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Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

∆P = F x R

A

Ohm’s law of hydrodynamics

P = pressure

F = Flow

R = Resistance

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2
Q

R1 + R2 + R3 +…

1/R1 + 1/R2 + 1/R3 +….

A

Resistance in series is additive

Resistance in parallel

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3
Q

The difference in pressure between two points along the axis of a vessel

A

Driving pressure

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4
Q

The difference in pressure between a point just inside the vessel and a point just outside the vessel

Also

The difference between the intravascular pressure and the tissue pressure. This is what governs vessel diameter.

A

transmural pressure

Radial pressure difference

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5
Q

pressure in a vertical column

A

hydrostatic pressure

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6
Q

cardiac output per square meter of BSA

A

cardiac index

at rest = 3.0 L/min/m2

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7
Q

∆V/∆T

A

Flow

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8
Q

Implications of Poiseuille’s law

A
  1. flow is directly proportional to the axial pressure difference
  2. flow is directly proportional to r4
  3. Flow is inversely proportional to the length of the vessel and the viscosity of the fluid

Note: Poiseulle only applies to rigid tubes

○ F= ∆P(πr4)/8ƞƖ

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9
Q

Assumptions for application of Poiseuille’s law to blood flow

A
  1. fluid must not be compressible
  2. tube must be straight, rigid, cylindrical, unbranched and with a constant radius
  3. velocity of the thin layer at the wall = 0
  4. flow must be laminar
  5. flow must be steady
  6. viscosity of the fluid must be constant
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10
Q

○ Re=(2r⊽ρ)/ƞ

A

Reynolds number describes turbulence

> 3000 = mostly turbulent

<2000 = mostly laminar

turbulence occurs when radius is large or the velocity is high (high CO) or the viscosity is low (anemia)

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11
Q

Describe mean pressure in the head and in the foot

A

The mean arterial pressure is 95 mm Hg. For a large vein in the head the mean pressure is lower (subtract 37), and for a vein in the foot the pressure is higher (add 95 mm Hg).

Note: although the arterial and venous pressures in the different location of the body are different, the driving pressure (aka pressure moving volume of blood from arteries to veins) is the same in both supine and standing positions.

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12
Q

As fluid flows along a horizontal tube with a narrow central region which has half the diameter of the two ends, the pressure in the central region is lower than pressure at the distal end of the tube.

A

Bernoulli effect

For the flow to occur from low pressure to high, the velocity in the center must be 4-fold higher. The fluid in the central region flows along an energy gradient (kinetic energy).

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13
Q

the lateral pressure in an artery in reference to atmospheric pressure

A

blood pressure

For catheters, blood pressure measurement is accurate when the opening of the transducer is perpendicular to the flow of blood

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14
Q

measure of the left atrial pressure

A

pulmonary wedge pressure

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15
Q

Equation for determining CO using the Fick principle (restatement of the law of conservation of mass)

A

Qp = VO2/(Cpv[O2] - Cpa[O2])

VO2 = amount of oxygen taken up by the lungs in ml/min

Cpv[O2] = pulmonary vein O2

Cpa[O2] = pulmonary artery O2

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16
Q

What is the reason the behavior of blood is non-Newtonian?

A

interaction of RBCs with fibrinogen

plasma is Newtonian, and the absence of fibrinogen eliminates shear stress

Relatively low Hct has increased viscosity due to stickiness of RBCs, whereas with high Hct viscosity increases due to cell deformation.

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17
Q

Do capillaries have a lower Hct than arterial Hct?

A

Yes. Branch vessels preferentially skim plasma from the main stream of the parent vessel.

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18
Q

Does blood have a high apparent viscosity at low flow?

A

yes.

The shear rate is also low when flow rate is low. This makes blood behave in a non-newtonian manner.

