DPT II Exam IV

STEMI infraction

transmural MI (entire thickness of the heart wall), ST segment elevation and pathologic Q waves

NSTEMI

subendocardal MI (affects the inner third of the heart muscle), non St segment

best biomarkers for outcome are

tropin I and T

how to tx STEMI

MONA

what does MONA stand for

morphine, oxygen, nitrate, aspirin

moriphine

analgesic and anxiolytic

statins

reduce LDL and have anti inflammatory effects

fibrinolysis

repercussion for STEMI

b blockers

decrease in HR, contractility, BP , and subsequently myocardial oxygen demand

ca channel blockers

arterial vasodilation, coronary vasodilation, decreasing peripheral resistance, after load, BP, and myocardial oxygen demand

arteriosclerosis

Chronic vascular disease characterized by abnormal thickening and hardening of the vessel wall

atherosclerosis

fat and fibrin deposits that harden over time

atherosclerosis is a BLANK disease

inflammatory with lesion progress

numerous factors are involved in atherolscleoris

non modifiable and modifiable

oxidized LDL plays

central role in the formation of fatty streaks

Ath-1 gene controls

oxidation and inflammatory process

HDL associated proteins apoj and paraoxonase may minimize

LDL oxidation

normal artery structure

1) intima (inner most layer)

2) media (middle layer)

3) adventitia (outer)

primary cause of SIHD

atherosclerosis, lesions decrease vessel diameter reducing perfusion in normal state when demand increases

microvascular angina

summer resistance sized vessels exhibit abdominal constriction resulting in ischemia

loss of endothelial integrity

structure and function, key to lesion development

the location of atherosclerotic lesion influences

extent of muscle involvement and clinical manifestation

collateral vessel development involves what growth factors

VEGF and BFGF

classical angina is due to

transient episode

MI is due to

response to significant or prolonged ischemia

what metabolic abnormalities are present in SIHD

lactate production, decreased IC pH, depletion of ATP, impaired cell transport

ECG abnormalities in SIHD

T wave inversion and or ST depression

chronic stable angina is caused by

transiet myocardial ischemia (exertion)

when can chronic stable agina occur

during rest and at night

what typically results from exertion/emotion and is relieved by rest?

chronic stable agina

chronic stable aging ECG is

normal in 50% at rest, changes in ST segment (depression) and T wave inversion occurs during episodes

are changes in cardiac enzymes resent in chronic stable angina?

no

primary indicators of chronic stable angin

left ventricular function as well as severity of stenosis

silent ischemia ECG

ST elevation or depression

why is there lack of symptoms in silent ischemia

altered pain afferents, pain perception, or less inflammation during episode

coronary vasospasm in SIHD

presence of mild/moderate fixed obstruction with occasional spasms at/near site of plaque, usually in the morning

Prinzemetal's Variant Angina

coronary vasospasm, no coronary artery obstruction (younger pts)

Prinzemetal's Variant Angina ECG

ST segment elevation

organic nitrates

NO activates guanylyl cyclase GC, increases cyclic GMO levels in cells, reduces phosphorylation of myosin light chain (MLC), decreases IC Ca and relaxation/vasodilation

ranolazine

selective inhibition of late Na current

all patients with PAD need

non pharmacist intervention, statin therapy, htn/diabetes management

what is beneficially in PAD symptomatic pts

antiplatelt +/- rivaroxaban/vorapaxar

stable

elicited by exertion or emotion

ischemic heart disease

artherosleoritc disease of coronary arteries, coronary artery disease

SIHD

chronic coronary disease

SIHD is a condition of

imbalance between myocardial oxygen supply and demand most often caused by atherosclerosis of the coronary artery.

prinzmetal

vasospastic angina without coronary artery obstruction

SNS intervention to the coronary arteries regulates

blood flow

determines the oxygen demand by the heart

contractility

LDL

oxidized during the first step of atherosclerosis

endothelin

potent vasoactive substance that c an cause vasoconstriction in the coronary circulation

abciximab

Glycoprotein IIb/IIIa inhibitor

APOJ

minimized LDL oxidation

intima

endothelial cells, NO PGY12

media

middle layer containing smooth muscles causes constriction/ contraction

adventitia

collagen rich that hardens connective tissues

ApoJ and paraoxonase

minimize LDL oxidation

direct effects of SNS intervention

smooth muscle dilation

indirect effects of SNS intervention

stimulate cardiac muscle beta receptors to increase HR and increase metabolic activity

coronary flow is greatest during

diastole

aortic pressure

important factor for perfusion to the coronary arteries (assist in blood flow)

radius of the vessel

primary determinant of overall flow

metabolic factors

adenosine, K ion, CO2, H+, prostaglandin, NO

endothelium

vasodilation through NO and PG12

grade I

ordinary physical activity does not cause aging, but strenuous work

Grade II

slight limitation of ordinary activity

Grade III

marked limitation

Grade IV

inability to carry any physical activity without discomfort, may be AT REST

what is the primary cause of SIHD

artherosclerosis

classic amnia is due to

transiet episodes

MI occurs in response to

significant or prolonged ischemia

SIHD metabolic abnormalities

low pH, depletion of ATP, lactate production

SIHD EKG

T wave inversion and ST depression

chronic stable angina

caused by transit myocardial ischemia and resolves at rest

silent ischemia

detected on routine exams, pain receptors or less inflammation during episode

PAD

most common form of peripheral vascular disease

caused by progressive narrowing of arteries due to atherosclerosis

characterized by stenosis and or occlusion of medium and large sized arteries excluding arteries that supply the heart and brain

PAD is due to

the oxygen demand greater than the oxygen demand

risk factors for PAD

Cigarette smoking

Hyperlipidemia

Hypertension

Diabetes mellitus

symptoms of PAD

intermittent claudication, fatigue, discomfort, cramping, relieved by rest, pain at lower extremities

claudication

pain within a specific group of muscles that is exacerbated by exercise and received by rest

clinical limb ischemia

pain at rest or tissues, limb loss

ABI

highest of DP or PT/ highest of brachial (take the lowest number)

ABI 0.7-0.99

mild

ABI 0.4-0.69

moderate

ABI under 0.4

severe

what vaccinations should patients either PAT receive

flu and covid

when should sympathetic patients receive surgery

imitating claudication or inadequate response to GDMT

what medications should PAD pts be on?

- high intensity statin

- diabetes management

- HTN management

- anticoagulant or antiplatlet

is antithromboric therapy recommended for asymptomatic pts?

No, unless other disease

is anti platelet therapy recommended for asymptomatic pts?

yes if there's other factors

clopidogrel

blocks P2Y12 receptor on platelet preventing GPIIb/IIIa activation leading to reduced platelet aggregation

what is vorapaxar C/E

stroke, ICH, TIA, bleeding

is warfarin indicated in PAD

no

when Is rivoraxaban indicated in PAD

symptomatic pts to reduce MALE/MACE

cilostazol MOA

inhibits PDE3 to increase cAMP to reversibly inhibit platelet aggregation and promotes vasodilation

Cilostazol C/E

Heart failure

Cilostazol used for

improvement of walking distance in claudication but NOT associated with benefit for MACE

pentoxifylline MOA

improves tissue oxygenation through improved blood flow (less blood viscosity and improved RBC flexibility)

what is petoxifylline used for

same as cilostazol, just less effective

what trial states that PAD is under diagnosed

PARTNERS