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Cardiology > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

When is the atrial pressure lowest and ventricular pressure highest?

A

ventricular systole

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2
Q

What happens when the ventricles contract and the Atrial-ventricular valves shut?

A

iso-volumic contraction

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3
Q

What happens during diastole?

A

Ventricle muscles relax –> ventricular pressure less than arterial –> forward-valves close –> iso-volumic relaxation –> pressure less than atria –> back valve opens –> atrial pressure fills up ventricles

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4
Q

What does S1 represent?

A

closing atrio-ventricular valves (tricuspid, mitral) = beginning of ventricular systole

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5
Q

What does S2 represent?

A

closing of ventricular-arterial valves (pulmonic, aortic) = beginning of diastole

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6
Q

What is physiological splitting?

A

Aortic and pulmonary valves do not close exactly at the same time (aortic first in normal)

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7
Q

What does pulmonary capillary wedge pressure estimate?

A

LAP - left atrial pressure (any other structures back to it)

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8
Q

What is the significance of PCWP?

A

PCWP is used to diagnose the severity of left ventricular failure and to quantify the degree of mitral valve stenosis (these elevate LAP)

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9
Q

What can a high LAP cause?

A

Pulmonary edema: increases in LAP are transmitted almost fully back to the pulmonary capillaries thereby increasing their hydrostatic pressure and filtration of fluid

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10
Q

Sarcomere is made of what two filaments?

A

thick and thin

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11
Q

Thick and thin filaments are made up of what?

A

myosin - thick

actin - thin

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12
Q

What are myofibrils?

A

bundle of sarcomere

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13
Q

What consists a muscle cells?

A

myofibrils, sarcoplasmic reticulum, T tubule system, mitochondria, and at least one nucleus

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14
Q

What is bead on a string?

A

actin molecules joined end on end

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15
Q

True or False: there are two beads on a string made of actin that wind around a tropomyosin molecule

A

True

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16
Q

Tropomyosin associates with what complex and what it made of?

A

Troponin complex, which is made of troponins I, T, C

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17
Q

True or False: under resting conditions tropomyosin blocks the myosin binding sites of the actin molecules

A

True

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18
Q

True or False: the troponin complex helps to destabilize the tropomyosin-actin complex

A

False: stabilises

troponin I binds to actin, troponin T binds to tropomyosin, troponin C binds to Ca

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19
Q

What is the composition of a myosin head?

A

two light chains, actin binding side, ATP binding site

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20
Q

What is a myosin filament?

A

300-400 myosin molecules held together by M-line proteins as well as the proteins nebulin and titin

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21
Q

Describe the cross-bridge cycle:

A
  • depolarization of myocardial cell (and its plasma membrane and t-bubule system)
  • Ca channels open in sarcoplasmic reticulum and t-tubules
  • Ca enters cells and binds to troponin C changing the troponin-tropomyosin-actin complex, and exposing the myosin-binding sites on actin
  • myosin binds to actin creating a cross-bridge
  • binding causes myosin head to bend and pull the actin filament as a result
  • ADP and Pi released –> power stroke
  • ATP binds to myosin head –> releases cross bridge
  • ATP hydrolysed –> myosin head returns to resting conformation (ie. re-cocking)
  • Ca is pumped back into the sarcoplasmic reticulum by Ca-ATPase
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22
Q

What molecules are critical for muscle contraction?

A

Ca and ATP

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23
Q

What are the 3 main factors to muscle fiber shortening?

A
  1. Pre-load (amount of filling before ventricular contraction)
  2. After-load (amount resistant to emptying)
  3. Contractility
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24
Q

How does pre-load affect the muscle fiber shortening?

A

The amount in ventricles prior to systole determines the length of each muscle fiber (ie. the amount of actin-myosin overlap, ideally is 2.2 micron for each sarcomere)

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25
Q

How is pre-load determined?

A

By measuring end-diastolic volume/pressure

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26
Q

What is Titin?

A

elastic protein that anchors the large heavy chain of myosin filament to the Z line

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27
Q

What factors determine the Frank-Starling Curve?

A

1) Titin: stretching the sarcomere increases elastic recoil of titin and hence contraction (important at the ascending part of curve)
2) Troponin C: higher Ca increases affinity of Troponin C; stretch of sarcomere also increases the affinity (ie. length dependent activation)
3) Stretch: brings actin and myosin filaments closer together making easier for interaction
4) Intracellular Ca

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28
Q

What is the best measure of after-load?

A

the wall tension needed to ‘pop’ aortic valve open and get forward flow (ie. related to systemic resistance)

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29
Q

What 3 factors determine wall tension?

