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
Dopamine Dose
1-30 mcg/kg/min IV infusion Dopaminergic = 0.5-2 Beta 1 = 2-10 alpha = > 10
26
Phenylepherine Dose
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
Ephedrine Dose
2. 5-10 mg IV adults 0. 1 mg/kg IV peds - longer onset due to indirect effects - tachyphylaxis possible on repeat doses
28
Dobutamine Dose
high dose (cardiac stress tests) = 10-20 m/kg /min low dose infusions: 5 mcg/kg/min
29
Milrinone Dose
50 mcg/kg IV bolus over 10-30 min 0.375-0.75 mcg/kg/min infusion
30
What kind of patients should NOT be subjected to hypotension
``` known carotid stenosis known valve disorders known heart failure known fixed CO known severe CAD ```
31
Factors that directly affect MAP
CO & SVR
32
Factors that directly affect CO
SV & HR
33
Factors that directly affect SV
Preload & Inotropy
34
Factors that directly affect Preload
Blood volume & venous compliance
35
What neurohumoral factors affect the physiology of blood pressure?
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
Volatile agents general effects on hemodynamics (HR, Preload, Afterload, Contractility)
HR - decrease Preload - vasodilation reduces volume return to heart Afterload - vasodilation reduces SVR Contractility - depress
37
Blood pressure control is due to 4 main factors including?
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
As anesthetists how can we control Frank-Starling Mechanism?
maintain optiumum preload
39
As anesthetists how can we affect SA & AV nodes?
antiarrhythmics
40
As anesthetists how can we affect nervous system factors?
sympathomimetics, anticholinergics, cholinergic
41
As anesthetists how can we affect baroreceptor reflexes?
be aware of bradycardia with pure alpha agonists
42
As anesthetists how can we affect chemoreceptor reflexes?
maintain optimal oxygen saturation, etco2, pH
43
As anesthetists how can we affect the atrial receptor (bainbridge) reflex?
maintain optimum preload
44
As anesthetists how can we affect humoral factors?
vasopressin
45
Describe the RAAS system
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
3 things that stimulate renin release by the kidneys
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
Diagram how we get from renin to ATII
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
How can dopamine cause both vasodilation and vasoconstriction?
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
non-catecholamine alpha1 agonist?
phenylephrine
50
Norepi dose
0.1 mcg/kg IV push bolus 2-20 mcg/min infusion 0.01-3 mcg/kg/min weight based infusion
51
Describe autoregulation of BP
-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
Describe Critical closing pressure
pressure at which vessels collapse and blood flow stops, this is what makes diastolic blood pressure an important variable
53
How do peripheral chemoreceptors regulate blood pressure?
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
How do central chemoreceptors regulate blood pressure?
- 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.