Ch 27: Disorders of Cardiac Function, Heart Failure, and Circulatory Shock

Disorders of Cardiac Function, Heart Failure, and Circulatory Shock

Disorders of the Pericardium

  • Definition of the Pericardium

    • A double-layered serous membrane

    • Separated by a space, the pericardial cavity

    • Contains about 50 mL of serous fluid

      • Acts as a lubricant that prevents frictional forces during heart contractions and relaxations

  • Functions of the Pericardium

    • Isolates the heart from other thoracic structures

    • Maintains heart's position in the thorax

    • Prevents overfilling of the heart

    • Contributes to the coupling of distensibility between the ventricles during diastole, ensuring both fill equally

  • Conditions Affecting the Pericardium

    • Congenital disorders

    • Infections

    • Trauma

    • Immune mechanisms

    • Neoplastic disease

    • Pericardial disorders often associated with other diseases in the heart or surrounding structures

  • Acute Pericarditis

    • Defined by clinical manifestations resulting from pericardial inflammation lasting less than 2 weeks

    • Diagnosis often includes ECG, chest radiography, and echocardiography

    • Friction rub (see Fig. 27.1) observed

  • Chronic (Relapsing) Pericarditis

    • Related to recurrent bouts of pericardial pain

    • May exhibit chronic and debilitating symptoms

    • Commonly associated with autoimmune disorders and viral infections

  • Pericardial Effusion

    • Accumulation of fluid in the pericardial cavity

    • Typically due to inflammatory or infectious processes

    • Signs and symptoms reflect right-sided heart failure

    • Can lead to life-threatening Cardiac Tamponade

      • Characterized by slow or rapid compression of the heart due to fluid, pus, or blood in the pericardial sac

      • Exhibits pulsus paradoxus (see Fig. 27.2)

  • Constrictive Pericarditis

    • Development of calcified scar tissue between the visceral and parietal layers of the pericardium

    • Results in fixed cardiac output and cardiac reserve

    • Symptoms may include ascites, pedal edema, dyspnea on exertion, fatigue, and Kussmaul sign

Assessment and Understanding of Conditions

  • Question #1

  • Which of the following conditions results in pathological changes due to pulseless electrical activity?

    • Pericardial effusion

    • Cardiac tamponade

    • Pericarditis

  • Answer to Question #1

    • B. Cardiac Tamponade

    • Rationale: Cardiac tamponade restricts muscle movement and inhibits ventricular contraction, while conduction remains intact leading to minimal to no stroke volume.

Coronary Artery Disease (CAD)

  • Definition

    • Heart disease caused by impaired coronary blood flow due to atherosclerosis

  • Coronary Circulation (see Figs. 27.3 and 27.4)

    • Supplies the heart muscle with oxygen and nutrients necessary for pumping blood

    • Major arteries involved include:

      • Left main coronary artery

      • Left anterior descending artery

      • Circumflex branch

      • Right coronary artery

      • Posterior descending artery

  • Consequences of Impaired Coronary Blood Flow

    • Angina

    • Myocardial infarction (heart attack)

    • Cardiac arrhythmias

    • Conduction defects

    • Heart failure

    • Sudden death

  • Evaluation of Coronary Blood Flow and Myocardial Perfusion

    • ECG: Changes in wave form patterns or orientation

    • Echocardiogram: M-mode, 2-D, Doppler, and esophageal echocardiography

    • Exercise Stress Testing: Motorized treadmill and bicycle ergometer

    • Transesophageal Echocardiography (TEE): A 2-D echocardiography transducer placed at the end of a flexible endoscope to obtain images from the esophagus

    • Nuclear Cardiovascular Imaging Methods:

    • Myocardial perfusion imaging

    • Infarct imaging

    • Radionuclide angiocardiography

    • Positron emission tomography

  • Atherosclerosis

    • A slow and progressive condition that begins early in life, affecting one or more of the major epicardial coronary arteries and their branches

  • Acute Coronary Syndromes (ACS)

    • Encompasses a spectrum of ischemic coronary diseases from unstable angina to myocardial infarction

  • Chronic Ischemic Heart Disease

    • Includes chronic stable angina, silent myocardial ischemia, variant or vasospastic angina, and ischemic cardiomyopathy

  • Determinants of ACS Status

    • Classifications into low risk or high risk based on:

    • Presenting characteristics

    • ECG variables

    • Serum cardiac markers

    • Timing of presentation

  • Unstable Angina/Non–ST-Segment Elevation Myocardial Infarction (UA/NSTEMI)