A

Pressure (biggest factor) in chamber
Radius = Size of chamber
Thickness of chamber wall

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30
Q

What is LePlace Law?

A

Tension is proportional to (P*R/t)
P = arterial pressure
R = heart size
t = thickness of heart wall

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31
Q

Why does an increase in afterload shift the Frank-Starling Curve to the right (ie. decrease stroke volume and increase LVEDP [ie.preload])?

A

Increase in afterload decreases the velocity of fiber shortening. Because the period of time available for ejection is finite (~200 msec), a decrease in fiber shortening velocity reduces the rate of volume ejection so that more blood is left within the ventricle at the end of systole (increased end-systolic volume –> added to the original preload –> high LVEDV and LVEDP).

32
Q

True or False: ventricular dilation would increase wall tension (and increased after-load)

A

True

33
Q

Contractillity depends on what factors?

A

Depends on pre-load / afterload, but also has independent factors (ie. ionotropy) for any given pre-load and after-load

34
Q

How is ionotropry measured?

A

Measured indirectly by % of ventricular volume ejected = EJECTION FRACTION

Directly measured by rate of fiber shortening = Δ Pressure / Δ Time (dP/dT)

35
Q

What is the main factor increasing ionotropy?

A

Calcium (more means more overlap between actin and myosin)

36
Q

What are some ionotropic factors?

A
  • Catecholamines (increase cAMP in cell, increase Ca++ storage)
  • Phosphodiesterase inhibitors (lead to increase cAMP in cell)
  • Digoxin (changes cell ion currents –> increase Ca++ influx)
  • Caffeine, stress hormone angiotensin II
37
Q

What are some chronic ionotropic factors?

A
  • the type of myosin light chains
  • the type of myosin (a vs b). For example, in heart failure, myosin a is lost and the proportion of myosin b (with slower ATPase activity) increases
  • the amount of ATP being generated in the cell
  • the release rate of calcium from troponin C
  • the re-uptake rate of calcium into the sarcoplasmic reticulum (the faster the uptake the greater the contractility)
  • the release rate of calcium into the sarcoplasmic reticulum (the faster the release the greater the contractility)
  • Various cytokines, hormones and paracrine factors (many from pericardial fat)
38
Q

What is lusitropy?

A

Speed of myocardial relaxation

39
Q

What is Ejection FRaction?

A

= % of ventricular volume pumped out in systole
= (volume end-diastole – volume end-systole) / (volume end-diastole)
= SV/LVEDV

40
Q

What is stroke volume?

A

Amount of blood pumped in each heart cycle

= (end-diastolic – end-systolic volume)

41
Q

What is cardiac output?

A

Cardiac Output (CO) = amount ejected with each heart beat x # heart beats / time

CO = Stroke volume x Heart Rate

42
Q

What is normal ejection fraction?

A

50-70%

43
Q

T or F: EF is an indirect measure of contractility?

A

T –> e.g., ↓ myocardial contractility → ↓ EF (seen in systolic heart failure, where EF is < 40%)

44
Q

What are the usual pressures in the heart compartments?

A

Right atrium: < 5 mm Hg
Right ventricle (pulmonary artery pressure): 25/5 mm Hg
Left atrium (pulmonary capillary wedge pressure): < 12 mm Hg
Left ventricle: 130/10 mm Hg

45
Q

What is the period of highest O2 consumption?

A

isolvolumetric contraction

46
Q

What is the dicrotic notch and when does it occur?

A

slight increase of aortic pressure in the early diastole (ie. isovolumetric relaxation) that corresponds to closure of the aortic valve

47
Q

At what point are all valves closed?

A

isovolumetric contraction/relaxation

48
Q

Which node is influenced by the ANS?

A

SA node

49
Q

Why is the delay at the AV node important?

A

Delays conduction for 60–120 ms (allowing the ventricles to fill with blood; without this delay, the atria and ventricles would contract at the same time)

50
Q

Which fibres allow for the synchronous contraction of ventricles?

A

purkinje fibres

51
Q

T or F: pacemaker cells have a resting membrane potential

A

F:
Pacemaker cells have no stable resting membrane potential. Their special hyperpolarization-activated cation channels (funny sodium channels) ensure a spontaneous new depolarization at the end of each repolarization and are responsible for the automaticity of the heart conduction system! In sympathetic stimulation, more If channels open, increasing the heart rate.

52
Q

Whats different about the upstroke and depolarization in pacemaker cells and cardiac muscle cells?

A

Upstroke and depolarization of a pacemaker cell are caused by the opening of voltage-activated L-type calcium channels. In other muscle cells and neurons, upstroke and depolarization are caused by fast sodium channels!

