Cardiac 1 Department of Rehabilitation Services Physical Therapy

Standard of Care: Cardiac

Department of Rehabilitation Services

Physical Therapy

Standard of Care: Cardiac

Inpatient Physical Therapy Management of the Surgical and Non-Surgical Patient with Cardiac

Disease

Case Type / Diagnosis: This standard of care applies to patients with cardiac disease including,

but not limited to: coronary artery disease (CAD), myocardial infarction (MI), valvular disease,

cardiomyopathy (CMP), heart failure (HF), arrhythmias, pulmonary hypertension, pulmonary

embolisms/deep vein thromboses, and congenital heart disease. It also applies to patients status

post (s/p) cardiac surgical and non-surgical procedures including, but not limited to: coronary

artery bypass graft (CABG), valve replacement or repair, percutaneous coronary intervention

(PCI), percutaneous transluminal coronary angioplasty (PTCA), aortic aneurysm repairs,

radiofrequency ablation (RFA), and transcatheter valve repairs. This standard of care does not

specifically address patients who are s/p mechanical circulatory support device (MCSD) or s/p

orthotopic cardiac transplant (OHT). For standards associated with Physical Therapy

management of these patient populations, please refer to the respective standards of care.

TABLE OF CONTENTS

Cardiac Pathologies:

• Coronary Artery Disease and Myocardial Infarction

• Valvular Disease

• CHF/Cardiomyopathy

o Cardiac Amyloidosis

• Arrhythmias

• Pulmonary Hypertension

• PE/DVT

• Pericardial Effusion/Tamponade

• Congenital Heart Defects

• Aortic dissection

• Cardiogenic Shock

Cardiac Tests & Procedures

• Common Cardiac Diagnostic Tests

o TTE/TEE

o Stress Test (MIBI)

o Cardiac MRI

o Cardiac PET Scan

o Cath/PCI

 
Standard of Care:  Cardiac 
 
Copyright © 2019 The Brigham and Women's Hospital, Inc., Department of Rehabilitation Services.  All rights reserved 
2 
•  Arrhythmia management 
o  Cardioversion   
o  Ablation  
•  Cardiac Surgery  
o  CABG 
o  Valve Repair/Replacement 
o  Aortic Arch Repair 
o  Maze 
o  ASD/VSD 
•  TAVR   
 
Cardiac Support Devices 
•  Chest Tubes  
•  PPM/ICDs  
o  Semi-permanent pacemakers 
o  Temporary pacemakers  
•  Pulmonary Artery Catheters  
•  IABP  
•  Impella  
•  ECMO  
Cardiac Physical Exam 
Physical Therapy Intervention 
Appendix 1: 
•  6MWT 
•  2MWT 
•  RPE 
Appendix 2: Cardiac and Critical Care Medications 
Appendix 3:Pulmonary Artery Catheter values  
 
 
Cardiac Pathologies:  
Coronary Artery Disease and Myocardial Infarction 
Definitions: 
•  Coronary Artery Disease (CAD), also known as atherosclerotic heart disease, is a 
progressive disease resulting in lipid deposits in coronary arteries resulting in coronary 
artery stenosis and ischemia. 
•  Acute Coronary Syndrome: an umbrella term used to describe events and symptoms 
related to cardiac ischemia 
o  Angina: typically presenting as chest pain, pressure, or discomfort. It can also 
present as jaw, back, neck, or left arm pain or stiffness. Can be mistaken for 
indigestion. Defined as stable, unstable, or variant angina. Symptoms can be 
masked by diabetes (silent MI) and can also present in atypical ways in women 

Standard of Care: Cardiac

A. Normal Sinus Rhythm

B. STEMI

C. NSTEMI

▪ Stable angina (angina pectoris): presents during activity/exercise at

predictable heart rates and blood pressures (known as rate pressure

product) and is relieved by coronary vasodilators or rest. Typically

managed by medication that reduces the cardiac workload (i.e.

vasodilators), stress management, and activity pacing.

▪ Unstable angina: can occur at rest, spontaneously, or with reduced

workloads, and may not be easily managed by rest or medication.

Typically indicates a blockage with intervention required, either

percutaneous or surgical

▪ Variant angina (Prinzmetal’s Variant Angina): typically occurs in the

younger population due to coronary artery vasospasm and most often

occurs at rest or overnight.

o Myocardial infarction (MI): typically classified as ST segment elevation (STEMI)

or non-ST segment elevation (NSTEMI), determined by 12-lead ECG, related to

elevation of the ST segment above the isoelectric line

▪ STEMI: An ST-elevation myocardial

infarction (STEMI) is a result of the

complete blockage of a coronary artery,

therefore typically has a higher risk of death

or disability due to increased myocardial

cell damage/death. Tissue damage tends to

extend through the full depth of the cardiac

wall local to the area of ischemia

▪ NSTEMI: A non-ST elevation myocardial

infarction (NSTEMI) is defined as when a

partial blockage of a coronary artery,

though severity within this group can vary

pending the level of occlusion.

Chart Review:

• Treatment: can include pharmacologic therapy, percutaneous intervention (i.e. stenting), or

coronary artery bypass grafting (see CABG below)

• MI rule out (R/O): Patients admitted with acute coronary syndrome (ACS), chest pain

(angina), or suspected MI are not appropriate for PT until they have either been ruled out for

a MI event, or until they are medically/surgically managed. During a R/O for MI, three sets

(one every 8 hours) of cardiac enzymes (creatinine kinase [CK-MB isoform], troponin [Tn-

I]) are drawn and electrocardiograms (ECGs) are performed.

1,3

o Creatinine Kinase (CK-MB isoform): Creatinine phosphokinase is an enzyme

released after cell injury or death of cardiac muscle. CK-MB measurement can assist

in the diagnosis of an MI, estimate the size of infarction and evaluate the occurrence

of re-perfusion. An early peak and rapid clearance from the blood can indicate re-

perfusion. Values may also be elevated due to other reasons. Communication with

the medical team should occur when there is question of the appropriateness of PT.

Standard of Care: Cardiac

o Brigham and Women’s Hospital has started using a troponin assay which is more

sensitive and specific for myocardial tissue necrosis. The numerical value associated

with myocardial necrosis has changed.

▪ Rule-in: troponin ≥ 52 ng/L, OR Δ >5 ng/L

▪ Rule-out: troponin <10 ng/L for women and <12 ng/L for men, AND Δ <3

ng/L

▪ If after q1h troponin neither rule-in or rule-out, obtain 3h troponin

o ECGs: Electrocardiography changes are almost always present in the event of an MI.

Early tracings typically show peaked or “hyperacute” T waves. As the MI progresses,

this is followed by ST-segment depression or elevation, Q-wave development and

lastly, T-wave inversions. Presentation can vary, with this progression occurring over

a few hours to several days, with Q-waves only developing in 30-50% of acute MIs.

▪ It is important to note that ST-segment depression or elevation can also be

caused by coronary artery spasm, electrolyte abnormalities, left ventricular

hypertrophy, interventricular conduction delays (BBB), atrial fibrillation or

flutter, Digoxin and pacemakers.

PT Examination:

• Determine medical stability:

o If the patient rules in for a MI, care must be taken to determine when a patient is

stable to participate in a PT examination or intervention. In general, it can be

expected that the patient may resume progressive monitored activity once cardiac

biomarkers have peaked and down trended for two sets and/or once the patient is

hemodynamically stable at rest.

o On occasion, once a patient has undergone intervention to treat the myocardial

ischemia (i.e.: heart catheterization with stenting), no further biomarkers will be

drawn, removing the ability to watch for down trending levels. In this event,

communication with the team is vital to determine whether it is medically appropriate

and safe to proceed with physical therapy evaluation and intervention.

o Of note, in some instances, cardiac enzymes may be elevated e.g., cardiac stress

related to volume overload (heart failure) or tachy-arrhythmias, or rise from

previously lower values e.g., after a cardiac catheterization, and may not indicate a

new MI event. Clarify appropriate activity orders with the responding clinician.

• Assessment of endurance

o Following ACSM Guidelines for Exercise Testing and Prescription

, it is appropriate

to evaluate a patient’s exercise tolerance soon after an MI occurs. Submaximal

exercise tests (such as a 6MWT, see Appendix 1) are recommended before hospital

discharge at 4-6 days after acute MI. Submaximal exercise testing can be used to

determine an appropriate exercise prescription and guide the medical team on the

effectiveness of their interventions, based on a patient’s hemodynamic response.

o See endurance/exercise testing.

Standard of Care: Cardiac

PT Intervention: Exercise Testing and Prescription

• Refer to PT Intervention/Aerobic Exercise Training for information regarding exercise

testing and prescription in the inpatient setting for a patient with cardiac dysfunction. A home

walking program should be established based on results of submax exercise test prior to

discharge.

• Post MI, a referral to a cardiac rehab program is highly recommended. Patients should be

educated on purpose of cardiac rehab, locations near their home (found on T-drive) and

provided with a referral prior to discharge.

Valvular Disease

Definitions:

• Any of the four valves of the heart can become diseased or dysfunctional for various

reasons, but commonly seen reasons include congenital abnormalities, progressive

calcification/atherosclerotic changes, rheumatic heart disease, infective endocarditis,

connective tissue disorders, and changes associated with heart failure and ventricular

dilation. Valve disease is typically diagnosed via echocardiogram which shows alterations

in a person’s blood flow.

Common terms of dysfunction/disease of heart valves:

• Insufficiency (or regurgitation): valves do not close properly, allowing blood to flow in

the reverse direction during ventricular systole or diastole. Consequences of insufficiency

include chamber hypertrophy and retrograde chamber dilation.

o Example: mitral insufficiency (mitral regurgitation): the mitral valve does not

close properly during systole, allowing leakage of blood backwards from the left

ventricle into the left atrium; it is the most common type of valvular heart disease.

▪ Mitral Valve Prolapse: the cusps of the mitral valve become enlarged and

floppy, bulging backward into the left atrium

• Stenosis: narrowing of the opening of the valve, often due to progressive calcification or

from rheumatic heart disease. This narrowing reduces forward blood flow, leading to

progressive dilation and hypertrophy of the chamber preceding the valve and potentially a

reduction in cardiac output

o Aortic valve stenosis is common and is classified in severity by a grading system

based on velocity of blood flow, pressure gradients from the left ventricle to the

aorta, and the aortic valve area. Cardiac output is preserved and the patient is

often asymptomatic until the stenosis is severe

Aortic Stenosis

Area

Mean gradient

Jet velocity

Mild

>1.5cm

<25 mmHg

<3.0 m/s

Moderate

1.0 – 1.5cm

35-40 mmHg

3.0 – 4.0 m/s

Severe

<1.0cm

>40 mmHg

>4.0 m/s

o Higher pressures on the left side of the heart lead to greater chance of valvular

dysfunction in the mitral and aortic valves, increasing the workload on the heart.

The heart can compensate for a time with chamber hypertrophy, dilation, and

Standard of Care: Cardiac

systemic BP adjustments however ultimately symptoms of heart failure can

develop.

Chart Review:

• Medical History:

o Etiology of valvular dysfunction

o Associated comorbidities

o History of management

• Chart Review:

o Reason for admission: typically related to progression of symptoms of heart

failure, admitted for medical management. Can be admitted for elective cardiac

surgery (see below).

o Type of valve dysfunction and severity. See grading system above

o Recent imaging including echo or right heart catheterization to evaluate for

progression

o Management plan, including changes in medication and/or progression to valve

repair or replacement.

▪ Diuretics for volume management or other plans for pharmacologic

management.

▪ Valvuloplasty (for aortic stenosis) – use of femorally inserted balloon

catheter to separate calcified leaflets or to stretch the annulus. This is a

palliative measure for patients not eligible for valve replacement

▪ Cardiac surgery

▪ Percutaneous valve replacement

• Aortic valves can be replaced transfemorally, particularly in older,

frail patients, due to risks associated with cardiac surgery. See

TAVR below. On occasion, patients undergo mitral valve

replacements with a similar technique

PT Examination:

• Prior level of function including most recent limitations. It is important, as with patients

with heart failure, to establish a baseline level of activity tolerance, both when a patient

has been feeling well and when they are feeling poorly, most likely due to symptoms

related to volume overload. See CHF section for further information

• Lung and heart sounds, listening for murmurs, pulmonary congestion, both pre and post

activity to assess for response to exertion

• Refer to endurance/exercise testing

PT Intervention:

• Refer to PT Intervention/Aerobic Exercise Training for information regarding exercise

testing and prescription

Standard of Care: Cardiac

Heart Failure/Cardiomyopathy

Definition/Pathology:

• The American Heart Association defines heart failure (HF) as a chronic, progressive

condition in which the heart muscle is unable to pump sufficient blood to meet the body's

metabolic demand. Heart failure is caused by conditions that damage or weaken the heart,

including coronary artery disease, myocardial infarction, hypertension, valvular disease,

cardiomyopathy, congenital heart defects, heart arrhythmias, myocarditis or other chronic

conditions such as diabetes, HIV, hyperthyroidism, hypothyroidism, or a buildup of iron

(hemochromatosis) or protein (amyloidosis).

• There are four types of heart failure, categorized by either a structural perspective (Left-

sided vs. Right-sided) or functional perspective (Systolic and Diastolic):

5-7

o Left-sided heart failure is caused by failure of the left ventricle to adequately

pump blood to periphery, which can lead to a backup of fluid on the lungs and

shortness of breath. Left ventricular failure and the resultant pulmonary

congestion is referred to as Congestive Heart Failure (CHF)

o Right-sided heart failure is caused by failure of right ventricle to pump

deoxygenated peripheral blood to the lungs, which can lead to back of fluid into

the abdomen, legs and veins. Right-sided heart failure can occur because of

progressive left-sided heart failure, pulmonary hypertension, valvular disease or

from pulmonary disease.

o Systolic heart failure is caused by impaired contractile function of the ventricle

resulting in reduced stroke volume, cardiac output and ejection fraction

o Diastolic heart failure is caused by impaired ventricular relaxation during

diastole leading to impaired filling and causes a reduced stroke volume and

cardiac output but the ejection fraction remains the same. Impaired ventricular

relaxation is often related to ventricular stiffness which is associated with older

age and amplified by HTN, diabetes mellitus and kidney disease.

• When treating a patient with heart failure, it is important to understand the type and cause

of heart failure to best design your education and treatment plan.

• Heart failure is typically classified based on the severity of the patient’s symptoms and

the effect the symptoms have on physical activity. The table below shows the most

commonly used classification system, the New York Heart Association Functional

Classification.

