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

Definition and Functions of the Pericardium

Definition

A double-layered serous membrane

Functions

Isolates the heart from other thoracic structures

Maintains its position in the thorax

Prevents it from overfilling

Contributes to coupling the distensibility between the two ventricles during diastole; they both fill equally

Types of Pericardial Disorders #1

Pericardial Effusion

The accumulation of fluid in the pericardial cavity

Cardiac Tamponade

Slow or rapid compression of the heart due to accumulation of fluid, pus, or blood in the pericardial sac

Pericarditis

An acute inflammatory process of the pericardium

Can be acute, chronic, or constrictive

Types of Pericardial Disorders #2

Constrictive Pericarditis

Calcified scar tissue develops between the visceral and parietal layers of the serous pericardium.

Cardiac output and cardiac reserve become fixed.

Ascites, pedal edema, dyspnea on exertion, and fatigue, Kussmaul sign

Clinical Manifestations

Acute pericarditis is based on clinical manifestations.

ECG, chest radiography, and echocardiography

Friction rub

Chronic pericarditis

No pathogen identified

Autoimmune disorders

Cardiac Tamponade

Pericardial effusion can lead to a condition called cardiac tamponade, in which there is compression of the heart due to the accumulation of fluid, pus, or blood in the pericardial sac.

Coronary Circulation

Left main coronary artery

Left anterior descending artery

Circumflex branch

Right coronary artery

Posterior descending artery

Coronary Heart Disease

Impaired coronary blood flow that may cause:

Angina

Myocardial infarction or heart attack

Cardiac arrhythmias

Conduction defects

Heart failure

Sudden death

Question #1

Which of the following conditions will result in pathological changes arising from pulseless electrical activity?

Pericardial effusion

Cardiac tamponade

Pericarditis

Answer to Question #1

B. Cardiac tamponade

Rationale: Cardiac tamponade is the result of restricted movement of the muscle and will inhibit ventricular contraction. The conduction is intact, but there will be little or no SV.

Basis for Diagnosis of Unstable Angina

Pain severity and presenting symptoms

Hemodynamic stability

ECG findings

Serum cardiac markers

The Evaluation of Coronary Blood Flow and Myocardial Perfusion

ECG

Changes in the pattern or orientation of wave forms

Echocardiogram

M-mode, two-dimensional, Doppler, and esophageal

Exercise Stress Testing

Motorized treadmill and bicycle ergometer

Nuclear Cardiovascular Imaging Methods

Myocardial perfusion imaging, infarct imaging, radionuclide angiocardiography, and positron emission tomography

Classification of Coronary Heart Disease

Chronic Ischemic Heart Disease

Chronic stable angina, silent myocardial ischemia, and variant or vasospastic angina

Acute Coronary Syndromes

Represent the spectrum of ischemic coronary disease ranging from unstable angina through myocardial infarction

Types of Angina

Chronic Stable Angina

Associated with a fixed coronary obstruction that produces a disparity between coronary blood flow and metabolic demands of the myocardium

Stable Angina

The initial manifestation of ischemic heart disease in approximately half of persons with CAD

Determinants of the ACS Status

Persons with an ACS are routinely classified as low risk or high risk for infarction based on the following:

Presenting characteristics

ECG variables

Serum cardiac markers

The timing of presentation

Characteristics of Pain Associated with Unstable Angina

The pain has a more persistent and severe course and is characterized by at least one of three features:

It occurs at rest (or with minimal exertion), usually lasting more than 20 minutes (if not interrupted by nitroglycerin).

It is severe and described as frank pain and of new onset.

It occurs with a pattern that is more severe, prolonged, or frequent than previously experienced.

