Unit 3 - Sources of Cardiac Muscle Dysfunction

Arrhythmia

• any irregularity in the heart's normal rhythm, whether that rhythm is too fast, too slow, or simply out of sync

• can arise spontaneously or in response to acute or chronic cardiac conditions

• can also arise as a side effect of medications or as a consequence of other medical conditions, such as electrolyte imbalances

• can originate from the atria or the ventricles

Atrial Arrhythmias

• Structural Issues: coronary artery disease (CAD), hypertensive heart disease, valvular defects

• Thyroid Dysfunction

  • Hyperthyroidism can increase excitability

• Substance Use

• Electrolyte Imbalances: K+, Mg2+

Ventricular Arrhythmias

• Ischemic Heart Disease

• Cardiac Remodeling: Dilated/hypertrophic myocardium

• Cardiomyopathies: Hypertrophic, dilated types

• Drug Effects: Antiarrhythmics, proarrhythmic drugs

Effective medical management of arrhythmias involves…

addressing underlying pathologies, adjusting lifestyle factors, and targeted pharmacotherapy

What is Atrial Flutter?

An atrial arrythmia characterized by rapid, regular atrial activity at a rate of 250-350 bpm

Atrial Flutter

• The structural and functional changes to the atrial myocardium following an MI or other sources of myocardial injury (e.g., surgery) can alter normal electrical conduction paths and set up a reentrant circuit.

• Can also occur in individuals with other preexisting heart conditions (e.g., valvular disease, pericarditis), have renal failure, hypertension, or chronic lung disease.

• May be paroxysmal/transient, persistent (lasting days or weeks), or permanent

Atrial Flutter ECG

• Because it is generally due to the regular depolarization of one area of the atria throughout each cycle (i.e., a single reentry circuit), the P waves appear identical to one another and give off a “sawtooth” appearance.

• Many of the fast impulses that reach the AV node occur during its refractory period and do not conduct to the ventricles, resulting in a slower ventricular rate (e.g., 2:1 or 3:1 atrial:ventricular rate).

What is Atrial Fibrillation?

• an erratic quivering or twitching of the atrial muscle that is caused by multiple ectopic foci and/or multiple reentry circuits

• the most commonly encountered arrhythmia in medical practice and accounts for 1/3rd of cardiac hospitalizations

  

Atrial Fibrillation ECG

• Since none of the ectopic foci actually depolarize the atria, no true P waves are found.

• The AV node acts to control the most of the impulses that initiate a QRS complex; therefore, a totally irregularly irregular rhythm exists between the AV node pacemaker activity and random bouts of electrical activity in the atria that summate to depolarize the AV node

Conditions that increase atrial pressures in Atrial fibrillation

• It is more common in enlarged atria with more space for dysfunctional circuitry. Following a myocardial infarction, inflammation and catecholamine release disrupt atrial electrophysiology and promote fibrosis, leading to structural changes like atrial dilation that exacerbate conditions favorable for the onset and persistence of atrial fibrillation.

  • Heart Failure

  • Hypertension

  • Pulmonary Disease

What to consider with atrial flutter and fibrillation?

• are not, in and of themselves, considered immediately life-threatening, they can lead to serious and potentially life-threatening complications if not properly managed

  • Stroke risk due to blood stasis

  • Induce heart failure via tachycardia-induced cardiomyopathy

Symptoms of both atrial flutter and fibrillation…

will largely depend on underlying ventricular rate

Medical options for treating atrial flutter and fibrillation include:

• Cardioversion: a medical procedure that aims to restore a normal heart rhythm

• Medications:

  • Rate Control Medications: beta-blockers (e.g., metoprolol) and calcium channel blockers (e.g., diltiazem)

  • Rhythm Control Medications: Antiarrhythmic drugs (e.g., amiodarone) work by altering the electrical signals in the heart to maintain a normal rhythm

  • Anticoagulants (e.g., warfarin, apixaban): prevent the formation of blood clots in the heart

PTs can play a critical role in managing patients with atrial flutter & fibrillation by ensuring safe and effective rehabilitation strategies:

• Activity Tolerance: fatigue, palpitations, shortness of breath, or chest pain can worsen with exertion.

• Pulse Monitoring: Pulse oximeters may be inaccurate in AFib. Consider assessment of physical pulse for a full minute.

  • Use stethoscope for apical pulse if still unsure.

  • Consider using RPE for exercise.

• RVR Concern: New-onset AFib with rapid ventricular response (RVR) >100 bpm at rest is concerning.

