3 - CV Physiology Flashcards

1
Q

Myocardium (key points)

A
  • 95% of the heart
  • responsible for pumping
  • cardiac muscle (involuntary)
  • fibers swirl diagonally around the heart
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2
Q

Cardiac muscle tissue (structural components of cell connections)

A
  • sarcolemma (cell wall)
  • cells connect at intercalated discs (1) containing:
    • gap junctions (allow cells to communicate)
    • desmosomes (keep fibers connected)

1-thickened sarcolemma

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3
Q

quiz on:
cardiac conduction system

A

see goodnotes

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4
Q

Sinoatrial (SA) node
(electrical signal)

A

fires constantly (100 times/min) which would translate to our bpm if nothing controlled it

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5
Q

cardiac conduction system anatomy

A
  • sinoatrial (SA) node
  • atriventricular (AV) node
  • bundle of HIS
  • right and left bundle branches
  • purkinje fibers
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6
Q

Action potential phases in ventricular myocyte

A

RMP roughly -90mV (1)
rapid depolarization (+20mV)
- Na+ channels open
- Na+ inflow depolarizes the cell
plateau (+10mV)
- Ca2+ inflow
- some K+ outflow
repolarization (90mV)
- Ca2+ channels close
- K+ outflow

refractory period (2) from depolarization to mid repolarization
contraction starts right after RP and ends right before

1-voltages are just examples, 2-cardiac AP cannot trigger

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7
Q

Electrocardiogram (ECG) 3 waves
(draw + label)

also called ECG or EKG, see goodnotes for graph

A

in order:
- P wave: small wave (+0.1mV/0.1s)
- QRS complex: 3 spikes (0.2,+1,-0.4mV/0.1s)
- T wave: large wave (+0.2mV/0.2s)
- U wave: tiny wave (not visible on most graphs)

voltages and times are just example values

info on how ECG functions is on avenue, not neccessary

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8
Q

Events corresponding to sections of the ECG graph

A
  • P: atria depolarize (action potential at SA node)
  • flat: atrial systole (1)
  • QRS: ventricles depolarize
  • flat: ventricular systole
  • T: ventricles repolarize
  • flat: ventricles relax

1-contraction

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9
Q

average values for adult:
- cardiac cycle length
- native bpm
- stroke volume
- blood pressure

A
  • 0.8s
  • 75bpm
  • 70mL
  • < 120/80 mmHG
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10
Q

Pressure waves vs ECG
(draw wave + label valve changes)

see goodnotes for graph

A

pressure waves: aortic, V, A
- AV close: R spike, first dip in LV/LA P
- SL open: QRS end, start of 1st wave for aortic P, 2nd wave peak LA
- SL close: mid T, dip in aortic P
- AV open: T end, end of wave in LV and aortic P, small wave in LA

systole –> increased pressure

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11
Q

aortic valve pressure wave
(notable points)

A
  • aortic valve opens
  • aortic valve closes
  • dicrotic wave due to rebound off valve closure
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12
Q

heart sounds

A

loudest
- S1: AV valves close
- S2: SL valves close
- S3: ventricles fill (much quieter
- S4: atrial systole (almost silent)

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13
Q

Pressure phases (cardiac cycle) in order

A
  • atrial contraction (AV open)
  • isovolumetric contraction (all closed)
  • ventricular ejection (SL open)
  • isovolumetric relaxation (all closed)
  • ventricular filling (AV open)
  • atrial contraction (AV open)…
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14
Q

Ventricular volume curve
(draw + label)

A
  • end diastolic volume (V systole start)
  • end systolic volume (V systole end)
  • stroke volume = EDV - ESV (∆volume in a V)
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15
Q

Cardiac output
(definition + equation)

A

volume of blood ejected from a ventricle into it’s respective vessel each minute
CO = HR x SV

heart rate x stroke volume

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16
Q

cardiac reserve
(definition + equation)

A

difference between our maximum HR and our resting HR
CR = HR(max) - HR(rest)

17
Q

Factors regulating stroke volume
(names + definitions)

A

increased x will increase SV:
- preload: stretch on heart before contracts
- contractility: contraction force of muscle fibers

increased x will decrease SV:
- afterload: pressure in V required to open SL valves

18
Q

Frank-Starling Law

A

stroke volume (SV) is proportional to muscle stretch and end diastolic volume (EDV)

only to a point, muscle can’t stretch indefinitely

19
Q

what affects preload?

A
  • duration of ventricular diastole
    • increase leads to slower HR
  • venous return
    • eg: increased by exercise, decreased by hemorrhage

increase in either leads to increased preload

20
Q

what affects contractility?

A

changes in cytosolic Ca2+
altered by inotropes:
- positive (increase C) eg: epinephrine
- negative (decrease C) eg: hypoxia(1)

1-low O2 levels in body tissues

21
Q

what affects afterload?

A
  • blood pressure
    • high BP –> increased afterload
  • vessel structure
    • vasoconstriction –> increased afterload
22
Q

qualities of the conductive fibers in the heart

A
  • autoarithmic: will depolarize spontaneously (act as pacemakers)
  • SA node is fastest and will set the pace
  • if preceding structures are impaired, the next structure sets a slower pace (eg: damaged SA node will lead to slower pace set by AV node)
23
Q

Factors regulating HR

A
  • Autonomic NS (+ symp. -parasymp.)

Chemical:
- Hormones ( +E&NE +Thyroxine)
- Cations (+Ca -Na -K)
- Hypoxia (-less oxygen)
- Acidosis (-excess H+)
- Alkalosis (-high pH)

Other:
- Age (+infants -older)
- Body Temp (+high T -low T)

24
Q

Nervous system control of the heart

A

Input:
- proprioceptors (monitor movement)
- chemoreceptors (measure blood chemistry)
- baroreceptors (monitor blood pressure)
Processing:
- cardiovascular center in medulla oblongata
Output:
- cardiac accelerator nerves (sympathetic) - increase HR and stroke volume
- vagus nerves (CN X, parasympathetic) - decrease HR

remember: SNS - adrenergic receptors, PSNS - cholinergic receptors