    • Onset: Abrupt

    • Characteristics: Severe, crushing pain (substernal), radiating to left arm, neck, or jaw

    • Accompanying symptoms: Nausea, vomiting, fatigue, weakness, tachycardia, anxiety, restlessness, and skin changes

  • ST-Segment Elevation Myocardial Infarction (STEMI)

    • Determining factors include:

    • Location and extent of occlusion

    • Amount of heart tissue supplied

    • Duration of occlusion

    • Metabolic needs of affected tissue

    • Extent of collateral circulation

    • Heart rate, blood pressure, and cardiac rhythm

  • Pathophysiology of Infarcts

    • Transmural Infarcts:

    • Involve full thickness of the ventricular wall

    • Occur due to obstruction of a single artery

    • Subendocardial Infarcts:

    • Involve inner one-third to one-half of the ventricular wall

    • More common in severely narrowed but patent arterial ductus

  • Populations Affected by Silent Myocardial Ischemia

    • Individuals asymptomatic without evidence of CAD

    • Individuals with history of myocardial infarction continuing silent ischemia episodes

    • Persons with angina who also have episodes of silent ischemia

  • Management of Acute Coronary Syndrome

    • Fibrinolytic therapy

    • Revascularization interventions:

    • Coronary artery bypass grafting (CABG)

    • Percutaneous coronary intervention (PCI)

    • Coronary stenting

    • Atherectomy

    • Post-infarction recovery protocols

    • Participation in cardiac rehabilitation programs

  • Types of Angina

    • Chronic Stable Angina:

    • Linked to fixed coronary obstruction causing disparity between coronary blood flow and myocardial metabolic demands

    • Stable Angina:

    • Initial ischemic heart disease manifestation for about half of CAD patients

    • Silent Myocardial Ischemia

    • Variant (Vasospastic) Angina

  • Basis for Diagnosis of Unstable Angina

    • Pain severity and presenting symptoms

    • Hemodynamic stability

    • ECG findings

    • Serum cardiac markers

  • Characteristics of Pain Associated with Chronic Stable Angina

    • Persistent and severe symptoms with one of three features:

    • Occurs at rest or with minimal exertion lasting over 20 minutes (if not interrupted by nitroglycerin)

    • Described as frank and severe new-onset pain

    • Exhibited pattern is significantly more severe, prolonged, or frequent than previously experienced

  • Causes of Unstable Angina

    • Atherosclerotic plaque disruption

    • Platelet aggregation

    • Secondary hemostasis

  • Nonpharmacologic Treatment of Angina

    • Smoking cessation for smokers

    • Stress reduction techniques

    • Regular exercise programming

    • Limiting dietary cholesterol and saturated fats

    • Weight reduction for obese individuals

    • Avoidance of cold or stress factors leading to vasoconstriction

  • Antiplatelet and Anticoagulant Therapy

    • Aspirin: Preferred antiplatelet agent, inhibits synthesis of prostaglandin and thromboxane A2

    • Ticlopidine and Clopidogrel: Used if aspirin is contraindicated, they irreversibly inhibit binding of ADP to platelet receptors without affecting prostaglandin synthesis

    • Platelet Receptor Antagonists: Target aggregation processes by blocking receptors in the final pathway for platelet function

Cardiomyopathies

  • Definition

    • Diverse group of diseases resulting from mechanical and/or electrical impairment leading to ventricular hypertrophy or dilatation

    • Genetic factors involved may relate solely to the heart or contribute to systemic disorders causing cardiovascular complications or heart failure

  • Types of Cardiomyopathies

    • Primary Cardiomyopathies: Heart muscle diseases of unknown origin

    • Secondary Cardiomyopathies: Cardiac abnormalities resulting from other cardiovascular diseases, such as myocardial infarction

  • Specific Types Include

    • Dilated

    • Hypertrophic

    • Restrictive

    • Arrhythmogenic right ventricular

    • Peripartum

  • Primary Types

    • Genetic Hypertrophic (see Fig. 27.14)

    • Arrhythmogenic right ventricular

    • Left ventricular noncompaction cardiomyopathy

    • Inherited conduction system disorders

    • Ion channelopathies

    • Mixed cardiomyopathy

    • Dilated cardiomyopathy (see Fig. 27.15)

