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Anesthesia Fast Facts > CV Phys & Vasopressors > Flashcards

CV Phys & Vasopressors Flashcards

1
Q

Drugs of choice for mild hypotension from general or regional anesthesia? (2)

A

Phenylephrine
Dose: 50-200 mcg
Infusion: 20-200 mcg/min

Ephedrine
Dose: 2.5-10 mg

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2
Q

Concentration: 1:1,000 epi

A

Dose Equivalent & Percent

1 mg/ml = 0.1%

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3
Q

Concentration: 1:10,000 epi

A

Dose Equivalent & Percent

0.1 mg/ml = 0.01%

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4
Q

Concentration: 1:100,000 epi

A

Dose Equivalent & Percent

0.01 mg/ml = 0.001%

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5
Q

Concentration: 1:200,000 epi

A

Dose Equivalent & Percent

0.005 mg/ml = 0.0005%

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6
Q

How many mg of epi are in 5mL of a 1:10,000 (g/mL) solution?

A

Convert 1:10,000 into mg/mL
1:10,000 = 1000mg/10,000mL = 0.1 mg/mL
5mL x 0.1 mg/mL = 0.5 mg

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7
Q

chronotropy

A

HR

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8
Q

inotropy

A

contractility

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9
Q

dromotropy

A

conduction velocity

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10
Q

lusitropy

A

rate of myocardial relaxation

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11
Q

Endothelial Vasodilators

A

NO and prostacyclin

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12
Q

Endothelial vasoconstrictors

A

thromboxane A2, leukotrienes, endothelin 1, ACE

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13
Q

(vascular) resistance is most affected by?

A

radius^4

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14
Q

PCWP is a good approximation of?

A

LA pressure and reflects the filling pressure of the L side of the heart

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15
Q

Bainbridge reflex

A

-atrial stretch can increase HR which may help match CO to venous return

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16
Q

Baroreceptor response

A

receptors in carotid sinus and aortic arch are activated by increased SBP that stimulates stretch receptors and sends signals through the vagus and glossopharyngeal nerves to CNS

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17
Q

Carotid sinus chemoreceptors

A

-stimulation due to atrial hypoxemia results in SNS stimulation

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18
Q

How low is too low of a decrease in BP in a healthy patient?

A

20-30% below baseline in normal healthy patient may be OKAY

hypotensive situations: keep MAP greater than 2/3 of normotensive MAP to prevent cerebral ischemia

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19
Q

Patient position and BP

A

blood pressure decreases 2 mmHg for every 2.5 cm (1 in) height above the point of measurement

BP in brain of a sitting pt is about 12-16 mmHg lower than the upper arm measurement

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20
Q

Endogenous catecholamine synthesis pathway:

A

phenylalanine > tyrosine > L-dopa > dopamine > norepi > epi

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21
Q

Common synthesized catecholamines:

A

dobutamine
isoproterenol
phenylephrine

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22
Q

Vasopressin Dose

A
  • 0.01-0.04 units/min IV infusion for vasodilatory shock
  • 1-8 unit bolus
  • elimination t1/2 10-20 min
23
Q

Great for refractory hypotension due to ACE/ARB-induced hypotension

A

Vasopressin

1-8 units IV push

24
Q

Epi Dose

A

20-100 mcg IV bolus

0.01-.1 mcg/kg/min infusion

25
Q

Dopamine Dose

A

1-30 mcg/kg/min IV infusion

Dopaminergic = 0.5-2
Beta 1 = 2-10
alpha = > 10

26
Q

Phenylepherine Dose

A

50-200 mcg IV bolus to treat BP that accompanies SNS blockade produced by anesthesia

20-200 mcg/min for continuous infusion

or if weight based infusion then 0.25-1 mcg/kg/min

27
Q

Ephedrine Dose

A
  1. 5-10 mg IV adults
  2. 1 mg/kg IV peds
  • longer onset due to indirect effects
  • tachyphylaxis possible on repeat doses
28
Q

Dobutamine Dose

A

high dose (cardiac stress tests) = 10-20 m/kg /min

low dose infusions: 5 mcg/kg/min

29
Q

Milrinone Dose

A

50 mcg/kg IV bolus over 10-30 min

0.375-0.75 mcg/kg/min infusion

30
Q

What kind of patients should NOT be subjected to hypotension

A 
known carotid stenosis 
known valve disorders
known heart failure
known fixed CO
known severe CAD
31
Q

Factors that directly affect MAP

A

CO & SVR

32
Q

Factors that directly affect CO

A

SV & HR

33
Q

Factors that directly affect SV

A

Preload & Inotropy

34
Q

Factors that directly affect Preload

A

Blood volume & venous compliance

35
Q

What neurohumoral factors affect the physiology of blood pressure?