53
Q

What happens if the output in RV is greater than LV?

A

If the output of the right ventricle is higher than the output of the left ventricle, this results in accumulation of blood in the lungs (lung edema).

54
Q

T or F: parasymp nerves activate both ventricles and atria

A

F:
Sympathetic fibers innervate both the atria and ventricles.
Parasympathetic fibers only innervate the atria.

55
Q

What is the effect of sympathetic stimulation on the heart?

A

↑ Heart rate, conduction, contractility, and relaxation

Activation of beta1 adrenergic receptors

56
Q

What is the effect of parasymp stimulation on the heart?

A

↓ Heart rate and atrial contractility (via SA and AV nodes)

Activation of parasympathetic muscarinic ACh receptors (subtype M2)

57
Q

What are two ways to increases preload?

A
  • venous constriction (During inspiration,
  • -> When changing from upright to supine position,
  • -> ↑ Skeletal muscle pump activity.
  • -> ↑ Venous tone (increased sympathetic activity)
  • increasing blood volume
58
Q

What are ways to decrease preload?

A

↓ Venous return

    - During expiration
    - When changing from supine to upright position
    - Nitroglycerin (venous vasodilatation)
    - Inferior vena cava obstruction during pregnancy or due to Valsalva maneuver
    - Due to ACE inhibitors or angiotensin II receptor blockers (?)
    - Hemorrhage

Tricuspid and mitral valve stenosis (↓ ventricular inflow)

Aortic stenosis (↑ diastolic ventricular pressure → ↓ ventricular filling because heart becomes stiff and cannot hold a lot)

Atrial tachycardia (e.g., atrial fibrillation ↓ ventricular filling time)

59
Q

How to decrease afterload?

A

↓ Systemic vascular resistance (e.g., due to vasodilators such as hydralazine, ACE inhibitors, angiotensin II receptor blockers) and/or pulmonary vascular resistance (e.g., due to vasodilators such as phosphodiesterase inhibitors)

60
Q

How to increase afterload?

A

↑ Systemic and/or peripheral vascular resistance (e.g., due to chronic hypertension)

Aortic valve stenosis

61
Q

How to increase myocardial contractility?

A

Sympathetic innervation (β1-receptor activation)

Catecholamines (e.g., epinephrine, norepinephrine, dopamine) through β1-receptor activation

High levels of blood and intracellular calcium

Thyroid hormones

Decreased extracellular Na+ (because subsequently, the activity of the Na+/Ca2+ exchanger will decrease)

Digitalis: inhibition of Na+/K+ pump → increased intracellular Na+ → decreased Na+/Ca2+ exchanger activity → increased intracellular Ca2+

62
Q

How to decrease myocardial contractility?

A
  • Parasympathetic stimulation
  • Acetylcholine
  • β1-receptor blockers: inhibition of adenylyl cyclase → ↓ cAMP → ↓ cAMP-dependent protein kinase A (PKA) activity
  • Nondihydropyridine Ca2+ channel blockers
  • Systolic heart failure
  • Hypoxia
  • Hypercapnia
  • Hyperkalemia
  • Acidosis
63
Q

T or F:

The Aortic pressure is lower in diastole and LV and LA higher

A

T

64
Q

T or F: in mitral stenosis the LAP is higher

A

T

65
Q

Why does the LAP abruptly rise during late systole in mitral regurgitation?

A

Because as the LV contracts blood goes back into LA raising volume and pressure

66
Q

T or F: the aortic pressure is much higher than LVP in aotic stenosis

A

F: LVP is (need to open stenoyic valve)

67
Q

What does a large A wave in venous tracing mean?

A

tricuspid stenosis, right heart failure, pulmonary HTN

68
Q

What does a cannon a wave mean?

A

AV dissociation (sometimes ventricle and atria not contracting in series), and ventricular tachycardia

69
Q

What happens to a wave in AV dissociation?

A

Infrequent peaks of a wave

70
Q

What causes an absence of a wave?

A

atrial fibrillation

71
Q

What happens to the venous tracing in tricuspid regurgitation?

A

giant v wave

72
Q

What increases contractility?

A

exercise and inotropes

73
Q

What decreases contractility?

A

MI, heart failure

74
Q

What is Torsades de Pointes?

A

AKA twisting of points that results in cardiac arrest usually due to hypokalemia or hypomagnesemia or induced by antiarrhythmic drugs (that prolong QT)

–> feared oucome of QT prolongation

75
Q

Which ion affects the QT segment?

A

calcium: [high] –> short QT

[low] then –> long QT

76
Q

What indices peaked t waves?

A

hyperkalemia, early ischemia

Cardiology (29 decks)

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