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135 Cards in this Set

  • Front
  • Back

Dietary modification, exercise program, cessation of smoking, drug therapy

Four general treatment measures for cardiac disorders

Interfere with clotting factor synthesis

Warfarin

Inhibit cardiac workload

Heparin

Percutaneous transluminal coronary angioplasty

Used in advanced atheromas

Coronary artery bypass grafting

Used in advanced atheromas

Laser angioplasty

Used in advanced atheromas

Angina pectoris

Chest pain

Decreased blood supply to heart, increased demand for oxygen by heart, or combination

Underlying pathology in angina pectoris

Most serious complication of angina pectoris

Myocardial infarction

Used to treat acute anginal attack

Coronary vasodilators

B-Adrenergic blockers (Lopressor)

Blocks B adrenergic receptors, slowing the heart rate, prevents sympathetic nervous system stimulation and increased demand on heart.

Calcium channel blockers (Adalat)

Vasodilator, blocks calcium channel, reducing cardiac contractility and work

Nitrates (vasodilators; transdermal or oral form, e.g.: nitroglycerin)

Reduces cardiac workload, decreases peripheral resistance by vasodilation

Digitalis (cardiac glycosides) e.g.: Lanoxin

Slows conduction through the atrioventricular node, increases the force of contraction (cardiotonic) to increase efficiency

Lower blood pressure and cardiac workload

Antihypertensive

Control blood pressure and prevent edema

Diuretic

Lower platelet aggregation and the chance of thrombus formation

Platelet inhibitor

Lower blood cholesterol and LDL levels and slow or arrest progression of atherosclerosis

Antihyperlipidemic

Angioplasty and stent insertion, coronary bypass graft

Surgical interventions that might be used in treatment of angina

Death of cardiac muscle resulting from prolonged ischemia

Myocardial infarction

Thrombus buildup obstructs artery due to atherosclerosis

Most common cause of myocardial infarction

Vasoplasm in presence of partial occlusion

Cause of myocardial infarction

Embolization of thrombus to smaller artery that is totally obstructed

Cause of myocardial infarction

Transmural infarction vs intramural infarction

Transmural infarction involves all three layers of heart

Most common site of myocardial infarction

Left ventricle

Pathophysiology of MI

Coronary artery is totally occluded, causing prolonged ischemia and cell death or infarction of myocardium

MI - area of necrosis is gradually replaced by

Fibrous (non-functional tissue)

ECG changes, and serum enzyme and isoenzyme levels. Serum levels of myosin and cardiac troponin are elevated, serum electrolyte levels may be abnormal, leukocytosis and elevated CRP and ESR are common. Arterial blood gas is altered. Pulmonary artery pressure measurements should be conducted to determine ventricular function

Diagnosis of myocardial infarction confirmed

Intracellular enzymes diffused from necrotic cells into the serum in a typical and predictable pattern that can be measured

Serum enzymes

Subgroups of a specific enzyme, found primarily in one type of tissue

Isoenzymes

Will be altered in areas of severe ischemia or necrosis

Electrical activity of myocardium

Complication of MI responsible for greatest number of deaths

Arrythmia

Cardiogenic shock, congestive heart failure, rupture of necrotic heart tissue, and thromboembolism

Other complications that may accompany MI

Treatment for MI - digoxin

Generally supports heart function

Usually precipitated by something that increases heart rate

Angina

May occur at rest or while asleep

Myocardial infarction

Relieved by nitroglycerin and rest

Angina

Not relieved by nitroglycerin and rest

Myocardial infarction

No tissue death

Angina

Cell death

Myocardial infarction

No changes in cardiac enzymes and isoenzymes

Angina

Cardiac enzymes and isoenzymes elevated

Myocardial infarction

No permanent ECG changes

Angina

Permanent ECG changes

Myocardial infarction

White blood cell count not elevated

Angina

Leukocytosis

Myocardial infarction

CRP and ESR elevated

With myocardial infarction, not elevated with angina

Serum levels of myosin and troponin elevated

With myocardial infarction, not elevated with angina

Atrial depolarization

P Wave

Ventricular repolarization

QRS complex

Ventricular depolarization

T wave

Alteration of cardia rate or rhythm

Dysrhythmia

May occur due to damage to the heart's conduction system or to systemic causes such as electrolyte abnormalities, fever, hypoxia, stress, infection, or drug toxicity

