Cardiac Physiology 4 Flashcards

1
Q

Diagram of an electron micrograph of a composit capillary in cross section

A
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2
Q

What are the factors responsible for for filtration and absorption across the capillary wall for formation of lymph?

A
  1. Capillary hydrostatic pressure ( Pc ) 2. Interstitial hydrostatic pressure ( Pi ) 3. Capillary oncotic pressure ( πz ) 4. Interstitial oncotic pressure ( πi ) 5. Filtration coefficient ( Kf ) 6. Reflection coefficient ( σ ).
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3
Q

How do oncotic pressure and hydrostatic pressure balance?

A

When hydrostatic pressure is greater than oncotic pressure, filtration predominates and fluid moves out. When oncotic pressure is greater than hydrostatic pressure, absorption predominates and water enters the capillary.

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4
Q

What would happen if the protein in the capillaries were not removed by the lymph vessels?

A

The large protein concentration gradient would accumulate in the interstitial fluid and act as an oncotic force to draw fluid from the blood capillaries to produce edema.

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5
Q

How does the rate of diffusion of small molecules relate to blood flow in the tissues?

A

40x greater, so any small molecule coming through by flow can be diffused across the capillary.

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6
Q

How do lipid-soluble substances pass through capillaries?

A

Directly through the lipid membrane. Rate is directly proportional to the lipid solubility of the substance.

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7
Q

What is the Starling Equation

A

Fluid movement== k[(Pc + πi) - (Pi + πp)], where Pc = capillary hydrostatic pressure, Pi = interstitial fluid hydrostatic pressure, πi = interstitial fluid oncotic pressure, and πp = plasma oncotic pressure. Filtration occurs when the algebraic sum of these terms is positive; absorption occurs when it is negative.

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8
Q

Pinocytosis definition

A

Process in which vesicles are formed from the lipid membrane of the capillaries to move large molecules across the capillary wall.

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9
Q

What is the technique to measure coronary blood flow?

A

Thermodilution

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10
Q

When is the coronary blood flow highest?

A

Right after the aortic pressure peaks. Right side follows more of the aortic flow.

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11
Q

How does coronary blood flow relate to coronary perfusion pressure?

A

Coronary blood flow is resiliant to changes in coronary perfusion pressures.

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12
Q

Graph A-What happens to the mean coronary blood flow and coronary sinus blood PO2 when ventricular systole is inhibited and constant pressure perfusion of the left coronary artery is maintained?

Graph B- What happens when sympathetic stimulation is added to A?

A

A-They both jump up. Otherwise there a lower wave as the heart pumps.

B-Coronary sinus blood PO2 drops temporarily then rises back up. Mean coronary blood flow dips from sympathetic coronary vasoconstriction then rises back up because it is overriden by metabolic vasodilation from the cardiomyocytes.

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13
Q

What factors increase and decrease coronary vascular resistance?

A

Increase: Alpha receptors, myogenic mechanism (intravascular pressure stretching vessel wall), systolic compression, other metabolic factors from increased metabolism from increased myocardial contractile activity (PO2, PCO2, H+, K+).

Decrease: Adenosine from decreased myocardial PO2 from increased metabolism and myocardial contractile activity, other metabolic factors, vagus nerves, myogenic mechanism, beta receptors.

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14
Q

How does coronary perfusion pressure affect myocardial lactate production, Pi levels, pH levels, and pressure in left ventricular contraction?

A
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15
Q

How are coronary collateral vessels formed?

A

From narrowing of coronary arteries in in response to wall stress and to chemical agents released by the ischemic tissue. They originate from preexisting small vessels that undergo proliferative changes of the endothelium and smooth muscle between branches of occluded and nonoccluded arteries. Prevent or reduce necrosis in ischemic myocardium.

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16
Q

How does the work of the left ventricle compare to the right ventricle?

A

7x, because pulmonary vascular resistance is much less than systemic vascular resistance.

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17
Q

In aortic stenosis, what is the energy demand of pressure work vs volume work?

A

High intraventricular pressure is developed during systole so LV O2 consumption is high while the volume work is the same. Coronary perfusion pressure and oxygen supply is normal or reduced because pressure drop across narrowed orifice of the aortic valve.