A

neural (autonomic) and humoral (circulating or hormonal) factors regulate the heart and vasculature

ANS = SNS & PSNS

Humoral = Renal Na+ and H2o handling by renin-angiotensin-aldosterone system (also circulating catecholamines, vasopressin (ADH), ANP, and endothelin)

36
Q

Volatile agents general effects on hemodynamics (HR, Preload, Afterload, Contractility)

A

HR - decrease
Preload - vasodilation reduces volume return to heart
Afterload - vasodilation reduces SVR
Contractility - depress

37
Q

Blood pressure control is due to 4 main factors including?

A
  1. intrinsic factors (frank starling, SA/AV node)
  2. nervous system (SNS, PSNS)
  3. reflexes (baroreceptor, chemoreceptor, atrial receptor/bainbridge)
  4. humoral factors (RAAS)
38
Q

As anesthetists how can we control Frank-Starling Mechanism?

A

maintain optiumum preload

39
Q

As anesthetists how can we affect SA & AV nodes?

A

antiarrhythmics

40
Q

As anesthetists how can we affect nervous system factors?

A

sympathomimetics, anticholinergics, cholinergic

41
Q

As anesthetists how can we affect baroreceptor reflexes?

A

be aware of bradycardia with pure alpha agonists

42
Q

As anesthetists how can we affect chemoreceptor reflexes?

A

maintain optimal oxygen saturation, etco2, pH

43
Q

As anesthetists how can we affect the atrial receptor (bainbridge) reflex?

A

maintain optimum preload

44
Q

As anesthetists how can we affect humoral factors?

A

vasopressin

45
Q

Describe the RAAS system

A

The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure. As the name implies, there are three important components to this system: 1) renin, 2) angiotensin, and 3) aldosterone. Renin, which is released primarily by the kidneys, stimulates the formation of angiotensin in blood and tissues, which in turn stimulates the release of aldosterone from the adrenal cortex.

46
Q

3 things that stimulate renin release by the kidneys

A

1) sympathetic nerve activation (acting through β1-adrenoceptors)
2) renal artery hypotension (caused by systemic hypotension or renal artery stenosis)
3) decreased sodium delivery to the distal tubules of the kidney.

47
Q

Diagram how we get from renin to ATII

A

Circulating Renin –> angiotensinogen –> angiotensin I –> [ACE enzyme in lungs] –> angiotensin II

renin is released into the blood, it acts upon a circulating substrate, angiotensinogen, that undergoes proteolytic cleavage to form the decapeptide angiotensin I. Vascular endothelium, particularly in the lungs, has an enzyme, angiotensin converting enzyme (ACE), that cleaves off two amino acids to form the octapeptide, angiotensin II

48
Q

How can dopamine cause both vasodilation and vasoconstriction?

A

Low doses - vasodilation via activation of DA1 receptors and inhibition of NE by activation of DA2 receptors

High doses - vasoconstriction via activation of alpha1 & alpha2 adrenoceptors on the postjunctional cell

49
Q

non-catecholamine alpha1 agonist?

A

phenylephrine

50
Q

Norepi dose

A

0.1 mcg/kg IV push bolus
2-20 mcg/min infusion
0.01-3 mcg/kg/min weight based infusion

51
Q

Describe autoregulation of BP

A

-the intrinsic ability of circulation to maintain a constant blood flow despite changes in perfusion pressure (MAP), vessel resistance is the regulated variable to keep flow constant

52
Q

Describe Critical closing pressure

A

pressure at which vessels collapse and blood flow stops, this is what makes diastolic blood pressure an important variable

53
Q

How do peripheral chemoreceptors regulate blood pressure?

A

They are sensitive to Pao2, Paco2, & pH

-decreased Pao2/incresaed Co2 causes co-activation of SNS and PNS causing SNS vasoconstriction and PNS decrease in HR

54
Q

How do central chemoreceptors regulate blood pressure?

A
  • exposed to CSF and not blood
  • stimulated by H+ concentrations in the CSF (not blood) and not PCo2/Po2
  • they do so via the products (increase in H+) of the henderson-hasselbalch equation that occurs with an increase in arterial PCo2 occurs leading to a reduction in pH.

Anesthesia Fast Facts (24 decks)

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