Cardiac arrythmias

Heart rate greater than 350 beats per minute

Fibrillation


Ectopic beat

Heart rate less than 60 bpm

Bradycardia

Heart rate between 160 and 350 bpm

Flutter

Heart rate between 100 and 160 bpm

Tachycardia

Slowing or no transmission of impulses between atria and ventricles

Heart block

Additional heartbeat originating in atria

Premature atrial contraction (PAC)

Extra heartbeat arising in ventricles

Premature ventricular contraction (PVC)

Restoration of normal cardiac rhythm by electrical shock

Cardioversion

Cessation of all activity in the heart, no impulse contraction, thus a flat ECG

Cardiac arrest

Causes: a problem in the heart itself (valve defect or MI) or a condition that increases the workload of the heart

Heart failure

Compensatory mechanisms in early heart failure

Reduced blood flow into systemic circulation to include kidneys, increased rennin and aldosterone secretion, resulting in vasoconstriction and increased blood volume. SNS response increases heart rate and peripheral resistance. Chambers of the heart dilate, and cardiac muscle becomes hypertrophied.

The chamber and blood vessels behind or "upstream" from the failing ventricle will not empty properly, resulting in the accumulation or congestion of blood and therefore an increased pressure in these areas

Backward effects

There will be decreased output of blood from the failing ventricle into the vessels "in front" of it, or "downstream".

Forward effects

Cause: Infarction of right ventricle, pulmonary valve stenosis, pulmonary disease (cor pulmonale)

Right-sided heart failure

Cause: Infarction of left ventricle, aortic valve stenosis, hypertension, hyperthyroidism

Left-sided heart failure

Backward effects: Dependent edema in feet, hepatomegaly and splenomegaly, ascites, distended neck veins, headache, flushed face

Right-sided heart failure

Backward effects: Orthopnea, cough, shortness of breath, paroxysmal nocturnal dyspnea, hemopytsis, rales

Left-sided heart failure

Forward effects: Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance

Right-sided heart failure

Forward effects: atigue, weakness, dyspnea, exercise intolerance, cold intolerance

Left-sided heart failure

Manifestations: See above forward and backward effects. Compensations: tachycardia and pallor, secondary polycythemia, daytime oliguria

Right-sided heart failure

Manifestations: See above forward and backward effects. Compensations: tachycardia and pallor, secondary polycythemia, daytime oliguria

Left-sided heart failure

Septal defect

A hole or defect in the atrial or ventricular septa

Valvular incompetence

Failure of a valve to close completely

Regurgitation

Backward flow or leaking of blood due to valvular incompetence

Prolapse

Abnormally enlarged and floppy valve leaflets that balloon backward with pressure or posterior displacement of the valve cusp

Stenosis

Narrowing of a valve

Heart murmur

Abnormal heart sounds due to leaky valves

Most detected by presence of a heart murmur

Congenital heart defect

Blood from the left side of the heart is recycled to the right side and to the lungs, resulting in increased volume in the pulmonary circulation, decreased cardiac output, and an inefficient system - an acyanotic condition

Left to right shunt

Unoxygenated blood from the right side of the heart bypasses the lung directly and enters the left side of the heart and hence the systemic circulation, producing varying degrees of cyanosis; death may occur in infancy in severe cases

Right to left shunt

Forward effects: Decreased cardiac output

Mitral stenosis, mitral regurgitation, aortic stenosis

Forward effects: Increased stroke volume and cardiac output

Aortic regurgitation

Forward effects: Decreased blood flow through pulmonary circulation, leading to decreased gas exchange and blood to left side of heart

Pulmonary stenosis

Forward effects: Decreased blood flow through pulmonary circulation, leading to decreased gas exchange and blood to left side of heart

Pulmonary regurgitation

Backward effects: Left atrial hypertrophy, atrial arrhythmias, mural thrombi, pulmonary congestion, pulmonary hypertension

Mitral stenosis, mitral regurgitation

Backward effects: Left ventricular hypertrophy, if severe, increased congestion in left atrium and pulmonary congestion

Aortic stenosis

Backward effects: Left ventricular hypertrophy, if severe, heart failure

Aortic regurgitation

Backward effects: Right ventricular hypertrophy, congestion in right atrium and systemic veins, leads to right-sided heart failure

Pulmonary stenosis, pulmonary regurgitation

Manifestations: Dyspnea, orthopnea, cyanosis, fatigue, arrhythmias, heart murmur, increased risk of stroke due to emboli originating in left atrium

Mitral stenosis

Manifestations: Dyspnea, orthopnea, cyanosis, fatigue, dizziness, arrythmias, heart murmur