This classification places patients in stages I-IV based on their physical

activity limitations.

NYHA

Class

Level of Clinical Impairment

No limitation of physical activity. Ordinary physical activity does not cause undue

breathlessness, fatigue or palpitations.

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity

results in undue breathlessness, fatigue or palpitations.

Standard of Care: Cardiac

III

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity

results in undue breathlessness, fatigue or palpitations.

Unable to carry on any physical activity without discomfort. Symptoms at rest can be

present. If any physical activity is undertaken, discomfort is increased.

Of note, Cardiac amyloidosis (CA) is a unique and rare form of heart failure that causes

thickening of the heart walls and leads, most commonly, to diastolic heart failure. Due to the way

amyloid affects the heart and other body systems, patients present differently than those with

more common forms of heart failure and therefore, our physical therapy approach should be

different. Patients with CA often have an impaired hemodynamic response to activity or

exercise, including exercise-induced syncope.

If you are treating a patient with this diagnosis, be

sure to consult a team lead or cardiopulmonary specialist when developing your plan of care. The

remainder of this section will focus on the more common presentation of heart failure.

Chart Review:

• Medical History

o Cause of heart failure and categorization based structure or function (e.g. -

ischemic vs. non-ischemic, congenital, systolic vs. diastolic, preserved vs.

reduced ejection fraction)

o Onset and duration of HF symptoms and NYHA Stage

• Hospital Course

o Reason for admission. Patients are often admitted due to symptoms related to

increased volume status, e.g. - progressive dyspnea on exertion, increased lower

extremity edema and decline in activity tolerance

o Take note of any relevant lab values, imaging or tests. Below are common

tests/measures done by the medical team in a patient with CHF:

▪ Chest X-ray: Determines the level of pulmonary congestion, common

findings include interstitial edema, atelectasis and pleural effusions.

▪ Echocardiogram

▪ Lab Values: Many lab values and electrolytes are affected by fluid

retention that occurs secondary to the inadequate cardiac output in CHF.

Fluid overload can lead to impaired renal function, hepatic function and

altered electrolytes.

• Below are common changes in lab values found in CHF:

o ↑ BNP, protein in urine (Albumin), BUN/Cr, PaCO2, liver

enzymes

o ↓ PaCO2, SpO2, Sodium

o ↑/↓ Potassium- may be increased or decreased

▪ Severe hypokalemia (< 2.5 mEq/L) or hyperkalemia

( >5 mEq/L) should be a precaution to PT

intervention due to the increased risk for cardiac

Standard of Care: Cardiac

arrhythmias. Be sure to collaborate with medical

team prior to intervention.

o Troponin can be elevated with heart failure, often due to

increased demand on the heart rather than acute myocardial

infarction. Be sure to trend troponin and look at clinical

picture to determine appropriateness for PT intervention.

• Patients with heart failure are at risk for gout due to the fluid

fluctuations, use of diuretics and potential for renal dysfunction.

Therefore, blood work may reveal hyperuricemia and the patient

may present with joint pain and inflammation.

▪ Cardiac Catheterization: may be done to determine the cause of heart

failure and potential for intervention (e.g. - valve repair/replacement,

CABG). Additionally, cardiac catheterizations can provide the medical

team with accurate information regarding ejection fraction, cardiac output,

stroke volume and filling pressures to assist in prognosis and to optimize

medical management.

• Medications*

o The focus of drug therapy in heart failure is on optimizing preload, improving

cardiac pumping performance and reducing afterload. Below are common

medications seen in patients with heart failure:

▪ Pre-load reducing agents: Diuretics

▪ Cardiac Pumping Enhancement: Ionotropic Agents

▪ Afterload Reducers: vasodilators (i.e. ACE inhibitors)

▪ Beta-Blockers (BB): are first line treatment (along with ACE inhibitors)

for patients with systolic heart failure, even when asymptomatic.

Prescription of a BB improves symptoms, reduces hospitalization, and

enhances survival.

14-15

The 3 FDA-approved BB to treat HF include

Bisoprolol (Zebeta), Carvedilol (Coreg), Metoprolol (Toprol)

o The patient may also be on an anticoagulant if they have a comorbid arrhythmia,

such as Atrial Fibrillation. Common anticoagulants seen in heart failure include:

aspirin, warfarin, rivaroxaban (Xarelto)

o *See the Appendix 2 for relevant medications, side effects and physical therapy

considerations for the categories/medications above.

• Determine Medical Stability - Some factors to consider related to heart failure include:

the patient’s level of dyspnea, resting vital signs, EKG pattern and any significant

changes in lab profile (CBC, electrolytes, kidney function)

o Patients admitted to the hospital are often in Acute (or Advanced)

Decompensated Heart Failure (ADHF), which is defined as “the sudden or

gradual onset of the signs or symptoms of heart failure requiring unplanned office

visits, emergency room visits, or hospitalization.”

Care must be taken as a

therapist when designing exercise programs, endurance programs and plan of care

for patients in ADHF. If patients are hospitalized with ADHF, they may be

Standard of Care: Cardiac

undergoing medication changes or introduction of inotropes requiring close

monitoring. These patients may have a PA line, A-line, PICC and/or CVC.

o Much of the research is focused on those with stable heart failure, therefore, the

therapist must consider the cause of the heart failure, severity of HF symptoms

(e.g. dyspnea and fatigue) and hemodynamic response to exertion when designing

interventions and plan of care for a patient in potentially decompensated heart

failure. Any questions regarding the medical stability of your patient should be

addressed with the medical team, team lead and/or cardiopulmonary specialist.

PT Examination:

• Determine prior level of function and impact of heart failure symptoms

o It is important to understand a patient’s lifestyle and past experiences with HF

management. Below are some good questions to ask a patient:

▪ How far can you walk before you need to rest? What causes you to rest?

SOB? Muscle weakness?

▪ Have you been to cardiac rehab?

▪ Do you exercise regularly?

o Objective Measurements of Quality of Life - it may not be realistic to perform

entire outcome measure in this setting but using the questions on these measures

may help guide your treatment, plan of care and goals.

▪ Kansas City Cardiomyopathy Questionnaire - quantifies the degree of

physical limitations associated with heart failure

▪ Minnesota Living with Heart Failure Questionnaire - total 50 or greater

may indicate a greater potential for successful rehabilitation.

• Vital Sign Assessment

o Be sure to monitor HR, SpO2, RR and BP at rest and with activity. Patients with

heart failure are at risk for oxygen desaturation and impaired hemodynamics due

to increased stresses on the heart, fluid overload and medication side effects.

o Be sure to check telemetry before, during (if possible) and after a physical therapy

session. Patients with heart failure are at increased risk for arrhythmias.

Additionally, patients are at risk for more life threatening ventricular arrhythmias

(such as VT and VFib). Be sure to know of baseline arrhythmias and any new

arrhythmias from this admission. Alert the medical team if an arrhythmia is noted

during physical therapy evaluation or treatment.

• Cognition/Mental Status

o Advanced heart failure and ionotropic medical support may have a negative

impact on cognition, specifically memory, motor response time and speed of

processing.

▪ In this case, you may want to consider the Mini Mental Status

Examination or consult Occupational Therapy

• Integumentary

o Patients in ADHF often present with lower extremity edema, which can be

quantified using the Pitting Edema Scale (0 to 4+), documented in EPIC by

Standard of Care: Cardiac

nursing or PT staff. It is important to consider how lower extremity edema is

affecting physical function and can be addressed by physical therapy intervention,

notably via imbalance, lower extremity fatigue, or gait deviations.

• Strength and Endurance

o Use of MMT strength assessment to identify any obvious weakness. Many

patients with heart failure will present with > ⅘ MMT strength, but will fatigue

quickly. Therefore, it is recommended to use an outcome measure to quantify

muscular endurance, such as: the 30 second sit to stand test or 5 Times Sit to

Stand test

o Quantify aerobic capacity and endurance. The results of a 6MWT can be used to

assist in determining discharge recommendations, exercise prescription and

prognosis. *See appendix 1 for patient instructions and appropriate performance

of this test.

o Be sure to quantify fatigue and dyspnea during functional mobility and

ambulation using the 0-10 RPE and DOE scales. These scales can help determine

a patient’s tolerance for activity and ADLs and can assist in discharge planning,

goal-setting and plan of care.

• Balance

o Patients at significant risk for balance impairments are older adults with ADHF.

This is due to the higher incidence of frailty in this population, leading to severe

deficits in all domains of physical function: balance, mobility, strength and

endurance.

o Use of standardized measures and gross observations of static and dynamic

balance to determine fall risk and balance impairments that can be addressed in

the therapist’s plan of care.

PT Intervention:

• Endurance Training

o Refer to PT Intervention/Aerobic Exercise Training for information regarding

exercise testing and prescription

• Strengthening

o It is recommended that patients with heart failure participate in a strengthening

program as an adjunct to aerobic exercise. Initial resistance training should begin

at a lower intensity, especially in the acute care setting, with close monitoring of

symptoms. Be sure to educate the patient on proper technique and breathing to

avoid valsalva. Below are the recommendations based on the updated literature:

▪ Mode: dynamic exercises targeting major muscle groups

• Be sure to include postural exercises to optimize positioning for

improved breathing and lower extremity muscle groups that

correlate to function

▪ Frequency: 2-3x/week

Standard of Care: Cardiac

▪ Intensity/Repetitions/Sets: 1 set of 10-15 reps to volitional fatigue or rated

3-5/10

• Initial resistance training should begin at a lower load and higher

repetitions. As tolerated the load can be increased with light

weights or resistance bands, which will decrease the number of

repetitions.

• Pacing/Energy Conservation

o Pacing and energy conservation techniques should be taught to avoid max fatigue

or shortness of breath with activity and to maximize participation in desired

activities. An analysis of all activities an individual performs helps to develop an

inventory to set priorities and organize the individual’s day.

o Attention should be paid to activities that create fatigue or dyspnea.

• Patient/Family Education

o Self-management techniques should be taught to manage the disease including:

▪ Signs and symptoms of decompensation (excessive SOB, fatigue,

peripheral swelling, waking at night with dyspnea/cough)

▪ Adherence to regular exercise program

• Create a home exercise program based on level of function at

discharge

• Include family member or caregiver on instruction of home

exercise plan to ensure compliance

• Referral to Cardiac Rehab. Patients must demonstrate 6 weeks of stable management of

heart failure to be deemed appropriate for initiating care.

Arrhythmias

Definitions and PT considerations:

• Cardiac arrhythmias represent an abnormal cardiac conduction that can potentially lead to

a decrease in cardiac output with activity, or at rest. Therapists should look at their

patient’s telemetry regularly as part of their pre-evaluation assessment and during

treatment to become familiar with patient responses. There are several factors that the

therapist should consider when deciding whether a patient with an arrhythmia is

appropriate for PT intervention, including:

o Acuity (how long this arrhythmia has been present)

o Symptoms

o Plans for management (what medications are being used, plans for electrolyte

replacements, cardioversion or ablation)

o Presence of a pacemaker or AICD.

o New or progressive arrhythmias during therapy should be noted and this

information relayed to the medical team.

• The following are additional clinical considerations for some specific arrhythmias to aid

in deciding whether the patient is appropriate for physical therapy. The therapist should

be aware that this is a list of some common arrhythmias but is not exhaustive. The

therapist should discuss appropriateness of PT intervention with the medical team, team

Standard of Care: Cardiac

lead and/or cardiopulmonary specialist in cases where the patient may be experiencing

any arrhythmia they are not familiar with.

o Atrial Fibrillation (AF): AF is a disorganized depolarization of the atria

resulting in an irregularly irregular heart rate and lack of effective atrial

contraction.

▪ Identify heart rate via telemetry or identify pulse rate by manual

inspection for one minute. Auscultation can also be used

▪ Considerations for PT intervention should include:

• Is the AF new?

• How high is the HR elevated due to AF at rest? With activity?

• Is the patient's BP affected by the arrhythmia?

• Is the patient having any symptoms due to an altered HR/BP such

as lightheadedness, shortness of breath, fatigue, exercise

intolerance?

o Heart Block (HB): Watch for progression of heart block or alteration in rhythm

in response to activity.

▪ First-degree heart block: Prolonged PR interval. Generally, there are no

precautions if the patient’s HR and BP are stable.

▪ Second degree heart block

• Type I (Mobitz I): PR interval increases until a ventricular

complex is dropped. This arrhythmia is frequently noticed with

increasing activity.

• Type 2 (Mobitz II): Several atrial contractions are needed to

propagate a single ventricular contraction (i.e. 2:1). This

arrhythmia can follow a Mobitz I or be a progression in a person

with first degree HB.

▪ Third degree (Complete heart block): There is a complete lack of

synchrony between atrial and ventricles observed on the EKG, resulting in

a greatly reduced ejection fraction and potential for hemodynamic

instability. PT is deferred until the patient has a PPM. If the patient

progresses to this rhythm during treatment they may become lightheaded

or syncopal, this is a medical emergency and the patient needs immediate

medical attention.

▪ First and second degree heart blocks may be stable and asymptomatic,

pacing sometimes required. Monitor patient throughout session

o Premature Ventricular Contraction (PVC): A PVC is a ventricular contraction

initiated by an abnormal focus within the ventricle rather than via the sinoatrial

node. PVCs are common, with a higher incidence observed in patients with

cardiac health conditions or after cardiac surgery.

PVCs can be palpated or

observed via ECG.

▪ While generally benign, considerations should include:

• Acuity

• Frequency at rest and with activity

Standard of Care: Cardiac

• Hemodynamic response

• Patient subjective response

• In general, an increase in frequency of PVCs with activity or

exercise should be noted in your documentation and reported to the

medical team as they can indicate increasing irritability in the heart

in response to exertion

o Ventricular Tachycardia (VT): VT is defined as four or more consecutive

premature ventricular contractions. VT can be palpated or observed via ECG.

Patients may also report a fluttering sensation in their chest or complain of feeling

lightheaded or dizzy. Sustained VT is a very serious arrhythmia that can result in

greatly decreased cardiac output due to ventricular contraction without time for

adequate refilling. Runs of VT are frequently seen in patients with heart failure

and may be considered baseline for certain patients.

▪ Consideration should include:

• Acuity, frequency, and duration of the runs of VT during the

hospitalization, particularly in a patient admitted with recurrent VT

• Patient symptomatology (i.e., lightheadedness/dizziness, syncope,

diminished exercise tolerance and/or confusion)

• Triggers of VT if known – electrolyte imbalance, exertion

• Current or planned pharmacological interventions including

addition of IV antiarrhythmic, beta blockers, electrolyte repletion.

