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Physiology > Chest Pain quiz > Flashcards

Chest Pain quiz Flashcards

1
Q

What is the equation for cardiac output

A

CO = HRxSV

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2
Q

Which side of the heart provides systemic circulation?

A

Left side

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3
Q

Which side of the heart provides pulmonary circulation?

A

Right side

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4
Q

What kind of circuit is between the pulmonary and systemic?

A

Series

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5
Q

What kind of circuit is between all the organs in systemic?

A

Parallel

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6
Q

What is the equation for Ohm’s law in hemodynamics?

A

Q = delta P / R

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7
Q

What is pressure difference in hemodynamics?

A

Delta P = MAP - CVP

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8
Q

What is normal BP (systole/diastole)?

A

130/80

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9
Q

What are the three main functions of cardiac action potentials?

A

Pacemaking by SA node, conduction of the impulse, initiating and controlling contraction

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10
Q

What demonstrates fast APs?

A

Atrial muscle, ventricular muscle, his/purkinje (LEFT SIDE)

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11
Q

What demonstrates slow APs?

A

Pacemaking (SA node), and slow conduction AV node (RIGHT SIDE)

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12
Q

What are the phases of a fast AP (0-4)?

A

0: Rapid depolarization activation of inward Na+
1: Initial repolarization (inactivate inward Na+, activate outward K+)
2: Plateau phase mediated by slowly activating inward Ca++
3: Repolarization due to inactivation of Ca currents and activation of several K+ currents
4: Resting membrane pot’l due to inward-rectivying K+ channels

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13
Q

What are the phases of a slow AP (0-4)?

A

0: slow depolarization due to activation of slowly-activating Ca++ channels
1: absent
2: absent
3: repolarization due to Ca++ channel inactivation and activation of K+ channels
4: slowly depolarizing resting potential

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14
Q

What effect does the parasympathetic NS have on phase 4 depolarization?

A

The parasympathetic NS releases ACh which reacts with muscarinic ACh recepters, increase in Igirk K currents, reducing the depolarization and HR (negative chronotropic effect)

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15
Q

What effect does the sympathetic NS have on phase 4 depolarization?

A

Sympathetic NS releases NorEpi and Epi at the heart which interact with B1 adrenergic recepts, increases both If (slow Na channels) and Ica leading to increase in HR and positive chronotropic effect

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16
Q

What is the P-wave?

A

It is the wave of depolarization from the SA node through the atria

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17
Q

What is the PR segment of an EKG?

A

It is the section after the P wave where there is no detectible signal as it is depolarizing the AV node

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18
Q

What is the Q-wave?

A

The depolarization wave along the bundle of his and purkinje fibers

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19
Q

What is the R-wave?

A

The peak, due to the mass of muscle involved. Wave of depolarization spreads throughout the ventricle, the deflection returns to zero.

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20
Q

What is the S-wave?

A

The last part of the ventricle to depolarize is near the atrium, a brief negative deflection occurs

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21
Q

What is the T-wave?

A

The ventricle repolarizes

22
Q

How do you measure heart rate?

A

The sinus rhythm is the interval between successive P-waves

23
Q

Where are the different leads located? (aVr, aVL, aVf, I, II, III)

A

aVr: -150, aVL = -30, I = 0, II = +60, aVf = +90, III = 120

24
Q

What is indicative of a heart block/AV nodal depression?

A

The PR-interval will increase, or the PR interval will not be followed by a QRS wave

25
Q

What causes an abnormal QRS complex?

A

Premature ventricular complex

26
Q

What is indicative of subendocardial injury?

A

ST depression

27
Q

What is indicative of a transmural epicardial injury?

A

ST elevation

28
Q

What is the equation for stroke volume?

A

EDV-ESV = SV (NORMAL = 60-100)

29
Q

What is the equation for ejection fraction/

A

EJ = SV/EDV (NORMAL = 55-70%)

30
Q

What is preload?

A

Preload s the load present before contraction has started, is provided by the venous return that fills the atrium and enters the ventricle during diastole. Preload represents ventricular stretching prior to contraction

31
Q

What is the law of LaPlace

A

Wall stress = (Pressure x chamber radius)/(2 wall thickness)

32
Q

What is afterload?

A

Afterload represents the force that the heart has to overcome to force blood into the aorta, technically, afterload is the wall stress present at peak systolic pressure

33
Q

What is inotrophy?

A

The ability to modulate the degree of force generation in cardiac muscle

34
Q

What effect does increasing preload have on SV and CO?

A

Increasing preload increases stroke volume to increase CO

35
Q

What is one pathophysiological example of increasing preload?

A

In the case of heart failure. The reduced CO triggers compensatory steps to increase blood vol thereby increasing preload and CO. (Can lead to hypertrophy by LaPlace law)

36
Q

What is one pathophysiological example of increasing afterload?

A

Aortic stenosis. Left ventricular emptying is impared due to narrowing of aortic valve leading to higher resistance, leading to compensatory increase in EDV limited by ventricular hypertrophy leading to a large increase with EDP

37
Q

What is one physiological example of increasing inotrophy?

A

Increase the amount of Ca that enter the cardiac myocyte during phase 2 of the AP leading to an increase in the amount of Ca released from the SR generating a larger force of contraction. This can be seen through symphathetic NS.

38
Q

What is Poiseulle’s equation?

A

Q=(deltaPpier^4)/(8Lviscosity) - not the prettiest I know I apologize

39
Q

What is the relationship between flow and radius?

A

If increasing radius by 2, you are increasing flow by 16

40
Q

What is normal viscosity and the factors effecting viscosity?

A

Normal - 38-54%, factors: altitude, polycythemia vera, severe dehydration, sickle-cell anemia

41
Q

What is resistance in series and in parallel?

A

Series = Rtot=R1+R2+R3, Parallel 1/RTOT=1/R1 + 1/R2 +1/R3

42
Q

What is the equation for total peripheral resistance?

A

TPR = (MAP - CVP)/CO

43
Q

How can MAP be calculated?

A 
MAP = DBP + (PP)/3
PP = SBP-DBP
44
Q

What is Starling’s law of the Capillary?

A

Bulk flow Q= K(Hydro Cap + tissue oncotic) - (Hydro tissue + Plasma oncotic)

45
Q

What are the two types of control of blood flow through the capillaries?

A

Local control and central control (CNS)

46
Q

What are the two main mechanisms of local control?

A

Metabolic - increase metabolic waste -> vasodilation -> increase blood flow
Myogenic - increased pressure, muscle contracts, resistance increases (autoregulation of blood flow)

47
Q

What are the two main mechanisms of central control?

A

Humoral mechanisms-everywhere and Neural mechanisms-fine control

48
Q

What does ANP cause?

A

Atrial natriuretic peptide - causes excretion of Na and water, also causes vasodilation to decrease TPR

49
Q

What does AngII cause?

A

Angiotensin II is a potent vasoconstrictor; stimulating aldosterone synthesis and release for retention of Na

50
Q

What does Epidnephrine cause?

A

released from adrenals via sympathetic stimulation vasodilation in live and skeletal muscle; increases heart rate

51
Q

What does NO cause

A

Gas produced by endotheliu, very short half life cause vascular relaxation and vasodilation

52
Q

What does Endothelin do?

A

ET-1 is a potent vasoconstrictor from endothelium

Physiology (6 decks)

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