cardiac Flashcards

1
Q

diastole

A

when blood returns to the heart and heart is relaxed

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2
Q

systole

A

when the heart is contracted

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3
Q

pulmonary system pressure

high or low

A

low pressure except for in utero

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4
Q

systemic system pressure

A

high pressure except for in utero

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5
Q

purpose of one way venous valves

A

to prevent pooling and backflow

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6
Q

factors affecting arterial resistance

A

diameter, length, blood viscosity

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7
Q

mean arterial pressure (MAP) =

A

cardiac output (CO) x systemic vascular resistance (SVR)

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8
Q

cardiac output (CO) =

A

stroke volume (SV) x heart rate (HR)

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9
Q

factors affecting cardiac output

A

preload, contractility and afterload

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10
Q

preload

A

amount of blood brought back to the heart

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11
Q

afterload

A

resistance that heart has to pump against (BP)

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12
Q

sympathetic receptors in heart

A

beta 1 receptors

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13
Q

parasympathetic receptors in heart

A

muscarinic receptors

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14
Q

stroke volume

A

amount of blood ejected by a ventricle with each contraction

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15
Q

stroke volume (SV) =

A

end diastolic volume (EDV) - end systolic volume (ESV)

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16
Q

starling’s law of the heart

A

higher end diastolic volume causes a stronger contraction and therefore a higher stroke volume due to myocyte stretch

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17
Q

blood pressure =

A

CO x systemic vascular resistance

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18
Q

RAAS system to control BP

A

decreased kidney perfusion –> renin released –> angiotensin I –> angiotensin II (arteriole constriction) (within hours) –> aldosterone (retention of Na+ and water; remodeling of heart muscle) (within weeks-months)

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19
Q

primary/essential hypertension

A

no single cause; 90-95% of cases; risk factors

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20
Q

hypertension risk factors

A

race, sodium intake, smoking, low potassium, family history, age, high cholesterol, too much caffeine, obesity, restricted activity, sleep apnea, alcohol use

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21
Q

secondary hypertension

A

has a direct cause; 5-10% of cases; precipitating conditions like cardiovascular, renal, and endocrine (high aldosterone) disorders; pregnancy; and medications

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22
Q

high blood pressure symptoms

A

headache (due to intracranial pressure), blurred vision (due to impeded optic nerve), chest pain (due to plaque build up in coronary arteries), nose bleeds (high pressure vessels rupture easily)

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23
Q

hypertension is also known as

A

“the silent killer”

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24
Q

end organ damage from hypertension

A

cerebrovascular damage (stroke, retinopathy), vasculopathy (atherosclerosis, aortic aneurysm), heart disease (left ventricular hypertrophy, coronary artery disease, HF), nephropathy/renal failure

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25
Q

ventricular hypertrophy

A

ventricular wall thickens due to having to work harder because of high peripheral vascular resistance; causes less volume in ventricle, decreasing CO and making heart work even harder

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26
Q

approaches to hypertension treatment

A

inhibit sympathetic impulses to decrease contractility, HR, and vasoconstriction; inhibit smooth muscle function; inhibit RAAS; inhibit retention of water

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27
Q

classes of antihypertensives

A

diuretics, calcium channel blockers, beta blockers, alpha 1 blockers, alpha 2 agonist, direct vasodilator, ACE/ARBs

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28
Q

goal of diuretics

A

move sodium into the tubules so that water follows and is excreted

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29
Q

furosemide (lasix)

A

loop diuretic; treat HTN, HF, renal disease, edema, and pulmonary edema; **not potassium or calcium sparing; **can cause orthostatic hypotension, electrolyte imbalances, photosensitivity, hyperglycemia, dehydration; caution - ototoxicity (hearing loss); monitor inputs and outputs

