First Aid - Cardiology

Front 1

heart sound which is the mitral and tricuspid valve closure

Back 1

S1

Front 2

heart sound which is the aortic and pulmonary valve closure

Back 2

S2

Front 3

heart sound which denotes the end of rapid ventricular filling

Back 3

S3

Front 4

heart sound that denotes high atrial pressure and stiff ventricle

Back 4

S4

Front 5

S3 is associated with what pathology

Back 5

dilated CHF

Front 6

heart sound which is associated with the "atrial kick" and is heard with a hypertophic ventricle

Back 6

S4

Front 7

what does S2 splitting mean and how does respiration influence this

Back 7

aortic valve closes before pulmonic (inspiration increases this difference)

Front 8

cardiac output =

Back 8

sv x hr

Front 9

mean arterial pressure =

Back 9

CO x TPR

Front 10

in terms of diastolic and systolic pressure MAP =

Back 10

2/3 diastolic pressure + 1/3 systolic pressure

Front 11

how does preload and afterload affect SV

Back 11

an increase in preload and decrease in afterload increase SV

Front 12

how does an increased in intracellular calcium affect contractility

Back 12

increase

Front 13

how does a decrease in extracellular sodium affect contractility

Back 13

increases it

Front 14

Phase 0 in the pacemeaker action potential represents what

Back 14

upstroke in which voltage-gated Ca2+ channels open

remember the pacemaker action potential does not involve fast voltage gated na+ channels

Front 15

how does a B1 blockade affect contractiligy

Back 15

decreases and decreases SV

Front 16

nitroglycerin affects preload how? why?

Back 16

decreases preload because it is a venous dilator

Front 17

how does hydralazine affect afterload and why

Back 17

it is a vasodilitor so it decreases afterload

Front 18

preload is affected how by exercise

Back 18

increased slightly

Front 19

acidosis affects contractility how

Back 19

decreases contractility and SV (H+ displace Ca+ in blood causing hypercalcemia in the blood (not heart)) hypercalcemia causes hyperkalemia a decrease contractility

Front 20

the palateau in a cardiac muscle action potential is Phas 2 and is due to

Back 20

Ca+ influx

Front 21

what is phase 1 in the mycardial action potential due to

Back 21

it is the initial repolarization whic his due to inactivation of voltage-gated Na+ channels. also the voltage gated K+ begin to open

Front 22

what is phase 3 in the myocardial action potential due to

Back 22

rapid depolarization which involves massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltae-gated Ca2+ channels.

Front 23

what phase in a myocardial action potential = resting potential and how does that relate to K+ permeability

Back 23

Phase 4 is the resting potential which and marked by high K+ permeability through the K+ channels

Front 24

the aortic arch detects what change in BP and transmits back to the medulla via what nerve

Back 24

detects a decrease in BP and transmits via the vagus

Front 25

the carotid sinus sense what change in BP and transmit back to the medulla via what nerve

Back 25

responds to an increase AND decrease in BP and transmits via the glossophyryngeal nerve back to the medulla

Front 26

how does hypotension affect baroreptor firing

Back 26

decrease in arterial pressure - decrease stretch - decrease in firing - increase in sympathetic firing - increase in HR, Contractiligy, and BP

important reaction to severe hemorrhage

Front 27

the carotid body is what kind of receptor

Back 27

chemoreceptor
carotid and aortic bodies resond to a decrease in PO2 (under 60mmHg) and an increase PCO2 and a decrease in the pH of blood

Front 28

what is measured with a Swan-Ganz catheter?

Back 28

Pulmonary capillary wedge pressure (PCWP) which is a good approximation of left atrial pressure

Front 29

what are the three local metabolites in the heart that determine autoregulation

Back 29

O2
adenosine
NO

Front 30

what is the one local metabolite which determine autoregulation in the brain

Back 30

CO2 (pH)

Front 31

in the lungs - hypoxia causes what

Back 31

vasoconstriction

in other organs hypoxia causes vasodilation)

Front 32

Net filtration pressure Pnet (using the starling forces idea) =

Back 32

(Pc-Pi) - (capillary oncotic pressure - interstitial oncotic pressure)

Front 33

how might you diagnose coartation of the aorta

Back 33

hypertension in the upper extremities and weak pulses in the lower extremeties

at least in adult type

in infantile type: aortic stenosis is proximal to insertion of ductus arteriosus.

Front 34

a ductus arteriosus patency is maintained by what two factors

Back 34

PGE synthesis
low O2 tension

Indomethacin (a prostagladin synthesis inhibitor) is used to close a PDA

Front 35

the kind of arteriosclerosis which includes calcification of the arteries (especially radial and ulnar). its usuallly benigh "pipestem arteries"

Back 35

monckeberg

Front 36

the kind of arteriosclerosis which includes fibrous plaques and atheromas forming in the intima or arteries

Back 36

atherosclerosis

Front 37

pale infarcts occur in what kind of tissues

Back 37

solid tissues w/ a single blood supply (brain, heart, kidney, spleen)

red infarcts occur in loose tissues w/ collaterals such as lungs, intestine, or following reperfusion.

Front 38

two things you might observe on an ECG right after a MI

Back 38

ST elevation (transmural infarct) or ST depression (endcardial infarct)

pathological Q waves (transmurel)

Front 39

what protein might rise 4 hours after in MI and stay elevated fro 7-10 days afterward

Back 39

troponin

Front 40

what is a cardiac tamponade

Back 40

fluid (e.g blood) accumulates in the pericardium and puts pressure on the heart decreasing diastolic filling. may lead to shock and death

seen after MI sometimes

Front 41

what is Dressler's syndrome

Back 41

an autoimmune phenomenon resulting in fibrinous pericarditis several weeks after a MI

Front 42

the most common cardiomyopathy - can be caused by Alcohol abuse, Beriberi, Coxsackie B virus, Cocain, Chagas disease

Back 42

dilated (congestive) cardiomyopathy)

leading to systolic dysfunction

Front 43

a cardiomyopathy which often causes death in young athletes

Back 43

hypertrophi cardiomyopathy

often asymmetric involving the intraventricular septum.
normal heart size
diastolic dysfunction
50% familial

Front 44

what three things might help you to diagnose hypertrophic cardiomopathy in a young person

Back 44

loud S4
apical impulses
systolic murmur

Front 45

how would you treat hypertrophic cardiomyopathy

Back 45

beta blocker

Front 46

this kind of cardiomyopathy might be caused by amyloidosis, endocardial fibroelastosis etc..

Back 46

restrictive/obliterative cardiomyopathy

Front 47

holosystolic high pitched "blowing"murmer

Back 47

mitral regurgitation

Front 48

mitral regurgitation can be heard the loudest where?

Back 48

apex

Front 49

crescendo-decrescendo systoli efection murmur following ejection click

Back 49

Aortic stenosis

LV is greater than aortic presusre during systole. pulse is weak compared to heart sounds - pulsus parvus et tardus

Front 50

the most frequent valvular sesion which causes a late systolic murmer with midsystolic click

Back 50

mitral prolapse

Front 51

The three types of drugs which are used to treat angina

Back 51

nitrats (decrease preload)
Beta blockers (decrease afterload)
Calcium channel blockers