cardiac patho - E3 Flashcards

1
Q

what area is the most concerning to get clogged for people w/ CAD

A

left anterior descending artery because it is the power house of the heart and determines perfusion to body
“widow maker”

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2
Q

CAD

A

the arteries branching off the aorta get clogged d/t atherosclerosis

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3
Q

do you have to have a heart attack to be able to have coronary artery disease

A

no, you can have CAD w/o having a heart attack but the disease can cause a heart attack

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4
Q

non modifiable risk factors for CAD

A

age, family hx, gender (men early years then equal post meni), ethnicity (AA), genetics

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5
Q

modifiable risk factors for CAD

A

HTN, cigarette smoking, diabetes, obesity/inactivity, diet, HDL, depression/stress

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6
Q

CAD etiology

A

atherosclerosis develops in the arteries supplying the myocardium causing the arteries to be blocked -> the damage causes decreased tissue perfusion and endothelial dysfunction (+the heart has to work harder than it is supposed to)

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7
Q

endothelial dysfunction

A

vessels become narrowed when they are supposed to dilate caused by DM, HTN, HDL, smoking
huge problem when paired w/ blocked arteries

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8
Q

when the heart doesn’t get the blood and oxygen it is supposed to -> what does it look like

A

angina
-can be asym
-chest pain, heart burn, irregular HR, weakness, anxiety, dizziness, cold sweat, nausea
if it becomes completely blocked -> MI

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9
Q

stable angina

A

coronary blood flow is diminished but not fully blocked -> sx occurs on exertion & relieved w/ rest

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10
Q

what to do if having a stable angina episode

A

stop activity & sit down (to decrease oxygen demand on the heart), take nitrate, call 911 if pain does not go away

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11
Q

what areas are associated w/ the heart that needed to be ruled not cardio before looking into other non cardiac problems

A

left arm, jaw, left shoulder, diaphoresis, pallor

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12
Q

what does cardiac pain present as

A

-pressure or tightness
-diffused, poorly localized
-associated w/ physical exertion or stress
-relieved w/ rest, prolonged could mean MI

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13
Q

what does non cardiac pain present as

A

-sharp or stabbing
-focal, well localized
-could be positional, spontaneous at rest
-no predictable relation to physical exertion
-can lasts seconds to days

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14
Q

atypical angina in women

A

-discomfort: hot, burning, tender
-location: not always the chest
-other: indigestion, heart burn, nausea, fatigue, lightheadedness, dyspnea

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15
Q

pain associated w/ a MI

A

-chest pain not brought on by exertion that can radiate
-pain not relieved in 2-5 mins
-N/v, SOA, diaphoresis

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16
Q

cardiomyopathy

A

disease that affects the myocardium that is usually idiopathic and can be caused by ischemia, htn, inherited disorders, infections, toxins, myocarditis, & autoimmune disorders that can lead to heart failure

17
Q

dilated cardiomyopathy

A

r/t ischemic problems, valve problems, alc/drugs, post/peri pts, heart failure issues & infections -> leads to heart failure w/ reduced ejection fraction

18
Q

hypertrophic cardiomyopathy

A

r/t htn causing the muscle to become enlarged -> leads to decreased ejection fraction and high risk of deadly arrhythmias and sudden cardiac death

19
Q

restrictive cardiomyopathy

A

r/t amyloid disease, the ventricles becoming resistant to filing & the muscle stops working / hardens -> leads to a right sided heart failure

20
Q

what is heart failure

A

a chronic, progressive condition in which the heart muscle is unable to pump enough blood to meet the body’s needs for blood and oxygen

21
Q

heart failures results in

A

decreased cardiac output, decreased myocardial contractility, increased preload & increased after load

22
Q

development of HF -> pathological changes that occur

A

-volume overload bc heart isn’t pumping effectively & you get a fluid back up
-impaired ventricular filling (which occurs during diastole aka in between the contraction)
-weakened ventricular muscle
-decreased ventricular contractile function (the squeeze during systole)

23
Q

etiology of HF

A

r/t repeated ischemic episodes (unstable angina or MIs), chronic htn, DM, copd (rvf), dysrhythmias, valve disorders (mitral insuf, aortic stenosis), pulm embolus (rvf)

24
Q

if a person has left sided heart failure, where does the back up of blood occur

A

into pulmonary circulation

25
Q

if a person has right sided heart failure, where does the back up of blood occur

A

into systemic circulation

26
Q

left sided heart failure symptoms

A

-cough, crackles, wheezes
-frothy sputum (possibly blood tinged)
-paroxysmal nocturnal dyspnea
-orthopnae (tripod position to breath)
-cyanosis, tachycardia, restlessness

27
Q

right sided heart failure symptoms

A

JVD, dependent edema (lower extremities), weight gain & anorexia, hepatosplenomegaly (enlarged spleen & liver)

28
Q

what is right sided heart failure most often caused by ; left sided

A

COPD ; HTN

29
Q

ejection fraction

A

the amount of blood pumped out of the left ventricle w/ each squeeze , normal is 55-65%

30
Q

Heart Failure: reduced ejection fraction (HFrEF) [systolic HF]

A

-EF <40% (seen on echo)
-caused by impaired contractile function, increased afterload, cardiomyopathy, & mechanical problems
-the left ventricle loses ability to generate pressure to eject blood & the weakened muscle cannot generate stroke volume which lower CO -> LV fails, blood backs up, caused fluid backup & accumulation

31
Q

Heart Failure: preserved ejection fraction (HFpEF) [diastolic HF]

A

-EF will be normal or mod decrease (40-49%)
-inability of the ventricles to relax & fill (ineffective muscle) during diastole caused by chronic HTN
-LV is stiff & noncompliant leading to high filling pressures which leads to decrease stroke volume & decreased CO -> fluid congestion

32
Q

ventricular remodeling in HF

A

a weakened heart muscle causing the heart to secrete molecular substances like angtiotensin II, aldosteron, andothelin, TNF alpha, epi & norepi, insulin like growth factor & growth hormone -> supposed to be protective but overtime provoke genetic changes, apoptosis, &hypertrophy of cardiac myocytes + as well as collagen deopsits & myocardial fibrosis which all worsen HF by causing enlargement & dilation

33
Q

S3 gallop in HF

A

-low pitch
-heard after S2 during rapid filing of the ventricle in the early part of diastole
fluid left in the ventricle after contraction