Heart Phys Flashcards

1
Q

major targets of cardiovascular drugs

A

voltage gated ion channels. anti-arrhythmic, anti-hypertensive, anti-angina.

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2
Q

three major channel conformations

A

resting (closed), activated (open), inactivated (closed). there is an inactivation gate as well as an activation gate.

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3
Q

phases 0-4 of the major active ionic current

A

0: depolarization
1: early repolarization
2: plateau
3: repolarization
4: resting (diastole)

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4
Q

slow response action potential

A

occurs in the nodes (SA and AV). only stages 0, 3, and 4. no plateau.

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5
Q

autonomic control of heart rate

A

Norepi and Epi increase heart rate (positive chronotropy)

ACh decreases heart rate (negative chronotropy)

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6
Q

threshold for excitation

A

amount of membrane depolarization required to produce an action potential

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7
Q

what does hypokalemia do to threshold?

A

hyperpolarizes, increases the threshold. this should decrease excitability, but gk decreases with low potassium causing increased excitability

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8
Q

what does hyperkalemia do to threshold?

A

depolarizes, decreases the threshold.

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9
Q

sodium current availability

A

resting membrane potential directly affects cardiac excitability. more depolarizing current required means increase in threshold, and vice versa.

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10
Q

resting membrane potential

A

can’t be determined by the Nernst equation. determined by the balance of inward Na+ and outward K+ ionic currents. resting myocardial membrane is 20 times more permeable to K than Na ions.

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11
Q

what happens in severe hyperkalemia?

A

depolarizes Vm, increases threshold through Ina inactivation, and decreases excitability

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12
Q

functional refractory period

A

minimum time duration after an action potential required for a threshold stimulus to produce a full response again

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13
Q

effective refractory period

A

no action potential may be elicited no matter how strong the stimulus

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14
Q

relative refractory period

A

higher than normal stimulus will elicit an action potential with reduced amplitude and duration

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15
Q

3 major determinants of conduction velocity

A

rate of phase 0 depolarization, resting membrane potential (more negative Vth = faster conduction), threshold potential (less negative Vth = slower conduction)

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16
Q

what is important about AV node delay

A

critical to ensure that atrial contraction finishes before ventricular contraction begins

17
Q

contraction

A
  1. Ca enter through Ica,L channel
  2. Ca ions activate the ryanodine receptor
  3. CaRC releases sarcoplasmic Ca into cytosol and initiates contraction
18
Q

relaxation

A

Cytosolic Ca is reduced back to resting levels by the SR Ca ATPase and the sarcolemmal Na/Ca exchanger

19
Q

sympathetic effects on heart

A

norepi/epi acts at beta 1 adrenergic receptor. increases cAMP and PKA. Increase IcaL and If. leads to positive chronotropy and increased AVN conduction. Increased IcaL and SERCA leads to positive inotropy and increased Ca sensitivity of contractile filaments

20
Q

parasympathetic effects on the heart

A

ACh acts at M2 muscarinic receptor. Decreased cAMP and PKA. activated IkaCh. Decreased Ica,L, If, increased IkaCh, leads to negative chronotripy and decreased AVN conduction. Decreased Ica,L and SERCA leads to negative inotropy and decreased Ca sensitivity of contractile filaments

21
Q

7 phases of the cardiac cycle

A

phase 1: atrial contraction

  1. isovolumetric contraction
  2. rapid ejection
  3. reduced ejection
  4. isovolumetric relaxation
  5. rapid filling
  6. reduced filling
22
Q

heart sounds

A

S1: closure of the mitral and tricuspid valves
S2: closure of the aortic and pulmonary valves
S3: when audible, occurs early in ventricular filling
S4: when audible, vibration of the ventricular wall during atrial contraction (ventricular hypertrophy)