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Anesthesia > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Name the 3 major effects of Angiotensin II.

A
  1. arterial and venous vasoconstriction
  2. aldosterone and ADH secretion
  3. remodeling of the myocardium with hypertrophy of cardiac myocytes and growth of fibroblasts
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2
Q

How to ACE inhibitors affect bradykinin?

A

Elevated levels of bradykinin

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3
Q

To which receptor do ARBs bind?

A

angiotensin receptor (AT1)

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4
Q

Describe the activation of the renin-angiotensin system.

A

Hypovolemia –> renin release from kidney

Renin converts angiotensinogen from the liver –> angiotensin I

Angiotensin I activated by ACE in the kidney and lungs –> angiotensin II

Angiotensin II –> arterial and venous vasoconstriction + aldosterone and ADH secretion

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5
Q

Name the 2 classes of calcium channel blockers.

A

Bind to L-type calcium channels

1,4-Dihydropyridine - binds to Ca channel in inactive closed state

Non-Dihydropyridine - active open state

Metabolized by liver

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6
Q

What are the primary effects of DHP calcium channel blockers?

A

end in -dipine

Primarily PERIPHERAL arteriolar + some coronary vasodilation

Dec SVR and MAP

Increase coronary blood flow

Direct negative ionotrope + after load reduction –> reflex inc HR and maintain CO

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7
Q

What are the primary effects site of non-DHP calcium channel blockers?

A

Diltiazem and Verapamil

myocardium, conduction system and coronary arteries, with less effect on systemic arterioles

Both - depress contractility, HR, AV node conduction

Dilt - coronary vasodilator = angina tx

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8
Q

What are some common indications for Nimodipine and Nicardipine?

A

Nimodipine - cerebral vasospasm in ICH

Nicardipine - alternative to nitroprusside and fenoldopam for arteriolar vasospasm, Tx HTN after cardiac surgery

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9
Q

What are some common side effects from DHP calcium channel blockers?

A

Flushing, nausea, headache

Reflex tachycardia –> undesirable in its w/ CAD

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10
Q

What are some common side effects from non-DHP calcium channel blockers?

A

bradycardia and systole

, heart block, hypotension and heart failure.

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11
Q

What are the major determinants of myocardial oxygen demand?

A

HR

Contractility

Wall stress - ventricular afterload and radius

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12
Q

What determines coronary blood flow?

A

Diastolic filling time

Coronary profusion pressure (aortic diastolic pressure and LV diastolic pressure gradient)

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13
Q

What is the mechanism of action of hydralazine?

A

Inhibits release of intracellular calcium in arteriolar smooth muscle cells –> diminished contraction and vasodilation

Baroreceptor –> inc HR, contractility and CO

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14
Q

What are the primary cardiovascular effects of sodium nitroprusside?

A

Metabolized –> NO –> activates guanylyl cyclase, increasing [cGMP]

Increased intracellular cGMP inhibits entry of Ca into smooth muscle + may increase Ca uptake by the endoplasmic reticulum –> relaxation of smooth muscle

dilates both arterioles and venues –> decreased myocardial preload and afterload

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15
Q

Why is coronary artery steal less of a problem with nitroglycerin than with sodium nitroprusside?

A

Reduces coronary perfusion pressure –> shunting blood away from narrowed myocardium

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16
Q

What are the hemodynamic effects of nesiritide?

A

arterial and venous vasodilation by binding to A and B natriuretic peptide receptors on vascular smooth muscle –> increase in cGMP

reduction of preload and afterload, reduces preload, PVR
natriuresis
diuresis
suppression of the renin-angiotensin-aldosterone system
increases CO w/ little or no change in HR

Can worsen dyspnea in patients with pulmonary edema from congestive heart failure

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17
Q

Where is vasopressin synthesized?

A

hypothalamus - paraventricular nuclei

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18
Q

What are the most important stimuli for vasopressin release?

A

increased plasma osmolality
decreased arterial pressure
reduced cardiac filling

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19
Q

What is the normal plasma osmolality? Which receptors are responsible for its regulation? Where are they located?

A

285 and 295 mOsm/kg

peripheral Cosmo-receptors - near the portal vein
central receptors - near the third ventricle

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20
Q

What agents also stimulate vasopressin release?

A 
acetylcholine
histamine
dopamine
prostaglandins
angiotensin II
nicotine
hypoxia
hyperthermia
pain
nausea
hypercapnia - stimulating carotid body chemoreceptors
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21
Q

Name the vasopressin receptor subtypes

A

V1a
V1b
V2

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22
Q

Where are the V1a receptors mainly located in the body?

A

vascular smooth muscle - vasoconstriction in mesenteric, skin and skeletal tissues

platelets
liver
adrenal gland
myometrium
brain - inhibit SNS
kidneys - constrict efferent arterioles --> inc GF, UOP
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23
Q

Where the the V2 receptors heavy distributed?

A

distal convoluted tubule and collecting duct –> increases water permeability

vascular endothelium –> arterial vasodilation.

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24
Q

Name three synthetic vasopressin analogs.

