Cardiology part 2 slide 173-287 Flashcards by Cinthia Duarte

what is the most common symptom assoc. with CAD

How well did you know this?

Not at all

Perfectly

if pain only occurs with exertion and is stable over a period of time is classified as

Stable angina

How well did you know this?

Not at all

Perfectly

if chest pain occurs at rest this is known as

unstable angina

How well did you know this?

Not at all

Perfectly

if cp persists without interruption for prolonged periods and irreversible myocyte damage has occurred is indicative of

myocardial infarction

How well did you know this?

Not at all

Perfectly

does chest pain worsen with deep breath?

How well did you know this?

Not at all

Perfectly

CAD can be assoc. with what other symptoms?

sob, diaphoresis, n/v

How well did you know this?

Not at all

Perfectly

what is the etiology of CAD (4)

which is most common?

atherosclerosis***, spasm, emboli, congenital

How well did you know this?

Not at all

Perfectly

the heart is responsible for what percentage of the body’s resting oxygen consumption?

How well did you know this?

Not at all

Perfectly

what occurs when there is either increased demand for oxygen relative to maximal arterial supply or an absolute reduction in oxygen supply

cellular ischemia

How well did you know this?

Not at all

Perfectly

fatty streaks in arterial walls are found mainly in areas exposed to increased ______ ____ like bending points and bifurcations and are thought to arise from _____________________

shear stress;

isolated macrophage foam cell

How well did you know this?

Not at all

Perfectly

which cells regenerate (remodel) to re-cover the exposed intima

endothelial cells

How well did you know this?

Not at all

Perfectly

at rest, pt have ischemia due to arterial lumen decreasing to what percentage?
what about during exercise?

90% at rest

50% with exercise

How well did you know this?

Not at all

Perfectly

what causes plt accumulation and occlusion? and how long can these episodes last?

fissuring of the atherosclerotic plaque

-10-20 min

How well did you know this?

Not at all

Perfectly

what has an important role in clinical presentation for artheroscleorsis??

plaque composition mediated by inflammation*

How well did you know this?

Not at all

Perfectly

how many seconds does it take for cells to fall to zero after coronary artery occlusion?

60 seconds

the longer the worse

How well did you know this?

Not at all

Perfectly

what occurs within seconds even BEFORE depletion of high energy phosphates occur

dysfxn of myocardial relaxation and contraction

How well did you know this?

Not at all

Perfectly

how long does it take for an inerreversible injury to occur if perfusion is not restored

40-60 min

How well did you know this?

Not at all

Perfectly

which vasoconstrictive factors release cause vasoconstriction and decrease flow?

thromboxane A, or serotonin

How well did you know this?

Not at all

Perfectly

explained “stunned” myocardium

ischemia after 1 hr taking 1 month to restore ventricular function

How well did you know this?

Not at all

Perfectly

what is the live vest vs AICD implantation

life vest would be after a stunned myocardium to monitor heart, after 3 months check it and if ef when up to 60-65% then it can be taken off
aicd implan- I think if its when tissue of affected area does not go back to normal and need defib to monitor heart

How well did you know this?

Not at all

Perfectly

what is the actual trigger for nerve stimulation seen in chest pain

adenosine

How well did you know this?

Not at all

Perfectly

chest pain that worsens with deep inspiration is indicative of

pericarditis

due to inflammation in pericardium

How well did you know this?

Not at all

Perfectly

what is the pericarditis sound

friction rub “to and fro” and high pitched squeaking sound

How well did you know this?

Not at all

Perfectly

continual inflammation of the pericardium leads to fibrosis and development of ______ pericarditis

constrictive pericarditis

How well did you know this?

Not at all

Perfectly

define kussmaul sign

inappropriate increase in the RAP and jugular venous pulsation level with inspiration

what are etiologies of pericarditis

infections, collagen vascular disease, neoplasm, metabolic, injury, idipathic

deposition of calcium in pericarditis indicates

scarring

where is "to and fro" rub most commonly heard? and why

in CP with pericarditis | - diastolic components merge, between visceral and parietal pericardial

what occurs during the filling of the ventricles in pericarditis known as a diastolic knock?