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30
Q

loop diuretic

A

inhibits sodium and chloride reabsorption in kidney; treat HTN, HF, renal disease, edema, and pulmonary edema; more potent than thiazides; rapid (effect in 30-50 mins); decrease vol. CO, and BP. furosemide (lasix)

otoxicity

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31
Q

thiazide diuretics

A

less potent than loop diuretic; inhibits sodium and chloride reabsorption; excretion of sodium, chloride and water; used with normal functioning, not for pt. in distress; treat HTN, peripheral edema, and cirrhosis of the liver

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32
Q

hydrochlorothiazide (HCTZ)

A

thiazide diuretic; calcium sparing; not for pt. in distress; may cause low K+, hyperglycemia, hypovolemia, photosensitivity; monitor input/output; monitor renal function and weigh daily; monitor blood sugar; use sunscreen and replace K+ as needed

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33
Q

potassium sparing diuretic

A

weak diuretic; promotes sodium and water excretion but potassium retention; blocks aldosterone (normally causes sodium resorption); use w/ HTN, edema, HF, ascites, hyperaldosteronism

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34
Q

spironolactone

A

potassium sparing diuretic; not as powerful as loop or thiazide diuretic; can cause hyperkalemia, hypotension, dry mouth, gynecomastia (breast enlargement in men); avoid foods high in K+

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35
Q

osmotic diuretic

A

most potent diuretic; pulls water into tubule for excretion without sodium loss; hypertonic solution; use for cerebral edema, acute renal failure and shock; only given IV

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36
Q

mannitol

A

osmotic diuretic; very intense diuresis; use for cerebral edema, acute renal failure and shock; causes sudden drop in fluids that may cause hypoTN, lightheadedness, confusion and HA; given IV; perform neuro assessment and LOC; caution in pt. w/ renal disease, anuria, intracranial bleeding or dehydration

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37
Q

carbonic anhydrase inhibitors

A

use at the same time as diuretic to cause more intense diuresis; block the effect of carbonic anhydrase; slow down movement of hydrogen ions; more sodium and bicarbonate lost in the urine; use for edema with heart failure, acute pulmonary edema, liver disease, and renal disease

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38
Q

acetazolamide (diamox)

A

carbonic anhydrase inhibitor; use in adjunct with diuretic for more intense diuresis; edema w/ HF, acute pulmonary edema, liver or renal disease; may cause metabolic acidosis due to less bicarbonate to be a buffer, hypokalemia, confusion; interacts with salicylates and lithium

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39
Q

ACE inhibitors

A

inhibits angiotensin converting enzyme which normally converts angiotensin I –> II and causes vasoconstriction; ACE inhibitor decreases vasoconstriction and BP; use for HTN and HF

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40
Q

lisinopril

A

ACE inhibitor; use for HTN and HF; lowers constriction and BP; may cause dry persistent cough, angioedema (swelling under skin), and hyperkalemia; monitor for hypoTN and K+ levels; can’t stop suddenly, causes rebound hypertension

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41
Q

angiotensin receptor blockers (ARBS)

A

blocks angiotensin II receptors in smooth muscle and adrenal cortex; blocks release of aldosterone to prevent peripheral vasoconstriction

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42
Q

losartan

A

angiotensin receptor blocker; treat HTN; blocks angiotensin II receptors; may cause angioedema, hyperkalemia, and renal failure

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43
Q

angiotensin II

A

causes vasoconstriction to increase BP

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44
Q

aldosterone

A

increases retention of sodium and water, remodeling of heart muscle over time to increase blood pressure

45
Q

angioedema

A

swelling beneath the skin

46
Q

beta blockers

A

inhibit beta 1 receptors in SNS to block norepinephrine and epinephrine; causes in HR, force of contraction, and velocity of impulse conduction; used for stable angina, HTN, HF, cardiac dysrhythmias, and sometimes performance anxiety; can be selective or non selective.

