Hemodynamics Flashcards

1
Q

Edematous fluid in pitting edema typically arises from. . .

A

. . . the arterial system via changes in Starling forces.

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2
Q

The balance of oncotic and osmotic pressures that work to keep fluid in the venous system

A

Interstitial space may pull some fluid out of the veins due to osmotic pressure differentials (higher osmotic pressure in the veins). When this happens, not only is the hydrostatic pressure of the vein reduced, but the albumin in the venous blood becomes more concentrated, along with all of its other solutes. This increases the oncotic pressure of the vein, forcing fluid back in.

This constant tug-of-war on fluid results in an equilibrium where most of the fluid is in the vein at any given moment.

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3
Q

What are some common causes of edema?

A

Increased hydrostatic pressure in the venous system, resulting from obstruction or heart defects.

Decreased oncotic force from reduced blood solute concentration. Albumin deficiencies may be caused by malnutrition, blood loss, or catabolic processes in the body taking up albumin as a resource.

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4
Q

Intravascular volume depletion

A

There is not enough volume in the circulatory system to maintain adequate blood pressure for optimal organ function.

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5
Q

Pressure cutoff for hypertension

A

a diastolic pressure consistently ≥90 mm Hg or a systolic pressure ≥140 mm Hg establishes the diagnosis of hypertension

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6
Q

Recent evidence suggests that ___ more accurately predicts cardiovascular complications

A

Recent evidence suggests that systolic pressure more accurately predicts cardiovascular complications

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7
Q

Blood pressure vs age (stratified by anatomical sex)

A
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8
Q

Mechanisms for regulating systemic blood pressure (diagram)

A
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9
Q

No matter how high the CO or TPR, ___ has the capacity to completely return blood pressure to normal by ___

A

No matter how high the CO or TPR, renal excretion has the capacity to completely return blood pressure to normal by reducing intravascular volume

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10
Q

pressure natriuresis

A

In the presence of normally functioning kidneys, an increase in blood pressure leads to augmented urine volume and sodium excretion, which then returns the blood pressure back to normal.

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11
Q

baroreceptor reflex

A

Mediated by receptors in the walls of the aortic arch and the carotid sinuses. If the arterial pressure rises, the baroreceptors are stimulated, relaying the signal to the medulla. Negative feedback signals are then sent back to the circulation, inhibiting sympathetic nervous system outflowandexciting parasympathetic effects.

The net result is (1) vasodilation and (2) reduction in CO

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12
Q

Baroreceptor signals from the carotid sinus receptors are carried by . . .

A

the glossopharyngeal nerve (cranial nerve IX)

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13
Q

Baroreceptor signals from the aortic arch receptors are carried by . . .

A

the vagus nerve (cranial nerve X)

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14
Q

Short-term blood pressure adaptation is mediated by ____. Long-term blood pressure adaptation is mediated by ____.

A

Short-term blood pressure adaptation is mediated by the baroreceptor reflex. Long-term blood pressure adaptation is mediated by kidney regulation and cardiomyocyte proliferation.

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15
Q

Why aren’t baroreceptors good for long-term blood pressure adaptation?

A

The reason for this is that the baroreceptors constantly reset themselves. After a day or two of exposure to higher-than-baseline pressures, the baroreceptor-firing rate slows back to its control value.

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16
Q

essential hypertension

A

Approximately 90% of hypertensive patients have blood pressures that are elevated for no readily definable reason. This is the diagnosis they receive.

The diagnosis of EH is one of exclusion. Heredity appears to play an important role, but good genetic markers have not been identified.

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17
Q

Negative chronotropic effect

A

Effect of decreasing the heart rate

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18
Q

The lusitropic effect

A

Downstream of beta-1 signaling and cAMP, PKA phosphorylates and inactivates phospholamban, increasing the activity of the SERCA pump.

This, in turn, speeds up the rate of calcium re-uptake, reducing the time of systole and increasing compliance of the ventricle.