18
Q

How is net efficiency of the heart calculated?

A

Total cardiac O2 consumption-O2 consumption of the nonbeating/asystolic heart.

19
Q

How does cardiac efficiency improve during exercise?

A

Improves because mean blood pressure and O2 consumption change only a little but CO and work change a lot.

20
Q

How does the uptake of a substrate in the heart influenced?

A

Directly proportional to arterial concentration, so depends on presence or absence of other substrates.

21
Q

How does substrate utilization in ischemia cause necrosis of myocardial cells?

A

In ischemia, lactic acid accumulates and decreases the intracellular pH. This condition inhibits glycolysis, fatty acid use, and protein synthesis and results in cellular damage.

22
Q

What are the components of the cardiovascular response to exercise?

A
  1. Increased stroke volume, 2. Increased HR/CO, 3. Redistribution of blood to working muscles and skin, 4. Increased metabolic rate of muscles, 5. Autoregulation from PO2, 6. Cardiovascular drift (decreased SV and plasma volume), 7. Increased systolic BP (unchanged diastolic), 8. Increased artery/vein O2 difference, 9. Incraesed blood viscosity, 10. Decreased blood pH level.
23
Q

How is stroke volume affected by exercise?

A

Increases to 40-60% of max capacity and then plateaus (reduced filling at higher HR). Increased volume of venous blood return (from muscle pumping, breathing-thoracic pressure, supine positioning). Increased enlargement capacity (F-S law), increased ventrical contractility, aortic or pulmonary artery pressure.

24
Q

How is heart rate/cardiac output affected by exercise?

A
  1. Anticipitory response- Increased HR before exercise by epinephrine release. 2. Steady state HR during steady exercise. Max HR=220-age.
25
Q

Where does the heart redistribute blood to and from during exercise?

A

To working muscles and to skin to maintain body temperature. Reduces blood flow to kidneys, stomach, liver and intestines. Due to decreased vagal tone and increased sympathetic tone.

26
Q

What is cardiovascular drift?

A

Increased HR compensates for decreased SV for decreased total blood volume to maintain flow caused by redistribution and decreased blood plasma.

27
Q

When in exercise does systolic blood pressure increase?

A

Valsalva maneuver and increased use of upper body musculature.

28
Q

Why is there an increased O2 difference between arteries and veins during exercise?

A

Represents the amount of O2 extracted from the blood to be used by muscles.

29
Q

Why is there a decreased plasma volume in exercise?

A

Increased blood pressure forces water from the vascular system to the interstitial spaces. Increased intramuscular osmotic pressure attracts fluid to the muscles, sweating.

30
Q

What is the result of decreased plasma volume?

A

Decreased performance, increased blood viscosity decreasing O2 transport.

31
Q

Equation for MAP relating to CO and TPR?

A

MAP=COxTPR

32
Q

What are the factors relating to CO in MAP?

A

Structure of the heart, Cardiac cycle, Control of heart rate, Control of stroke volume.

33
Q

Factors of total peripheral resistance in MAP

A

Functions of vessels, Local control of resistance, Central control of resistance.

34
Q

What is the autonomic NS effect on SV?

A

Sympathetic neurones: Release norepinephrine + circulating epinephrine, Act on b receptors, Increases contractility, Stronger & shorter systole. Parasymp: none.

35
Q

What is the major affector of capacitance?

A

Venoconstriction

36
Q

What are the individual neurological controls of CO and TPR in the medullary cardiovascular center?

A

Afferent: Glossopharyngeal nerve, carotid sinus baroreceptors, vagus nerve (afferent and efferent), aortic arch baroreceptors. Efferent: sypmathetic nerves, adrenal medulla, venoconstriction and arteriolar constriction.

37
Q

How is contractility increased in exercise?

A

increased sympathetic tone and circulating adrenaline.

38
Q

How is EDV maintained during exercise?

A

Shortened systolic phase, sympathetic venoconstriction, skeletal muscle pump, respiratory pump

39
Q

What are the changes in afterload during exercise?

A

Depends on balance between arteriolar constriction (tends to increase TPR), vs arteriolar dilation (tends to decrease TPR).

40
Q

What is the increase in CO and the corresponding increase in skeletal muscle during exercise?

A

3x, 10x