Unit 6 - Management Considerations in Cardiac Rehab and Special Topics

Cardiac Rehabilitation Re-assessment:

PTs should routinely review a patient's progress to:

• make program adjustments

• identify remaining risk factors

• set new short-term goals

Cardiac Rehabilitation Re-assessment:

PTs should perform reexaminations and consider diagnostic tests to determine whether patients are progressing

• Vital signs and telemetry – rest and in response to physical activity

• Subjective reporting with activity (e.g., dyspnea, RPE)

• Outcome measures

• Quality of Life (QoL) measures

• Physical activity behavior

• Absolute measures of strength or aerobic capacity where available

• Medical diagnostic tests (e.g., echocardiography, radiographs, blood glucose, lipids) as applicable

Cardiac Rehabilitation Re-assessment

• Each clinical note should include documentation of patient progression to justify the ongoing need for skilled services

• Consider Minimal Clinically Important Differences (MCID)

Outcomes: What are our expectations?

• Cardiac rehabilitation should be able to improve on many of an individual’s body structure/function impairments, activity limitations, and participation restrictions where they are related to cardiorespiratory and some musculoskeletal impairments (e.g., weakness) and decreased health knowledge and behaviors.

  • We should generally expect that a competently structured plan of care should improve an individual’s functional capacity, exercise tolerance, and overall quality of life

  • Some changes should be expected within the short term and others take longer

Outcomes: Expectations for objective measurements

• Exercise training has been shown to reduce myocardial oxygen demand during submaximal efforts via decreased heart rate and blood pressure responses.

• Increases in aerobic capacity should provide for an increased tolerance for daily life activities consisting of repeated submaximal physical exertion

• Cardiac rehabilitation has been shown to improve on measures of physical capacity and health knowledge

  • Examples: 6 Minute Walk Test, peak oxygen consumption, 1-RM assessment, functional strength (e.g., Five Times Sit to Stand), Cardiac Knowledge Questionnaire

The greatest improvements are often found in patients with the lowest initial maximum oxygen consumption levels.

Making Adjustments

PTs should consistently correlate outcome assessments with goals established by the therapist and patient

Making Adjustments:

When patient progress falls short of expectations, we should consider

• Patient compliance with our recommendations

  • Are there any modifiable barriers to compliance?

• Our dosage of interventions

  • Is the dosage sufficient enough to create the change we’re looking for?

  • Are there signs that the dosage is excessive (e.g., overtraining)?

• If our assumptions regarding how anatomical and physiological abnormalities relate to the desired activity and participation outcomes are valid

Heart Transplant

• First successfully performed in 1967

• 3700 per year performed in the United States

• 90% 1-year survival rate

Why Might Someone Need a Heart Transplant?

• End Stage Heart Failure

• Congenital Heart Defects

• Restrictive Cardiomyopathy

• Significant Heart Valve Disease

• Pulmonary Arterial Hypertension

• Damage from Infection/Chemo

• Chronic Lung Disease

Anatomical Changes (Heart Transplant)

New Heart Innervation

• Preganglionic sympathetic and parasympathetic fibers are severed

• Postganglionic fibers remain

• Higher resting heart rate

• Alpha and Beta receptors are still present

PT Implications (Heart Transplant)

• No sympathetic or parasympathetic innervation

• Ionotropic input remains

  • Frank Starling mechanism to increase Stroke Volume

  • Circulating catecholamines increase heart rate

• Increased warm-up and cool-down times

• Heart Rate and Blood Pressure monitoring is essential

• Your patient can and SHOULD still exercise!

PT Implications (Heart Transplant): Signs and Symptoms of Organ Rejection

• Constitutional

  • Fatigue, weakness, fever, chills, malaise, nausea, loss of appetite

• Respiratory

  • Shortness of breath, cough, decreased peak flow or incentive spirometry, decreased O2 saturation