In modest flow, RBCs move toward the center of the stream and lower viscosity

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19
Q

Flow relationship of arteries and capillaries

A

According to the principle of continuity (mass action again), the total volume flow of blood must be the same at any level of arborization. The mean linear velocity of flow is a mirror image of the profile of the total cross-sectional area. Because the smaller vessels (capillaries and venules) have a smaller diameter but collectively have a much larger cross-sectional area than the parent vessel, in order for flow to be conserved, the flow in each smal vessel must be significantly lower than the parent. Note: postcapillary venules have the largest total cross-sectional area.

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20
Q

Application of Poiseulle to radius of a vessel

A

The resistance on an individual unbranched vessel is inversely proportional to r4. Therefore, vessel with small radius has high resistance. BUT the number of vessels in parallel determines the overall resistance to flow. Since the diameters of arterioles are larger than capillaries, it would appear their resistance is lower. There are more capillaries in parallel than arterioles, so the resistance of the capillaries is lower. The arterioles are where the steepest pressure change occurs and these are the vessels of highest resistance.

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21
Q

How are smooth muscle cells arranged in elastic arteries vs muscular arteries?

A

In elastic arteries, the VSMCs are arranged in spirals with varying pitch. In muscular arteries, they are in concentric rings or helices. Vascular elastic tension is determined by the elastin and collagen fibers. VSMCs exert tension by contraction.

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22
Q

Relationship of artery and veins to transmural pressure and volume

A

Arteries have a low volume capacity but can withstand high transmural pressure. Veins have high volume capacity but can withstand only small transmural pressure differences.

This is the relationship of compliance.

C = (change in volume)/(change in pressure)

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23
Q

Laplace’s law

A

The transmural pressure is the distending force that increases the circumference of a vessel. Force opposing this distension is tension. The equilibrium between transmural pressure and tension depends on the radius.

T = (change in P) x r

The wall tension increases as the radius increases. High wall tension is required to withstand high pressure. In order to withstand higher tension, the vessel must contain a higher amount of elastic tissue. Aorta has a larger radius, higher wall tension, withstands high pressure and contains higher amount of elastic tissue.

Elderly have decreased elasticity of vessels due to increased collagen and crosslinking of collagen fibers.

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24
Q

Locations of highest capillary density

A

myocardium

lungs

The myocardium capillary density is 7x that of skeletal muscle

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25
Q

[O2]a - [O2]v/ [O2]a

A

Extraction ratio

the amount of O2 that the tissues remove is an expression of the A-V difference normalized to the arterial content of a substance.

The extraction ratio decreases with increased flow but increases with increased metabolic demand (greater tissue extraction).

Only 20% of capillaries are perfused at rest, but precapillary sphincters dilate in exercise.

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26
Q

the amount of solute that crosses a particular SA of a capillary per unit time

A

flux

The Px (permeability coefficient) describes the ease with which the solute crosses the capillary by diffusion.

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27
Q

Relationship between hydrostatic pressure and colloid osmotic pressure with movement of fluid across capillary wall

A

When the difference between the intravascular pressure and the extravascular pressure (hydrostatic pressure) is positive, fluid moves from the vascular space to the tissue. If the osmotic pressure exerted by the plasma proteins is greater than the extravascular pressure exerted by proteins and proteoglycans, fluid moves into the capillary lumen from the tissue space.

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28
Q

The ratio of colloid osmotic difference observed over the colloid osmotic difference in theory

A

reflection coefficient

if it is 0, water moves the solute

if it is 1 the barrier completely excludes the solute

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29
Q

Why is interstitial fluid pressure slightly negative in most tissues?

A

fluid removal by the lymphatics

lymphatics return 2-4 L of fluid and 100-200 g of proteins to the circulation per day

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30
Q

How does endothelin cause vasoconstriction?

A

It binds to ETa receptor and increases intracellular calcium, promoting vasoconstriction

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31
Q

Calcium influx in cardiac muscle

A

unlike skeletal muscle, cardiac muscle requires extracellular calcium to enter L-type calcium channels in the T tubule membrane. This influx of calcium triggers release of calcium from the SR and intiates muscle contraction

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32
Q

How do catecholamines exert positive inotropic effect?