Premature Ventricular Contractions (PVC)

occur when an ectopic focus (or foci, in the case of multifocal PVCs) creates an impulse from somewhere in one of the ventricles. It occurs early in the cardiac cycle before the SA node actually fires

Premature Ventricular Contractions (PVC) ECG

• The QRS complex is wide and bizarre and occurs earlier than normal sinus beat would have occurred.

  • It is wide because of slow cell-to-cell connections rather than through the normal rapidly conducting His-Purkinje system

• **There are no P waves**

PVCs are…

common even among healthy people and are often asymptomatic and benign. In patients without heart disease, they usually pose no risk of life-threatening arrhythmias

PVCs can indicate…

underlying cardiac disorder and may suggest increased risk of serious ventricular arrhythmias, especially if frequent or multifocal

Serious PVCs

• More than 10 per minute at rest

• Occur consecutively

• Multifocal origin

  

Physical exam note on PVCs

can be palpated as a skip or pause in the pulse. This may misleadingly suggest a lower HR during exercise when, in fact, arrhythmias have increased

Trigeminy

every third beat is a PVC, with two normal beats in between

Bigeminy

• every other beat is a PVC, creating an alternating pattern between a normal beat and a PVC.

• Because it has a higher PVC frequency, it is generally more concerning

  

Couplet

• two PVCs occur consecutively

• suggest heightened ventricular ectopy, their clinical significance depends on the underlying cardiac condition

• may indicate increased ventricular irritability and a higher risk of progressing to sustained arrhythmias, such as ventricular tachycardia

  

Triplet

• three PVCs occur consecutively

• considered a brief run of what is called non-sustained ventricular tachycardia if they occur at a rate of 100 beats per minute or higher

  

Multifocal PVC

• originate from multiple ventricular foci from different areas of the ventricles

• clinically more concerning than unifocal PVCs because they suggest greater ventricular irritability, increasing the risk of more serious arrhythmias, particularly in patients with underlying heart disease

• considered a red flag in clinical practice

  

Ventricular Tachycardia (V-Tach)

• a life-threatening arrhythmia defined as three or more consecutive PVCs at a rate exceeding 100 beats per minute, often reaching between 150 and 250 beats per minute

• indicates extreme electrical instability in the ventricles and is often a precursor to even more lethal arrhythmias, like ventricular fibrillation

  

The rapid heart rate Ventricular Tachycardia (V-Tach)…

• shortens ventricular filling time and leads to inefficient, uncoordinated contractions, drastically reducing cardiac output

  • This results in a significant drop in blood pressure, hemodynamic instability, and, without intervention, rapid progression to loss of consciousness, cardiac arrest, or sudden death

V-tach symptoms

lightheadedness and syncope, as reduced cardiac output can impair perfusion to vital organs

Ventricular Fibrillation (V-Fib)

• chaotic, uncoordinated electrical activity in the ventricles, causing the heart to, essentially, just quiver rather than pump blood

• results in virtually no cardiac output, depriving vital organs of blood flow

• Without immediate intervention, it is fatal within minutes

  

Ventricular Fibrillation (V-Fib) ECG

a rapid, erratic waveform with no recognizable QRS complexes, P-waves, or T-waves

Asystole

• the most severe form of cardiac arrest, characterized by complete absence of electrical activity in the heart

• indicates that the heart is no longer generating impulses, resulting in no cardiac output and no blood flow to the body

• non-shockable, meaning defibrillation is ineffective

• treatment focuses on immediate CPR to manually circulate blood and administration of emergency medications, such as epinephrine, to stimulate the heart and restore electrical activity

AV heart blocks

• conduction disorders caused by delays or interruptions in the heart's electrical system, disrupting the coordination between the atria and ventricles

• vary in severity based on the exact location and extent of conduction impairment

• first-degree, second-degree, third-degree

First-degree AV block

PR interval > 200 ms; delay at the AV node

Second-degree AV block

• Mobitz Type 1 (Wenckebach): Progressive PR lengthening until a beat is dropped (P wave not conducted).

  

• Mobitz Type 2: Fixed PR interval; intermittent non-conduction of P waves. Often involves a bundle branch block

  

Third-degree AV block

• Complete block

• No AV conduction; atrial and ventricular rhythms are independent

  

Cardiac rhythm assessment is used to…

identify and understand common to life-threatening arrhythmias. A regular rhythm expected during exercise; changes in arrhythmia with activity require careful evaluation

Considerations for clinical decision-making

• Is the arrhythmia new or changing in character with increased activity?

• Is the arrythmia benign or life-threatening?