    • Restrictive cardiomyopathy

  • Acquired Cardiomyopathies

    • Myocarditis: Inflammation of heart muscle

    • Peripartum Cardiomyopathy: Develops in the last month of pregnancy or within 5 months postpartum

    • Stress Cardiomyopathy: Also known as Takotsubo syndrome, often triggered by emotional or physical stress

    • Idiopathic Forms

  • Secondary Forms

    • Conditions leading to cardiac abnormalities include drugs, diabetes mellitus (DM), metabolic disorders (MD), autoimmune diseases, and cancers (see Chart 27.2)

  • Treatment

    • Depends on type; may include:

    • Medication

    • Implanted pacemakers

    • Defibrillators

    • Ventricular assist devices

    • Ablation procedures

    • Goal is often symptom relief; heart transplant may be necessary for some patients

  • Question #3

  • Which may contribute to the development of a cardiomyopathy?

    • Valvular stenosis

    • Valvular regurgitation

    • Myocardial Infarction (MI)

    • Ischemia

    • All the above

    • None

  • Answer to Question #3

    • E. All the above

    • Rationale: All listed conditions can lead to cardiomyopathy development.

Infectious and Immunologic Disorders

  • Predisposing Factors for Endocarditis

    • Damaged endocardial surface

    • Portal of entry for organisms to access circulatory system

    • Valvular disease, prosthetic heart valves, congenital heart defects provide conducive environments for bacterial growth

    • Simple gum massage or innocuous lesions may give bacteria access to bloodstream in individuals with existing defects

  • Infective Endocarditis (IE)

    • Invasion of heart valves and endocardium by microbial agents (see Fig. 27.16)

    • Formation of bulky, friable vegetations leading to destruction of underlying cardiac tissue

    • Systemic manifestations caused by various organisms:

    • Streptococci

    • Enterococci

    • Haemophilus sp.

    • Actinobacillus actinomycetemcomitans

    • Cardiobacterium hominis

    • Eikenella corrodens

    • Kingella kingae

    • Gram-negative bacilli

    • Fungi

  • Manifestations of Rheumatic Fever

    • Acute Stage: History of initiating streptococcal infection; affects connective tissues in heart, blood vessels, joints, and subcutaneous tissues

    • Recurrent Phase: Extension of cardiac effects of the disease

    • Chronic Phase: Permanent deformities develop in heart valves

Valvular Heart Disease

  • Definition

    • Hemodynamic disturbances that promote directional blood flow through heart chambers

    • Dysfunction causative from:

    • Congenital defects

    • Trauma

    • Ischemic damage

    • Degenerative changes

    • Inflammation

  • Mechanical Disruptions

    • Narrowing of valve opening leading to improper function:

    • Stenosis

    • Distortion of valve causing improper closure:

    • Incompetent or regurgitant valve: Allows backward flow when valve should be closed

  • Valve Disorders Include:

    • Mitral Valve Disorders:

    • Mitral valve stenosis (see Fig. 27.18)

    • Mitral valve regurgitation (see Fig. 27.19)

    • Mitral valve prolapse (see Fig. 27.20)

    • Aortic Valve Disorders:

    • Aortic valve stenosis (see Fig. 27.18)

    • Aortic valve regurgitation (see Fig. 27.18)

  • Diagnosis and Assessment

    • Cardiac auscultation detects blood flow turbulence from valvular disorders

    • Echocardiography: Widely used to assess structure and function using inaudible ultrasound signals

Heart Failure (HF) and Circulatory Shock

  • Compensatory Mechanisms

    • Frank-Starling mechanism (see Fig. 27.25)

    • Neurological responses (sympathetic nervous system)

    • Renin-angiotensin-aldosterone mechanism

    • Natriuretic peptides

    • Endothelins (see Fig. 27.26)

    • Myocardial hypertrophy

    • Remodeling

  • Types of Dysfunction

    • Systolic Dysfunction: Impaired cardiac blood ejection during systole

    • Diastolic Dysfunction: Impaired cardiac filling during diastole

    • High Output: Increased demand for cardiac output, with potentially supranormal heart function; often linked to excessive metabolic needs

    • Low Output: Disorders impairing heart pumping; manifests as systemic vasoconstriction with cold, pale, or cyanotic extremities

  • Left-Sided Heart Failure:

    • Leads to decreased cardiac output and elevated pulmonary venous pressure

  • Right-Sided Heart Failure Symptoms:

