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Clin Med Exam 2 > coronary artery disease > Flashcards

coronary artery disease Flashcards

1
Q

ischemia

A

decrease in blood flow to the myocardium

angina is a symptom

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2
Q

infarction

A

is death of myocardium caused by lack of blood flow

angina is a symptom

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3
Q

angina

A

90% of cases caused by CAD

when cardiac workload exceeds the oxygen supply to the myocardial tissue, ischemia occurs causing chest pain

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4
Q

chronic stable angina

A

classic

exertional

occurs at predictable levels of physical or emotional stress

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5
Q

new onset angina

A

has developed in the past 2 weeks

unstable

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6
Q

nocturnal angina

A

awaken a person from sleep w/ same sensation experienced during exertional

unstable

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7
Q

postinfarction angina

A

after an MI

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8
Q

periinfarction angina

A

a symptom of worsening cardia ischemia

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9
Q

prinzmetal’s angina

A

vasospastic/variant

cuased by coronary artery spasm

not arthrosclerosis

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10
Q

decubitus (resting) angina

A

occurs often at rest and at same time everyday

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11
Q

clinical manifestations of angina

A

pain or discomfort (dermatome from C3-T4)

sensation described as squeezing, burning, pressing, heartburn, indigestion or choking

recognizing symptoms more difficult in women

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12
Q

diagnosis angina

A

history

supported by sublingual nitroglycerin shortening attack

DO NOT TAKE VIAGRA

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13
Q

treatment of angina pectoris

A

drugs that help restore or maintain balance b/w myocardial oxygen supply and demand

organic nitrates

beta-adrenergic blockers

calcium channel blocker

anticoagulants

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14
Q

organic nitrates (angina)

A

decrease myocardial oxygen demand

dilates the veins and decreased the amount of blood returning to the heart

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15
Q

beta-adrenergic blockers (angina)

A

decrease HR and force of myocardial contraction by antagonizing Beta-1 receptors

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16
Q

calcium channel blockers (angina)

A

increase coronary blood flow

increasing myocardial oxygen supply by dilation

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17
Q

anticoagulants (angina)

A

heparin

aspirin to prevent further blockage of the coronary arteries

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18
Q

implications for PT

A

watch out for orthostatic hypotension

monitoring vital signs

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19
Q

myocardial infarction

A

development of ischemia w/ resultant necrosis of myocardial tissue

heart attack

occur more frequently in early morning hours, holiday season

genetics play a major role in CVD

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20
Q

what percent of MIs result from coronary thrombosis

A

80-90%

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21
Q

risks of MI

A

upper reparatory tract illnesses

periodontal disease

acute respiratory tract infections

increased PAI-1 in people with diabetes

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22
Q

PA-1 (MI)

A

plasminogen activator inhibitor 1

increases the risk of thrombosis

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23
Q

one of the best indicators for heart attack risk

A

bigger waist to hip ratio

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24
Q

pathogenesis of MI

A

occlusion of the coronary arteries (esp left coronary artery) and its branches effecting the left ventricle

MI/reperfusion injury accompanies by inflammatory response

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25
Q

clinical manifestations of MI

A

sudden sensation of pressure

chest pain (occasionally radiating to the arms, throat, neck and back)

may be accompanied by pallor, shortness of breath and perspiration

post-infarction complications

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26
Q

post-infarction complications

A

arrythmias

cardiogenic shock

pericarditis

rupture of the heart

sudden death

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27
Q

gender differences of MI

A

female hearts are smaller and constructed differently

LV mass increased with age

women delay seeking help, receive less aggressive therapy, therefore death rate for bypass is 2x higher

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28
Q

common symptoms of women MI

A

gripping chest pain and breaking out in a cold sweat

symptoms less recognizable (such as pain or discomfort in the stomach, jaw, neck or back, nausea)

CHRONIC UNEXPLAINED FATIGUE

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29
Q

other considerations for women and MI

A

hormonal status

hypertension

cholesterol

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30
Q

hormonal status

A

estrogen has be considered to have a cardioprotective benefit

31
Q

hypertension

A

more common in women

32
Q

cholesterol

A

guidelines for on lipid levels have not been standardized in women

except HDL

33
Q

diagnosis of MI

A

measurement of serum levels of cardiac enzymes such as cardiac troponin (TnI)

cardiac troponin T (TnT)

myocardial isoenzyme of creatine kinase (these are released during a heart attack)

34
Q

treatment MI

A

thrombolytic agents that dissolve clots

promote vasodilation

reduce infarct size

35
Q

chart angina v. MI

A

signs and symptoms

pathogenesis

in notes

36
Q

congestive heart failure

A

heart is unable to pump sufficient blood to supply the body’s needs

4 types

most common cause for hospitalization in people older than 65

37
Q

4 types of congestive heart failure

A

systolic heart failure

diastolic heart failure

left sided heart failure (CHF)

right sided heart failure

38
Q

systolic heart failure

A

contractile failure of myocardium

39
Q

diastolic heart failure

A

increased filling pressures are required to maintain adequate cardiac output

40
Q

left sided heart failure

A

left ventricle can no longer maintain normal cardiac output

41
Q

right sided heart failure

A

right-sided ventricular dysfunction secondary to either left-sided heart failure or to pulmonary disease

Cor pulmonale

42
Q

cor pulmonale

A

abnormal enlargement of the right side of the heart as a result of a disease of the lungs or pulmonary vessels