Manifestations of ST-segment Elevation AMI

Abrupt onset

Severe and crushing pain, usually substernal, radiating to the left arm, neck, or jaw

Gastrointestinal complaints (nausea and vomiting)

Complaints of fatigue and weakness

Tachycardia, anxiety, restlessness, feelings of impending doom

Pale, cool, and moist skin

Causes of Unstable Angina

Atherosclerotic plaque disruption

Platelet aggregation

Secondary hemostasis

Factors Determining the Extent of an Infarct

Location and extent of occlusion

Amount of heart tissue supplied by the vessel

Duration of the occlusion

Metabolic needs of the affected tissue

Extent of collateral circulation

Heart rate, blood pressure, and cardiac rhythm

Involvement of Heart Muscle in an Infarct

Transmural Infarcts

Involve the full thickness of the ventricular wall

Occur when there is obstruction of a single artery

Subendocardial Infarcts

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

Occur more frequently in the presence of severely narrowed but still patent arterial ductus

Populations Affected by Silent Myocardial Ischemia

Persons who are asymptomatic without other evidence of CAD

Persons who have had a myocardial infarct and continue to have episodes of silent ischemia

Persons with angina who also have episodes of silent ischemia

Medical Management Following Infarct

Thrombolytic therapy

Revascularization interventions

Coronary artery bypass grafting (CABG)

Percutaneous coronary intervention (PCI)

Atherectomy

Cardiac rehabilitation programs

Nonpharmacologic Treatment of Angina

Smoking cessation in persons who smoke

Stress reduction

Regular exercise program

Limiting dietary intake of cholesterol and saturated fats

Weight reduction if obesity is present

Avoidance of cold or other stresses that produce vasoconstriction

Antiplatelet and Anticoagulant Therapy #1

Aspirin

The preferred antiplatelet agent for preventing platelet aggregation in persons with CAD

Inhibits synthesis of prostaglandin, thromboxane A2

Ticlopidine and clopidogrel

May be used when aspirin is contraindicated

Irreversibly inhibits the binding of ADP to its receptor on the platelets; no effect on prostaglandin synthesis

Antiplatelet and Anticoagulant Therapy #2

Platelet Receptor Antagonists

Target a single step in the aggregation process

Block the receptor involved in the final common pathway for platelet adhesion, activation, and aggregation

Treat acute coronary syndrome

Question #2

Which type of angina is brought about by exercise or stress?

Stable

Unstable

Answer to Question #2

A. Stable

Rationale: Stable angina does not present as a problem until there is an increase in workload.

Myocardial Diseases

Myocarditis

Inflammation of the heart muscle and conduction system without evidence of myocardial infarction

Primary Cardiomyopathies

Heart muscle diseases of unknown origin

Secondary Cardiomyopathies

Conditions in which the cardiac abnormality results from another cardiovascular disease, such as myocardial infarction

Types of Cardiomyopathies

Dilated

Hypertrophic

Restrictive

Arrhythmogenic right ventricular

Peripartum

Cardiomyopathies

A heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and that are due to a variety of causes that frequently are genetic.

Cardiomyopathies either are confined to the heart or are part of generalized systemic disorders, often leading to cardiovascular death or progressive heart failure–related disability.

Primary and Secondary Cardiomyopathy

Primary

Genetic

Hypertrophic

Arrhythmogenic right ventricular

Left ventricular noncompaction cardiomyopathy

Inherited conduction system disorders

Ion channelopathies

Mixed cardiomyopathy

Dilated cardiomyopathy

Restrictive cardiomyopathy

Secondary

Acquired cardiomyopathies

Myocarditis

Peripartum cardiomyopathy

Stress cardiomyopathy

Alcoholic cardiomyopathy

Treatment of Cardiomyopathy

Treatment depends on the type of

Medication

Implanted pacemakers

Defibrillators

Ventricular assist devices

Ablation

The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant.

Question #3

Which of the following may result in the development of a cardiomyopathy?

Valvular stenosis

Valvular regurgitation

Ischemia

All the above

None of the above

Answer to Question #3

E. All the above

Rationale: All the above can contribute to the development of a cardiomyopathy.

Predisposing Factors for Endocarditis

A damaged endocardial surface

A portal of entry by which the organism gains access to the circulatory system

The presence of valvular disease, prosthetic heart valves, or congenital heart defects provides an environment conducive to bacterial growth.

