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Pathophysiology > Exam 2: Ch 19 CHD, Fetal & Congenital Disorders > Flashcards

Exam 2: Ch 19 CHD, Fetal & Congenital Disorders Flashcards

1
Q

__% of deaths in high income countries from heart disease

A

1 killer in USA

40%

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2
Q

the left and right coronary arteries begin just ____ to the ______ valve

A

distal, aortic

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3
Q

left main coronary artery gives rise to the ___ & ______

A

LAD, circumflex

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4
Q

left anterior descending supplies

A

septum and anterior wall of the LV

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5
Q

circumflex supplies

A

lateral (free) wall of LV

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6
Q

right coronary artery supplies

A

RV and gives rise to posterior descending artery

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7
Q

posterior descending artery supplies

A

posterior wall

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8
Q

gradual occlusion of CA does not produce symptoms until…

A

late because collaterals form

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9
Q

which artery BP reflects aortic pressure?

A

CA

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10
Q

CA flow is controlled by…

A

aortic BP: particularly DBP (intra myocardial vessels compressed during systole)

auto-regulation: CA flow increases to meet metabolic needs (O2 extraction high)

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11
Q

inadequate DBP leads to

A

ischemia

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12
Q

dilators include

A

NO and metabolites

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13
Q

CHD is divided into….

A

chronic ischemia heart disease

acute coronary syndromes

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14
Q

ischemia

A

any time cardiac oxygen demands are greater than supply

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15
Q

CHD caused by plaque categories

A

stable plaque

unstable plaque

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16
Q

fixed stable plaque

A

leads to stableangina

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17
Q

unstable plaques

A

rupture and form clots

lead to unstable angina and MI (ACS)

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18
Q

plaque rupture

A

can be spontaneous but often 2ndary SNS activity

vulnerable to rupture when they have a lipid core, inflammation, low SMC

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19
Q

plaque rupture occurs most often …

A

in the morning

during or after exercise

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20
Q

plaque rupture mechanisms

A

rupture exposes lipid core, causing platelets to adhere and release ADP and prostaglandins

more platelets leads to a thrombus

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21
Q

___ blocks prostaglandin synthesis

A

ASA – aspirin

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22
Q

_____ blocks ADP receptors on platelets

A

Plavix

23
Q

3 types of acute coronary syndrome (ACS)

A

Q-wave MI (ST elevation)

non Q-wave MI (non ST elevation)

unstable angina

24
Q

Q-wave MI generally occurs from a, and others from…

A

Q-wave: complete coronary artery occlusion

non Q-wave, unstable angina: incomplete or intermittent occlusion

25
Q

T wave inversion

A

ischemia

26
Q

ST changes in general

A

damage

27
Q

ST depression

A

subendocardial injury

28
Q

ST elecation

A

transmural injury

29
Q

Q wave

A

old MI

30
Q

serum markers

A

necrotic cells release contents into blood

myoglobin increased at 1hr, peaks in 4-8 hrs

not cardiac specific

31
Q

will a Q-wave MI and non Q-wave MI show increased serum markers?

A

yes, then classified as MI

32
Q

how is the area of infarct determined in Q-wave MI

A

which CA is blocked

33
Q

cause and symptoms of non Q-wave MI and unstable angina

A

from: plaque disruption with clot and/or arterial spasm

pain occurs at rest and is severe, persistent (>20 min), not relieved by NTG

called MI if serum markers are elevated

34
Q

symptoms of MI

A

acute pain, not relieved by rest or NTG

female more likely to have “discomfort”

elderly likely to have SOB (shortness of breath)

GI symptoms

30-50% die from VF (ventricular fibriliation) in 1st few hours

35
Q

extent of pathologic changes in ACS determined by

A

which vessel is occluded

time of occlusion

metabolic needs of tissue

extent of collaterals

36
Q

pathologic changes in ACS

A

immediate loss of contractility

irreversible damage and necrosis in 20-40min

reperfusion can reestablish blood flow, but “stuns” tissue

stunned tissue non functional

37
Q

goal of managing ACS

A

prevent extent of injury/necrosis

prevent sudden cardiac death

cells may not die if reperfusion achieved in 20-40min

38
Q

what happens in ER for ACS

A

evaluate for reperfusion w/ 12 lead ECG

watch for ST/T wave changes and PVCs (premature ventricular contractions)

O2 optimizes hemoglobin saturation

39
Q

drugs given in ER for ACS

A

analgesia with MS (IV) relieves pain, decrease anxiety

beta blockers decrease myocardial O2 needs

aspirin inhibits prostaglandin syn. by platelets

Plavix blocks ADP receptor on platelets

NTG decreases preload/afterload

MS for pain and anxiety

40
Q

management of ACS: fibrinolytic therapy

A

dissolves clots

limits infarct size

reduces mortality

best if begun within 90min of 1st symptoms

41
Q

PCI - percutaneous coronary intervention

A

balloon tip catheter introduced to femoral or brachial artery

catheter advanced to blockage under fluoro

expand balloon to dilate stenosis

statins prevent vessel collapse when catheter withdrawn

42
Q

acute and long term complications of PCI

A

acute: thrombosis, vessel dissection

long-term: restenosis (recurrence of stenosis)

43
Q

CABG

A

done on or off the pump

graft from aorta to CA distal to blockage

venous or arterial graft

mammary artery used, saphenous vein

44
Q

recovery from ACS

A

at 4-7 days the infarct is soft and can rupture

~7 weeks necrotic tissue replaced with granulation tissue (fibrous scar)

45
Q

recovery complications of ACS

A

HF and cardiogenic shock from decreased contractility

Dressler’s syndrome

LV aneurysm and rupture from weakened wall

ventricular septal rupture

papillary muscle (mitral valve) rupture

46
Q

Dressler’s syndrome

A

pericarditis – hypersensitivity to tissue necrosis

47
Q

3 subtypes of chronic ischemia heart disease

A

stable angina

silent MI

vasospastic angina

48
Q

stable angina

A

caused by fixed obstruction of CA, plaque > 75%

precipitated by increased O2 demands from exercise or emotional stress

generally relieved within 10 min of rest + NTG

49
Q

silent MI

A

MI without angina

lack of pain may indicate high pain threshold or DM

50
Q

vasospastic angina

A

spasm of CAs –> angina

occurs at rest

associated with life-threatening arrythmias

51
Q

angina classification (4)

A

class 1: pain with prolonged exercise

class 2: slight limitation of normal activity

class 3: marked limitation of ordinary activity

class 4: pain at rest/any physical activity

52
Q

diagnosis of chronic ischemic heart disease

A

rule out (R/O) non-cardiac pain – reflux, muscular

exercise stress test produces ST changes

holter monitor for vasospastic angina

53
Q

treatment goal for chronic ischemic heart disease

A

reduce symptoms and prevent MI

54
Q

treatment for chronic ischemic heart disease

A

angioplasty (PTCA) or CABG

therapeutic lifestyle changes (TLC)

anti-platelet drugs

beta blocks to decrease cardiac work

calcium channel blockers dilate arteries

NTG decreases preload/afterload

Pathophysiology (24 decks)

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