43
Q

risk factors of CHF

A

hypertension

pre-existing heart disease

pulse pressure elevation

Paget’s disease

HIV medication

44
Q

CHF pathogenesis

A

structural changes such as loss of myofilaments, apoptosis, disturbances in calcium homeostasis and alteration in collagen synthesis

neurohormonal compensatory mechanisms

45
Q

neurohormonal compensatory mechanisms (MI)

A

first compensatory phase: ventricular dilation, pulmonary congestion

second compensatory phase: sympathetic nervous system increases stimulation the heart muscle

third compensatory phase: activation of renin-angiotensin-aldosterone system, kidneys retain water and sodium to increase blood volume

46
Q

clinical manifestations CHF

A

left sided heart failure: dyspnea, fatigue, muscular weakness, renal changes, PULMONARY EDEMA

right-sided heart failure: edema, jugular venous distension, abdominal pain, right upper quadrant pain, cyanosis, PERIPHERAL EDEMA (most prominent in lower extremities)

47
Q

treatment of CHF

A

goal is to improve the heart’s pumping ability

48
Q

drugs that increase myocardial contraction force

A

positive inotropic agents

digitalis

phosphodiesterase inhibitors

dopamine and dobutamine

49
Q

digitalis

A

increase intracellular calcium concentration to enhance contractility and increase the heart’s mechanical pumping ability

50
Q

phosphodiesterase inhibitors

A

allow c-AMP concentrations to increase, allowing calcium concentrations to increase

51
Q

dopamine and dobutamine

A

stimulate beta-1 receptors on the myocardium to increase contractility, usually reserved for pts w. advanced cases

52
Q

agents that decrease cardiac workload

A

drugs affects the renin-angiotensin system

beta blockers

diuretics

vasodilators

53
Q

drugs that affect the renin-angiotensin system

A

ACE inhibitors: limits peripheral vasoconstriction, decreased the pressure against which the heart has to pump

angiotensin II receptor blockers (ARBS): used as an alternative for those who cannot tolerate ACE inhibitors

54
Q

beta blockers (CHF)

A

normalize sympathetic stimulation of the heart

reduce HR and myocardial contraction force

55
Q

diuretics (CHF)

A

reduce congestion in the lungs and peripheral tissues by exerting excess fluid

56
Q

vasodilators (CHF)

A

reduce peripheral vascular resistance

57
Q

implications for PT CHF

A

prevent complications of bedrest, monitor vital signs

exercise should be avoided immediately after eating or taking vasodilators

58
Q

sudden cardiac death

A

death resulting from abrupt loss of heart function

electrical impulses in the diseased heart become rapid (ventricular tachycardia) or chaotic (ventricular fibrillation) or both

59
Q

what can mimic cardiogenic pain

A

GI distress

anxiety (panic attack)

muscular strain

infectious disease

60
Q

helpful screen

A

if symptoms worsen w/ effort and abates with rest, its more likely cardiogenic

symptom is constant, probably not cardiogenic

symptom comes and goes on its own, it is hard tot ell

symptom is reproducible w/ pressure, less likely to be cardiogenic

61
Q

cardiomyopathies

A

conditions affect the heart muscles so that contraction and relaxation of myocardium are impaired

primary and secondary

62
Q

primary cardiomyopathies

A

include genetic, mixed and acquired

confined to heart muscle

63
Q

secondary cardiomyopathies

A

involve myocardial pathology as part of generalized systemic disorders that affect the heart along w/ other organs

64
Q

clinical manifestations cardiomyopathies

A

dyspnea

orthopnea

tachycardia

palpitations

peripheral edema

distended jugular vein

65
Q

3 cardiomyopathies

A

dilated

hypertrophic

restrictive

66
Q

dilated cardiomyopathy

A

occurs most often in black men

b/w 40 and 60 years old

obesity

long-term alc abuse

systemic hypertension

smoking

infections

pregnancy

SECONDARY TYPE

fatigue, weakness, chest pain (unlike angina), BP normal or low

67
Q

hypertrophic cardiomyopathy

A

autosomal dominant trait on chromosome 14

most common cause of cardiac sudden death in the young

primary type

usually asymptomatic, sudden death being the presenting sign

68
Q

restrictive cardiomyopathy

A

result of myocardial fibrosis, hypertrophy, infiltration or defect in myocardial relaxation

can be either primary or secondary

exercise intolerance, fatigue, shortness of breath, peripheral edema

69
Q

nonpenetrating trauma (cardiomyopathy)

A

any blunt chest trauma, the pain is similar to an MI and is often confused w/ musculoskeletal pain from soft tissue consequences of chest trauma

treated similar to MI

70
Q

penetrating trauma (cardiomyopathy)

A

d/t external objects (bullets or knives), complications include arrythmias, aneurysm formation, death from infection

71
Q

myocardial neoplasm (cardiomyopathy)

A

primary cardiac tumors are rare

95% malignant tumors are sarcomas

5% of malignant tumors are lymphomas

sarcomas replace functional cardiac tissue w/ cancerous cells, may not produce any symptoms or present w/ arrythmias and conduction disturbances

benign primary cardiac tumors occur 3x more often than malignant primary tumors

72
Q

cardiac neoplasms come to the attention of the therapist when

A

progressive interference w/ mitral valve function results in exercise intolerance/ exertional dyspnea

embolus causes stroke

73
Q

systemic manifestations of cardiac neoplasms

A

muscle atrophy

arthralgias

malaise

Raynaud’s phenomena

Clin Med Exam 2 (9 decks)

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