• Cardiac

  • Tachycardia at rest, new arrhythmias, drop in blood pressure

• Typical S&S of Heart Failure

  • Fluid Overload/Hypervolemia

PT Implications (Heart Transplant): New Comorbidities

• Type 2 Diabetes

• Viral Infections

• Immune suppression

• Anxiety

• Osteoporosis

• Wounds

• Airway Clearance

• Frailty

Common Cardiac Rhythm Disturbances that Impact Athletes

• PVCs

• SVT

• V-Tach

• Atrial Fibrillation

Atrial Fibrillation in Athletes

• 6 times more likely but typically asymptomatic

• Not impacted by position played

• Significant Increase in risk for clotting

  • CVA

  • Heart Failure

  • MI

• Often significantly tachycardic when symptomatic

  • Usually seen as SVT

• Cause is unknown but…

Potential Causes of A-Fib in Athletes

• Exercise-Induced Atrial Hypertrophy and Fibrosis

• Left Ventricular Hypertrophic Cardiomyopathy

• Left Ventricular Hypertrophic Cardiomyopathy: Congenital Hypertrophic Cardiomyopathy

• Hypertension due to long-term NSAID use

Potential Causes of A-Fib in Athletes: Exercise-Induced Atrial Hypertrophy and Fibrosis

• Scarring due to prolonged preload

  • Microinflammation of atrial lining

  • Scarring creates ectopic foci

    • Reduces control of SA node

    • Increased parasympathetic drive and decreased sympathetic drive

    • Persists for decades

Potential Causes of A-Fib in Athletes: Left Ventricular Hypertrophic Cardiomyopathy

• Can be a normal side effect of intensive cardiovascular training but…

  • Can be dangerous when it progresses too far

  • Impaired cardiac conduction

    • Tissue dysfunction

    • Rhythm disturbances

    • Reduced Cardiac Output

Potential Causes of A-Fib in Athletes: Left Ventricular Hypertrophic Cardiomyopathy: Congenital Hypertrophic Cardiomyopathy

• Second most common cardiomyopathy in children

• Typically goes undetected

• Can result in sudden cardiac death

• RED FLAGS:

  • SOB with activity, presyncopal/syncopal episodes, palpitations, chest pain/tightness

Potential Causes of A-Fib in Athletes: Hypertension due to long-term NSAID use

• NSAID use starts early

• Contributes to Maladaptive Cardiovascular Changes

• Influence of COX-2 pathway inhibition

  • “-coxib” drugs

  • COX-1 drugs: “-dac” and “-fen” drugs (+others)

• AHA Recommendations for judicious use

Commotio Cordis

“Shot to the Heart”

• A sudden and violent impact to the chest causes electrical abnormality to the point of stopping electrical activity in the heart.

  • Hockey puck

  • Tackle

  • Kick/Punch

• Extremely Rare but…

  • Baseball has highest risk, followed by football

Identifying Commotio Cordis

• Athlete displays a drop after a blow to the chest

• Pulseless and unconscious

• AED and CPR are critical to ROSC

• ICD not helpful, return to play after cardiac clearance

Sickle-Cell Trait: Training Considerations

• Slow start to training

• Hydration is critical

• Avoid very intense training sessions

• Gradual accommodation to elevation, heat, or humidity

• Avoid stimulants (energy drinks)

Sickle-Cell Trait: Symptoms of Exacerbation

• Muscle tenderness, pain, weakness, or cramping

• Inability to cool down, even with rest

• Prolonged fatigue after activity

• Rapid respirations

Concussion

• Type of tissues impacted

  • Midbrain

  • Brainstem (Diffuse Axonal Injury)

  • Cranial Nerves

• These contribute to heart rate modulation and vasodilation/constriction!

  • HR, Rhythm, and BP all impacted

  • Leads to A-fib and other arrythmias

The Role of the PT in Sideline Management

• Screening & Prevention

• Emergency Response

• Intervention

Role of the PT in Emergency Response

The Smart Heart Sports Coalition Initiatives

• Emergency Action Plans (EAPs) for each athletic venue

• Clearly marked automated external defibrillator (AEDs) at each athletic venue

• CPR and AED education for coaches

Ventricular Assist Device (VAD)

• sed in patients who have endstage heart failure

• Can be Right, Left, or Both (BiVAD).

• External power sources provide power through a drive line into the body that runs a pump that circulates blood, offloading the work of the heart.