47
Q

cardio selective beta blockers

A

metoprolol, atenolol; blocks only beta 1 receptors in heart; reduce CO

48
Q

non-selective beta blockers

A

propranolol (inderal), carvedilol; blocks both beta 1 and 2 receptors; may cause bronchoconstriction and blood sugar masking; caution in pt. w/ diabetes; may be used for performance anxiety

49
Q

calcium channel blockers

A

blocks movement of calcium to cause relaxation and less nerve impulses; often couples w/ beta blockers; lowers HR and BP; may be dihydropyridines or non-dihydropyridines

50
Q

dihydropyridines

A

amlodipine and nifedipine; calcium channel blockers that act only on arterial smooth muscle cells (not on cardiac calcium channels); vasodilates arteries to lower BP; used for angina and HTN; may cause ankle edema,** gingival hyperplasia** (overgrown gums), proteinuria, and hypoTN

51
Q

non-dihydropyridines

A

verapamil and diltiazem; calcium channel blockers that act on arterial SMCs and cardium; causes arterial vasodilation, slowing of HR in SA node (chronotropic), slowing of conduction in AV node (dromotropic), and reduction in contractility of myocardium (ionotropic); used for stable angina, HTN and dysrhythmias; may cause bradycardia and heart block; interacts with beta blockers and digoxin

52
Q

chronotropic

A

alter rhythm

53
Q

dromotropic

A

alter conductivity

54
Q

ionotropic

A

alter contractility

55
Q

adrenergic blockers

A

block postsynaptic alpha 1 receptor sites in arteries, bladder and urethra; dilates peripheral arteries to lower peripheral resistance and BP; treat HTN, benign prostatic hyperplasia, and raynaud’s

56
Q

prazosin (minipress)

A

adrenergic blocker used to treat HTN, benign prostatic hyperplasia, and raynaud’s; lowers BP; may cause orthostatic hypoTN (give at night), reflex tachycardia (inc HR in response to dec. BP), nasal congestion, impotence (erectile dysfunction), or rebound hypoTN (take at same time every day)

57
Q

hydralazine

A

arterial vasodilator; decrease afterload to reduce workload; inc. perfusion of heart

58
Q

nitroprusside, nitroglycerine, isosorbide

A

venous vasodilators; reduce venous return, reduces preload

59
Q

vasodilators

A

used to treat HTN, HF, MI, and angina; different ones chosen for different reasons; may cause postural hypoTN, reflex tachycardia, and HA; combine with diuretic to avoid blood volume inc.

60
Q

arteriosclerosis

A

loss of arterial elasticity; hardening of the vessel walls; natural process of aging; calcium deposited into cytoplasm and causes elasticity loss

61
Q

atherosclerosis

A

inflammatory disease; small tears in inside of arteries then fill with fatty streaks and fibrous plaque; made up of cholesterol; can be reversed

62
Q

manifestations of atherosclerosis

A

no s/s until severe; claudication (leg pain caused by dec. blood flow); reduced exercise tolerance and shortness of breath; HTN, stroke, MI

63
Q

atherosclerosis risk factors

A

smoking (stiffens vessels), obesity, high fat diet, HTN, diabetes, lack of exercise, family history

64
Q

atherosclerosis modes of treatment

A

treat BP and cholesterol, anticoagulant

65
Q

peripheral artery disease

A

narrowing or blockage of artery causing decreased blood flow towards tissue; creates ischemia below the occlusion; can cause ischemic ulcers and changes in skin, swollen grey feet, hair loss; pulses are diminished or absent; sharp stabbing pain

66
Q

peripheral artery disease treatment

A

vasodilators, antiplatelets

67
Q

peripheral venous disorders

A

deoxygenated blood can’t get back to heart; pooling in extremities; areas of ischemia and necrosis due to low O2; dull and achy, edema, diminished/absent pulses, warm legs, ulcer risk.