▪ New onset of VT, long runs of VT and patient symptoms may indicate that

the patient may not be clinically appropriate for PT.

o Ventricular Fibrillation (VF): VF is defined as absence of organized ventricular

activity and presents as irregular undulations of varying contour and amplitude on

ECG. There is no cardiac output and the patient will usually die within 3-5

minutes if a more normal cardiac function is not restored.

Pulmonary Hypertension

Definition:

• Pulmonary hypertension (PH) is defined as an increase in resting mean pulmonary artery

pressure (mPAP) of > 25mmHg, measured via right heart catheterization. Normal mPAP

can range between 14-20mmHg at rest.

• Increased pressure in the pulmonary arteries can be due to changes in endothelial lining

of the vasculature, leading to arteries that become narrowed, blocked, or destroyed.

25,26

Increased pressure can also result from hypoxic vasoconstriction, occlusion of the

pulmonary vascular bed, or parenchymal disease with loss of vascular surface area.

• Over time, increasing resistance in the pulmonary vasculature can lead to right heart

dysfunction and failure with its resultant clinical picture

• Classification: Pulmonary hypertension is classified into 5 types, dependent upon the

underlying cause. They are grouped based on clinical presentation, pathological findings,

hemodynamics, and treatments strategies.

Standard of Care: Cardiac

Group

Clinical Classification

Group 1: pulmonary arterial hypertension

Group 1

: pulmonary veno-occlusive and/or

pulmonary capillary hemangiomatosis

Idiopathic (or primary)

Heritable (genetic mutation)

Drug or toxin induced

Associated with:

• Connective tissue disease

• Portal hypertension

• Congenital heart disease

Group 2: pulmonary hypertension due to left heart

disease – pulmonary vascular hypertension

Left ventricular systolic and/or diastolic dysfunction

Valvular disease

Congenital/acquired left heart inflow/outflow tract obstruction

and congenital cardiomyopathy

Congenital/acquired pulmonary vein stenosis

Group 3: pulmonary hypertension due to lung diseases

and/or hypoxia

COPD

Interstitial lung disease (ILD)

Other pulmonary diseases with mixed restrictive and obstruction

patterns

Sleep-disordered breathing

Alveolar hypoventilation disorders

Developmental lung diseases

Group 4: chronic thromboembolic pulmonary

hypertension (CTEPH) and other pulmonary artery

obstructions

CTEPH

Angiosarcoma or other intravascular tumors

Arteritis

Congenital pulmonary artery stenosis

Parasites

Group 5: Pulmonary hypertension with unclear and/or

multifactorial mechanisms

Hematologic disorders

Systemic disorders: sarcoidosis, neurofibromatosis

Metabolic disorders: thyroid disorders

Chronic renal failure (w/ and w/out dialysis)

• Pulmonary hypertension associated with another pathology is more common than Group

1 or idiopathic PH

• Symptoms are generally non-specific and related more to the underlying pathology or the

progression of right heart dysfunction and failure.

• WHO Pulmonary Hypertension Classifications

25,26

Class I – No limits

Diagnosed, but no symptoms

Class II – slight/mild limits

No symptoms at rest, (+) shortness of breath,

fatigue, chest pain during physical activity

Class III – noticeable/marked limits

Comfortable at rest, (+) symptoms during normal

activity

Class IV – severe limits

Symptomatic at rest

Standard of Care: Cardiac

Chart Review:

• Medical History

o Etiology of PH and categorization based on above classifications

o Other potentially associated cardiopulmonary conditions

o Onset and duration of PH symptoms and symptom class, if noted

o Take note of any recent or frequent hospitalizations. Information gathered here

can include home medication management, use of home oxygen

• Hospital Course

o Reason for admission. Patients are often admitted due to symptoms related to the

underlying pathology, i.e. increased volume status, or change in symptomatic

presentation

o Take note of any relevant lab values, imaging or tests. Below are common

tests/measures done by the medical team in a patient with PH:

▪ Chest X-ray: Used to determine condition of the lungs in underlying

pathology, i.e. the level of pulmonary congestion. Depending on the cause

of PH, abnormalities on CXR may not correlate with the degree of PH.

▪ Echocardiogram: Used to evaluate the effects of PH on the heart,

particularly the right sided anatomy, including chamber dilation, as well as

to estimate pulmonary artery pressure.

▪ Right Heart Catheterization: allows for more direct visualization of the

functioning of the right heart and can also be used to assess congenital or

acquired intracardiac shunting

▪ Pulmonary Function Tests: Used to identify the contribution of

underlying airway disease to a patient’s symptomatic presentation, and can

be useful in diagnosing new PH. Patients with Group 1 PAH can show

mild to moderate reduction in lung volumes and frequently show reduced

lung diffusion capacity for carbon monoxide, or DLCO, while patients

with PH secondary to COPD will show PFT changes consistent with that

pathology, namely airway obstruction and increased lung volumes. A

decreased DLCO can indicate an interstitial lung disease as an underlying

pathology.

▪ Lab Values: many lab values are assessed in patients with known or

suspected PH, depending on underlying etiology. During the work-up for

new or existing PH, arterial blood gases are often evaluated and can show

a variety of issues. Rates of O

diffusion vary depending on pathology,

therefore PaO

can be reduced or normal, while PaCO

can be normal,

reduced, or elevated. An understanding of a patient’s blood gas readings

can help determine likely functional status, need for supplemental O

, and

potential for CO

retention.

• Medications

o Treatment of PH depends upon etiology and includes management of the

underlying condition in Groups 2-5, optimizing hemodynamics, lung function,

and volume status.

Standard of Care: Cardiac

o Common medications used to treat PH*:

▪ Pulmonary vasodilators: epoprostenol (Flolan, Veletri), Treprostinil

(Tyvaso, Remodulin)

▪ Phosphodiesterase inhibitors: increases lung production of intrinsic

vasodilators. Examples include: sildenafil, tadalafil

▪ High-dose calcium channel blockers: relax smooth muscle in vasculature.

Examples include: amlodipine, diltiazem

▪ Anticoagulants, digoxin (rate control), beta blockers, ACE inhibitors, O2

therapy, and diuretics can also be employed

o *See the Appendix 2 for relevant medications, side effects and physical therapy

considerations for the medications above.

o Lung transplant is the only definitive cure for Group 1 PH (pulmonary arterial

hypertension), considered only after failure of medical management

• Determine Medical Stability

o Patients admitted to the hospital are often in an exacerbation of their underlying

condition, including a heart failure or COPD exacerbation, and medical stability

and appropriateness for PT will depend upon the management of those conditions.

o Understanding the anticipated management plan can assist in determining

appropriateness for PT. For instance, patients who are going to be initiated on IV

pulmonary vasodilators may benefit from PT assessment following the start of

drug therapy.

o Additionally, patients with progressive disease in need of more advanced care can

rapidly move from the stepdown floors to the ICUs depending on stability, with a

progression of care that can include surgery (atrial septostomy, lung transplant) or

mechanical support (VV ECMO). Patients being worked up for lung transplant

may have PT consults placed for 6MWT. Discuss appropriateness of this with

your team lead or cardiopulmonary specialist

o Any questions regarding the medical stability of your patient should be addressed

with the medical team, team lead and/or cardiopulmonary specialist.

PT Examination:

• Determine prior level of function and impact of PH symptoms

o It is important to understand a patient’s lifestyle and past experiences with

medical management. Questions can include:

▪ How far can you walk before you need to rest? What causes you to rest?

SOB? Muscle weakness?

▪ Do you exercise regularly?

▪ Have you attended a formal rehab program, cardiac or pulmonary as

appropriate?

• Vital Sign Assessment

o Be sure to monitor HR, SpO

, RR and BP at rest and with activity. Patients with

PH are at risk for oxygen desaturation and impaired hemodynamics due to

increased stresses on the heart, fluid overload and medication side effects.

Standard of Care: Cardiac

• Lung auscultation: assessing for pulmonary congestion both before and after treatment in

the case of left heart dysfunction.

• Signs and symptoms of progressive right heart failure, particularly in later stages of PH:

jugular venous distension, peripheral edema, ascites, and systemic hypotension due to

impaired cardiac output (note hemodynamic response to exertion).

• Endurance

o Exercise tolerance can be limited in these patients, as with increasing workloads,

pulmonary pressures increase, further restricting cardiac output and limited

oxygen supply to skeletal muscles. Patients can be subject to lactic acidosis at

lower workloads

o The 6MWT can be used to quantify aerobic capacity and endurance. *See

appendix 1 for patient instructions and appropriate performance of this test.

PT Intervention:

• Exercise intolerance in patients with PH is associated with reductions in maximal O

uptake and other factors similar to those with advanced heart failure. Increased resting

pressures in the pulmonary vasculature lead to more dramatic increases during activity

which can result in reduced pulmonary blood flow and subsequently reductions in cardiac

output, with output insufficient to meet increasing demands. Patients with PH have

additionally been found with skeletal muscle abnormalities with impaired oxygen

utilization, further exacerbating the intolerance.

• Physical Activity recommendations:

o Evidence has demonstrated that exercise is safe for patients with PH however it is

suggested that patients should be encouraged to be active within symptom limits

and should avoid excessive physical activity that leads to a progression or

exacerbation of symptoms. Patients should be treated with the best standard of

pharmacological treatment and in stable clinical condition before starting a

supervised rehab program.

o Exercise training has been shown to improve 6MWT distances and quality of life,

as well as several physiologic measures of aerobic capacity and cardiopulmonary

health.

29,30

Presumed negative effects of exercise on the right ventricle have been

demonstrated to be short-lived, with function normalizing within days.

Exercise

training has been shown to be highly effective in patients with more severe

symptoms, with patients able to improve their WHO classification.

o Training protocols include progressive endurance training, either walking or

cycling, at low to moderate workloads, measured as % peak VO

or heart rate.

Successful programs have also included respiratory muscle training.

o In this setting, it is often more practical to prescribe exercise based on the RPE,

targeting workloads at less than 5/10 on the modified Borg scale, pending

appropriate hemodynamic response as determined on exercise testing including

the 6MWT.

Standard of Care: Cardiac

PE/DVT

Definition:

• Venous thrombi are intravascular deposits composed mainly of fibrin and red blood cells,

usually located in the deep veins. They can lead to complications, including deep vein

thrombosis (DVT) or pulmonary embolism (PE). DVTs occur in regions of slow or

disturbed blood flow, often in the lower extremity. The majority are confined to the calf

and are asymptomatic, small and not associated with major complications. However,

venous thrombi in the proximal veins (popliteal, femoral, iliofemoral), may break off,

leading to a blockage in the pulmonary circulatory system, called a PE.

Chart Review:

• DVT: The major signs and symptoms of LE DVT include pitting edema, pain,

tenderness, swelling, warmth, redness or discoloration (erythema), and prominent

superficial veins.

o Diagnosis: The Wells criteria for LE DVT are the most commonly used tool to

determine likelihood of DVT. The results of the Wells criteria should guide the

selection of medical testing, including the D-dimer test to measure the breakdown

or degradation of cross-linked fibrin (increases in the presence of a thrombosis)

and then a duplex ultrasound.

▪ If the ultrasound confirms an LE DVT, medical treatment should be

initiated and mobilization is often postponed, however this should be

considered on a case by case basis, as the risks of immobility have been

shown often to outweigh the risks associated with mobilizing someone

with a DVT.

o Treatment: Anticoagulation therapy is effective in the prevention of extension,

embolization, and recurrence of DVT.

▪ Options include subcutaneous low-molecular weight heparin (Lovenox,

Fragmin), monitored IV or subcutaneous unfractioned heparin (Heparin

Sodium), or fondaparinux (Arixtra)

▪ Lab Values:

• Heparin is measured by clotting times such as activated partial

thromboplastin time (APTT or PTT).

Warfarin (Coumadin) is measured using the International

Normalized Ratio for Prothrombin Time (PT INR)

o INR Reference Ranges

▪ 2.0-3.0 = desired range

▪ 2.5-3.5 = heart valve in place

▪ >4.0 = risk of hemorrhage

o If the INR is between 4.0 and 5.0, resistive exercises should

be avoided, with participation in light exercise only due to

increased risk of bleeding. Ambulation should be restricted

if gait is unsteady to prevent falls.

Standard of Care: Cardiac

▪ Placing a filter in the inferior vena cava is a treatment that is used when a

patient has a PE or acute proximal DVT and anticoagulant therapy is not

indicated because of the risk of bleeding.

• Pulmonary Embolism (PE): major signs and symptoms include tachycardia, sudden

change in breathing, chest pain, coughing

o Categories:

▪ Massive: Acute PE that causes hemodynamic instability including SBP

<90 mmHg, pulselessness, bradycardia, tachycardia, tachypnea,

bradypnea, respiratory failure, right ventricle failure. Damaged lung tissue,

combined with less available area for pulmonary perfusion can cause high

pulmonary artery pressures, dramatically increasing right ventricular work

and leading to right-sided heart failure.

▪ Submassive: Acute PE, patient remains hemodynamically stable without

systemic hypotension (systolic blood pressure >90 mm Hg) but with either

RV dysfunction or myocardial necrosis.

▪ Nonmassive: no signs of clinical instability, hemodynamic compromise, or

right ventricular strain.

o Diagnosis: The most frequent diagnostic testing for PE is serial computed

tomography, followed by ventilation/perfusion scans, or pulmonary angiography

o Treatment: Heparin therapy is most commonly used to treat PE, however

massive and submassive PEs can also be treated with endovascular catheter

directed thrombolysis via an EKOS device. To maintain adequate tissue

oxygenation, mechanical ventilation with supplemental oxygen may be required.

In addition, if the patient is hypotensive or in shock, fluid therapy and

vasopressors may be needed.

▪ Pulmonary embolectomy may be indicated in patients who have large

emboli and cannot receive heparin therapy or have overt right ventricular

heart failure leading to cardiac arrest.

PT Examination/Intervention:

• As physical therapists in the acute care setting, we play a role in the prevention of DVTs

by educating patients on their risk, mobilizing and providing LE exercises

• We can also be a first line for screening patients for DVTs. If your patient presents with

signs and symptoms of a DVT, be sure to communicate these with the medical team.