• Pump Settings can be read externally on device interface

Ventricular Assist Device (VAD): Purpose

• Bridge to Transplant

• Terminal Device

Ventricular Assist Device (VAD): PT Implications

• Increased risk of infection

  • Take temperature

• No heart rate or pulse

• No diastolic BP (if left-sided)

  • Will have systolic

  • Must use Doppler to take SBP

• No BP (if right-sided or BiVAD)

• VAD settings are the patient’s vitals

• Native vitals may still be measurable

VADs in Pediatrics

• there isn't enough space in the mediastinum for the VAD

• cannulas are used to reach the heart while the pump is located outside of the body

VADs: What you need to know

• Not an entry-level skill

• Ongoing on-the-job training required

• Can be seen in any setting!

• Patient is the expert on their device

Introduction to Congenital Heart Defects: Prevalence and Impact

• Occurs in 6-8 per 1,000 live births.

• Accounts for 3% of all infant deaths and 46% of deaths from congenital malformations

Introduction to Congenital Heart Defects: Classification

• Cyanotic: Reduced oxygen saturation (e.g., cyanosis).

• Acyanotic: Normal oxygen saturation but potential for cardiac strain

Introduction to Congenital Heart Defects: Key Fetal Circulatory Structures

• Foramen ovale: Right-to-left atrial shunt bypassing the lungs.

• Ductus arteriosus: Connects pulmonary artery to the aorta

Introduction to Congenital Heart Defects: Clinical Relevance

• Defects result in disrupted blood flow, shunting, or mixing of oxygenated and deoxygenated blood.

• Impacts exercise tolerance, oxygen delivery, and fatigue level

Septal Defects

• Atrial Septal Defect (ASD)

• Ventricular Septal Defect (VSD)

Septal Defects: Atrial Septal Defect (ASD)

• Patent foramen ovale → left-to-right atrial shunting.

• Symptoms: Heart murmur, pulmonary artery enlargement

• Typically asymptomatic early; surgery by age 2-3 if not closed

Septal Defects: Ventricular Septal Defect (VSD)

• Openings in ventricular septum → left-to-right shunting.

• Small defects may close spontaneously; large defects → CHF, pulmonary complications.

• Symptoms: Feeding issues, poor weight gain, rapid breathing, irritability

• Surgery if symptoms persist or defect remains after early childhood

Septal Defects: Clinical Implications for PT

• Monitor for activity intolerance: tachypnea, fatigue, cyanosis.

• Consider cardiopulmonary limitations even after repair.

• Tailor interventions to improve endurance and safety during activity

Obstructive Defects

• Coarctation of the Aorta

• Hypoplastic Left Heart Syndrome (HLHS)

Obstructive Defects: Coarctation of the Aorta

• Narrowing of the aorta → increased proximal pressure, decreased distal pressure.

• Symptoms: Upper body hypertension, weak/absent lower extremity pulses.

• Management: Surgical repair

• PT Considerations: Monitor for hypertension and poor lower extremity perfusion

Obstructive Defects: Hypoplastic Left Heart Syndrome (HLHS)

• Underdeveloped left ventricle, aortic and mitral valve stenosis/atresia.

• Dependent on PDA for systemic blood flow; ductus closure → severe CHF.

• Management: Mechanical ventilation, palliative surgeries.

• PT Considerations: Tailor interventions to address cardiopulmonary limitations; prevent overexertion

Patent Ductus Arteriosus (PDA): Pathophysiology

• Failure of ductus arteriosus to close → blood shunting from aorta to pulmonary artery.

• Leads to increased pulmonary blood flow and heart/lung workload

Patent Ductus Arteriosus (PDA): Risk Factors

Prematurity, respiratory distress syndrome (RDS), hypoxia

Patent Ductus Arteriosus (PDA): Symptoms

• Tachycardia, respiratory distress, poor weight gain (large PDA).

• May be asymptomatic if the opening is small

Patent Ductus Arteriosus (PDA): Management

• Medical: Indomethacin or ibuprofen to reduce prostaglandin production.

• Surgical: Minimally invasive closure (ligation) if symptoms persist

Patent Ductus Arteriosus (PDA): Clinical Implications for PT

• Monitor for signs of activity intolerance (fatigue, dyspnea, tachypnea).

• Address residual cardiopulmonary limitations through carefully tailored interventions