68
Q

deep vein thrombosis (venous thromboembolism)

A

clot in vein preventing return of blood to heart; platelets adhere to damaged wall and form platelet plug, clotting factors create clot, can become dislodged and enter right atrium and enter pulmonary system(pulmonary emboli); test for D-dimer levels to assess risk

69
Q

virchow’s triad

A

risk factors for DVT; hypercoagulability; venous stasis; vascular damage

70
Q

deep vein thrombosis symptoms

A

pain (w/ dorsiflexion of foot), swelling, redness, warmth of lower extremities

71
Q

DVT treatment

A

thrombolytic enzymes (break up thrombus); thrombectomy (surgery to remove thrombi); IVC filter; compression stockings (prevent venous stasis); calf exercises; anticoagulants, low dose aspirin

72
Q

coronary artery disease (CAD)

A

atherosclerosis in 1 or more coronary arteries; narrowing/obstruction; causes dec. perfusion of myocardium; leads to HTN, MI, HR, death (more lethal in younger pt.); s/s don’t occur until there’s enough blockage to cause ischemia

73
Q

coronary artery disease risk factors

A

modifiable: BMI >30, diabetes, HTN, alcohol use, high LDL, low HDL, smoking – cause inc. inflammation and clotting factors
non-modifiable: age 65+, family history

74
Q

coronary artery disease treatment

A

nitrates, calcium channel blockers, cholesterol-lowering medications

75
Q

variant (prinzmetal) angina

A

most severe; pain at rest without provocation; triggered by smoking; associated with AV block or ventricular arrhythmias; with or without CAD; treated with calcium channel blockers and stopping smoking

76
Q

stable angina

A

myocardial atherosclerosis (CAD); pain with exertion; aggravated by exercise, cold temps, stress; stable pattern; relieved by rest; 1st line of treatment is nitrates (vasodilation) and aspirin (prevent clots)

77
Q

unstable angina (pre-infarction angina)

A

angina of increasing intensity, frequency, or duration; what used to make it stop doesn’t anymore; at rest or with minimal activity; lasts >15 mins; unresponsive to nitroglycerin (NTG)

78
Q

angina medications

A

nitrates (vasodilate); beta blockers (dec. O2 consumption); calcium channel blockers (relax); antiplatelet (prevent thrombosis formation)

79
Q

nitrates (nitro-bit, nitrostat)

A

antianginal; vasodilation of veins and large arteries; does not dilate coronary arteries; decrease preload and afterload to dec. work of heart; sublingual, take up to 3 tabs and call 911 if still have pain; store in a dark tightly capped bottle

80
Q

myocardial infarction risk factors

A

atherosclerosis, CAD, high cholesterol, smoking, HTN, obesity, sedentary, stress

81
Q

myocardial infarction

A

myocardial tissue abruptly and severely deprived of O2; thrombus lodged in coronary artery; sudden crushing chest pain radiating to shoulder (in men) or jaw (in women); NV, shortness of breath, sweating

82
Q

MI signs in older adults

A

shortness of breath, pulmonary edema, dizziness, altered mental status, dysrhythmias

83
Q

low density lipoproteins (LDL)

A

bad; tightly packed cholesterol, triglycerides, and lipids; carried by proteins that enter circulation; healthy level: under 100

84
Q

high density lipoproteins (HDL)

A

good; loosely packed lipids; used for energy; pick up remanent of fats and cholesterol left in periphery by LDL breakdown; healthy level: above 60

85
Q

HMG-CoA Reductase inhibitors (statins)

A

atorvastatin (lipitor); blocks enzyme HMG-CoA (normally helps synthesize cholesterol); used in hyperlipidemia, CAD prevention (primary), stabilize plaques in pt. w/ CAD (secondary)

86
Q

atorvastatin (lipitor)

A

HMG-CoA reductase inhibitor; treat hyperlipidemia, prevent CAD, stabilize plaques in pt. w/ CAD; limit cholesterol synthesis; may cause flatulence, abd. cramps, constipation, dizziness, HA, pruritus (itching), hepatotoxicity; teratogenic; grapefruit juice inc. toxicity risk

87
Q

bile acid sequestrants

A

cholestyramine; binds to bile acid to force liver to use cholesterol to make more bile; decreases serum cholesterol levels; prevention of CAD; dissolves gallstones

88
Q

cholestyramine

A

bile acid sequestrant; decreases cholesterol levels to prevent CAD; gritty power must be dissolved; take w/ lots of fluids; usually combo with statin; may cause constipation; malabsorption of fat soluble vitamins (A, K, E, D), diuretics, digoxin, warfarin, thyroid hormones, and corticosteroids