early filling occurs but the filling suddenly stops by the non elastic thickened pericardium makes v wave more prominent on ekg

during pericarditis, does the systemic venous pressure increase or decrease

INCREASES bc blood entering heart is limited so increasing RA pressure Normally: inspiration there's a decrease in pressure to allow filling bUT this is prevented due to the inflammation

pericardial effusion and tamponade define

too much fluid in pericardial space | - sudden filling of heart limits ventricular filling (tamponade)

what are the Becks Triad | what dz has this

- hypotension - elevated JVP - muffled heart sounds - pericardial effusion and temponade

what causes pericardial effusion

any cause of pericarditis

what are the names of the layers of the arterial vessels and what are they made up of

adventitia- outer layer of connective tissue media- middle layer of smooth muscle intima- containing the layer of endothelial cells

resistance vessels vs capacitance vessels

resistance vessels: arteries | capacitance: venues and veins--> walls distend

what is the smooth muscle surrounding the capillary openings called

precapillary sphincters

arterioles is to ___ as veins is to oncotic

hydrostatic

prostacyclin is produced by ___ and thromboxane A2 is produced by ____

- endothelial cells | thrombi: platelets

prostacyclin promotes ____ where as thromboxane causes plt aggregation and vasoconstriction

vasodilation

nitric oxide is a potent ___

dilator

NO produces cGMP which in turn mediates ____

relaxation of vascular smooth muscle --> vasodilation

due to vasodilation from NO, it leads to ___

hyperemia

what is the most potent vasoconstrictor

endothelia-1 ET1

what are the principal vasoconstrictors vs principal vasodilators

constrict: norepinephrine and epi dilators: vasoactive peptide, kinins, natriuretic peptides

what are bradykinin and Lysyl-bradykinin

vasodilators

what type of vasodilator is used as a marker to see if there's an improvement of Heart Failure after natriuresis

BNP- brain natriuretic peptide | --- if bnp levels are elevated its consisted with HF so if it shows that it is going down then less likely to have HF

a discharge of noradrenergic vasomotor nerves lead to ___ of BP and inhibits effect of ____ stimulation which ____ CO

inc | vagal; dec

C-reactive protein are a marker for ____

inflammation or plaques

whenever you see foam cells think ____

LDL - fatty streaks

explain pathogenesis of atherosclerosis in terms of foam cells, endothelial, and thrombosis

smooth --> foam --> endothelial cells (plaque) --> rupture --> pltl aggrgt --> block blood flow (thrombosis)

chylomicrons

protein coat of cholesterol and triglycerides in intestinal epithelial cells

thrombotic strokes are due to

blockage of cerebral circulation

intermittent claudication is seen in

circulation of legs --> pain and fatigue when walking

where do you see frank gangrene

in extremities in atherosclerosis

what main body parts do clot formation and obstruction occur

brain, kidney, heart

how is progression of atherosclerosis less rapid in premenopausal women than in men

ESTROGEN- increases cholesterol removal

homocysteine levels are associated with

accelerated atherosclerosis / inflammation

diabetes, smoking, nephrotic syndrome, and hypothyroidism is seen in acceleration of

atherosclerosis

is HTN a syndrome or disease

syndrome

renal artery constriction increases blood pressure which in turn activates ----

RAS system - false HTN | its really due to the obstruction of blood flow

pill HTN

normally renin secretion is dcreased to compensate but this compensation is inadequate and BP is high

conns disease ( hyperaldosteronism)

tumor in adrenal that secretes large amounts of aldosterone aka Na retention and inc fluid and HTN

pheochromocytoma- excess secretion of catecholamines leads to

increase secretion of norepinephrine and inc pressure

three main causes of HTN

sugar, cholesterol, BP, and diet and smoking play a role

**which type of shock causes warmth of the skin

Distributive Shock due to vasodilation***

hypovolemic shock

inadequate volume to fill vascular system --- stab wound loosing blood like crazy

distributive shock (3 types)

- anaphylactic (allergies) - neurogenic (head and spine injuries, loss of activity) - septic shock

cariogenic shock

inadequate pumping of the heart -- usually LV infarct

obstructive shock

Pumonary/vascular | -right sided heart failure --> PE, pulm HTN

virchows triad seen in thrombosis

- endothelial damage (Abnl vessel wall) - abnl blood flow - inc coag of blood

canalization

new lumen form within the thrombus

embolization

part of thrombus becomes dislodged and travels distal to site of formation and can produce obstruction

thromboembolism from left side of heart vs right side of heart

left side: stroke (goes to aorta to cerebral artery) | right side: PE (DVT to right side to pulmonary)

Deep Vein Thrombosis location and etiology and S&S

begin in the lower extremities and pelvis etiology: virchows triad S&S: edema, heat to site, Homan's sign

etiology of Peripheral apertural disease (PAD)

atherosclerosis

6 Ps in PAD

``` pain pallor pulselessness paresthesia's poikilothermic paralysis ```

Cardiology part 2 slide 173-287 Flashcards

(76 cards)