• Is the arrhythmia producing new or worsening symptoms?

Clinical tips

• Individuals experiencing intermittent arrhythmias might not exhibit arrhythmic events during every bout of increased activity.

• Arrhythmias that are effectively managed with medication while at rest can sometimes become less controlled or more pronounced during physical exertion

Hypertensive Heart Disease

• Left Ventricular Hypertrophy (LVH)

  • Thickening of the left ventricle wall to counteract increased vascular resistance; stiffens myocardial structures

  • creates a continuous afterload challenge

Hypertensive Heart Disease Results

• Decreased Compliance & Diastolic Dysfunction:

  • Impaired ventricular filling and relaxation, reducing preload and stroke volume, particularly during exertion.

• Impaired Coronary Reserve:

  • Limited oxygen supply during exercise heightens the risk of myocardial ischemia, atrial fibrillation, and ventricular dysrhythmias.

• Reduced Cardiac Output:

  • Symptoms include lightheadedness, dizziness, dyspnea, and decreased exercise tolerance

Valvular dysfunction can…

develop acutely (e.g., valvular rupture) or chronically (e.g., due to atherosclerotic changes)

Valvular dysfunction can lead to…

• Stenosis:

  • Narrowing of the valve opening, increasing pressure gradients and leading to ventricular hypertrophy.

• Regurgitation:

  • Valve fails to close properly, causing backflow, volume overload, and potential dilation of chambers.

• Prolapse:

  • Valve leaflets bulge backward, disrupting the seal, often seen in the mitral valve.

• Chronic pressure or volume overload can lead to structural changes in the heart that can cause issues in both systole and diastole

Acute Valvular Dysfunction

Sudden cardiac output impairment; requires immediate surgical intervention.

Acute Valvular Dysfunction: Clinical Presentation

Sudden heart failure, severe dyspnea, chest pain, hypotension.

• Example: Acute mitral regurgitation → volume overload → cardiogenic shock.

Acute Valvular Dysfunction: Management

Emergency valve repair/replacement

Chronic Valvular Diseases

Gradual onset due to degeneration, calcification, or congenital anomalies

Chronic Valvular Diseases: Clinical Presentation

Gradual symptoms like exertional dyspnea, fatigue, angina.

• Example: Chronic aortic stenosis → left ventricular hypertrophy → compensated cardiac output

Chronic Valvular Diseases: Management

Monitoring, medical therapy, timely surgical intervention

Diagnostic Techniques for Valvular Function Assessment

integral to the medical clinical decision-making process as they guide the timing and type of interventions, from medical management to surgical procedures valve repair or replacement

• Echocardiography

• Cardiac Catheterization

• Other diagnostics: ECG, chest X-ray; vital for assessing cardiac function

Early recognition and management of valvular problems are crucial to prevent catastrophic outcomes

Echocardiography

• TTE: Non-invasive, visualizes valve anatomy, function, and blood flow.

• TEE: Detailed images, especially for mitral valve and prosthetic valves.

• Stress Echo: Evaluates valvular function under stress conditions

Cardiac Catheterization

Assesses severity of stenosis/regurgitation, critical for surgical planning

Medical Management of Severe Valvular Disease

• Surgical Interventions

• Percutaneous Interventions

Medical Management of Severe Valvular Disease: Surgical Interventions

• Valve Repair: Preserves the native valve; techniques include annuloplasty and chordal procedures.

• Valvulotomy: Incisions to relieve stenosis, often for congenital issues.

• Valve Replacement:

  • Mechanical Valves: Durable, require lifelong anticoagulation.

  • Bioprosthetic Valves: Made from animal tissue, no long-term anticoagulation needed, shorter lifespan

Medical Management of Severe Valvular Disease: Percutaneous Interventions

• Transcatheter Aortic Valve Replacement (TAVR): Minimally invasive for severe aortic stenosis, especially in high-risk patients.

• Percutaneous Balloon Valvuloplasty: Dilation to improve valve function and flow

Medical Management of Severe Valvular Disease: Advancements

Minimally invasive techniques and potential innovations like regenerative medicine aim to
improve outcomes

PT Considerations in Acute Recovery from Valvular Surgery

• Minimally invasive surgeries and repairs

• Valvular Replacements

PT Considerations in Acute Recovery from Valvular Surgery: Minimally invasive surgeries and repairs

• Smaller incisions are associated with less pain and quicker recovery which can allow for faster progression of activities toward pre-operative function.

