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revision ime-kah general > Cardiology physiology > Flashcards

Cardiology physiology Flashcards

1
Q

Describe the organization of the myocardium

A
  • Lattice network, with intercalated disks between muscle cells (continuous mb + gap junctions)
  • T tubules @ level of Z lines
  • Lots of mitochondrias
  • Actin (troponin, tropomyosin) +Myosin
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2
Q

What is the role of tropomyosin

A

Blocks myosin binding sites on actin

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3
Q

What is the particularity of ventricular systole contraction

A

LV twist or rotation (due to different dirrections of layers) with clockwise contraction and counterclockwise contraction during SYSTOLE. Relaxation : springs

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4
Q

Phase 0 of cardiomyocyte

A

Depolarisation : opening of sodium channels , influx of sodium. ends at +20

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5
Q

resting membrane of cardiomyocyte

A

-80

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6
Q

phase 1 of action potential of cardiomyocyte

A

initial repolarization - opening of potassium channels (efflux of potassium)

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7
Q

phase 2 of action potential of cardiomyocyte

A

plateau - calcium channels (l type) open , decreased permeability of potassium due to close of potassium channels. This also allows contraction.
this is why ventricular contraction x15 longer skeletal muscle

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8
Q

phase 3 of action potential of cardiomyocyte

A

Repolarization - closed Ca channels, opening K channels (outward current of K)

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9
Q

what is a refractory period

A

during the plateau. it explains why cell cannot be excited again once it already is. it is shorter in the atria than ventricule. A cell can be excited in the relative refractory period if strong impulse.
N.B absolute refractory period is due to closed Na,Ca channels (unavailable) so no PA can be initiated

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10
Q

what pump opens to initiate contraction of cardiomyocyte

A
  • RYR (ryanoside receptor) on sarcoplasmic reticulum. - due to inward current of Ca by L type of Ca
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11
Q

what pumps out calcium during relaxation

A

-SERCA 2 on sarcoplamic reticulum
- Ca/Na pump on membrane (Ca out, Na in) (with pre-established gradient by Na/K ATPase)

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12
Q

What are p, qrs, t assocaited with

A

p : depolarization of atria
qrs : depolarization of ventricles
t : repolarization of ventricles (happens slightly before contraction of ventricles)

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13
Q

what does q-t represent

A

contraction of ventricle

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14
Q

what closes the aortic valve

A

it is a lunar valve. it closes due to distended large arteries which push back blood into the ventricles (backward pressure gradient) . not due to pressure differential

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15
Q

ejection fraction

A

EF = stroke volume (volume that empties from ventricles during systole) / end diastolic volume

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16
Q

role of papillary muscles

A

to prevent bulging inwards of a-v valve , contract also in systole

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17
Q

explain wigger’s diagram

A
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18
Q

label diagram

A
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19
Q

frank starling law

A

the more the heart is stretched during filling the greater the force of contraction and blood pumped into the aorta (due to actin myosin overlap being more optimal)

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20
Q

preload

A

degree of tension when muscle contractions (end diastolic pressure) or = degree of the ventricular stretch when the heart is at the end of diastole

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21
Q

Afterload

A

sum of all forces opposing ejection (RPT, compliance of arterial tree, and volume of ventricule at onset)

22
Q

Loi de laplace

A

Tension = pressure (left ventricule) x radius/2xwall thickness
N.B if chronic increase in pressure, there will be increased wall thickness, decreased radius and decreased wall tension

23
Q

role of sympathetic system

A
  • increased heart rate
    -increased conduction
  • increased contractibility
  • increased sinus discharge rate
24
Q

what receptor for sympathetic system, where and what does it do

A

b1 receptor (NE)
the whole heart (mostly the ventricles)
increases Na/Ca permeability