• A patient with a known DVT who develops unexplained breathlessness, desaturation,

hemoptysis, pleuritic pain, arrhythmia, or fever should be suspected of having developed

a PE and the medical team should be notified.

• Early ambulation and compression stockings are recommended for patients with acute

DVT once medical treatment has been initiated (anticoagulation or IVC filter) and may

provide even faster improvement with less pain, swelling, and minimize the extension of

a DVT.

• In patients with diagnosed massive and submassive PEs, mobility is only indicated when

the patient is stabilized after all interventions other than anticoagulation therapy (ex:

Standard of Care: Cardiac

thrombectomy or thrombolysis) have been performed, or when optimum symptom

management and right heart function have been achieved.

• If out of bed activity orders are written for someone with a known DVT or PE who is not

being treated medically, be sure to clarify activity orders and document these in your note

Pericardial Effusion/Tamponade

Definition/Pathology:

• A pericardial effusion refers to excess fluid that develops between the pericardium and

the heart itself. Injury to the pericardium can cause acute pericarditis (inflammation in the

pericardial sac surrounding the heart), which can lead to a pericardial effusion. Some

common causes of pericardial inflammation include: heart surgery, infection,

inflammatory disorders such as RA or Lupus, metastatic cancer and kidney failure with

excessive nitrogen levels.

o A rapid or significant accumulation of fluid can lead to cardiac tamponade, which

is a life-threatening condition characterized by elevated intracardiac pressures,

progressively limited ventricular diastolic filling, reduced stroke volume and

pulsus paradoxus.

10,35

Chart Review:

• When reviewing a chart for a patient with a known pericardial effusion, it is important to

note the cause and current or planned treatment. How the effusion is managed can help

you determine the severity of the effusion and the patient’s expected hospital course. The

goal of medical treatment is to address the underlying cause of the effusion.

• Some common treatments of pericardial effusion include:

10,36

o Initiation of NSAIDs, corticosteroids, colchicine (commonly used to treat gout),

diuretics or antibiotics

o If the effusion is related to cancer, radiation or chemotherapy may be used

o For larger pericardial effusions:

▪ Pericardiocentesis: a needle and catheter is inserted into the pericardial

space to drain the effusion. The catheter and drain may remain in place

temporarily for ongoing drainage.

• Some indications for removal of catheter by nursing include:

o Pericardial drainage less than 25-30 mL over 24 hours.

o Hemodynamic stability: SBP greater than 100 mmHg, no

pulsus paradoxus (< 10 mm Hg)

o Absence of pericardial effusion.

▪ Pericardial Window: a surgical procedure for recurrent effusions,

involves removing a portion of the pericardium to allow the effusion to

drain continuously into the peritoneum or chest.

• Check activity orders. Activity may be restricted while monitoring for tamponade.

o If a patient is without a procedure (e.g. with close monitoring, medications or

chemo/radiation), be sure that the effusion is stable and the patient has been

Standard of Care: Cardiac

hemodynamically stable. Check in with nursing, in addition to the chart, to ensure

hemodynamic stability and updated activity orders.

o If a pericardial drain was placed, the patient is often on bedrest to allow for

frequent vital sign assessment by nursing.

Pt will be cleared for progression of

activity when deemed stable by medical team. Be sure to get updated activity

orders on a case-by-case basis depending on the duration of the drain.

o When a pericardial drain is removed, the patient should remain on bed rest for 1

hour and defer physical activity/therapy for 2 hours.

Be sure to seek updated

activity orders from medical team.

PT Examination:

• Careful monitoring of vital signs and patient response to activity is essential to monitor

for progression to tamponade.

• Be sure to look out for signs and symptoms of tamponade, including: jugular vein

distention, hypotension, tachycardia, fatigue/malaise, lightheadedness, rales at lung bases,

shortness of breath and tachypnea. Alert nursing immediately if cardiac tamponade is

suspected.

PT Intervention:

• Be sure to look at the whole clinical picture and the reason for pericardial effusion when

designing your intervention and plan of care.

• For example, someone with recent heart surgery who developed a pericardial

effusion may have a different plan of care then someone who known metastatic

cancer who also developed a pericardial effusion

• Patient’s should be educated on the signs and symptoms of Tamponade and on

appropriate activity progression in order to achieve their goals

• Out of bed mobility and ambulation is not contraindicated in these patients and should be

encouraged, just be sure to clarify all activity orders based on their treatment and

hemodynamic stability as noted above

Congenital Heart Defects

Definition:

• Congenital heart defects include any structural abnormality of the heart, present at birth,

and typically forming early in gestational development. They can cause a variety of

signs and symptoms and are of varying severity and prevalence. They are typically

classified into acyanotic and cyanotic lesions. Management is dependent upon the

severity of the presentation.

• Acyanotic lesions: this group of defects result in increased flow of blood through the

pulmonary vasculature through left to right shunting, with fully oxygenated blood

circling back to the lungs as well as into systemic circulation. Signs and symptoms can

include increased respiratory rate, low peripheral PO

, low stroke volume, and increased

work load on the heart leading to progressive heart failure.

Standard of Care: Cardiac

o Septal defects: Includes both atrial and ventricular septal wall abnormalities that

allow mixing of blood between 2 chambers and decreasing the amount of fully

oxygenated blood that that leaves as cardiac output.

▪ Atrial septal defects (ASD)/Ventricular septal defects (VSD): small ones

present at birth are generally asymptomatic and close with growth. Larger

defects allow for greater mixing of deoxygenated blood, and in adults,

increase the risk for stroke, heart failure, pulmonary hypertension, and

endocarditis.

39,40,41

• The most common atrial septal defect is a patent foramen ovale, often

going undiagnosed but placing a patient at increased risk for stroke,

requiring surgical closure.

39,40

• In adults, small unrepaired defects or childhood repairs of larger ASDs

rarely cause problems. Previously undiagnosed defects can lead to

heart failure in adults and are often closed, even when asymptomatic.

• Late or adult complications of childhood VSD closures are rare. Large

unrepaired defects can lead to pulmonary hypertension in adults, and

small defects left open are at increased risk for endocarditis.

o Patent Ductus Arteriosus (PDA) is a common heart defect, due to failure of the

ductus arteriosus to close after birth, leading to mixing of oxygenated blood from the

aorta with deoxygenated blood in the pulmonary artery with subsequent increased

pressure and pulmonary hypertension. The defect can close without treatment, but is

often managed with medication or minimally invasive surgical or catheter assisted

closure.

39,42

Long term prognosis in childhood repairs is good, and cardiology follow

up is usually not needed.

o Coarctation of the Aorta is a narrowing of the aorta, creating a left ventricular

outflow obstruction and leading to progressive left ventricular hypertrophy.

Additionally, upper body hypertension can occur which can lead to progressive heart

failure. There are typically normal to low blood pressures in the supply distal to the

constriction.

39,43

▪ Surgery is required to correct the defect and is performed as soon as the

coarctation is diagnosed, which can happen in adulthood.

▪ Patients with early repair will require long-term cardiology follow up for BP

management and monitoring due to the risk of recoarctation or aneurysm.

• Cyanotic lesions: this classification of defects involves right to left shunting whereby most

of the blood bypasses the lungs and enters systemic circulation without being fully

oxygenated. Chronic hypoxemia leads the body to increase its red blood cell production,

leading to polycythemia and an increase in blood viscosity, increasing the risk for stroke.

o Tetralogy of Fallot: This complex CHD includes pulmonary valve stenosis, a large

ventricular septal defect, an overriding aorta (aorta leaves the heart between the right

and left ventricles, directly over the septal defect), and right ventricular hypertrophy

(due to the narrowing of the pulmonary valve). This defect requires early surgical

management to redirect blood flow and surgical techniques are continuously

evolving.

39,44

Standard of Care: Cardiac

▪ Patients admitted at BWH as adults are often admitted to the heart failure

service for management of the long-term consequences of the

abnormal/repaired blood flow, including right sided heart failure, arrhythmia,

and repair of continued areas of stenosis.

o Hypoplastic left-heart syndrome: this syndrome includes an underdeveloped or

hypoplastic left ventricle, aortic and mitral valve stenosis or atresia, and coarctation

of the aorta. This syndrome is largely asymptomatic until the ductus arteriosus closes.

Medications can be used to keep the ductus arteriosus open and surgery or transplant

is required for survival.

Surgical correction includes staged procedures that allow

for the right ventricle to pump systemically and to redirect blood flow to the lungs.

o Transposition of the Great Arteries (TGA): the key component of this defect is a

reversal of the positions of the pulmonary artery and the aorta, leading to separate

pulmonary and systemic circulatory systems with variable communication via PDA,

ASD, or VSD. Without communication to allow mixing of the blood inside the heart,

severe cyanosis occurs and the defect is incompatible with life. Prostaglandin E

can

be given to maintain a PDA however surgical treatment is required early.

▪ Adults with a history of repaired TGA require lifelong cardiology follow up

due to risk of heart failure, tachy and bradyarrhythmias, endocarditis and for

blood pressure management. Surgical baffles can also become obstructed

requiring stenting or further surgery for management.

Chart Review:

• Medical History:

o Review to gain an understanding of the patient’s CHD and surgical history or

management of the defect. This should include an understanding of the patient’s

current medication management such as beta blocker therapy, inotropic therapy,

diuretic use, anti-arrhythmics, etc

o Number of recent admissions and reason, as this can indicate a decline in cardiac

function and the potential for progression to advanced therapies

• Hospital Course:

o Reason for admission, often a progression of symptoms associated with heart

failure (refer to CHF)

o Planned surgical procedures, if any.

o Changes to current medical management including pharmacologic and potential

for progression to advanced therapies such as mechanical circulatory support

and/or transplant

PT Examination: refer to heart failure

PT Intervention: refer to heart failure and PT Intervention/Exercise Training

Standard of Care: Cardiac

Aortic Dissection

Definition:

• Aortic dissections involve a tearing of the intimal lining of the aorta, allowing for blood

to enter the lining, leading to further separation of the walls of the vessel, which at high

pressures, can cause an aortic rupture.

• Dissections are typically classified as:

o Type A: occurring in the ascending aorta, distal to the aortic valve, and along the

arch. Medical emergency that requires surgery, via sternotomy, to manage given

the acuity and risk for neurologic compromise

o Type B: occurring in the descending aorta past the bifurcation of the left

subclavian artery. Often medically managed, however may also require surgery

3,47

Chart Review:

• Medical History:

o Presenting symptoms of an acute or chronic dissection can mimic those of an MI,

so be sure that medical work up is complete before seeing these patients.

Symptoms can include sudden chest or back pain, change in pulse, shortness of

breath, or syncope.

• Hospital Course:

o Diagnostic work up to rule in dissection can include CT angiography, MRI and/or

transesophageal echo (TEE).

o If an MI is suspected, check lab values (see above)

o Plan for management:

▪ Typically, patients with Type A dissection will be referred for urgent

surgical management to the cardiac surgery team. Please refer to cardiac

surgery below

▪ Management of Type B dissections often involves aggressive

pharmacologic management for BP and HR control to prevent progression

of the tear. Type B dissections that have ruptured, are causing severe pain,

or have led to distal organ ischemia may also require surgical management

o Review of vitals to determine how well controlled the patient’s HR and BP have

been under current medical management

PT Examination:

• It is extremely important to establish hemodynamic parameters for patients with

medically managed aortic dissections prior to initiating mobility

o Heart rate and BP parameters are often provided by the managing medical team;

however, those parameters may not take response to activity into consideration

o A conversation should be had with the responding clinician or other member of

the medical team to establish reasonable parameters for HR and BP in response to

functional mobility

• Establish baseline and current level of functional mobility with frequent VS monitoring

throughout examination

Standard of Care: Cardiac

PT Intervention:

• Restore baseline level of mobility as appropriate given hemodynamic response to activity

• Education, specifically around limitations and expectations for return to prior level of

function.

o These patients are often counseled to minimize exertion and while basic

functional mobility is acceptable, a return to a high-level exercise program may

not be recommended

o Avoid valsalva

Cardiogenic Shock

Definition/Pathology:

• Cardiogenic shock (CS) is a clinical condition of inadequate end organ perfusion due to

cardiac dysfunction.

It can present across a spectrum of severity from mild

hypoperfusion to profound shock,

with the reduction in tissue perfusion resulting in

decreased oxygen and nutrient delivery to the tissues and, if prolonged, leading to multi-

organ failure. Acute myocardial infarction (AMI) is the most common cause of CS,

usually associated with severe ventricular dysfunction (anterior wall STEMI). There are

multiple other causes of CS as well.

• Clinical criteria for diagnosing CS include:

o Persistent hypotension

▪ Systolic blood pressure (SBP) <80-90 mmHg for 30 minutes OR mean

arterial pressure (MAP) <65 mmHg for 30 minutes OR vasopressor

required to achieve a SBP ≥90 mmHg OR MAP 30 mmHg or lower than

baseline

o Severe reduction of cardiac index

▪ 1.8 L/min/m

without support

▪ 2.0-2.2 L/min/m

with support

o Elevated filling pressures of left, right, or both ventricles

o Signs of impaired organ perfusion with at least one of the following criteria:

▪ Altered mental status

▪ Cold extremities

▪ Oliguria

▪ Increased serum-lactate

• The diagnosis of CS is usually made with clinical signs and symptoms as well as help

from monitoring hemodynamics via pulmonary artery catheter (PAC), electrocardiogram

(ECG), chest x-ray, blood tests (ABG, electrolytes, CBC, and troponin), echocardiogram,

and cardiac catheterization.

Chart review:

• It is important to note the cause, or suspected cause, as well as the current and/or planned

treatment. If an intervention such as PCI, CABG, valve surgery, VAD placement, or heart

Standard of Care: Cardiac

transplant is planned, it should be noted. If the patient is pending an intervention check

the activity orders and speak with the responding clinician as deferring mobility until

after the intervention may or may not be indicated. Patients with CS are often critically ill

and in the ICU.

• Trends and current vitals and lab values should also be noted to ensure a patient is

hemodynamically appropriate for mobility. There are often hemodynamic parameter

goals that are individualized to each patient given their clinical presentation.

• Patients diagnosed with CS have increased likelihood of requiring mechanical ventilator

support as well as increased likelihood of worsening renal failure, which could require

renal replacement therapy.