A

make SR calcium channels more sensitive to cytoplasmic calcium

Stimulate SERCA, increasing calcium stores for later release

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33
Q

leads with upright QRS on normal 12-lead EKG

A

I, II, aVL, aVF, V3, V4, V5 V6

V3 is almost isoelectric

34
Q

transverse plane leads

A

precordial leads (V1-V6)

35
Q

frontal plane

A

limb leads: aVL, aVR, aVF, I, II, III

36
Q

atrial depolarization on EKG

A

P wave

37
Q

length of time for conduction through the AV node before activation of the ventricles

A

PR interval

38
Q

depolarization wave spread through the ventricles, as seen on EKG

A

QRS

39
Q

on EKG, how long the ventricles stay depolarized

rough measure of the overall action potential of the ventricles

A

QT interval

40
Q

the potential at which no current would flow even if the ion channels were open

A

reversal potential

41
Q

relationship of potassium to ectopic pacemakers

A

hyperkalemia slows or stops the pacemaker

hypokalemia facilitates ectopic pacemaker

42
Q

What causes a flattened or inverted T wave? What causes a tall T wave?

A

Flattened or inverted: digoxin, pericarditis, PE

Tall: hyperkalemia, MI

43
Q

PR interval gradually lenthens from one cycle to the next until the AV node falls off completely and a ventricular depolarization is skipped

A

Second degree heart block Mobitz type I

44
Q

PR interval is constant

every nth ventricular depolarization is missing

A

second degree heart block Mobitz type II

45
Q

ECG finding with enlarged right atrium

A

enlarged p wave

46
Q

When do you see T wave inversion in MI?

A

within 1-2 days

47
Q

Describe the ECG of MI several weeks after event

A

ST segment and T wave are normal

Q wave persists

48
Q

Reversible causes of prolonged PR (first degree block)

A

increased vagal tone

transient AV ischemia

beta blockers

calcium channel blockers

digitalis

antiarrhythmics

49
Q

How do you treat third degree heart block?

A

pacemaker

50
Q

What produces S3 heart sound?

A

rapid filling of the ventricles during diastole making the ventricle walls recoil

can be heard in adults with overfilled ventricles at end systole (70 mL)

51
Q

S1-S2-S3

A

ventricular gallop

“Kentucky”

52
Q

S4-S1-S2

A

atrial gallop

“Tennessee”

53
Q

What produces S4 heart sound?

A

strong atrial contraction against a low compliance ventricle (stiff ventricle)

pathologic

54
Q

What does arterial impedence reflect?

A

ventricular afterload

Impedence = resistance

55
Q

Why is pulsation absent from capillaries?

A

pressure is dampened and blood flow is continuous

56
Q

Pressure waves in the venous system are produced by:

A
  1. retrograde action of the heartbeat during the cardiac cycle
  2. respiratory cycle
  3. contraction of the skeletal muscles
57
Q

Why is S2 split during normal inspiration?

A

The lower impedence of the pulmonary circulation and the increased volume return to the right heart creating a larger EDV that requires more time to eject, postponing closure of pulmonary valve (P2)

58
Q

Order of pumping and valve closures

A

right atrium contracts before the left

left ventricle contracts before the right

mitral valve closes before the tricuspid

pulmonic valve opens slightly before the aortic, because the right ventricle doesn’t have to generate as much pressure to open the pulmonic valve

59
Q

the mechanical energy set free in the passage from resting length to active state is a function of the length of the fiber

The length of the myocardial fibers is proportional to the EDV.

The tension of the myocardial fibers is proportional to systolic pressure

A

Starling’s law

60
Q

How much of the CO is represented by the coronary blood flow?

A

5%

61
Q

Which is dominant in coronary blood flow: local autoregulation or influence of sympathetic innervation (alpha)?

A

local metabolic influence and autoregulation is dominant in the coronary blood flow

Note: signs of ischemia are best viewed as the coronary blood flow not meeting demand

62
Q

an increase in SV for a given preload and afterload is due to

A

increase in contractility

(he makes a point that these 3 variables need to be in the description of contractility to portray it accurately)

63
Q

syncope is associated with

A

abrupt arteriolar dilation causing a drop in SVR, lowering MAP significant enough to cause cerebral hypoperfusion

64
Q

at what HR does SV begin to decline?