• Repairs preserve native valve tissue, leading to more physiological function and quicker activity progression compared to replacements

PT Considerations in Acute Recovery from Valvular Surgery: Valvular Replacements

• Open-heart valve replacements or complex multi-valve surgeries often require longer recovery times and a more conservative approach to physical therapy to prevent excessive strain on the heart and surgical site.

• PTs should be cautious in advancing activities, considering the higher risk of post operative complications and slower healing

PT Considerations in Acute Recovery from Valvular Surgery: Monitoring Considerations

• Hemodynamic Stability:

  • Monitor for changes in cardiac output, dyspnea, fatigue, or abnormal rhythms.

• Incision Sites:

  • Inspect for infection or dehiscence.

• Bleeding:

  • Long-term anticoagulation increases bleeding risk. PTs should monitor for bleeding and educate patients on recognizing warning signs

Cardiomyopathies

• Structural & functional abnormalities are not primarily due to CAD, HTN, valvular disease, or congenital defects.

  • Leads to systolic or diastolic dysfunction, heart failure, arrhythmias, or sudden death.

• Differentiated by:

  • Functional Categories: Dilated, hypertrophic, restrictive.

  • Causal Viewpoint: Genetic, acquired, or mixed

Cardiomyopathies: Diagnostic Tools

Echocardiography and myocardial biopsy distinguish between types

Dilated Cardiomyopathy (DCM)

• Mitochondrial Dysfunction and Dilation:

  • primarily involves mitochondrial dysfunction in the heart muscle, reducing energy availability and impairing the heart's ability to pump effectively, leading to ventricular dilation as the heart compensates for decreased contractility.

• Systolic Dysfunction:

  • The primary concern is systolic dysfunction leading to reduced ejection fraction and cardiac output

Hypertrophic Cardiomyopathy (HCM)

• Myocardial hypertrophy:

  • characterized by asymmetrical myocardial hypertrophy, myocardial disarray, rapid ventricular emptying and a preserved or slightly elevated ejection fraction.

• Diastolic Dysfunction:

  • Increases LV end-diastolic pressure and predisposes to arrhythmias and sudden cardiac death. It is the leading cause of sudden cardiac death in young athletes in the USA

Common Concerns in both Dilated Cardiomyopathy (DCM) & Hypertrophic Cardiomyopathy (HCM)

• Arrhythmias:

  • require vigilant monitoring for arrhythmias; adjusting exercise based on risk

• Hypotension:

  • Both present a significant risk of exercise-induced hypotension due to their respective impacts on cardiac output, necessitating careful monitoring and cautious progression in exercise intensity to prevent sudden drops in blood pressure

Conditions that can contribute to heart failure

• HTN

• CAD

• cardiac dysrhythmia

• renal insufficiency

• cardiomyopathy

• heart valve abnormality

• pericardial effusion

• pulmonary embolism

• pulmonary hypertension

• spinal cord injurt

• age-related conditions

Heart Failure: Systolic

• impaired cardiac contractile function, where the left ventricle cannot pump blood effectively, resulting in a reduced ejection fraction

• Some Causes

  • Ischemic Heart Disease

    • Myocardial Infarction, Transient/persistent myocardial ischemia

  • Dilated Cardiomyopathy

    • Idiopathic (~50% of cases), Viral, Familial/Genetic, Alcohol, and many more

  • Valvular Heart Disease

    • Aortic valve stenosis or regurgitation, mitral valve stenosis or regurgitation

Hear Failure: Diastolic

• impaired filling of the left or right ventricle due to hypertrophy and/or changes in the composition of the myocardium

• Some causes

  • Left Ventricular Hypertrophy

  • Restrictive Cardiomyopathy

  • Myocardial fibrosis

  • Pericardial effusion or tamponade

Heart Failure: HFrEF vs HFpEF

Due to overlap between systolic and diastolic dysfunction (i.e., many patients with HF suffer from both) and the widespread use of echocardiograms

HFrEF

Heart Failure with reduced ejection fraction

• <40% EF

• indicating impaired contractility and systolic dysfunction

• falls below 40% due to weakened or damaged ventricular muscle, reducing the heart's ability to contract forcefully and expel sufficient blood during systole

HFpEF

Heart Failure with preserved ejection fraction

• >50% EF

• reflects preserved contractility but impaired relaxation and filling characteristic of diastolic dysfunction

• Thickened and stiffened ventricular walls, as seen in conditions like left ventricular hypertrophy, limits the heart's capacity to accommodate returning blood

Heart failure with midrange ejection fraction

• intermediate zone between 40% and 50%

• shares characteristics of both HFrEF and HFpEF

Responses to decreased cardiac output include the activation of sympathetic nerves and the renin-angiotensin-aldosterone system in order to:

• Increase myocardial contractility and heart rate

• Produce arterial vasoconstriction (to help maintain arterial pressure)

• Produce venous constriction (to increase venous pressure)

• Increase blood volume (to increase preload/ventricular filling)

Increase activity in sympathetic nervous system wil…

stimulate myocardial contractility, heart rate, and arterial/venous tone which results in an increase in central blood volume which serves to further elevate preload (to attempt to increase cardiac output).