• While reviewing the chart, therapists should also take notice of:

48,50

o Lines, including central venous catheter, arterial line, and pulmonary artery

catheter. The therapist should note the location of the line as frequently lines are

placed via femoral access and may alter or impair a patient’s ability to participate

o Pharmacologic Support*

▪ IV fluids

▪ Vasoactive Medications including vasopressors and inotropes

▪ Antiarrhythmics

▪ *See the Appendix 2 for relevant side effects and physical therapy

considerations for the medications above.

o Mechanical ventilation – level of support, recent changes to indicate improvement

or worsening of condition, and presence of sedating medications

o Renal replacement therapy, continuous versus intermittent

o Mechanical circulatory support devices (left ventricular, right ventricular, or

biventricular devices) including IABP, Impella, VA ECMO (see support devices

below for therapy considerations for each device). The ProtekDuo Tandem Heart

or CentriMag can also be used for temporary support as a bridge to recovery or

more durable support, see Mechanical Circulatory Support Devices Standard of

Care for further information.

PT Examination:

• Once physical therapy is indicated it is essential to monitor the patient’s hemodynamic

response to exercise and mobility. ROM testing or mobility may be limited if the patient

has certain lines or mechanical circulatory support devices present. Beyond a traditional

examination a therapist should focus on:

o Cognition

▪ Increased likelihood of altered mental status and decreased command

following (reference?)

o Skin integrity: note change in color and/or temperature, presence and severity of

edema

o Peripheral pulses: likely to be irregular, rapid, and/or faint

o Jugular vein distension

Standard of Care: Cardiac

o Pulmonary assessment including auscultation of lung sounds as able, assessing for

presence of inspiratory crackles indicating pulmonary edema, and ventilatory

pattern and effort

o Auscultation of the heart: distant or faint heart sounds, presence of S3 or S4 heart

sounds

PT Intervention

• Treatment should be based on the patient’s impairments and hemodynamic response to

mobility with the goal of maximizing functional mobility, independence, and safety prior

to discharge. As a patient recovers, formal exercise testing and prescription may be

indicated, however functional mobility assessment can be used to provide guidance for an

exercise program. See PT Intervention/Exercise Training for further information.

Cardiac Tests and Procedures:

Common Cardiac Diagnostic Tests

Echocardiogram

• An echocardiogram is one of the most common diagnostic tests to visualize the heart,

aorta, and other blood vessels. The device emits ultrasound waves to create a single or

two-dimensional image.

51,52

It allows for examination of the chambers of the heart, blood

flow, valve function, and volume status to provide information about heart function

including cardiac output, ejection fraction, and diastolic function or to diagnose

conditions such as a blood clot or mass in the heart, pericardial effusion, congenital heart

diseases, or active infections of the heart valves.

51-53

• Types of Echocardiograms include:

o Transthoracic Echocardiogram (TTE)

-Transducer is placed on the chest and

ultrasound must travel through the chest wall and lungs to reach the heart. This is

the most common type of echocardiogram utilized and can be performed at

bedside.

o Transesophageal Echocardiogram (TEE)

- under sedation, a transducer is passed

through the esophagus, which sits posterior to the heart. This allows for less

interference, superior image quality and visualization.

Stress Test -MIBI

• A sestamibi or MIBI is a nuclear perfusion scan that looks at myocardial blood flow via

IV injection of technetium sestamibi, a pharmacological agent which contains a type of

radioactive isotope. Sestamibi distributes in the myocardium proportional to the

myocardial blood flow.

Single photon emission computed tomography (SPECT)

imaging of the heart is completed by detecting the gamma rays emitted by the isotope as

it decays.

• Two sets of images are taken:

o One set of images is taken when the patient is at rest.

Standard of Care: Cardiac

o The second set is taken once the patient’s heart is stressed. This is done by having

the patient exercise on a treadmill or pharmacologically (with use of a vasodilator

or dobutamine).

• The images of the heart at rest and during peak stress are compared. From the comparison

one can distinguish ischemic versus infarcted areas of the myocardium with high

sensitivity.

Cardiac MRI

• A cardiac magnetic resonance imaging (MRI) is used to create a detailed image of the

heart’s structures including chambers, muscle, valves, as well as how blood is flowing

through the heart and vessels. It can help diagnose conditions including atherosclerosis,

cardiomyopathy, congenital heart disease, heart failure, aneurysm, heart valve disease,

cardiac tumor, or infiltrative disorders like cardiac sarcoid or cardiac amyloid.

Cardiac PET Scan

• A cardiac positron emission tomography (PET) scan is a test where radioactive tracers

are injected intravenously into a patient and a gamma detector picks up images from the

tracer. A computer converts the signals into an image that shows the size, shape, position,

and some function of the heart.

• A cardiac PET scan show if the heart is getting enough blood flow, if coronary artery

disease is present, and can identify areas of damage or ischemia.

Cardiac Catheterization

• A catheter is inserted into the left or right side of the heart for diagnostic and interventional

purposes. It is important to determine whether only a cardiac catheterization was performed

or if additional procedures were performed as well e.g., percutaneous transluminal coronary

angioplasty (PTCA) or insertion of coronary artery stents, prior to PT examination or

intervention. Activity precautions are aimed at protection of the incision site and are as

follows:

o Left heart catheterization (LHC) is used to diagnose left ventricular, atrial,

pulmonary vein, and coronary artery impairments.

▪ Due to the arterial incision site via the femoral artery, these patients are on

bed rest for 6-8 hours with involved LE straight. Patient may have a knee

immobilizer donned to minimize hip flexion. The patient is monitored for

groin hematomas, and pain.

▪ Use of the radial artery is also common and the patient can ambulate with

assistance if vital signs are stable and there is no signs of bleeding or other

complications, or if not otherwise stated in the physician orders.

▪ Complications associated with a left heart catheterization include groin

hematoma and retroperitoneal or intramuscular bleeding in the LE or

intramuscular bleeding in the forearm. Also, consider a patient’s response to

the general anesthesia while examining functional mobility.

Standard of Care: Cardiac

o Right heart catheterization (RHC) is used to diagnose right atrial, ventricular, and

pulmonary artery impairments including flow rates and pressures. The incision site is

generally via the external jugular vein and there are no activity restrictions. RHC can

also be used to estimate left heart pressures

Arrhythmia Management

Cardioversion

• Electrical Cardioversion [Direct-Current Cardioversion (DCCV)] or Pharmacological

Cardioversion

o Medical interventions, either by cardiac electrical shock (DCCV) or with medication

(e.g. Ibutilide) are aimed at restoring normal sinus rhythm to optimize cardiac output.

o Due to potential return of arrhythmias, or patient fatigue associated with anesthesia

for DCCV, PT is generally held the day of cardioversion. Make sure to check for

changes to activity orders and monitor for resumption or progression of cardiac

arrhythmia.

Ablation

• Catheter ablation is a procedure that uses radiofrequency energy, laser light or extremely cold

temperatures (cryoablation) to destroy a small area of heart tissue that is causing arrhythmias

when medicines are not tolerated or effective.

o Venous access (either femoral, subclavian, or internal jugular) is achieved through

cardiac catheterization.

• Most commonly used in treating supraventricular tachycardia, atrial flutter and atrial

fibrillation.

• If patient had femoral access, they are on bed rest with leg straight for 6-8 hours.

Cardiac Surgery and Sternal Precautions

1,3

Common Cardiac Surgeries requiring median sternotomy

• Coronary Artery Bypass Graft: CABG is a surgical intervention used to treat a

completely occluded coronary artery that cannot be treated by, or has failed treatment

with a percutaneous intervention. It uses a vascular graft (typically the saphenous vein or

left internal mammary artery) to revascularize the myocardium. CABG can be performed

for one or more vessels as typically documented in a patient’s chart by CABG x4 or

4vCABG.

• Valve Repair/replacement: Valve repair or replacement surgery is a treatment for

valvular disease. Valves can be replaced by mechanical valves (bileaflet, tilting disc)

which are known for a longer life span and durability, but need lifelong anticoagulation,

or with biological valves (cadavers, porcine or bovine) which carry a benefit of not

needing life time anticoagulation therapy. Minimally invasive valve replacements via a

partial sternotomy (aortic and mitral valve), and mitral valve repair/replacement via a

thoracotomy approach can be utilized in appropriate patients

• Aortic arch repair: An aortic arch repair can be done using synthetic material to replace

the diseased or damaged portions of the vessel. A minimally invasive approach would

Standard of Care: Cardiac

entail a metal wire mesh stent being inserted percutaneously via an artery. This minimally

invasive approach is typically seen in pts who would not tolerate an open surgical

approach, see TAVR below.

• Maze: The Maze procedure is performed to treat atrial fibrillation. It is an open

procedure that entails the etching of lines by heat (radiofrequency energy), cold

(cryoablation) or a scalpel to the atria to create patterns of scar tissue (maze) to block the

abnormal electrical impulses associated with atrial fibrillation. This procedure is often

combined with other open-heart procedures and rarely performed on its own.

• ASD/VSD: Atrial and ventricular septal defects are often repaired surgically. Small

defects are closed via internal sutures while larger defects may require patching that may

be created from the patient’s own tissue or use synthetic material. These repairs can be

performed on their own but are often performed in conjunction with other procedures

during the open sternotomy surgery.

Sternal Precautions

• The exact origin of sternal precautions is not known and current literature does not

support all the imposed restrictions, many of which are anecdotal “or based on expert

opinion”. Multiple recommendations and protocols exist across institutions, with some

limited consensus.

• Current recommendations for sternal precautions at Brigham and Women’s Hospital to

be followed for up to 12 weeks:

o No lifting more than 10 lbs

o Avoid excessive pushing/pulling (such as closing/opening heavy doors,

vacuuming, dog walking, shoveling snow, carrying groceries or laundry baskets)

o Avoid excessive twisting through your trunk, such as reaching behind you

o Avoid excessive coughing, laughing or sneezing; be sure to hug a pillow across

your chest when performing these activities.

o Avoid sit-ups. Log roll to get in and out of bed.

o Avoid driving or sitting in the front seat of a car with an airbag for 3-4 weeks

o Avoid excessive overhead or lateral arm movements, however patients are

encouraged to perform functional arm movements and active ROM exercises in a

pain free range

• Consideration should be taken to identify those patients who have multiple risk factors

for sternal wound dehiscence and these patients should be encouraged to strictly adhere

to sternal precautions:

59,60

o Use of internal mammary artery (IMA) in the bypass graft

o Females with pendulous breasts

o Morbid obesity

o Barrel chest

o History of poorly controlled diabetes mellitus

o Osteoporosis

o Redo operation for bleeding or repeat cardiothoracic surgery

• Signs of impaired sternal healing:

Standard of Care: Cardiac

o A crunch, pop or click in your sternum

o Bleeding that does not stop even with pressure applied

o Signs of infection, such as fever, redness or warm skin around the incision

• The therapist should use sound clinical judgment to allow for safe progression of

mobility to optimize functional return, and individual patient limitations should be

considered and discussed with the medical team and the patient. At this time, patients s/p

full sternotomy without signs of sternal infection should follow sternal precautions for up

to 12 weeks, pending follow up with the surgeon and potentially earlier liberalization of

precautions. Patients with minimally invasive (partial) sternotomies should follow sternal

precautions until surgeon clearance.

• Current literature has shown that restrictive sternal precautions may in fact worsen

functional limitations due to impairments in muscle performance, poor healing of

connective tissues across the sternal incision, and long-term impairments in pulmonary

function and thoracic cavity mobility.

58,61

TAVR

• Transfemoral/Transcatheter Aortic Valve Replacement (TAVR) is a less invasive method

for replacing the aortic valve in patients with aortic stenosis when compared to a standard

cardiac surgery for replacement of the valve. This method is currently approved for use in

patients with severe symptomatic aortic stenosis (AS) who are at intermediate to high

surgical risk or are otherwise inoperable.

• Performed via femoral artery catheter access to deploy a mechanical valve across the pre-

existing diseased valve. Imaging is required to ensure the vascular pathway is clear

without stenosis, calcification, or tortuosity

• A balloon is expanded to seat the valve in position before the catheter is withdrawn

• PT implications:

o Monitor patients for post-op bleeding and/or tamponade

o This technique is performed without a sternotomy, therefore there are no sternal

precautions post-procedure. However, because the technique is performed via a

femoral approach, the patient should avoid any heavy lifting (>5-10lbs) for 1

week following the procedure.

o Activities promoting sudden or extreme hypertension should be avoided

o Lower incidence of arrhythmias as compared to open approach

o As this procedure is performed in a higher risk population, baseline frailty should

be noted and may significantly impact functional performance post procedure.

o Length of stay is typically very short following the procedure and patients may be

discharged the following day

Standard of Care: Cardiac

Cardiac Support Devices:

Chest Tubes

• Chest tubes (CT) on the cardiac service are primarily placed post-operatively in the

pleural or mediastinal cavity to remove excess fluid or blood associated with surgery. The

chest tube unit provides negative pressure to assist with drainage.

• Maintaining the integrity of this closed system by keeping the chest tube upright and the

water seal trap in place prevents fluid buildup and potential lung compression and

ensuing respiratory distress. Use of low wall suction may be employed to maintain a

closed system when there is a large air leak from the lung to the thoracic cavity. When

the air leak is small or when the necessity of continued chest tube use is being evaluated,

the CT may not require suction but remain on water seal or have temporary surgical

clamps in place on the tubing.

• Prior to PT examination or treatment, clarify if the chest tube needs to remain to suction.

If continuous suction is necessary, either use a portable suction unit if walking in hall, or

extended tubing to allow increased patient activity in room.

• Chest PT, shoulder ROM, and deep breathing exercises to patient tolerance are beneficial

in the management of ventilation and airway clearance.

• Removal of a CT may result in the development of a pneumothorax or exacerbation of

the initial air leak related to lung tissue injury. A follow-up chest x-ray (CXR) is

performed and read by a physician assistant (PA) or physician (MD) to rule out a

pneumothorax following CT removal.

o If a PT works with a patient before the CXR has been read, activity orders should

be clarified with the PA. If the decision is made to treat the patient, monitor for

signs of acute pneumothorax (acute shortness of breath, new or increased palpable

crepitus felt anywhere in the thorax, precipitous drop in SPO2 from baseline or <

80%).

Permanent Pacemaker and/or Implantable Cardioverter-Defibrillator

• The insertion of a permanent pacemaker (PPM) or implantable cardioverter-defibrillator

(ICD) may occur to maintain appropriate cardiac conduction or prevent cardiac

arrhythmias.

• A PPM or ICD has three main components: a pulse generator, leads, and electrodes.

