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BMS 130 > assist cardio-heart > Flashcards

assist cardio-heart Flashcards

1
Q

what is the PR interval

A

time it takes for electrical impulse generated in the SA node to travel through the atria and across the AV node to the ventricles

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2
Q

what is a PR segment

A

AV nodal DELAY

it weirdly stops bfeore q, it stops BEFORE the QRS complex starts!!!!!!!!! so between atrial dep and ventricular dep

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3
Q

what occurs in the atria at the same time as qrs

A

atria is simultaneously repolarizing but we cant see it

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4
Q

what occurs in the T wave

A

ventricular repolarization

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5
Q

what is P to T

A

one cardiac cycle (heart beat)

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6
Q

how should q and s appear

A

q shsould be small. s is small and may not be present

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7
Q

what is the QT interval

A

time it takes from the beginning of QRS complex to the END of the T wave.

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8
Q

what occurs in the ST segment- between the end of the QRS and the beginning of the T wave?

A

from the end of the QRS to the begining of the T wave; ventricles are contracting and emptying, plateau phase of action potential!!!!

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9
Q

what is the plateu plase of the action potential in terms of the ecg letters

A

ST segment!!!!! its between the end of the QRS segment and the beginning of the T segment

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10
Q

what happens between the end of the T wave and the beginning of the P wave? (TP segment)

A

from the END of the T wave to the BEGINNING of the P wave- ventricles are RELAXING and filling!!!!!! (t wave is ventricular repolarization!)

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11
Q

at what distance between qrs complexes is there tach/bradychardia

A

tach: >100 beats/min
brad: <60 beats/min

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12
Q

what is arrhythmia

A

variation from normal rhythym and sequence of excitation of the heart (flutters, fibrillations-a and v, heart block, complete heart block)

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13
Q

what is atrial flutter

how it appears

A

rapid but regular sequence of atrial depolarization. ventricles can’t keep up, inadequate filling of ventricles and lessened cardiac output is the result..
-can increase the HR

appearance on ecg is just lots of p waves in between regularly spaced qrs complexes

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14
Q

what is atrial fibrillation

A

uncoordinated atrial depolarization-> chaotic asynchronized atrial contractions.

  • impulses reach AV note erratically and ventricular rhythym is irregular too.. (bc they are reaching it erratically)
  • atria “QUIVERS” rather than fully conttracts so its HARD TO FIND THE P WAVE
  • QRS DOES NOT appear at regular intervals.
  • lowers cardiac output tooo..
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15
Q

what is ventricular fibrillation

A
  • uncoordinated ventricular depolarization-> chaotic asynchronized ventricular contractions.
  • difficult to determine Heart rate- atrial depolarization and repolarization are normal but hard to discern on ECG. cardiac output goes DOWN!!!!!
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16
Q

what is a primary heart block

A

A heart block is where artia beat regularly but the ventricles are not stimulated– issue in CARDIAC CONDUCTING SYSTEM!!!!!!! reduced ventricular contractions.

primary: PR interval is prolonged; the time for impulse to travel from atria to ventricles is longer (through AV) but most signals of SA do pass to AV!!! (damage not bad)

17
Q

what is a secondary heart block

A

A heart block is where artia beat regularly but the ventricles are not stimulated– issue in CARDIAC CONDUCTING SYSTEM!!!!!!! reduced ventricular contractions.

-2ndary: some SA impulses do not reach the AV node. P wave may be followed by another p wave (no QRS in between) QES is not spaced evenly.

(looks like a atrial flutter except with abnormal qrs spacings.. or a atrial fibrillation with normal ps)

18
Q

what is a tertiary heart block

A

A heart block is where artia beat regularly but the ventricles are not stimulated– issue in CARDIAC CONDUCTING SYSTEM!!!!!!! reduced ventricular contractions.

tertiary: complete dissociation of atrial and ventricular activity.
ventricles become dependent on autorhythmic cells of bundle of his and perkinje so it goes MUCH slower than the atria. rhythmic atria and ventricles but the ventricles are a lot farther apart and less frequent. both are regularly spaced.

