pvd-up to Cardiomyopathy Flashcards
where does PVD usually occur
lower limbs. usually in arteries but can also be in veins, cap, lymphatics
how are PVD and atherosclerosis different
the changes are atherosclerotic but they take place in diff vessels.
similar to changes int he coronary artery
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
atherosclerotic occlusive disease
develops gradually
occurs in lower extremities
inc in elderly and diabetes mellitus pts
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
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)
collateralization=
formation of new vessels around an obstruction which may or may not be useful
compensation for atherosclerotic occlusive disease
vasodilation, anaerobic metabolism and collateralization
what happens if theres no Tx for atherosclerotic occlusive disease
leads to ulceration and gangrene and then amputation
aneurysms=
localized dilation of an artery that is permanent
d/t degenerative changes in the vesel wall
where do aneurysms generally develop
in certain regions of the vessel where they bend or bifurcate
risks for aneurysms
HTN, atherosclerosis, congenital defects
C-HTN-Aneurysms everywhere?
3 types of anuerysms
fusiform eg abdominal aorta
saccular
dissecting
common sites of aneurysms
abdominal aorta thoracic aorta femoral iliac popliteal
are aneurysms always detectable
if in a body cavity they may go undetected within limits
what is a dissecting aneurysm and how is it different from fusiform and saccular
dissecting seem to bleed in between the vessel layers
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
do complications always develop for a disease
no
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
2 types of CAD
acute coronary syndromes
chronic ischemic heart disease
acute coronary syndrome is what type of CVD
wat is it
CAD
what is CAD
it is heart disease caused by impaired coronary blood flow
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
chronic ischemic heart disease vs acute coronary syndromes
fig 4-5
-stable angina has a fixed atherosclerotic plaque (it is CIS)
-
chronic ischemic heart disease
stable angina
congestive heart failure (issue with blood flow)
why is stable angina stable
because the atherosclerotic plaque isnt going anywhere
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
angina pectoris is a _____ of CAD
is a mnft of CAD
etiology of angina pectoris
- atherosclerosis mostly
- vasospasm
- thrombosis
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
mnfts of angina pectoris
chest pain (triggered by exertion, emotion, cold) (cold because it causes vasoconstriction)
stable angina
is
triggered by
- fixed plaque
- perfusion impeded
- transient pain (~5 min)
- triggered by exertion, relieved by rest
how could you assist a pt w stable angina nonpharmacologically
relax, stop exerting yourself
come out of cold
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
stable and unstable angina
what is the other kind of angina called
variant/vasospastic/Prinzmetal’s angina
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
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)
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
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
etiology of STEMI
atherosclerosis
hemmorhage
coronary vessel spasm
the problem is that the heart isnt getting eough blood
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
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)
2 Types of MI infarction
-subendocardial infarction
transmural infarction
subendocardial infarction
inner 1/3 to 1/2 of ventricle wall distal occlusion (branches)
transmural infarction
1 artery is obstructed
the entire ventricle wall is affected
the occlusion is proximal
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
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
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
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
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
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
CKMB vs CKMM
CKMM is nonspecific to heart vs CKMB
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)
how do diuretics help the heart post MI
diuretics lead to fluid loss->dec blood volume which allows dec cardiac workload
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
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
revascularization surgery on the heart is aka
angioplasty or bypass
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.)