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19
Q

Concentric hypertrophy

A

The type of cardiac wall thickening you see as a result of increased pressure in the ventricles. Results from the adding of additional muscle fibres to the ventricular wall, which aid in doing pressure work (high pressure with low or normal volume).

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20
Q

Eccentric hypertrophy

A

Type of hypertrophy in which, rather than thickening of the ventricular wall, the ventricular radius increases. This type of hypertrophy is a response to mitral regurgitation, and aids in doing volume work (high stroke volume with low or normal pressure).

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21
Q

Hypertrophy becomes maladaptive when. . .

A

. . . cellular structural changes of hypertrophy result in mismanaging calcium. In short, an over-hypertrophied heart eventually becomes energy inefficient. Other pathological changes include:

  • Diastolic filling is impaired
  • Capillarity is decreased
  • Shift towards apoptosis
  • Increase in arrhythmia frequency (partially related to the above, manifestation of interference in conduction system)
  • Increased susceptibility to ischemia-reperfusion injury
22
Q

Heart failure on a Starling plot

A
23
Q

Capillarity

A

of blood vessels / # of cardiomyocytes

If muscle is proliferating and hypertrophying faster than the endothelium can grow to supply it, risk of ischemia greatly increases.

24
Q

Both ___ and ___ increase cardiac contractility.

A

Both epinephrine and norepinephrine increase cardiac contractility.

25
Q

If you wanted to increase the cardiac contractility of a patient under general anestesia for an operation, what are you probably going to use?

A

digoxin (a classical positive inotrope)

26
Q

Consequences of increased contractility

A
  1. Increased ejection fraction
  2. Increased stroke volume
27
Q

Indicator dilution method of measuring cardiac output

A

Put a catheter in and deliver indicator in the right atrium, then remeasure in the pulmonary artery. Typically cooled saline is used for this, and temperature is measured via IR light to visualize (thermodilution).

28
Q

Fick method for measuring cardiac output

A

Measure 1) the pulmonary arterial ppO2, 2) the venous ppO2, and 3) the oxygen consumed by the individual over the period of time.

29
Q

Normal ejection fraction range

A

55-70%

30
Q

Ejection fraction may be measured by. . .

A
  • echocardiography
  • radionucleotide ventriculography
31
Q

Blood pressure ‘set point’

A

Point to which blood pressure will return from minute-to-minute variations. Mediated by baroreceptor reflex.

32
Q

Which baroreceptors are functionally more important in humans?

A

The carotid

33
Q

Outputs via which the CNS responds to baroreceptor signals

A
  1. Heart rate
  2. Stroke volume
  3. Systemic vascular resistance
34
Q

Arginine vasopressin (aka antidiuretic hormone / ADH)

A

Brain hormone synthesized in the supraoptic and paraventricular neurons in the hypothalamus. Travels down the hypothalamic-pituitary axis and is released from the posterior pituitary.

Major regulator of vascular tone, maintaining it at a certain level (positive effect). Also regulates kidneys via vasopressin receptors (V2R) in the kidney collecting ducts, resulting in AQP2 insertion and water re-uptake.

35
Q

Baroreceptors and vasopressin

A

Under normal conditions, the cardiovascular control center inhibits production and release of vasopressin in the hypothalamus, keeping levels low.

An acute fall in blood pressure results in interruption of this inhibition, increasing vasopressin levels. It then increases blood pressure by 1) increasing SVR and 2) increasing intravascular volume.

36
Q

Renin-angiotensin-aldosterone system

A

Renin is released by the kidney, and converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II is a powerful vasoconstrictor, and also promotes aldosterone synthesis by adrenal cortex. Aldosterone acts on mineralocorticoid receptors in kidney tubules, increasing Na and water reuptake (raising intravascular volume).

37
Q

Baroreceptors and the renin-angiotensin-aldosterone axis

A

If blood pressure falls abruptly, baroreceptors mediate increase in sympathetic tone. SNS stimulation of the kidney results in renin production, feeding into the axis. This restores blood pressure in two ways: 1) vasoconstriction from angiotensin II, and 2) increase in intravascular volume from aldosterone.