-GREATEST reduction in cardiac output.

19
Q

when is ventricular systole on the ecg

A

from R (spike in qrs) to middle of T

– basically from middle of depolarization of ventricles to middle of repolarization of ventricles !

20
Q

when is ventricular diastole on ecg

A

from middle of t all the way to the next R spike

– from ventricular repolarization to ventricular depolarization

21
Q

what does sympathetic stimulation act on that parasympathetic system DOES NOT when it comes to heart rate stimulation

A
  • ventricular conduction (Para- NO EFFECT) sympathetic; increases excitability and hastens conduction thru bundle and perkinje
  • ventricular muscle (para - NO EFFECT) sympathetic increases contractility, strengthens contraction
  • adrenal medulla (para-NO EFFECT) sympa stims epinephrine release

BTW do not forget that it DOES act on atrial muscles! decreases contractility and weakens the contraction!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

22
Q

what is cardiac output

A

volume of blood pumped out by heart per minute
depends on:
-heart rate
-stroke volume (volume of blood pumped per min)

23
Q

what is cardiac reserve

A

diff between volume at rest pumped and maximum volume pumped per minute out of the heart (differences in stroke volume)

24
Q

what is sympathetic system effect on venous return

A

increase venous return by increasing BP ?

25
Q

how does increaes in venous return impact end diastolic volume?

A

through intrinsic control, it increases end diastolic volume ? – more in there.

26
Q

how does sympathetic system impact stroke volume

A

through extrinsic control it increases stroke volume

27
Q

what is the mechanism by which parasympathetic system acts on the SA node

A
  • slows depolarization towards threshold :

- depresses Na ( If, funny) channels and T-typee calcium channels so calcium influx initially. increases K+ permeability

28
Q

what is the mechanism by which parasympathetic acts on AV node

A
  • decreases av node excitablity :
  • prolongs transmission of impulse to ventricles
    • INCREASES K+ permeability!
29
Q

how does the parasympathetic system act on the atrial contractile cells?

A

-shortens plateau phase of action potential – mech; reduce slow inward current (calcium) through L type channels
this slows contraction (contraction occurs during repolarization?)

–less strong (sympathetic increases calcium flux so that its a longer stronger contraction)

30
Q

how does parasympathetic system act on the ventricular contractile cells

A

-sparsely innervated by vagus nerve so ventricular contraction is NOT IMPACTED trick question!! DOES NOT

(but dont forget that sympathetic DOes and it increases contractility, strengthens contraction!

31
Q

how does the sympathetic system act on the SA node

A

speeds depolarization to threshold
-more rapid, frequency goes up
mechanism; greater Na (funny) channels and calcium t type channels influx.

32
Q

how does sympathetic system act on the AV node

A

reduce AV nodal delay; increases conduction velocity and increases slow calcium influx

33
Q

how does symp act on conduction

A

increeases spread of action potential through conduction pathways - spread faster at bundle and perkinje

34
Q

how does symp system act on atrial and ventricular contractile cells during contraction

A

increase contractile strength

-increases calcium permeability thru prolonged opening of L type calcium channels

35
Q

what does sympathetic system do to atrial and ventricular contractile cells during relazation

A

enhance relax
-increase activity of sarcoplasmic reticulum, calcium back into the sarcoplasmic reticulum to help relax (important for relaxing)

36
Q

whats the franklin starting law sequence

A

increased venous return -> stretch cardiac muscle fibers -> EDV goes up -> stronger contraction -> more blood leaves heart (stroke volume)

stretched cardiac muscle- optimal length!! length tension relationship - amount of ejection depends on this.

37
Q

what drives the coronary circulation

A
  • during diastole 70% of flow– aortic blood pressure

- during systole; 30% driven by ventricular contraction

38
Q

how does the coronary artery get dilated?

A

0activity increases, adenosine is formed and released
adenosine acts as a paracrine hormone and induces dilation of coronary blood vessels!! blood flow to cardiac muscles increasess.

BMS 130 (3 decks)

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