25
role of parasympathetic system
It decreases HR and strength of contraction
26
what receptor for sympathetic system, where and what does it do
by vagal nerve - Ach On the S-A (+++) and AV nodes increases potassium permeability (K leaks out of cells creating hyperpolaziration) and longer time to reach threshold
27
impact of temperature and BP on HR
Hypothermia decreases heart rate BP does not do anything
28
impact of potassium on HR
hyperkaliemia = bradycardia , weaker cardiac contraction (dilated flaccid heart) - resting membrane potential is less negative (e.g closer to threshold due to less potassium leaking out of cell because the concentration gradient is decreased) - decreased intensity of AP (Less reactive Na channels) - weaker cardiac contraction
29
impact of hypercalcemia
- stronger longer contractions (hypertension, arrythmias) due to increased calcium entering during plateau - shorter QT (speeds repolarization) => arrhythmias?
30
impact of hypocalcemia
- weaker contractions - prolonged QT (torsade de pointe)
31
different phases of action potential of nodal fiber
32
resting membrane potential of nodal cell
-55
33
are AV node also pacemakers? if so why do they not set the electrical activity?
- yes - they dont because they have slower rythm
34
what makes nodal AV cells pacemakers
instable resting membrane due to funny sodium channels= slow influx of Na until threshold
35
reason for delay of impulse from A to V
contraction of atrium finishes before contraction of ventricle
36
what is the major determinant of cardiac output
venous return (sum of all tissue blood flow which depends on o2 demands/metabolic demand) others : blood volume, HR (sympathetic system... also increases RPT and contractility)
37
what are determinants of venous return
- Frank starling law - Brainbridge reflex : stretch in right sinus node in RA activates vasomotor center, and sympathetic system, leading in an increased HR - right atrial pressure (VR = Psf - PRA / RVR) PsF : Systemic Filling Pressure , pressure right atria (backward force), RVR : resistance of blood flow between peripheral vessels + right atrium. - mean circulatory filling volume (blood volume, nervous system vasoconstriction)
38
Ohm's law
Cardiac output = Arterial pressure / Total peripheral resistance Arterial pressure = ( Mean arterial - right atrial pressure)
39
Increases in CO (due to decreased in RPT or increased pressure)
RPT : - thiamine deficiency (metabolic => vasodilation) - anemia (decreased blood viscosity) BP : hyperthyroidism
40
Mechanism of maintaining BP during exercice
- increased metabolism in skeletal muscle leads to vasodilatation of arteries which decreases RPT = decreased BP - Activation of nervous system : increased HR, large vein constriction (increased venous return ) + arterial (increased TPR) => increased BP Globally there is an increased Cardiac output
41
Other formula for cardiac output
CO = HR x Stroke volume
42
systemic filling pressure
The pressure in the venous system when there is no blood flow (a measure of how much the venous system is "filled" with blood)
43
what is the major determinant of RPT
arterioles ! = control circuits due to innervated smooth muscle walls (alpha 1 : splanchnic, renal, skin ; beta 2 : skeletal muscle)
44
compliance
C= ΔP/ ΔV ​- distensibility (mostly veins, less arteries)
45
pulse pressure mean pressure
pulse pressure : difference systolic - diastolic pressure (depends on stroke volume and compliance of arterial tree) mean pressure : diastolic P + 1/3 pulse pressure
46
baroreflex
- carotid sinus baroreceptors : very se to variation in BP - vasomotor center : brain stem, to 1/3 pons - decrease firing rate of carotid sinus nerve activates sympathetic system, inhibits parasympathetic system
47
baroreflex is acute or chronic correction
acute
48
Consequences of increased Ang II and mechanism on increasing BP
- increases aldosterone secretion : increases na reabsorption at renal distal tubule - increases Na-H exchange and Na reabsorption at proximal convoluted tubules - increases thirst - vasoconstriction of arterioles : increased TPR ** its slow (requires new protein synthesis**
49
consequence of atrial stretch
- increased HR (brainbridge reflex) - decreased ADH secretion (V2 receptors) - increased atrial natriuretic peptice - decreased renal sympathetic activity
50
causes of fluid retention in HF
- RAAS activation (decreased BF to kidneys but also increased K and acth) - Aldosterone (by RAAS) - increased ADH (low BP?) - decreased glomerular pressure (low bp?, intense vasoconstriction of afferent arterioles sympathetic)

revision ime-kah general (4 decks)

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