BSC physiology Flashcards by Andrea Parsons

what are the characteristics of 1st degree AV block

long PR interval

PR interval greater than .2 seconds

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sinus bradycardia

less than 60

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what is the normal PR interval

.12-.2

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atrial flutter

multiple p waves before every QRS and looks fairly regular

abnormal conduction

R-R interval is constant from beat to beat

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atrial fibrillation

no distinct p waves

saw tooth

reentry is setting up this pathway (ectopic focus taking over normal SA rate of depolarization)

irregularly irregular

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2:1 AV block Mobitz II

conduction system block

PR interval of conducted beats is normal

every other P wave is conducted

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2:1 secondary AV block Mobitz I

longer PR interval with each cycle to the next until the AV node fails completely

slower rate

AV block meaning you drop a QRS because it doesn’t get to the ventricle

Wenckebach

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third degree AV block

no pattern, no association
complete block

AV dissociation

regularly paced P waves
irregularly spaced QRS and T waves

completely variable PR interval

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multiformed PVC’s

QRS complexes are irregular and not the same (the ones that are PVC’s)

PVC’s not preceded by p waves that don’t look the same so they are coming from different ectopic areas that are acting out

QRS duration is longer, ectopic foci are spreading depolarization cell to cell (via gap junctions and this is taking longer)

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unifocal PVC

unusual QRS’s in the middle of everything

ectopic focus, originating in the ventricles

premature
No p wave precedes PVC QRS

QRS greater than .12 sec b/c cell to cell spread and not following the normal conduction system which takes longer

same shape PVC indicates one ectopic focus

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torsades de pointes

different amplitudes of QRS’s

type of ventricular tachycardia

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ventricular tachycardia

faster rate than normal originating in the ventricles

only seeing QRS’s

cell to cell spread b/c of wide QRSs

the QRS’s appear the same

more organized, probably have time for filling

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ventricular fibrillation

abnormal conduction

no discernable P-waves

no discernable QRS complexes
bag of worms

not good!! NO FILLING DEAD

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what does an AED do

resets putting everything into refractory

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know***

tachy
brady
atrial flutter
afib
uniformed multiformed pvcs
ventricular tachy
v-fib
one more

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case 56 year old female with heart palpitations
light headedness shortness of breath
bp 95/70
her ECG shows supraventricular tachycardia
what does this mean

normal p wave?

no normal p wave (covered by t wave)

SA node is not the pacemaker

how can the automaticity of the SA node be over-riden

site with intrinsic rate of depolarization that is greater than the SA node

what does an essentially normal PR interval suggest about the location of an ectopic focus

located near the AV node, allowing AP’s to reach ventricles via the normal pathway

ventricular rate is matching ectopic rate w

which factor most likely promotes an ectopic focus to develop into a re-entrant circuit

decreased conduction velocity

b/c there is time for the area to get out of refractory

3 requirements for reentry

partial depolarization of a conduction pathway

unidirectional block

timing : reentrant current must occur beyond the ERP

what 3 things promote reentry

lengthened conduction pathway
decreased conduction velocity (hyperkalemia)
reduced refractory period

why does a patient with supraventricular tachycardia lightheadedness, dizzy, and short of breath

because she was hypotensive b/c her CO is decreased

MAP how do you calculate

DBP + 1/3 (Pulse pressure) (SBP- DBP)

which variable best explains the girl’s audible murmur in a left to right shunting (patent ovale) LA to RA

increased blood flow velocity (narrowing opening) that is audible as a murmur

decreased viscosity

anemia causes increased turbulence

the largest decrease in blood pressure across a given segment of peripheral vasculature occurs in the arterioles due to the fact that they have the greatest ...

resistance arterioles are the resistance vessels greatest area of regulation (with vasodilation and all that jazz)

an increase in which starling force is most likely contributing to edema

capillary hydrostatic pressure

why does the guy have increased capillary hydrostatic pressure?

b/c he has pooling in his venous system, so the pressure is higher and maintained in the capillary beds AND he has low blood pressure he has a fistula-- arteriole side right to venous side and getting backed up

what could explain hypotension (when discussing ohm's law)

total peripheral resistance

why is radius so key to distributing CO is because....

radius to the 4th power is key for blow flow

which most directly contributes to the functional syctium of the heart

intercalated disks consist of low-resistance pathways through which a depolarizing current is spread GAP junctions - allow depolarizing current not to die out

what best describes the characteristic of an AP that is generated earlier than normal within the relative refractory period before repolarization is complete

lower amplitude of upstroke

longer duration of the AP of the heart contributes to...

the hearts inability to produce tetanus

which change would increase the liklihood of his aneurysm to rupture

increased wall tension increased vessel radius decreased wall thickness

augmented Ca channel opening hyperkalemia k channel blockers na inactivation gate mutations all do what?

all promote long QT syndrome all ventricular events

what is afterdepolarizations

occur in refractory period and set up series of extra ventricular contractions can lead to Vfib both early afterdepolarization and delayed afterdepolarizations stay depolarized longer

in wolf-parkinson white syndrome with an accessory conduction pathway that bypasses the AV node and relies on ventricular depolarization cell-to- cell via gap junctions what would you expect to see?

widening of the QRS complex alternate path around the AV node (bundle of kent) AP conducted directly from atria to ventricle why spread to atria to ventricles via an accessory pathway in WPW syndrome compared to AP conduction via the AV node? --> because the cells in the atria itself (myocytes and ventricular cells are fast AP type) and the nodal cells are slow type AP

what physical properties of AV nodal cells contribute to slower conduction velocity

smaller diameter, increased internal resistance to current flow

how do you calculate the total peripheral resistance

first determine MAP then use the equation TPR= MAP/CO