In persons with preexisting valvular or endocardial defects, simple gum massage or an innocuous oral lesion may afford the pathogenic bacteria access to the bloodstream.

Infective Endocarditis

Invasion of the heart valves and endocardium by a microbial agent

Formation of bulky, friable vegetations and destruction of underlying cardiac tissues

Systemic manifestations

Streptococci

Enterococci

Haemophilus sp.

Actinobacillus actinomycetemcomitans

Cardiobacterium hominis

Eikenella corrodens

Kingella kingae

Gram-negative bacilli

Fungi

Manifestations of Rheumatic Fever

Acute Stage

History of an initiating streptococcal infection

Involves mesenchymal connective tissue of the heart, blood vessels, joints, and subcutaneous tissues

Recurrent Phase

Extension of the cardiac effects of the disease

Chronic Phase

Permanent deformity of the heart valves

Function and Disorders of the Heart Valves

Function: Promote directional flow of blood through the chambers of the heart

Dysfunction results in disorders:

Congenital defects

Trauma

Ischemic damage

Degenerative changes

Inflammation

Disruptions Occurring with Valvular Heart Disease

Narrowing of the valve opening, so it does not open properly

Stenosis

Distortion of the valve, so it does not close properly

Incompetent or regurgitant valve: permits backward flow to occur when the valve should be closed

Valve Disorders

Mitral Valve Disorders

Mitral valve stenosis

Mitral valve regurgitation

Mitral valve prolapse

Aortic Valve Disorders

Aortic valve stenosis

Aortic valve regurgitation

Cardiac Auscultation and Echocardiography

Valvular heart disorders produce blood flow turbulence and often are detected through cardiac auscultation.

Echocardiography is still the most widely used diagnostic test to check for structure and function of the heart. It uses ultrasound signals that are inaudible to the human ear.

Adaptive and Maladaptive Mechanisms in Heart Failure

Frank-Starling mechanism

Sympathetic nervous system

Renin-angiotensin-aldosterone mechanism

Natriuretic peptides

Endothelins

Myocardial hypertrophy

Remodeling

Heart Failure #1

High Output

Extensive need for cardiac output

Function of heart may be supranormal

Excessive metabolic needs

Low Output

Disorders that impair pumping of the heart

Systemic vasoconstriction with cold, pale, and sometimes cyanotic extremities

Heart Failure #2

Systolic dysfunction—impaired ejection of blood from the heart during systole

Diastolic dysfunction— impaired filling of the heart during diastole

Heart Failure #3

Right-sided

Pulmonary edema, weight gain, congestion of viscera, jugular vein distention

Cor pulmonale

Left-sided

Decreased cardiac output, elevated pulmonary venous pressure

Factors Affecting Postnatal Pulmonary Vascular Development

Prematurity

Alveolar hypoxia

Lung disease

Congenital heart defects

Signs and Symptoms of Childhood Congenital Heart Disease

Symptoms associated with altered heart action

Heart failure

Pulmonary vascular disorders

Difficulty in supplying the peripheral tissues with oxygen and other nutrients

Chronic versus Acute Heart Failure

Chronic—long-term condition characterized by decreased cardiac function

Volume overload

Venous congestion become more prominent in both pulmonary and systemic circulations

Acute—represents a gradual or rapid change in heart failure signs and symptoms, indicating need for urgent therapy

Pulmonary congestion due to elevated left ventricular filling pressures, with or without a low cardiac output

Fetal Blood Flow

Parallel rather than in series

The right ventricle delivering most of its output to the placenta for oxygen uptake

The left ventricle pumping blood to the heart, brain, and primarily upper body

Umbilical vein and two umbilical arteries

Foramen ovale

Ductus arteriosus

Cyanosis and Shunting

Defects that increase resistance to aortic outflow increase left-to-right shunting.

Defects that obstruct pulmonary outflow increase right-to-left shunting.