    • Pulmonary edema

    • Weight gain

    • Congestion of viscera

    • Jugular vein distention

  • Chronic vs. Acute Heart Failure

    • Chronic Heart Failure: Long-term, characterized by sustained cardiac function decline

    • Volume overload accompanied by venous congestion in pulmonary and systemic circulation

    • Acute Heart Failure: Gradual or rapid change in heart failure symptoms, indicating need for urgent treatment

    • Results in pulmonary congestion due to raised left ventricular pressures, with or without low output

  • Development of Postnatal Pulmonary Vascular Changes

    • Influences include prematurity, alveolar hypoxia, lung diseases, and congenital heart defects

  • Congenital Heart Defects Types

    • Patent ductus arteriosus

    • Atrial septal defects

    • Ventricular septal defects

    • Endocardial cushion defects

    • Pulmonary stenosis

    • Tetralogy of Fallot

    • Transposition of great vessels

    • Coarctation of the aorta

    • Kawasaki disease

  • Signs and Symptoms in Childhood Congenital Heart Disease

    • Altered heart action

    • Heart failure indications

    • Pulmonary vascular disorders leading to supply difficulties for peripheral tissues

  • Kawasaki Disease

    • Primarily affects skin, brain, eyes, joints, liver, lymph nodes, and heart

    • Characterized by vasculitis affecting small vessels, sometimes progressing to larger arteries

    • Immunologic origin with three distinct phases:

    • Acute phase: Fever, conjunctivitis, rash, oral mucosal involvement, hand and foot swelling, and engorged cervical lymph nodes

    • Subacute phase: Fever resolution and desquamation

    • Convalescent phase: Complete symptom resolution, generally after about 8 weeks

  • Causes of Heart Failure in Children

    • Inability to maintain required cardiac output for metabolic demands

    • Structural (congenital) defects

    • Surgical correction of defects increasing heart failure risk

  • Aging Process Effects on Cardiac Function

    • Increased vascular stiffness and reduced beta-adrenergic response limiting heart’s ability to increase heart rate and contraction

    • Changes include left ventricular hypertrophy and decreased heart compliance

  • Heart Failure in Infants and Children

    • Embryonic heart development considerations

    • Fetal circulatory path dynamics

    • Congenital heart defects impacting pathological blood flow leading to cyanotic and acyanotic disorders

Circulatory Failure (Shock)

  • Definition and Consequences

    • Leads to organ hypoperfusion and inadequate oxygen/nutrient supply for cellular activities

  • Compensatory Mechanisms

    • Engage sympathetic and renal systems to respond to shock states

  • Types of Shock

    • Circulatory Shock: Heart failure in pumping action, loss of vascular fluid (hypovolemic shock), flow obstruction (obstructive shock), or increased vascular compartment size causing distribution issues (distributive shock)

    • Cardiogenic Shock: Heart’s inability to pump blood adequately to meet body demands

    • Hypovolemic Shock: Represents diminished blood volume causing insufficient filling of vascular compartments

    • Neurogenic Shock: Decreased sympathetic control of vessel tone

    • Anaphylactic Shock: Vasodilation and increased capillary permeability secondary to allergies

    • Septic Shock: Severe infection triggering systemic responses

  • Complications Related to Shock

    • Potential outcomes include pulmonary injury, acute renal failure, gastrointestinal ulceration, disseminated intravascular coagulation (DIC), and multiple organ dysfunction syndrome (MODS)

  • Acute Lung Injury (ALI)/Acute Respiratory Distress Syndrome (ARDS)

    • A potentially lethal pulmonary condition producing rapid onset of profound dyspnea occurring 12 to 48 hours post-trigger

    • Focus on intervention is critical

  • Acute Renal Failure

    • Usually stems from impaired renal perfusion or kidneys’ direct injury

    • Degree of failure correlates with shock severity and duration

  • Gastrointestinal Complications

    • Associated with loss of appetite, nausea, vomiting

    • Mucosal lesions may develop in stomach/duodenum leading to sepsis and ischemia

  • Disseminated Intravascular Coagulation (DIC)

    • Involves the extensive activation of the coagulation cascade leading to widespread clot formation and potential vessel occlusions

  • Multiple Organ Dysfunction Syndrome (MODS)

    • A severe complication of shock, progressively depleting the body’s compensatory capabilities affecting various organ systems (lungs, kidneys, liver, brain, heart)

    • Risk factors include sepsis, prolonged hypotensive states, hepatic dysfunction, infarcted bowel, advanced age, severe trauma, and history of substance abuse.