Mitral regurgitation

Manifestations: Dizziness, fainting, fatigue, heart murmur, if severe, dyspnea, orthopnea, cyanosis, angina

Aortic stenosis

Manifestations: Very strong, bounding pulse, heart murmur, may develop symptoms of heart failure

Aortic regurgitation

Manifestations: Weakness, fatigue, cyanosis, swelling of feet and ankles, symptoms of right-sided heart failure, heart murmur

Pulmonary stenosis

Manifestations: Weakness, fatigue, cyanosis, swelling of feet and ankles, symptoms of right-sided heart failure, heart murmur

Pulmonary regurgitation

Associated with heart murmurs

Valvular defect, septal defect

Pulmonary valve stenosis, ventricular septal defect, dextroposition of the aorta, right ventricular hypertrophy, present in

Tetralogy of Fallot

Microorganism that generally causes rheumatic fever

Group A B-hemolytic streptococci

High risk individuals for rheumatic fever

Ages 5-15

Pathophysiology of rheumatic fever

Acute systemic inflammatory condition resulting from abnormal immune reaction of untreated infection. May include inflammation in large joints, migratory polyarthritis, nonpruritic skin rash, nontender subcutaneous nodules of extensor surfaces of wrists, elbows, knees, ankles, and inflammation of basal nuclei, causing involuntary jerky movements. Rheumatic heart disease can develop years later.

Aschoff bodies

Myocarditis as result of rheumatic fever, inflammation develops as localized lesions in the heart muscle

Endocarditis from rheumatic fever

May lead to permanent scarring of heart valves, which leads to rheumatic heart disease. Causes high risk for infective endocarditis

Heart valve most commonly affected by rheumatic heart disease

Mitral valve

Defective heart valves infected by organisms with low virulence, i.e. Streptococcus viridans

Subacute infective carditis

Normal valves attacked by highly virulent pathogens, i.e. Staphylococcus aureus

Acute infective carditis

Insidious onset, various new heart murmurs, low grade fever, fatigue, anorexia, splenomegaly, Osler's nodes on fingers, signs of vascular occlusion or infection (abscesses) in remote areas, intermittent high fever

Subacute infective carditis

Sudden onset, sudden, spiked fever, chills, drowsiness. Heart valves badly damaged and may be torn, causing severe impairment of heart function. Septic emboli may cause infarctions and abscesses in remote sites with corresponding signs and symptoms of infection.

Acute infective carditis

High blood pressure (values)

Systolic above 120 and diastolic above 70

Essential Hypertension (values)

Consistently above 140/90 mm Hg

Idiopathic hypertension

Essential hypertension

Hypertension that results from renal or endocrine disease, or pheochromocytoma

Secondary hypertension

Furosemide, Hydrochlorothiazide

Diuretics

Enalaprilm, Ramipril, Captopril, Fosinopril

ACE inhibitors

Nifedipine, Amlodipine, Diltiazem

Calcium channel blockers

Metoprolol, Atenolol, Propranolol, Nadolol

B-Adrenergic blockers

Localized dilation of an arterial wall

Aortic aneurysm

Causes include atherosclerosis, trauma (particularly car accidents), syphilis, or congenital defects

Aortic aneuryms

Development of a thrombus in a vein in which inflammation is present

Thrombophlebitis

Spontaneous thrombus development in the absence of inflammation

Phlebothrombosis

Blood stasis and sluggish blood flow, endothelial injury, and increased blood coagulability contribute to

Thrombophlebitis

A blood clot or sometimes other material that blocks a pulmonary artery or one of it's branches

Pulmonary embolus

Hypotension resulting from decreased circulating blood volume, resulting in decreased tissue perfusion and general hypoxia.

Shock

Ascites - present in

Right-sided heart failure

Positive Homan's sign - present in

Thrombophlebitis

ECG changes - present in

Myocardial infarction, arrythmias

Positive blood cultures - present in

Rheumatic fever, endocarditis

Claudication - present in

Thrombophlebitis

Hemoptysis - present in

Heart failure

Heart murmur

Congenital defects, rheumatic fever, rheumatic heart disease, tetralogy of Fallot, septal defects, valvular defects - stenosis and regurgitation

Elevated cardiac enzymes - present in

Myocardial infarction

Subcutaneous nodules - present in

Rheumatic fever

Pulmonary edema - present in

Left sided heart failure, mitral stenosis, mitral regurgitation