Crying, defecating, or stress of feeding may increase pulmonary vascular resistance and cause an increase in right-to-left shunting.

Resulting cyanosis

Types of Congenital Heart Defects

Patent ductus arteriosus

Atrial septal defects

Ventricular septal defects

Endocardial cushion defects

Pulmonary stenosis

Tetralogy of Fallot

Transposition of the great vessels

Coarctation of the aorta

Kawasaki disease

Kawasaki Disease

The skin, brain, eyes, joints, liver, lymph nodes, and heart

Vasculitis in the small vessels and progresses to involve some of the larger arteries

Immunologic in origin

Acute phase: fever, conjunctivitis, rash, involvement of the oral mucosa, redness and swelling of the hands and feet, and enlarged cervical lymph nodes

Subacute phase: defervescence and desquamation

Convalescent phase: complete resolution of symptoms until all signs of inflammation have disappeared after about 8 weeks

Causes of Heart Failure in Children

Inability of heart to maintain the cardiac output required to sustain metabolic demands

Structural (congenital) heart defects

Surgical correction of heart defects may cause heart failure

Aging Process and Cardiac Function

Increased vascular stiffness

Reduced responsiveness to beta adrenergic stimulation that limits the heart’s capacity to maximally increase heart rate and contractility

Left ventricular hypertrophy

Heart compliance decreases

Circulatory Failure (Shock)

Results in hypoperfusion of organs and tissues

Insufficient supply of oxygen and nutrients for cellular function

Compensatory mechanisms: sympathetic and renal systems

Heart Failure in Infants and Children

Embryonic development of the heart

Fetal and perinatal circulation

Congenital heart defects

Pathophysiology

Abnormal shunting of blood

Cyanotic versus acyanotic disorders

Disruption of pulmonary blood flow

Manifestations and treatment

Circulatory Shock

Pathophysiology

Clinical manifestations

Treatment

Cardiogenic Shock

Pathophysiology

Clinical manifestations

Treatment

Hypovolemic Shock

Pathophysiology

Clinical manifestations

Treatment

Types of Shock

Distributive shock

Neurogenic shock

Anaphylactic shock

Etiology

Clinical manifestations

Treatment

Prevention

Sepsis and Septic Shock

Pathophysiology

Clinical manifestations

Treatment

Obstructive Shock

Circulatory shock that results from mechanical obstruction of the flow of blood through the central circulation

Causes: dissecting aortic aneurysm, cardiac tamponade, pneumothorax, atrial myxoma, and evisceration of abdominal contents into the thoracic cavity

Complications of Shock

Pulmonary injury

Acute renal failure

Gastrointestinal ulceration

Disseminated intravascular coagulation (DIC)

Multiple organ dysfunction syndrome (MODS)

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

Potentially lethal form of pulmonary injury that may be either the cause or result of shock

Rapid onset of profound dyspnea that usually occurs 12 to 48 hours after the initiating event

Definition

Intervention focus

Acute Renal Failure

Most cases due to impaired renal perfusion or direct injury to the kidneys

Degree is related to severity or duration of shock

Gastrointestinal Complications

Loss of appetite, nausea, vomiting

Superficial mucosal lesions of the stomach and duodenum

Development of sepsis and shock

Ischemia

Disseminated Intravascular Coagulation (DIC)

Widespread activation of the coagulation system with resultant formation of fibrin clots and thrombotic occlusion of small and midsized vessels

Systemic formation of thrombin

Multiple Organ Dysfunction Syndrome (MODS)

Ominous complication of shock

Rapidly depletes the body’s ability to compensate and recover from a shock state

Affects multiple organ systems—lungs, kidneys, liver, brain, heart

Risk factors: sepsis, prolonged periods of hypotension, hepatic dysfunction, infarcted bowel, advanced age, severe trauma, alcohol abuse

Treatment Measures to Correct and Reverse Shock

Fluid resuscitation

Restore blood flow

Improve oxygen delivery

Hemodynamic stability