Generators are usually described as being either single-chamber or

dual-chamber.

o Single-chamber systems have one lead, which is usually placed

in the right ventricle or right atrium.

o Dual-chamber systems have two leads, one of which is

implanted in the right atrium and the other in the right

ventricle.

• The device is usually inserted under the skin in the left subclavian

pocket, with leads inserted into the right side of the heart via the left

subclavian vein to the superior vena cava. In instances where insertion

Standard of Care: Cardiac

via a left subclavian pocket is not possible or after an infection of a left pocket, the new

device may be inserted via the same routes on the right side.

• Precautions in movement following placement are focused on incision healing and lead

fixation. Although current literature has not investigated the time frame for the leads to

firmly attach into the myocardium, current recommendations from physicians indicate

that 4-6 weeks allows incision healing and firm adhesion of pacemaker leads.

• Current pacemaker precautions at BWH are:

o Keeping the involved UE in a standard sling for 24 hours

o No therapeutic exercise to involved shoulder for 4-6 weeks unless approved by

the Electrophysiology Service (EPS).

o Involved UE may be used functionally but limit shoulder flexion and abduction to

90 degrees for 4-6 weeks.

o Patient may use minimal weight bearing (10-15 lbs.) into UE while using an

ambulatory assistive device, however use of axillary crutches are not

recommended due to venous pressure in the axilla region and incisional stress. In

rare instances, use of axillary crutches to safely negotiate stairs may be indicated.

o No lifting greater than 5 lbs. with involved UE for 4-6 weeks.

• Leadless pacemakers are small self-contained devices that are inserted

in the right ventricle of the heart. A leadless pacemaker does not require

leads or a generator, or the creation of a surgical pocket on the chest.

Currently, the device is available for patients who need single-chamber

pacing only. Because there are no wires or generator, there are no upper

body activity limitations after the implantation so typical pacemaker

precautions do not apply.

• Semi-permanent pacemakers

o Generally used as a bridge therapy when a patient is not clinically able to tolerate

a permanent pacemaker placement (e.g. infection with positive blood cultures).

The device wires are placed transcutaneously with the pacemaker external and

secured with subcutaneous sutures and a dressing. Given the location and lack of

permanent fixation, mobility of the ipsilateral shoulder is generally

contraindicated. Seek clarification of activity orders out of bed with MD and

EPS.

• Temporary Cardiac Pacing

o Used to treat bradyarrhythmias and rarely a tachyarrhythmia, until it resolves or

until long-term therapy can be initiated.

o Two types are typically seen at BWH:

▪ Transvenous pacing wires (typically used more emergently in the CCU):

Introduced through the internal jugular or subclavian veins, therefore no

ROM assessment or therapeutic exercise to the involved shoulder is

allowed.

• More comfortable and more durable in patients in whom the

Standard of Care: Cardiac

anticipated duration of temporary cardiac pacing may be several

days to weeks.

• Most patients will be restricted to bed or chair and cannot

ambulate.

▪ Epicardial pacing wires (typically seen post-cardiac surgery): often left in

place after cardiac surgery when the risk of cardiac arrhythmias is most

great.

• Patients may be dependent on this pacemaker for cardiac rhythm,

or the device may be in place to take over in the event of an

adverse cardiac rhythm (usually bradycardia) and just sensing

(a.k.a. “back-up mode”)

• Leads may be attached to the atrium, ventricle, or both chambers,

with the wires tunneled and externalized.

• No UE ROM restrictions as the wires are transthoracic.

• Mobilization of a patient with temporary epicardial pacing wires is

considered appropriate, however caution should be taken to avoid

dislodging the wires. The therapist should be aware of the

patient’s underlying cardiac rhythm, and activity orders should be

clarified. Most importantly, orders should be clarified in patients

who have more serious arrhythmias (ex: heart blocks) who are

dependent on the pacing for adequate cardiac function.

• When no longer needed, the epicardial pacing wires may also be

detached from the temporary pacing device, capped with insulating

wire caps, and taped to patient’s chest. When epicardial pacing

wires are removed, they are either cut at the skin level or pulled

through the skin. When removed through the skin, there is a risk

of bleeding where they were attached to the myocardium and

therefore these patients are monitored for signs of cardiac

tamponade (i.e., tachycardia, lightheadedness, dyspnea) and follow

this progression of activity to allow for monitoring:

o Patient may be out of bed with RN in room after 1 hour of

bed rest.

o Patient may participate with PT after 2 hours.

o Patient may initiate or resume stair training after 4 hours.

Pulmonary Artery catheter (or Swan-Ganz catheter)

• Pulmonary artery catheters (PAC) are the most commonly used tool for in-depth

hemodynamic assessment. They allow for a rapid evaluation of the effectiveness of

interventions used to manipulate circulatory volume and pressure, including the

administration of fluids and diuretics as well as vasoactive and inotropic medications.

• The catheter is flexible, balloon tipped, and is most commonly inserted in the jugular or

subclavian vein. It travels to the superior vena cava, right atrium, right ventricle, and

Standard of Care: Cardiac

pulmonary artery. The catheter is connected to a transducer that measures many

hemodynamic parameters including:

o Direct measurement of pulmonary artery pressure, pulmonary capillary wedge

pressure (during balloon inflation), central venous pressure, and mixed venous

oxygen saturation

o Estimates stroke volume, cardiac output, and cardiac index.

o See Appendix 3 for full description of PAC values and interpretation

• Potential complications with PAC insertion are

o Ventricular arrhythmias, right bundle branch block, pneumothorax.

• Potential complications with the ongoing use of PACs are

o Pulmonary artery infarction, pulmonary artery rupture, line infection, movement

within the pulmonary artery causing injury to the vessel or accidental

dislodgement into the right ventricle, or dysrhythmias.

• Therapists treating patients with PACs should be aware of the normal waveforms for

atrial, pulmonary artery and pulmonary capillary wedge pressure measurement, although

artifact is commonly seen when mobilizing the patient due to changes in leveling of the

transducer. Physical therapy is contraindicated if the catheter is in the wedged position.

See Appendix 3 for a picture of various waveforms

• The actual risk of potential PAC complications arising from positional changes is not

known, as there are limited reports directly measuring the effects of positional changes

and mobility however one 2015 study did demonstrate safe mobility, including

ambulation, without PAC complications.

• At Brigham & Women’s Hospital, when the patient is medically appropriate for PT and

continues to have a PA line in place, activity orders are often for therapeutic exercise

and/or bed to chair transfers. However, patients at times are liberalized to ambulation.

The therapist should seek appropriate activity orders. To minimize movement in a locked

PA line, ipsilateral shoulder flexion and abduction is limited to 90 degrees.

• Patients being admitted for management of acute decompensated heart failure or pending

orthotopic heart transplant often have PA lines placed long-term for tailored medical

therapy. In these instances, a standing exercise program and/or seated stationary biking

is often utilized for optimization of the patient’s aerobic capacity.

IABP

• Intra-aortic balloon pump (IABP) are temporary devices used to support cardiac pump

function and improve blood flow to the myocardium. A flexible catheter with a balloon

mounted on its end is inserted, usually through the femoral artery, and passed into the

descending thoracic aorta. Rapid inflation and deflation of the balloon in synchrony with

cardiac contraction causes counterpulsation due to volume displacement and pressure

changes within the aorta.

Balloon deflation augments forward flow, balloon inflation

redirects flow into the coronary arteries.

• Patients with IABPs are typically hemodynamically unstable and inappropriate for

therapeutic exercise and mobility programs. Protection of the catheter’s integrity is of

Standard of Care: Cardiac

utmost importance.

In specific cases, the therapist may receive a consult from the MD

for therapeutic exercise to uninvolved extremities. In these instances, movement and

activity should be limited to avoid disruption of the catheter, balloon rupture, or incision

site infection.

o Minimize extreme joint range of motion where the IABP is present.

o Avoid hip flexion greater than 70 degrees on the side where the catheter is

inserted.

o Other institutions have demonstrated safe mobility with patients with femoral

IABP placements, however current practice at BWH is for these patients to

remain on bedrest. Use of this type of support is often transient, as either a bridge

to recovery or transition to a more durable level of support

Impella

• The Impella devices are a continuous flow axial pumps contained within a pigtail catheter

that are designed to offload pressure from the ventricle by augmenting forward blood

flow and increasing cardiac output.

• They are most commonly used as a left ventricular support device with the catheter

placed in a retrograde fashion, with the inlet pump sitting in the left ventricle and outlet

in the ascending aorta. This creates a continuous flow of blood from the left ventricle to

the proximal ascending aorta.

o The three most common versions available are the Impella 2.5, CP, and 5.0 which

have a maximum flow of 2.5 L/min, 3-4 L/min, and 5.0 L/min respectively.

▪ The Impella 2.5 and CP devices can be deployed percutaneously via the

femoral artery and the 5.0 device requires a surgical cutdown but can be

placed either via the femoral or axillary artery.

o The external controller system allows for manual adjustments in rotational speed

to alter flow and cardiac output, and houses the infusate of heparin and dextrose,

designed to prevent clotting and contamination of the motor by blood.

• This device is employed in situations of clinical deterioration or progressive cardiogenic

shock not otherwise managed pharmacologically. It has been documented for use in

patients with cardiogenic shock for a variety of reasons including acute and post MI,

ischemic cardiomyopathy, myocarditis, and acute cardiac transplant graft failure, used as

either a bridge to recovery or a transition to another more durable device. Impella can

also be employed as a transition from IABP or EMCO, in cases where longer recovery

time is needed. The device is approved for 6 hours of use, however has been used off-

label for days to weeks.

• Mobilizing patients who require Impella support with an axillary cannulation has been

documented as safe and feasible with benefits to the patient.

73,75,76

However, it is

recommended that a patient with a femorally inserted Impella maintain bedrest.

• At BWH, patients with femorally inserted devices are on bedrest; however, if the device

is thought to be needed long term, they have been converted, when able, to proximal

cannulation to allow for mobility.

Standard of Care: Cardiac

• There are no standard mobility protocols or precautions for these devices however

typically ipsilateral shoulder movement is kept to a minimum, maintained below 90°.

Monitoring vital signs for response to exercise and device flow is important.

• Working with the Impella specialists can help identify changes to device settings that

may be important during PT sessions in order to support adequate cardiac output with

potentially increased venous return due to exercise

ECMO

• Extracorporeal Membrane Oxygenation (ECMO): Utilized in cases of severe acute

respiratory failure or cardiac failure/cardiogenic shock, when other forms of life support

are insufficient for sustaining body functioning. ECMO can be placed either venoarterial

(VA) and venovenous (VV) for support. Both methods of cannulation provide respiratory

support (i.e. support for gas exchange), but only VA ECMO provides hemodynamic

support by supporting both the lungs and the heart.

This standard of care will focus on

VA ECMO cannulation for support of significant cardiac compromise.

• Indications for VA ECMO include:

o Cardiac/circulatory failure and refractory cardiogenic shock

o Massive PE with cardiac compromise

o Cardiac arrest

o Failure to wean from cardiopulmonary bypass after surgery

o As a bridge to recovery, cardiac transplant, or placement of durable VAD

support.

• With VA ECMO support, venous blood will enter the external device to be oxygenated

and then recirculated back into the arterial circulation to supply all body tissues. As stated

above, this system augments the heart and lungs to provide respiratory and hemodynamic

support. In the oxygenator, hemoglobin is saturated with O

and CO

is removed.

Oxygenation of the blood is determined in part by the flow rate through the device. CO

elimination is determined by the sweep gas, typically 100% oxygen, and the sweep flow

rate.

• VA ECMO cannulation:

o Venous cannula is placed in either the inferior vena cava or the right atrium,

preferably via the femoral vein.

o Arterial cannulation: The blood is returned to arterial circulation typically via the

right femoral artery to the left ventricle or aorta.

▪ Although femoral access is preferable due to ease of insertion, the primary

complication associated with this is the risk for ipsilateral lower extremity

vascular compromise and ischemia. A reperfusion cannula can be used,

placed distally to the femoral artery cannula, redirecting part of the infused

blood directly back to the leg.

o Additional complications of VA ECMO, with the blood return to the aorta

potentially competing with native, antegrade circulation, are a separation of upper

Standard of Care: Cardiac

and lower body perfusion (watershed phenomenon), left ventricular distention,

and pulmonary edema.

• VA ECMO cannulation can occur proximally as well, via the R common carotid or

subclavian arteries, allowing increased ease of mobility.

• Literature supports mobilization on VA ECMO, including ambulation, even with femoral

cannulation,

however current practice at BWH is still largely on a case by case basis. It

has been demonstrated as feasible and safe in a small population of patients.

• PT considerations for patients on ECMO:

o Please note, treating a patient on ECMO support is an advanced skill and requires

consultation by a team lead or clinical specialist. Please work in consultation with

respiratory therapy as well for documentation of sweep, SvO

, and flow rates

o Sweep: gas exchange measured in flow (L/min) and FiO2. The flow is indicative

of rate of gas exchange (removal of CO2) and the fraction of delivered O2 is

FiO2.

o SvO

: measure of mixed venous oxygen saturation, normal values are ~75%.

Drops in SvO

can be seen with activity and increasing exertion however care

should be taken to minimize the drop. Seek parameters with the ECMO team.

Often changes to the sweep can help maintain appropriate levels.

o Arterial BP: can be low and relatively static with minimal to no difference

between systolic and diastolic readings, depending upon the flow rate through the

ECMO circuit (i.e. how much is the device unloading the heart).

o Flow: monitoring flow rates through the circuit is important with all activity to

ensure adequate functioning of the device and perfusion of the body

o Range of motion for femoral cannulation: although no formal guidelines have yet

been developed, PT intervention has maintained a hip flexion angle of less than

90° due to risk of compressing the cannula and creating a permanent kink in the

line.

o Collaborate with the ECMO specialists to make appropriate adjustments to

ECMO settings to support mobility and exercise. This can include increasing the

sweep for improved SvO

with activity

o Ensure safety and security of the ECMO cannulas to the patient with an

appropriate device (including but not limited to: Foley strap, drain secure,

headband, abdominal binder) prior to and during mobilization

Medications

Therapists should review and be familiar with a patient’s current medication list. The therapist

should especially be aware of any intravenous medications being used, and become familiar with

their actions and potential side effects. The administration of certain medications generally

indicates that the patient is hemodynamically unstable and/or has complex medical issues.

