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Flashcards in pvd-up to Cardiomyopathy Deck (58):
1

where does PVD usually occur

lower limbs. usually in arteries but can also be in veins, cap, lymphatics

2

how are PVD and atherosclerosis different

the changes are atherosclerotic but they take place in diff vessels.
similar to changes int he coronary artery

3

acute arterial occlusion
does it occur quickly or slowly

may be due to a clot which has developed elsewhere (embolism) or my form in vessel (thrombosis)
-quickly. it leads to inadequate perfusion and tissue is compromised

4

atherosclerotic occlusive disease

develops gradually
occurs in lower extremities
inc in elderly and diabetes mellitus pts

5

why does atherosclerotic occlusive disease inc in elderly adn diabetic pts

elderly because atherosclerotic changes only mnft after decades
in diabetics because one of the chronic complications of diabetes is vascular damage

6

mfft of atherosclerotic occlusive disease

-intermittent claudication
(pain upon walking.)
- tissue distant to occlusion gets ischemic due to impeded perfusion which leads to infarction and pain
-dec venous return -> venous stasis. the pressure will build up and cause edema. the lymphatics get overwhelmed and this leads to lymph stasis and wastes and fluids accumulate

-intermittent claudication
-ischemia (infarction & pain)
-edema (lymph stasis, waste, fluid accum)

7

collateralization=

formation of new vessels around an obstruction which may or may not be useful

8

compensation for atherosclerotic occlusive disease

vasodilation, anaerobic metabolism and collateralization

9

what happens if theres no Tx for atherosclerotic occlusive disease

leads to ulceration and gangrene and then amputation

10

aneurysms=

localized dilation of an artery that is permanent
d/t degenerative changes in the vesel wall

11

where do aneurysms generally develop

in certain regions of the vessel where they bend or bifurcate

12

risks for aneurysms

HTN, atherosclerosis, congenital defects

C-HTN-Aneurysms everywhere?

13

3 types of anuerysms

fusiform eg abdominal aorta
saccular
dissecting

14

common sites of aneurysms

abdominal aorta
thoracic aorta
femoral
iliac
popliteal

15

are aneurysms always detectable

if in a body cavity they may go undetected within limits

16

what is a dissecting aneurysm and how is it different from fusiform and saccular

dissecting seem to bleed in between the vessel layers

17

complications of aneurysms

-pressure on adjoining structures
-the most serious complication is rupture
-thrombosis (with a bulge the speed of flow will be dec which puts pt at risk of clotting and thrombi)
-distal embolization

18

do complications always develop for a disease

no

19

coronary artery disease
causes what
due to what
where does it occur

major cause of death
mostly d/t atherosclerosis
occurs in coronary artery and other branches of coronary circuit

20

2 types of CAD

acute coronary syndromes
chronic ischemic heart disease

21

acute coronary syndrome is what type of CVD
wat is it

CAD

22

what is CAD

it is heart disease caused by impaired coronary blood flow

23

which types of conditions fall under acute coronary syndrome
char of ACS

MI
unstable angina
sudden cardiac death

hppens quickly but whatever is predisposing the person doesnt have to happen quickly

24

chronic ischemic heart disease vs acute coronary syndromes

fig 4-5
-stable angina has a fixed atherosclerotic plaque (it is CIS)
-

25

chronic ischemic heart disease

stable angina
congestive heart failure (issue with blood flow)

26

why is stable angina stable

because the atherosclerotic plaque isnt going anywhere

27

stable angina is pain on exertion T or F
what is it?
how is unstable angina different in rt pain

true
stable is transient pain

unstable is pain at rest and during exertion
-it is severe, longer, also at rest & or nocturnal

28

angina pectoris is a _____ of CAD

is a mnft of CAD

29

etiology of angina pectoris

-atherosclerosis mostly
-vasospasm
-thrombosis

30

pathophysiology of angina ectoris

-inadequate perfusion->myocardial ischemia->angina
(under normal circumstances the arteries would dilate on demand but they are unable to dilate d/t atherosclerosis

31

mnfts of angina pectoris

chest pain (triggered by exertion, emotion, cold)
(cold because it causes vasoconstriction)

32

stable angina
is
triggered by

-fixed plaque
-perfusion impeded
-transient pain (~5 min)
-triggered by exertion, relieved by rest

33

how could you assist a pt w stable angina nonpharmacologically

relax, stop exerting yourself
come out of cold

34

unstable angina

unstable plaque
-plaque collects platelets, fibrin and cellular debris
-if ruptured it leads to thrombosis
-platelets aggregate->prostaglandin release->vasospasm
(int he capillary it had the effect of inc cap permb, vasodilation)
-pain is severe, longer, also at rest and or nocturnal. it can lead? to acute coronary syndrome and therefore MI if not managed well