89
Q

cholesterol absorption inhibitors

A

ezetimibe (zetia); inhibit absorption of cholesterol; treat hypercholesterolemia, sitosterolemia

90
Q

ezetimibe (zetia)

A

cholesterol absorption inhibitor; treat hypercholesterolemia; may cause abd. pain, diarrhea, muscle aches and pain; caution in combo with statin; interacts w/ cholestyramine, fenofibrate, gemfibrozil, and warfarin

91
Q

niacin

A

vitamin B3; inhibits release of free fatty acids from adipose tissues; inc. rate of triglyceride removal from plasma; may cause flushing

92
Q

fenofibrates

A

inhibits triglyceride synthesis in liver to lower LDL; inc. uric acid secretion; stimulate triglyceride break down

93
Q

omega 3-acid ethyl esters (lovaza)

A

inhibits liver enzyme system to dec. synthesis of triglyceride

94
Q

omega 3-carboxylic acid (epanova)

A

fish oil mixture; free fatty acid approved as an adjunct to diet to reduce triglyceride levels with severe hypertriglyceridemia

95
Q

QRS complex

A

ventricular contraction

96
Q

arrhythmia (dysrhythmia)

A

disruption in cardiac rate or rhythm; due to electrolyte imbalances, medications, hypoxia of myocardium, aging, or structural damage; results in lower cardiac output and the associated symptoms

97
Q

sinus arrythmias

A

can still sustain life; tachycardia or bradycardia

98
Q

ectopy

A

type of arrhythmia; early contraction; premature atrial contraction (PAC) or premature ventricular contraction (PVC); can be harmless if not over time

99
Q

junctional rhythms

A

originates from AV node or bundle of his; atria and ventricles fire at different rates; another node fires separately from the SA node

100
Q

amiodarone (potassium channel blocker)

A

block potassium channels and slow outward movement of K+ during phase 3 of the action potential; first line for V-fib maintenance; works for atrial and ventricular; can cause HF, N/V, hypoTN

101
Q

adenosine

A

antiarrhythmic; for emergency situation; for supraventricular tachycardia (SVT); short half life so give as close to heart as possible (antecubital) and follow w/ flush

102
Q

digoxin

A

only cardiac glycoside in the US; troublesome-narrow therapeutic range; use for HF, A. fib, A. flutter, A. tachycardia; inc. force of contraction; vagal stimulation; high K+ reduces effect (ACE inhibitor); low K+ inc. toxicity risk (diuretics); hold if apical pulse <60bpm

103
Q

ways to stimulate vagal nerve (to dec. HR + conduction)

A

knees to chest, vomiting, ice on face (kids), straining to stool (elderly)

104
Q

left ventricular failure (congestive HF)

A

most common HF; BP drops; back up into lungs; cyanosis, pulmonary congestion, dyspnea, orthopnea, fatigue, confusion

105
Q

right ventricular failure (cor pulmonale HF)

A

back up in venous system, can lead to venous congestion of organs (liver); right HF is the most common cause; inc. peripheral venous pressure, ascites, distended jugular veins, edema, weight gain, red

106
Q

systolic HF

A

problem with contraction and ejection results in dec. ventricular output –> baroreceptors stimulate SNS to inc HR; heart tries to compensate by releasing natriuretic peptides

107
Q

diastolic HF

A

problem with relaxing and filling; cardiac cells die during systolic HF and muscles become fibrotic –> diastolic HF; fibrotic ventricle resists filling leading to dec. CO; low CO inc. work for the heart and perpetuates HF

108
Q

diagnosing HF

A

history + physical assessment; echocardiogram, chest x ray; EKG; enzyme labs; stress test; cardiac catheter

109
Q

heart failure treatment

A

ACE inhibitor/ARB; aldactone (K+ sparing diuretic); digoxin (cardiac glycoside); Lasix (loop diuretic); beta blocker