38
Q

Baroreceptor-independent renin release

A

The glomerulus also contains its own form of pressure sensor, independent of the CNS-coupled receptors. This is important for maintaining kidney function, as kidneys must adjust renal arterioles in series to regulate pressure and achieve filtration. These sensors may pick up a decreased blood pressure and increase renin production independent of the CNS.

39
Q

The vasoconstrictive properties of angiotensin II and vasopressin respond within ___ to a change in blood pressure.

A

The vasoconstrictive properties of angiotensin II and vasopressin respond within minutes to hours to a change in blood pressure.

So, not a rapid as the CNS’s system, but not chronic by any means.

40
Q

Effective arterial blood volume

A

The volume perceived by the body’s baroreceptors to be arterial. May be low even when the total vascular volume is high, as with patients with cardiac failure. If the heart isn’t working well, blood will be trapped in the venous system.

This is a problem the kidneys can’t solve, since the intravascular volume is fine, and adding more fluid will just result in increased edema (for the most part). But, the kidneys have no way of knowing this, and so they increase water retention anyway.

41
Q

Natriuretic peptides produced in the heart

A

Peptide hormones produced in the heart in response to high blood pressure (measured as chronic atrial stretching). Include atrial natriuretic peptide and B-type natriuretic peptide. Act on the kidney to increase salt and water elimination, reducing intravascular volume.

ANP also inhibits the renin-angiotensin-aldosterone axis and vasodilates.

42
Q

Endothelins

A

Synthesized by mural cells. Act at ETAR on vascular smooth muscle to potently vasoconstrict. Can also act in the CNS to increase arterial pressure and vasopressin secretion.

Can also act at ETBR on endothelial cell membranes, causing eNOS stimulation and NO-mediated vasodilation.

43
Q

BP in supine position

A

Body does not have to work against gravity to return blood from the legs to the heart.

44
Q

Lying/sitting down to standing BP response

A

Blood initially pools more in the legs and abdomen, causing decreased venous return and thus blood pressure drop. This is called orthostatic hypotension when it is pathologically large, clinically greater than a 10 mmHg drop in pressure.

45
Q

BP measured while standing is always ___ than BP taken supine or sitting.

A

BP measured while standing is always lower than BP taken supine or sitting.

46
Q

You’re on an airplane and a woman a few rows in front of you develops chest pressure (“this is my angina”). She tells you she has a history of CAD and high blood pressure, but she has missed all of her meds for the last few days because of her travel. You check her blood pressure and it is 190/110 mm Hg and her pulse is 98 bpm. The flight attendant gives you the airplane first aid kit; what would you give right now?

A

Nitroglycerin and metoprolol

Nitroglycerin will widen the coronary arteries, metoprolol will decrease the oxygen demand by lowering heart rate and contractility.

47
Q

As cardiac output increases, pulmonary artery pressure. . .

A

. . . doesn’t change very much. It increases a bit, but not by as much as one might expect if the tubes were rigid. This is because pulmonary vessels have a greater compliance than most, so the pulmonary vessels are expanding. Intuitively, if the work being done on the fluid is greater and the pressure isn’t changing much, we can infer that the velocity is going up much more.

48
Q

Phenylephrine

A

α1 agonist. Used clinically to constrict blood vessels in the periphery, increasing SVR / afterload. This is one way to raise blood pressure and to shift the Starling curve down.

49
Q

Agents that increase contractility

A

Catecholamines and β1 agonists

50
Q

Effects of afterload on the starling curve

A

Shifts the Starling curve down.

51
Q

During exercise, the systemic vascular resistance. . .

A

Might go up or down. If the individual is very warm, then thermoregulatory dilation will have a powerful effect on decreasing resistance. β2 activity opens up vessels to skeletal muscle, while α1 activity constricts vessels to the enteric system.