chapter 24 disorders of cardiac function. definition and functions of the pericardium definition –...

Chapter 24Disorders of Cardiac Function

Definition and Functions of the Pericardium

• Definition– A double-layered serous membrane

surrounding the heart• 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

• 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 pericardial sac

Pericarditis

• An acute inflammatory process of the pericardium – Can be acute, chronic, or constrictive– May be due to autoimmune disease, infection,

Rheumatic fever– Difficulty breathing, swelling of legs and ankles,

dry cough, fatigue, anxiety, chest pain

Types of Pericardial Disorders (cont.)

• Constrictive pericarditis – A disorder caused by inflammation of the

pericardium– Eventual thickening, scarring and contracture of the

pericardium occurs causing it to be less elastic.– This prevents the pericardium from stretching and

results in reduced filling of the chambers of the heart. – This reduces the amount of blood pumped by the

heart and causes blood to back up behind the heart, resulting in symptoms of heart failure.

– Constrictive pericarditis may be life threatening if untreated.

Clinical Manifestations

• Acute pericarditis is based on clinical manifestations– ECG, chest radiography, and echocardiography – Friction rub

• Chronic pericarditis– No pathogen identified– Autoimmune disorders

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

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

a. A. Pericardial effusion b. B. Cardiac tamponade c. C. Pericarditis

Answer

a. Pericardial effusion

b. B. Cardiac tamponade: 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.

c. Pericarditis

The Evaluation of Coronary Blood Flow and Myocardial Perfusion

• ECG– Changes in 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– Variant or vasospastic

angina

Acute coronary syndromes (ACS)

– Represent the spectrum of ischemic coronary disease

– Ranges from unstable angina through myocardial infarction

– Chest pain (angina) that feels like burning, pressure or tightness and lasts several minutes or longer

– Pain elsewhere in the body, such as the left upper arm or jaw (referred pain

– Nausea– Vomiting– Shortness of breath (dyspnea– Sudden, heavy sweating

(diaphoresis)

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 people with CHD

Populations Affected by Silent Myocardial Ischemia

• Persons who are asymptomatic without other evidence of CHD

• 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

Non-pharmacologic 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

Anti-platelet and Anticoagulant Therapy

• Aspirin – The preferred anti-platelet agent for preventing

platelet aggregation in persons with CHD – Inhibits synthesis of prostaglandin and

thromboxane A2

Anti-platelet and Anticoagulant Therapy (cont.)

• 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

Determinants of ACS (Acute Coronary Syndrome) Status

• Persons with an ACS are routinely classified as low risk or high risk for infarction based on– Presenting characteristics– ECG variables– Serum cardiac markers– Timing of presentation

Causes of Unstable Angina

• Atherosclerotic plaque disruption• Platelet aggregation• Secondary hemostasis

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:

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

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

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

Basis for Diagnosis of Unstable Angina

• Pain severity and presenting symptoms• Hemodynamic stability• ECG findings• Serum cardiac markers

Manifestations of ST-Segment Elevation Acute Myocardial Infarction

• 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

doom • Pale, cool, and moist skin

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 – Involves the full thickness

of the ventricular wall – Occur when there is

obstruction of a single artery

– Associated with atherosclerosis involving major coronary artery

Subendocardial infarcts

• Involves the inner one third to one half of the ventricular wall

• Occur more frequently in the presence of severely narrowed but still patent arteries

Medical Management Following Infarct

• Thrombolytic therapy– The use of drugs to break up or dissolve blood clots,

which are the main cause of both heart attacks and stroke.

• Revascularization interventions– Coronary artery bypass grafting (CABG)– Percutaneous coronary intervention (PCI)– Atherectomy

• Cardiac rehabilitation programs

Question

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

a. A. Stableb. B. Unstable

Answer

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

b. Unstable

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

Cardiomyopathy Development (American Heart Association)

• Heterogeneous group of diseases of the myocardium• Associated with mechanical and/or electrical dysfunction• Usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation • 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 lead to cardiovascular death or progressive heart failure–related disability

Primary and Secondary Cardiomyopathies

• Primary – Genetic • Hypertrophic–The Heart Muscle thickens

• Arrhythmogenic right ventricular –progressive fibrofatty replacement of the myocardium

that predisposes to ventricular tachycardia and sudden death

• Left ventricular non-compaction cardiomyopathy– the muscular wall of the main pumping chamber of

the heart (the left ventricle) appears to be spongy

Secondary

• Acquired cardiomyopathies –Myocarditis • Inflammation of the heart muscle• Symptoms– Abnormal Heart Beat– Flu-like Symptoms– Leg Swelling– Fainting

• Stress cardiomyopathy – Caused by rapid and severe heart muscle weakness

• Alcoholic cardiomyopathy

Mixed cardiomyopathy

• Dilated cardiomyopathy–A condition in which the heart becomes

weakened and enlarged, and it cannot pump blood efficiently–Due to alcohol, lupus, rheumatoid arthritis,

coronary artery disease• Restrictive cardiomyopathy– A group of disorders in which the heart

chambers are unable to properly fill with blood because of stiffness in the heart

Treatment of Cardiomyopathy

• Treatment depends on the type – Medication– Implanted pacemakers– Defribillators– Ventricular assist devices – Ablation– The goal of treatment is often symptom relief, and

some patients may eventually require a heart transplant.

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

• Streptocococci • 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

Fetal Blood Flow

• Parallel rather than in series• Right ventricle delivering most of its output to the

placenta for oxygen uptake • Left ventricle pumping blood to the heart, brain,

and primarily upper body • Umbilical vein and two umbilical arteries • Foramen ovale – Allows blood to enter the left atrium from the right

atriumDuctus arteriosus – A shunt connecting the pulmonary artery to the aortic

arch

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

Factors Affecting Postnatal Pulmonary Vascular Development

• Prematurity• Alveolar hypoxia• Lung disease• Congenital heart defects

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

Question

• Which of the following might result in the development of a cardiomyopathy?

a. A. Valvular stenosisb. B. Valvular regurgitationc. C. MId. D. Ischemiae. E. All the above

Answer

a. A. Valvular stenosis

b. B. Valvular regurgitation

c. C. MI

d. D. Ischemia

e. E. All the above: Any of these conditions can contribute to the development of a cardiomyopathy.

Kawasaki Disease

• Vasculitis in the small vessels; 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

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