35

stable and unstable angina
what is the other kind of angina called

variant/vasospastic/Prinzmetal's angina

36

variant/vasospastic/Prinzmetal's angina

-pin can occur nocturnally, at rest

-differs from the other two types of angina in that theres no atherosclerosis
-the coronary vessels undergo vasospasm
-to detect ECG changes the patient must be in pain at tht time

37

mnfts of vasospastic angina

-transient, mild to moderate chest pain
-squeezing, burning (heartburn or indigestion? this is what the pt often think and they dont seek attention because of this)
-can radiate to L shoulder and upper arm
-the pain can be migratory (starts somewhere and moves elsewhere)

38

tx of variant or Prinzmetal's angina

dec activity
use ntroglycerin (a vasodilator)

the more episodes of angina a person has the more likely they are to hve an MI

39

Myocardial infarctions (STEMI)
where is this in r/t CAD
how does this affect life
is it acute or chronic

it is end point of CAD
its life threatening
it has acute onset

40

etiology of STEMI

atherosclerosis
hemmorhage
coronary vessel spasm

the problem is that the heart isnt getting eough blood

41

patho of STEMI

atherosclerosis->complicated lesion->ischemia->cardiac hypoxia->anaerobic metb->acidosis??->arrythmias (irreg heart rate)->inability to pump and infarction

some area of heart wall will die and it is irreplaceable

42

size of infarction is based on

-affected vessel-how much tissue is affected
-extenet of occlusion
-duration of occlusion
-metabolic status of hert
-HR, BP and rhythm (status of person)
-collateral circulation (two vessels supplying area or more this would give alternate routes for the blood to arrive)

43

2 Types of MI infarction

-subendocardial infarction
transmural infarction

44

subendocardial infarction

inner 1/3 to 1/2 of ventricle wall
distal occlusion (branches)

45

transmural infarction

1 artery is obstructed
the entire ventricle wall is affected
the occlusion is proximal

46

what is a STEMI

an acute STEMI is char by the ischemic death of myocardial tissue assoc w elevation of the ST-segment of the ECG, and serum markers (cardiac) indicating myocardial damage

47

sme mnfts of MI

-chest pain (radiate to L shoulder, neck, jaw, arm)
-crushing pain that is severe
-anxiety, tachycrdia
-nausea, vomiting, fatigue
( severe pain is often assoc w nausea and vomiting. The electrical activity that is taking place in the centre in the brain that senses pain will affect the nearby vomit reflex center)
-less common (from him talking) palor, dizziness, palpitations, SOB, weakness. women often present with some of these symptoms as well as the pain often radiates to back

48

review ECGs and what happens when

at minimum during the St segment there is no electrical activity
the atria is in diastole and filling since the Av valves are closed
the ventricles are in systole ad building up pressure until semilunar valves can open
the ventricles eject blood into the pulmonary and aortic arteries

49

dx of Mi

-ECG (can show you where occlusion is and the extent of it. eg look for St depression and know it is subendocardial injury or St elevation and it is transmural
-angiogram (insert a catheter into an artery. Once near the occlusion or heart, release contrast medium. Then visualize the circuit on the screen. Dangerous because most pts have atherosclerosis. v precise. If obstruction found they will fix it)
-serum markers: Troponin I &T, myoglobin, CKnB

50

TRoponins T& I and MI
when do they peak and appear

troponins are regulatory proteins in the heart. (specifica to heart)
difficult to use as a serum marker because they are present in blood in various amounts depending on the time post MI
-I & T will begin to appear 3-4hrs after and peak 8-12hrs

51

myoglobin as a serum marker for MI
peaks and appears

it is a resp pigment in the blood nonspecific to the heart. Stores oxygen. appears 1-2hrs after Mi and peaks early

52

CKMB vs CKMM

CKMM is nonspecific to heart vs CKMB

53

Tx of MI

-stat attention to preserve life
-thrombolytics, anti-arrythmics & anticoagulants
-oxygen for hypoxia
-morphine PRN
-post-stabilization: IV diuretics, inotrope + vasodilator
-revascularization Sx (angioplasty, bypass)

54

how do diuretics help the heart post MI

diuretics lead to fluid loss->dec blood volume which allows dec cardiac workload

55

inotrope

a drug class :affects the force of contraction but not the rate
-there are positive inotropes and negative.
Negative will dec the force of contraction.
if the heart was failing and not forceful enought then could give positive inotrope

56

is nitroglycerin useful post MI or during MI

it is not useful during MI because the thrombus has already caused vasodilation but once it is gone post MI it can be useful to have a vasodilator

57

revascularization surgery on the heart is aka

angioplasty or bypass

58

types of surgery to help with MI

balooning angioplasty (isnt used as often now
-stent. (a metal bracket put into vessel to hold it open. may have platelet aggregation.)