A

around 150-180 in normal sinus rhythm

In healthy athletes it declines around 180

Note: it is the rhythm that really determines the rate at which SV is compromised. NSR is coordinated and SV is adequate. Vtach at a similar rate reduces SV from baseline and can have hemodynamic compromise after 30 seconds

65
Q

chemoreceptors and tachycardia

A

Peripheral chemoreceptors sense hypoxia and increase ventilation

Central chemoreceptors sense increased CO2 and stimulate ventilation.

Pulmonary stretch receptors sense increased stretch which leads to inhibition of the cardioinhibitory center -> tachycardia

Decreased CO2 in the brain from hyperventilation also inhibits the cardioinhibitory center -> tachycardia

Bottom line: net response to hypoxia is tachycardia

66
Q

Driving pressure and RAP relationship to venous return

A

driving pressure: CVP-RAP

increased arteriolar tone decreases CVP (lower blood volume)

decreased arteriolar tone increases CVP (increases blood flow and therefore volume in the system and thus venous return)

67
Q

Effects of ANG II

A
  1. vasoconstriction
  2. reduction of renal blood flow resulting in increased Na reabsorption
  3. stimulates release of aldosterone
  4. stimulates release of vasopressin
  5. stimulates release of NE
  6. acts as a cardiac growth factor
68
Q

Does extracellular potassium promote vasodilation or vasoconstriction?

A

vasodilation

so does adenosine and CO2

69
Q

How is ascites produced?

A

The pressure in the hepatic portal vein is 10-12 mm Hg. When the right side of the heart fails, increased vena cava pressure causes transudate fluid from the liver to enter the peritoneal cavity (Starling forces)

70
Q

What is the triple response?

A
  1. blanching of skin from pressure
  2. red reaction from local dilation of vessels in response to sensed pressure
  3. flare reaction is axon reflex of branching nerve fiber resulting in spread to the surrounding area
71
Q

index of the functional capacity of the body to generate aerobic power

A

VO2 max

normal: 30-40 mLO2/min kg

72
Q

How do positive g forces affect cardiovascular system?

A

• Shifts the blood volume away from direction of acceleration

can result in transient shift of blood flow away from the brain and loss of consciousness

73
Q

How does negative g affect cardiovascular system?

A

• blood volume redistributes toward the head
○ Expands the central blood volume (away from the legs), increases preload, increases water in the interstitium of the face -> bloats the face

Causes headache and nausea

74
Q

diastolic pressure + 1/3 pulse pressure

A

mean arterial pressure (MAP)

75
Q

reduced S1 intensity causes

A

long PR in 1st degree block

mitral regurgitation

LVH causing stiffness and decreased distance of movement of the leaflets

76
Q

fixed splitting of S2

A

stays the same throughout the resp cycle

ASD can cause volume overload which increases the capacitance of the pulmonary system and delays closure of pulmonic valve

77
Q

widened splitting of S2

A

audible separation of A2 and P2 in expiration

delayed closure of pulmonary valve due to pulmonic stenosis or RBBB

78
Q

sharp, high-pitched sound that does not vary with respiration

hear 3 sounds in succession at the pulmonic area

present with rheumatic heart disease

A

opening snap
of mitral or tricuspid valves

is time internal between OS and A2 is narrow the stenosis is severe

79
Q

audible separatin of A2 and P2 in expiration with sound fusion in inspiration

reflects a delay in aortic valve closure

aortic stenosis or LBBB

A

paradoxical splitting

80
Q

What causes a prominent v wave?

A

tricuspid regurgitation

81
Q

What causes a prominent a wave?

What causes a small a wave?

A

tricuspid stenosis

cardiac tamponade

RVH

small a wave caused by volume depletion and is absent in afib

82
Q

symptoms of pericardial effusion

A

dysphagia

dyspnea

hoarseness

hiccups

dull constant ache on left side of chest

Cardiology (10 decks)

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