Discussion regarding the goals of PT intervention on a case-by-case basis should occur prior to

PT treatment session with staff mentor, clinical specialist, or PT supervisor and/or a member of

the physician team. Clarify with the MD an appropriate activity level for patients on vasoactive

Standard of Care: Cardiac

medications: vasodilator, inotropic/vasopressor, antiarrhythmic, and antianginal. Common

cardiac medications are listed in Appendix 2.

Cardiac Physical Exam

The outline below is designed to guide the therapist through relevant components of a physical

exam on a patient with cardiac dysfunction, or to assist with interpretation of a chart review.

Note that components may not apply to all patients.

• General appearance

o Body type

o Posture- tripod, semi-fowler

o Skin tone

o Equipment, lines, and support devices

• Neck

o JVD

▪ Assessment for distention of the right Internal Jugular vein (IJ)

is a difficult skill. Its importance lies in the fact that the IJ is in

straight-line communication with the right atrium. The IJ can

therefore function as a manometer, with distention indicating

elevation of Central Venous Pressure (CVP). This in turn is an

important marker of intravascular volume status and related

cardiac function.

• Position: Sitting or recumbent in bed with HOB elevated

at least 45 degrees, head turned to left.

https://www.youtube.com/watch?v=NH8YM8DDhkk

o Accessory muscle use, SCM hypertrophy

• Chest

o AP diameter (i.e. barrel chest), scoliosis/kyphosis, pectus excavatum vs pectus

carinatum

o Hands on lower lobes to assess excursion, respiratory rate, and breathing pattern

▪ Common breathing patterns

• Tachypnea: increased respiratory rate

• Hyperpnea: normal rate but deeper, seen with emotional stress,

diabetic ketoacidosis

▪ Fremitus: vibration that is produced by the voice or by presence of

secretions in airways and is transmitted to the chest wall and palpated by

hand.

o Cough (and how to document)

▪ Types: productive, non-productive, dry, congested, moist, persistent,

strong, weak, spontaneous

▪ Sputum: color, amount, smell

o Auscultation of lungs (using diaphragm of stethoscope)

▪ For examples of general abnormal sounds:

https://www.youtube.com/watch?v=gOB0nM0PRTc

Standard of Care: Cardiac

▪ Listen for normal, abnormal or adventitious sounds

• Diminished, caused by:

o Hyperinflation: COPD

o Hypoinflation: acute lung disease- atelectasis,

pneumothorax (PTX), pleural effusion

• Absent: Pleural effusion, PTX, severe hyperinflation, obesity

• Adventitious:

o Bronchial: Consolidation, atelectasis with adjacent patent

airway

o Crackles/Rales/Ronchi:

https://www.youtube.com/watch?v=5wEMGd1PRrg

▪ Secretions if biphasic

▪ Deflation or edema if monophasic

o Wheezes

▪ Diffuse airway obstruction if polyphonic

▪ Localized stenosis if monophonic

▪ Extrapulmonary adventitious sounds

• Crunch: mediastinal emphysema

• Pleural rub: pleural inflammation or reaction:

https://www.youtube.com/watch?v=36t0vMrcrKU

• Pericardial rub: pericardial inflammation

o Auscultation of heart (bell of stethoscope)

▪ Normal sounds: S1/S2 “lub-dub”

• S1 is the sound which marks the approximate beginning of systole,

and is created by the closing of the tricuspid and mitral due to

increased intraventricular pressure during systole. The ventricles

continue to contract throughout systole, forcing blood through the

aortic and pulmonary, or semilunar valves. At the end of systole,

the ventricles begin to relax, the pressures within the heart become

less than that in the aorta and pulmonary artery, and a brief back

flow of blood causes the semilunar valves to snap shut, producing

S2.

▪ Abnormal sounds: S3/S4

• An S3 is most commonly associated with left ventricular failure

and is caused by blood from the left atrium rushing into an already

overfilled ventricle during early diastolic filling,

“S3, Slosh-ing-in”. The S4 is a sound created by

blood trying to enter a stiff, non-compliant left

ventricle during atrial contraction

(beginning of systole). It is most frequently

associated with left ventricular hypertrophy

Standard of Care: Cardiac

that is the result of long standing hypertension, “S4 A-Stiff-Wall”.

▪ Murmurs and mechanical valves

• https://www.youtube.com/watch?v=6YY3OOPmUDA

• Extremities – assess for:

o Digital clubbing

o Coloration

o Cyanosis – Perioral, distal extremities

o PAD: Pale, loss of hair, shiny, diminished pulse, cold,

painful (claudication), ulceration (heel, malleoli, anterior

shin), numbness/tingling

o PVD: Brownish coloration, edema, ulceration (above medial malleolus, calf,

dorsum of foot), sometimes numbness/tingling

o Edema

▪ None

▪ Non-pitting

▪ 1+ Mild pitting, barely perceptible impression when finger is pressed into

the skin

▪ 2+ Moderate pitting, slight indentation, skin rebounds <15 seconds

▪ 3+ Deep pitting, deeper indentation, skin rebounds 15-30 seconds

▪ 4+ Very deep pitting indentation, skin rebounds >30 seconds

o Pulses: Brachial, radial, PT, DP

Exercise/endurance testing:

• Assess baseline level of function, both just prior to admission and when last feeling well,

as appropriate

o Take note of any recent or frequent hospitalizations. Be sure to check in “Chart

Review” in EPIC to see PT notes from previous admissions, if applicable, to help

guide understanding of functional status and assist in determining a change in

status.

• Use of standardized endurance testing is encouraged for all patients as clinically stable

and able.

81-84

o 6MWT: The 6MWT can be used to quantify aerobic capacity and endurance.

Results of the test can be compared to age-predicted norms using an equation

developed by Gibbons et al

for all patients 22-79. A spreadsheet for calculating

this information is located on the T drive. The spreadsheet additionally calculates

average gait speed and average METs.

▪ Documentation should include: distance walked in feet and meters,

percent predicted, ability of the patient to complete the test, adverse

events, and vital signs per/during/post including rate of perceived exertion

(RPE).

▪ Gait speed and METs can be used to help with the development of goals

and patient education regarding return to activity.

Standard of Care: Cardiac

o For patients unable to tolerate or otherwise complete a 6MWT, the 2-minute walk

test is an option. See Appendix 1

• Monitor patient for significant tachy- or bradycardia that is new or changed from baseline

as this may indicate an abnormal response to the activity being performed or identify a

person not ready to participate in activity with PT.

• Use of HR for exercise prescription in patients with cardiac health conditions is not

always effective given the effects of cardiac medications, specifically Beta Blockers

, on

heart rate. Use of the RPE scale to monitor exertion levels is the best way to determine

safe exercise parameters in the acute care setting, since peak HR cannot always be

determined by a pharmacological or exercise stress test.

o In general, however, the ability for the heart rate to respond to changing activity is

considered a good prognostic factor after cardiac event, while a decrease in heart

rate (>5 beats/min) with increased activity or abnormal HR increase for the level

of work being done is considered a poor prognostic indicator.

PT Intervention/Aerobic Exercise Training:

Endurance Training:

• Whenever exercise testing is utilized, it is important to monitor the patient closely for

symptoms of exercise intolerance and hemodynamic response. Data extracted from

exercise testing will then assist the therapist in providing the patient with an appropriate

and safe exercise prescription, likely in the form of a home exercise program.

• Designed by choosing the mode, intensity, frequency and duration based on patient

presentation and previous tests and measures, such as the 6MWT or 2MWT. Be sure to

include a warm-up and cool-down. The recommendations below are based on the ACSM

recommendations for an inpatient exercise program for patients with cardiac

dysfunction.

o Mode: Walking

▪ You could consider a stationary bike or restorator depending on the

patient’s prior level of function or symptom burden

o Intensity/Duration: Determined by patient’s symptoms (DOE) and RPE during

exam or during a 6MWT in combination with HR response. It is recommended to

start an exercise program at a lower intensity (RPE </= 5/10).

▪ Consider using interval training with multiple short bouts of exercise with

rest breaks in between to allow for longer duration of exercise without

excessive symptoms. If using interval training, the goal would be to

increase the time of the exercise bout and decrease the rest time. You

should attempt to achieve a 2:1 ratio of exercise/rest. A good starting point

would be 3-5 min of work, followed by 1-3 min of rest (slower walk or

complete stop, at the patient’s discretion).

▪ If a patient can walk for 6 minutes with a low RPE, then intervals of time

greater than 6 minutes are indicated. If the patient is unable to complete

the 6-minute interval, intervals based on 6MWT results can be used to

Standard of Care: Cardiac

achieve an aerobic training effect (may only be 1-2 or 5-6 intervals to

achieve this aerobic training effect). Rest intervals can also be determined

using the 6MWT and should be included in the exercise prescription.

o Frequency: 2-4x/day, 5-7x/week

o Progression: When continuous exercise duration reaches 10-15 min, increase

intensity as tolerated within the recommended RPE and HR limits.

• Be sure to quantify fatigue and dyspnea during functional mobility and ambulation using

the 0-10 RPE and DOE scales. These scales can also help determine a patient’s tolerance

for activity and ADLs and can assist in discharge planning, goal-setting and plan of care.

Cardiac Rehab:

• Cardiac rehab (CR) is a comprehensive outpatient program offered to patients with a

variety of diagnoses of cardiac dysfunction, designed to improve physical, psychological,

social and vocational functioning. The emphasis is on monitored exercise training,

however programs additionally offer education on smoking cessation, diet and nutrition,

weight loss, stress management, and management of diabetes, lipids, and hypertension.

• CR programs have been shown to reduce all-cause mortality and cardiovascular

mortality, decrease symptoms, reduce recurrent MI, improve adherence with medication

management, increase exercise tolerance, mood and health-related quality of life, and to

reduce hospitalizations.

o CR programs additionally show great benefits on risk factor modification,

including lipid profile, obesity, and psychosocial stress.

88-91

• Thirty-six sessions are covered, however MI risk reduction has been seen with fewer

sessions attended.

• ACCF/AHA clinical guidelines:

o Class IA recommendation for management of stable ischemic heart disease

o Class IIA recommendation for chronic stable heart failure

• Covered diagnoses:

o MI/ACS

o CABG

o s/p PCI

o stable angina

o Heart valve repair/replacement

o Heart failure (EF < 35%),

o Heart or heart/lung transplant

o PAD

• Patients and their families should be educated on the purpose and benefits of cardiac

rehab and referred prior to discharge as appropriate.

• A list of certified cardiac rehab centers in Massachusetts, New Hampshire, Maine,

Connecticut and Rhode Island can be found on the T-drive and printed for patients to

reference based on where they live. Centers are certified by the American Association of

Cardiovascular and Pulmonary Rehabilitation (AACVPR), https://www.aacvpr.org/.

Standard of Care: Cardiac

Authors: Reviewers:

Michelle Tagerman, PT, GCS Elizabeth Powers, PT

Jessica Rydingsward, PT, CCS Jessica Rydingsward, PT, CCS

Jenna Stuebe, PT, CCS Jenna Stuebe, PT, CCS

Elizabeth Powers, PT

Laurel Mangelinkx, PT

Allison Trzaskos, PT

Alison Kras, PT

Appendix 1:

Six-Minute Walk Test

Purpose: The purpose of the 6MWT is to have patients perform a standardized test to assess

aerobic capacity and to assist in the prescription of an exercise program based on test results. The

results of the 6MWT have been shown to aide in the prognosis of medical conditions such as CHF

and COPD

• The test consists of standardized instructions to the patient (available on the T drive), with

the patient allowed to self-pace the walk based on the instructions.

• The therapist measures distance walked, vital signs pre/during/post walk, and the number of

rests required. For practical purposes, HR, SpO

, and RPE are collected during the walk at 2

minute intervals, with BP measurements taken prior to the test, just after the test, and after a

period of recovery if indicated. The test is performed without benefit of a warm-up.

• Document distance ambulated by recording the number of completed laps on a pre-measured

hallway. Pace off the additional distances as needed (2ft floor and ceiling tiles in Shapiro)

• Conditions for stopping the test include:

o Drop in SpO

< 80% or if other signs/symptoms of significant desaturation are

present (i.e. confusion, stupor)

o Lightheadedness

o Level III/IV angina

o Marked dyspnea or fatigue

o Severe musculoskeletal pain or vascular insufficiency such as LE claudication

o Greater than moderate discomfort from any cause

o Patients on telemetry who demonstrate:

▪ Increasing multifocal premature ventricular contractions (PVCs), coupled

PVCs, or ventricular tachycardia (3 consecutive PVCs)

▪ Rapid atrial dysrhythmias

Normative Values/Prognosis:

• Patient’s with chronic heart failure walked an average distance of 310-427 meters

depending on the severity of the disease

• Distance walked on the 6MWT has an inverse correlation with the NYHA functional

class

Standard of Care: Cardiac

Modified Borg Scale

Rate of Perceived Exertion (RPE)

0 Nothing at all

0.5 Very, very slight

1 Very slight

2 Slight

3 Moderate

4 Somewhat hard

5 Hard

7 Very hard

10 Very, very hard, Maximal

• A recent study by McCabe et al. found that 6MWD in patients with HF performed in the

inpatient setting prior to discharge can predict hospital readmission in 30 days. Patients

with a 30-day readmission walked less than 536ft. Subjects who walked >984ft had a

probability of readmission in 30 days < 13%. It has been suggested that persons who

ambulate less than 300 meters have significantly increased mortality and morbidity

regardless of sex.

Two Minute Walk Test

Purpose: The 2-minute walk test exists as an alternative to the 6MWT for patients who are

otherwise unable to complete the longer time/distance due to symptomatic presentation, level of

aerobic conditioning, or time constraints. Normative values have recently been established in a

small population and work is ongoing to build a robust comparative dataset.

Instructions for

performing the test are similar to the 6MWT, as are the values collected by the therapist and the

ability to utilize the results as an objective starting point for creating an exercise prescription.

Age matched norms for healthy, community dwelling adults age 18-85.

