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Patho Test 1 > Chapter 4 Cardio > Flashcards

Chapter 4 Cardio Flashcards

1
Q

Increase in electrical charge
Accomplished through cellular ion exchange
Generates cardiac contraction

A

Depolarization

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2
Q

Cellular recovery

Ions returning to the cell membrane in preparation for depolarization

A

Repolarization

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3
Q

Atrial depolarization

A

P wave

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4
Q

Ventricular depolarization

A

Qrs complex

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5
Q

Ventricular repolarization

A

T wave

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6
Q

Rate of contraction

A

Chronotropic

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7
Q

Rate of electrical conduction

A

Dromotropic

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8
Q

Strength of contraction

A

Inotropic

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9
Q

Pressure needed to eject the blood

A

Afterload

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10
Q

Amount of blood returning

A

Preload

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11
Q

Carries deoxygenated blood away from the heart

A

Pulmonary artery

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12
Q

Carries oxygenated blood to the heart

A

Pulmonary vein

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13
Q

Inflammation of the pericardium
Triggered by viral infection, thoracic trauma, MI, TB, malignancy, and autoimmune conditions
Fluid accumulates in the space between pericardial sac and heart

A

Pericarditis

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14
Q

Cardiac compression from excessive fluid accumulation

Life-threatening

A

Cardiac tamponade

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15
Q

Formally called bacterial endocarditis
Infection of endocardium and heart valves
Vegetation forms on internal structures and creates small thrombi

A

Infective Endocarditis

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16
Q

Inflammation of the myocardium

Uncommon; poorly understood

A

Myocarditis

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17
Q

Conditions that weaken and enlarge the myocardium

Can be acquired or inherited

A

Cardiomyopathy

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18
Q

Most common type

Cardiomegaly and ventricular dilation damage myocardium muscle fibers, resulting in decreased CO and blood stagnation

A

Dilated cardiomyopathy

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19
Q

Mainly affects systolic function
More common in men and those who are sedentary
Ventricle wall becomes stiff and unable to relax

A

HYPERtrophic cardiomyopathy

20
Q

Common in South and Central American, India, Asia, and Africa
Caused by rigidity of ventricles, leading to diastolic dysfunction

A

Restrictive cardiomyopathy

21
Q

Inadequate pumping

Leads to decreased CO, increased preload, and increased after load

A

Heart Failure

22
Q

Compensatory mechanisms activated
activation of the sympathetic nervous system
renin-angiotensin-aldosterone system
ventricular hypertrophy
The compensatory mechanisms help at first but create a vicious cycle

A

Heart failure

23
Q

Cardiac output fails

Blood backs up to the pulmonary circulation

A

Left-sided failure

24
Q

Blood backs up to the peripheral circulation

A

Right sided failure

25
Q

Structural issues present at birth

Most common type of birth defect

A

Congenital heart defects

26
Q

Weakening of an artery

common in the abdominal aorta, thoracic aorta, and cerebral, femoral, and popliteal arteries

A

Aneurysms

27
Q

High levels of lipids in the blood
Increases risk for many chronic diseases
Lipids come from dietary sources and are produced by the liver

A

Dyslipidemia

28
Q

Chronic inflammatory disease characterized by thickening and hardening of the arterial wall
Inflammatory process is triggered by a vessel wall injury
Lesions develop on the vessel wall and calcify over time

A

Atherosclerosis

29
Q

Narrowing of peripheral vessels

A

PVD

30
Q

Atherosclerotic changes of the coronary arteries

Impairs myocardial tissue perfusion

A

CAD

31
Q

Intermittent chest pain resulting from myocardium ischemia

A

Angina

32
Q

Stationary blood clot consisting of platelets, fibrin, erythrocytes, and leukocytes

A

Thrombus

33
Q

Engorged veins resulting from valve incompetency
Most common in the legs
May also occur as esophageal varies and hemorrhoids
Increased venous pressure and blood pooling and lead to vein enlargement and valve stretching
Valves become incompetent, leading to reversal of blood flow and increased distinction
Capillary pressure increases, which leads to fluid leak, resulting in edema and skin discoloration

A

Varicose veins

34
Q

Swelling due to a lymph obstruction

A

Lymphedema

35
Q

Deal of the myocardium

Coronary artery blood flow is blocked due to atherosclerosis, thrombus, or vast spasms

A

MI

36
Q

Prolonged elevation in blood pressure
Excessive cardiac workload due to vasoconstriction, which leads to increased afterload
Vasoconstriction decreases renal blood flow, leading to inappropriate activation of the renin-angiotensin-aldosterone system

A

HTN

37
Q

Especially intense form
Does NOT respond well to treatment
Type of htn

A

Malignant HTN

38
Q

Decreased blood volume or circulatory stagnation resulting in inadequate tissue and organ perfusion

A

Shock

39
Q

Sympathetic nervous system and renin-angiotensin-aldosterone system are activated

A

Compensatory shock

40
Q

Compensatory mechanisms fail

Tissues become hypoxia, cells switch to anaerobic metabolism, lactic acid builds up, and metabolic acidosis develops

A

Progressive Shock

41
Q

Organ damage occurs

A

Irreversible Shock

42
Q

Loss of vascular sympathetic tone and autonomic function lead to massive vasodilation

A

Neurogenic (distributive)

43
Q

Bacterial endotoxins activate an immune reaction

A

Septic

44
Q

Excessive allergic reaction

A

Anaphylactic shock

45
Q

Left ventricle cannot maintain adequate cardiac output

A

Cardiogenic shock

46
Q

Venous return reduces because of external blood volume losses

A

Hypovolemic shock

Patho Test 1 (5 decks)

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