Over time, though, the heart becomes insensitive to B-adrenergic stimulation, which results in a decreased force of myocardial contraction and an inability to attain higher heart rates during physical exertion

Declining cardiac output causes…

a reduction in renal blood flow and glomerular filtration rate, which leads to sodium and fluid retention. The RAAS is also activated, leading to further increases in peripheral vascular resistance and LV afterload as well as sodium retention

As cardiac muscle dysfunction worsens…

the heart becomes less and less able to tolerate the increases to afterload/systemic vascular resistance that aims to maintain arterial pressure

The body has ways to compensate for declining cardiac output and include increasing B-adrenergic stimulation and activation of the RAAS system:

B-adrenergic stimulation becomes less effective over time and the RAAS system can eventually work against the heart’s function

As cardiac muscle dysfunction worsens, the heart becomes less sensitive to preload and less able to tolerate increases to afterload. This should help us remember that we should be vigilant in monitoring for:

• Fluid Status: reduced sensitivity to preload impairs the heart's ability to pump efficiently, leading to fluid retention as the kidneys compensate for perceived low blood volume.

• Conditions that create excessive afterload such as unmanaged hypertension which can place additional strain on the heart, exacerbating myocardial workload and potentially worsening heart failure

Heart Failure: ACC/AHA Staging

Stage A to D

ACC/AHA Staging: Stage A

• high risk for developing CHF

• no structural disorder of heart

ACC/AHA Staging: Stage B

• structural disorder of heart

• never developed symptoms of CHF

ACC/AHA Staging: Stage C

• past or current symptoms of CHF

• symptoms associated with underlying heart disease

ACC/AHA Staging: Stage D

• end-stage disease

• requires specialized treatment strategies

Heart Failure: NYHA Staging

Class I to IV

NYHA Staging: Class I

no limitation of physical activity

NYHA Staging: Class II

• slight limitation of physical activity

• comfortable at rest

NYHA Staging: Class III

• marked limitation of physical activity

• comfortable at rest

• Class IIIa or IIIb

NYHA Staging: Class IIIa

no dyspnea at rest

NYHA Staging: Class IIIb

recent dyspnea at rest

NYHA Staging: Class IV

• inability to carry on any physical activity without discomfort

• symptoms present even at rest

The most common symptom experienced by individuals living with heart failure?

dyspnea

What can cause dyspnea?

• Interstitial edema

• Pulmonary edema

• Reduced respiratory muscle blood flow

Interstitial edema

Lungs become heavy and difficult to move

Pulmonary edema

Fluid transudation into alveoli increases the work of breathing

Reduced respiratory muscle blood flow

Decreased cardiac output and lactic acid accumulation exacerbate dyspnea

What can cause Pulmonary Crackles/Rales?

• fluid in alveolar spaces

• Heard at lung bases

Pulmonary Crackles/Rales: Caused by fluid in alveolar spaces

due to elevated pulmonary pressures

Pulmonary Crackles/Rales: Heard at lung bases

potentially extending upward with increased severity or changes in position

Orthopnea

• Dyspnea when lying flat due to fluid redistribution from the abdomen and legs to the lungs.

• Relief:

  • Sitting up or sleeping with extra pillows

    • number of pillows used indicates severity

Paroxysmal Nocturnal Dyspnea (PND)

• Severe breathlessness and coughing that wake the patient 1-3 hours after lying down.

• Cause:

  • Reabsorption of interstitial fluid from the lower extremities back into circulation, increasing venous return and load on the heart.

• Relief:

  • Sitting upright or standing provides relief, but symptoms can persist

Extra Heart Sounds: S3

• (aka ventricular gallop) indicates a more compliant left ventricle. Thought to occur as blood passively fills a quickly distending left ventricle that makes contact with the chest wall during early diastole.

  • May be normal (“physiologic S__”), particularly in young people, but in the presence of other indicators of heart disease, it is one of the most sensitive indicators of significant ventricular dysfunction