Age

Women’s Distance (m)

Men’s Distance (m)

18-54

183

200.9

55-59

176.4

191.0

60-64

166.4

179.1

65-69

155.2

184.2

70-74

145.9

172.4

75-79

140.9

157.6

80-85

134.3

144.1

Modified Borg RPE

Standard of Care: Cardiac

METs

If a patient’s functional capacity is >/4 METs, here is an example of how to progress exercise in

setting of recent cardiac hospitalization or surgery:

Week

%FC

Total exercise

time (min) at

%FC

Exercise bout

(min)

Rest bout

(min)

Number of

exercise/rest bouts

1-2

40-50%

10-20

3-7

3-5

3-4

50-60%

15-30

7-15

2-5

2-3

60-70%

25-40

12-20

• METs reference points:

o 1 MET: self-care, ADLs, household ambulation, walk 1-2 blocks on level ground,

stationary bike very low resistance

o 2-5: carrying up to 2-5 lbs, cleaning windows, raking leaves, golf, tennis, biking

up to 8 mph

o <4 METs: do light housework

o >/4 METs: climb a flight of stairs, walk uphill, walk at 4 mph, heavier

housework, moderate recreational activities

Standard of Care: Cardiac

Appendix 2:

Common Cardiac Medications

Class

Drug

Indication

Mechanism

Admin

Route

Onset

Implications

ACE Inhibitors

(-pril)

Captopril

Lisinopril

-CHF

-HTN

Decrease cardiac workload

Decrease peripheral vascular

resistance.

Also prevent Na+ and water retention

Promote vasodilation

15-60

minutes

Hypotension

Skin rash

Dry Cough

Beta Blockers

(-lol)

Metoprolol*

Atenolol*

Esmolol*

Labetalol

Carvedilol

*Indicates cardio-

selective*

-Arrhythmias

-CHF

-Angina

-HTN

Decrease cardiac workload

Decrease heart rate and contractility.

Some may also produce peripheral

vasodilation

IV (see IV

meds below)

15-60

minutes

Bradycardia

Hypotension

Arrhythmias

Excessive

negative

inotropic effect

Calcium

Channel

Blockers

Amlodipine

Diltiazem

Verapamil

-Arrhythmias

-Angina

-HTN

Decrease rate of discharge of SA

node. Inhibit conduction velocity

through AV node. Causes coronary

vasodilation by blocking Ca+ from

entering vascular smooth muscle,

which increases O2 supply

IV (see IV

meds below)

30-60

minutes

Cough

Hypotension

Dry mouth

Edema

Diuretics

Hydrochlorothiazide

Furosemide

-CHF

-HTN

Decrease cardiac workload.

Decrease volume of fluid that heart

30-60

Hypotension

Standard of Care: Cardiac

Torsemide

Spironolactone

must pump. Decreases fluid

accumulation

IV (see IV

meds below)

minutes

Electrolyte

imbalance

Vasodilators

Nitrates

(ie Nitroglycerin)

Hydralazine

Milrinone

Nifedipine

-CHF

-HTN

-Angina

Decrease cardiac workload. Promote

dilation of peripheral vasculature –

decreased cardiac preload and

afterload

Decreases peripheral and vascular

resistance

IV (see IV

meds below)

Nitro: 1-3

minutes

20-45

minutes

Tachycardia

Hypotension

Palpitations

Fluid Retention

Angiotensin II

Receptor

Antagonist

Losartan

Valsartan

-HTN

-CHF

Block effects of angiotensin II on

vasculature, which causes blood

vessels to dilate

1-2

hours

Hypotension

Cough (less

likely than with

use of ACE

inhibitors)

Positive

Inotropic

Agents

Digoxin

Milrinone

-CHF

-Afib

Increase myocardial contractility. May

also help normalize autonomic effects

on the heart

IV (see IV

meds below)

30-120

minutes

Hypotension

Arrhythmias

Toxicity

(Digoxin)

Anti-

arrhythmic

Amiodarone

-Arrhythmias

Delay repolarization of cardiac cells –

slows and stabilizes heart rate

IV (see IV

meds below)

3-7 hours

Increase in

arrhythmias

Pulmonary

toxicity

Pulmonary

Vasodilators

Sildenafil

Tadalafil

Remodulin

Flolan/Veletri

-Pulmonary

HTN

Dilates pulmonary arteries

IV (see IV

meds below)

1-2 hours

Dry Mouth

Irregular HR

Hypotension

Lipid

Management

Atorvastatin

Lovastatin

-HLD

Increased LDL-receptor activity

Inhibits cholesterol Synthesis

1-2 hours

Myopathy

Standard of Care: Cardiac

(-statins)

Pravastatin

Simvastatin

Anti-platelet

agents

Aspirin

Clopidogrel (Plavix)

Ticagrelor

-unstable

angina

-s/p MI

-s/p CVA

Decreased platelet aggregation and

inhibit thrombus formation

Within

two hours

Increased risk

for bleeding

Anti-

coagulants

“Blood

thinners”

Coumadin

Apixaban

Xarelto

-DVT/PE

-s/p

Mechanical

heart valve

replacement

-Afib

Prolong time it takes for blood to clot

and inhibits blood clot formation.

12-24

hours

For Coumadin:

monitor INR

levels

Increased risk

for bleeding

For Heparin:

Monitor PTT

Lovenox

Subcutaneous

Injection

3-5

hours

Heparin

Bivalirudin

Subcutaneous

Injection

IV (see IV

meds below)

20-60

minutes

Common Cardiac/Critical Care IV Medications

Clas

Drug

Indication

Mechanism

Dosing

(gtt)

Onset

Half Life

PT Implications

Vasopressors

/Inotropes

Dobutamine

Hypotension

Shock

Low cardiac

output

CHF

Increases the strength and

force of the heartbeat,

causing more blood to

circulate through the body.

Does not cause

2-20

mcg/kg/min

1-10

min

2 min

Trend BP

Can be administered on

step down floor

Standard of Care: Cardiac

Augment diuresis

vasoconstriction or

tachycardia

Dopamine

Hypotension

Bradycardia

Low doses increase

myocardial contractility to

increase cardiac output.

High doses cause

vasoconstriction to

increase BP.

2-20

mcg/kg/min

5 min

2 min

Trend BP

Can be administered on

step down floor

Epinephrine

Decreased atrial

& ventricular

contractility

Bradycardia

Increases the coronary

artery pressure thereby

promoting increased

coronary blood flow

0.05-1

mcg/kg/min

Rapid,

w/in

mins

Trend BP*

Levophed

(Norepinephrine)

Decreased cardiac

output

Bradycardia

Hypotension

Decreased

coronary artery

flow

Causes heart muscle

vasodilation and peripheral

muscle vasoconstriction

0.01-3

mcg/kg/min

Rapid,

w/in

secs

Trend BP*

Neosynephrine

(Phenylephrine)

Bradycardia

Decreased cardiac

output

Exhibits rapid and

extended vasoconstrictor

actions

10-220

mcg/min

Rapid,

w/in

secs

1.5 hours

Trend BP*

Vasopressin

Hypotension

Increases peripheral

vascular resistance to

increase arterial BP

0.01-0.1

Units/min

Rapid,

w/in

mins

<10

minutes

Trend BP*

Standard of Care: Cardiac

Primacor

(Milrinone)

Acute CHF

Inotropic vasodilator,

increases contractile force

in the heart muscles

0.375-0.75

mcg/kg/min

5-12

min

2.4 hours

Trend BP

Vasodilators

Nipride

(Nitroprusside)

Acute CHF

Hypertensive

crisis

Hypotensive

induction (for

surgery)

Hypotensive agent relaxes

smooth muscle of blood

vessels, dilate peripheral

arteries and veins;

promotes peripheral

pooling and decreases

venous return to reduce

preload (left ventricular

end-diastolic pressure and

pulmonary capillary wedge

pressure); decrease in

afterload (systemic

vascular resistance, systolic

and MAP)

0.3-4

mcg/kg/min

min

2 min

Trend BP

Nitroglycerin

Angina

CHF

HTN

Hypotension

induction

(intraoperative)

Vasodilating agent that

relieves tension on vascular

smooth muscle and dilates

peripheral veins and

arteries; improves the

contractile state in smooth

muscle which results in

vasodilation

1-200 mcg/min

Rapid,

w/in

secs

~ 3 minutes

Exercise tolerance may be

blunted; angina; HR, BP,

wedge pressure

Standard of Care: Cardiac

Antiarrhythmic

Amiodarone

(Similar meds:

Sotalol)

Supraventricular

arrhythmias

(afib/flutter)

lengthen the cardiac action

potential

initial 300 mg

IV over 1 hour,

f/b 10-50 mg/hr

IV over 24

hours, then

switch to p.o.

For CV of Afib

or for vent

arrhythmias:

150 mg IV over

10 min, then 1

mg/min IV for 6

hours, then 0.5

mg/min IV for

18 hours or

switch to p.o

10-50 days

HR, SpO2

Digoxin

Afib

Heart Failure

Reduced sympathetic

response

8 to 12 mcg/kg

1.5-2 days

Renal function, electrolyte

levels

Brevibloc

(Esmolol)

-Angina

-Acute MI

-CHF

-Hypertension

Beta Blocker; Block

sympathetic activity;

reduces rate and

conduction

50-200

mcg/kg/min

2-10

min

~9 mins

BP, HR

Lidocaine

-Ventricular

arrhythmias (a/w

MI/ischemia)

-Ventricular

fibrillation

Depresses diastolic

depolarization and

automaticity in the

ventricles. Has little effect

on atrial tissue.

1-4 mg/min

45-90

second

~2 hours

ECG

Standard of Care: Cardiac

Quinidine

-Afib/flutter

Sodium-channel blockade

0.25 mg/kg/min

6-8 hours

ECG, BP

Procainamide

-Ventricular

arrhythmias

increases effective

refractory period and

reduces impulse

conduction velocity and

excitability in the atria,

His-Purkinje fibers and

ventricular muscle of the

heart

20 to 50

mg/min

3-4hours

BP, ECG

Cardizem

(Diltiazem)

-Atrial

Arrhythmia

-HTN

-Paroxysmal

supraventricular

tachycardia

-Stable angina

Channel Blocker;

most effective at SA & AV

nodes; reduce rate and

conduction

5-20 mg/hr

minute

3.4-4.9

hours

Vitals

Cardene

(Nicardipine)

HTN

Stable angina,

chronic

Channel Blocker;

affects the contractile

functions of cardiac and

vascular smooth muscle

2.5-15mg/hr

10 min

14.4 hours

Vitals

Isoproterenol

(Isoprel)

Bronchospasm

Cardiac Arrest

Heart Block

Beta Agonist; lowers

peripheral vascular

resistance and diastolic

pressure; prevents

bronchoconstriction

2-10 mcg/min

second

BP, HR, ECG, CVP, ABG

Standard of Care: Cardiac

Diuretic

Bumex

(Bumetanide)

Edema (CHF)

Potent loop diuretic,

inhibits reabsorption of

sodium and chloride,

enhances excretion of

potassium; increases serum

uric acid and reduces uric

acid excretion

1mg/hr

2-3

min

1-1.5 hours

Ototoxicity may occur,

Check labs (electrolytes)

Lasix (Furosemide)

Edema (CHF,

renal failure)

HTN

Pulmonary

Edema

Potent diuretic blocks the

absorption of sodium and

chloride; increases urine

output

10-20 mg/hr

5 min

~2 hours

Ototoxicity may occur,

Check labs (electrolytes)

Anticoagulant

Heparin

Afib

PE/DVT

Inhibits blood clotting

Weight or PTT

based

Secon

1.5 hours

Increased risk of bleeding;

check PTT

Bivalirudin

Angina

PCI

Can be used when

patients have HIT

Helps prevent the

formation of blood clots

0.75 mg/kg as

an IV bolus

dose, followed

immediately by

1.75 mg/kg/hr

second

25 minutes

Increased risk of bleeding

Pulmonary

Vasodilators

Remodulin

Pulmonary HTN

Dilates arteries and

decreases amount of blood

clotting platelets

1.25 ng/kg/min

4 hours

Hypotension

Arrythmias

Flolan/Veletri

Pulmonary HTN

Synthetic prostaglandin

that dilates blood vessels

and decreases stickiness of

platelets

2 ng/kg/min

Within

minute

3-5

minutes

Hypotension

Tachycardia

Chest pain

Standard of Care: Cardiac

Sedatives

Diprivan (Propofol)

Procedures

requiring sedation

Mechanically

vented adults

Short acting. Decreases

level of consciousness

5-50

mcg/kg/min

second

3-12 hr

Consider dose and ability

to follow commands/

participate in PT

Precedex

(Dexmedetomdine)

Procedures

requiring sedation

Mechanically

vented adults

Can provide semi-arousal

sedation.

Provides sedation without

high risk of respiratory

depression

0.2-0.7

mcg/kg/hr

1 min

~2 hours

Consider dose and ability

to follow commands/

participate in PT

Versed

(Midazolam)

Used to produce

amnesia

Anxiety

Depresses the CNS. Used

commonly for procedures

that do not require general

anesthesia; causes

relaxation

1-30

mg/hr

1-5

min

~3 hours

Consider dose and ability

to follow commands/

participate in PT

Nimbex

(Cisatracurium)

Surgical

procedures

Mechanically

assisted

breathing, or

insertion of

breathing tube.

Skeletal muscle relaxant

that blocks the effects of

acetylcholine.

1-10

mcg/kg/min

2-3

min

22 minutes

Hold PT, pt paralyzed and

unable to participate

Standard of Care: Cardiac

Appendix 3

Parameter

Normal Range

Clinical Significance

Pulmonary Artery

Pressure (PAP)

20-30 mmHg/0-6

mmHg

Indicates state of resistance in pulmonary vasculature and

right ventricle function

↑: pulmonary artery hypertension, COPD or emphysema,

PE, pulmonary edema

Pulmonary Artery

Wedge Pressure

(PAWP)

4-12 mmHg

Indicates left ventricle function

↑: LV failure with pulmonary congestion

↓: LV compliance (hypertrophy, infarction)

Central Venous

Pressure (CVP)

0-6 mmHg

Indicates volume status and right ventricle function

↑: overhydration, increased venous return, RV failure

↓: hypovolemia, decreased venous return

Stroke Volume (SV)

60-80 mL/beat

Amount of blood ejected during systole

↓: impaired cardiac contractility, valve dysfunction

Cardiac Output

(CO) = Stroke

Volume (SV) x Heart

Rate (HR)

4-8 L/min

Amount of blood ejected from the left ventricle in 1

minute

↓: decreased volume, decreased strength of ventricular

contraction

Cardiac Index (CI)

2.5- 4 L/min

Relates cardiac output (CO) to body surface area (BSA);

CI = CO/BSA

↑: high-output failure due to fluid overload, renal disease,

septic shock

↓: CHF, hypovolemia, cardiogenic shock

Mixed Venous

Oxygen Saturation

(SvO2)

60-75%

Index of oxygenation status that measures that relationship

between O2 delivery and O2 demand; reflects

cardiovascular tissue perfusion

PAC wave forms

Standard of Care: Cardiac

References:

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