A

argipressin (AVP)
terlipressin (TP)
desmopressin (DDAVP).

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25
Q

What is the plasma half-life of exogenous vasopressin?

A

4-20 minutes - continuous infusion is necessary for maintenance

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26
Q

Name some of the common indications for vasopressin use.

A
  1. Vasodilated states - sepsis (w/ norepi)
  2. Refractory hypotension - can restore SNS response
  3. Cardiac arrest
  4. Bleeding esophageal varices
  5. central diabetes insipidus
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27
Q

What is terlipressin?

A

synthetic analogue of AVP - greater selectivity for the V1 receptor

28
Q

What are some of the side effects of vasopressin?

A

Skin necrosis after extravasation

Anaphylaxis
bronchospasm
urticaria
ischemia of the GI tract

29
Q

How does methylene blue (MB) work?

A

selective inhibitor of inducible nitric oxide synthase (iNOS) –> reduces the formation of NO

Inhibits guanylate cyclase in vascular smooth muscle –> vasoconstriction

  • reverse hypotension in septic shock
  • helpful in profound vasoplegia following cardiopulmonary bypass
30
Q

Name some of the side effects of methylene blue.

A

contraindicated in severe renal insufficiency

cardiac arrhythmias (transient nodal rhythm and ventricular ectopy)
angina pectoris
coronary vasoconstriction
decreased cardiac output
decreased renal blood flow
increased mesenteric vascular resistance
31
Q

Which receptor is the target of the majority of cardiac inotropes?

A

Beta-1

inc Ca –> excitation-contraction coupling
+ lusitropy (relaxation)
+ chronotropy (HR)
+ dromotropy (conduction velocity)

32
Q

High dose dopamine primarily effects which receptor?

A

alpha receptors at >10ug/kg/min

33
Q

What is the effect of milrinone on SVR?

A

PDE-III inhibitor
Systemic vasodilation –> DEC SVR
Inc HR and CO

34
Q

How does digoxin increase inotropy?

A

inhibits Na+/K+-ATPase in cardiac myocytes –> increases intracellular Na+, –> so more Na+ can exit through the Na+/Ca+ exchanger –> increasing intracellular Ca2+ –> augmenting excitation-contraction coupling

35
Q

Digoxin toxicity is more likely in which disease state?

A 
Renal insufficiency
Hypokalemia
loop and thiazide diuretics
amiodarone
advanced age.
36
Q

What is the digitalis effect on EKG?

A

classic (nonischemic) downward slope of the ECG ST-segment

37
Q

What is the pathognomonic ECG finding in digitalis toxicity?

A

paroxysmal atrial tachycardia with 2:1 atrioventricular (AV) block

38
Q

What are two limiting side effects of dobutamine?

A

Tachycardia

Hypotension

39
Q

What are the main actions of PDE-III inhibitors on the myocardium?

A

Inc SV, CO,HR, contractility

Dec SVR, PVR, MvO2, Preload

40
Q

Can you use milrinone in renal insufficiency?

A

Cautiously - may –> hypotension as effects may persist long after d/c

41
Q

List two differences between milrinone and amrinone.

A

Amrinone = thrombocytopenia

Milrinone - shorter half-time

42
Q

Milrinone is best used to treat which of the following:

  1. HTN w/ normal LV fxn
  2. Vasoplegia
  3. Pulm HTN
  4. Biventricular HF
A

4 - Biventricular HF –> dec filling pressures = “off-loading” the heart and inc stroke work

Also beneficial in low cardiac index, high SVR patients

2 = methylene blue

43
Q

What are the primary ions involved in the cardiac action potential?

A

Na
Ca
K

44
Q

What are the two different types of action potentials?

A
  1. Slow response
    - cell w/ automaticity
  2. Fast response
    - muscle and purkinjie fibbers
45
Q

True or False: The resting membrane potential for cells with automaticity is more negative than cells without automaticity.

A

False - slow response = automaticity = less negative

46
Q

What are the primary etiologies of arrhythmias?

A

reentrant phenomena and enhanced automaticity.

47
Q

Describe the phases and ion movements in myocyte and pacemaker cells

A

Phase zero: sodium in

Phase one: potassium out

Phase two: calcium in

Phase three: potassium out

Phase four: if slow response fiber, then sodium leaks in to the cell - regulated by ANS

48
Q

Describe the 4 classes of antiarrhythmics

A

Class I - Na channel blockers

Class II - beta-blockers

Class III - K channel blockers

Class IV - Ca channel blockers.

49
Q

What is the objective and main mechanism of antiarrhythmics?

A

changing action potential duration

changing properties of automaticity

50
Q

What is a unique side effect of procainamide?

A

Lupus-like syndrome

51
Q

What is the effect of the potassium channel blockers on APD (action potential duration) and ERP (effective refractory period)?

A

Ex: amiodarone, sotalol, ibutilide, dofetilide, and bretylium

lengthen the APD, and the ERP

52
Q

Class II antiarrhythmics effect what phase of the action potential?

A

Beta-blockers –> Phase 4 of the slow response AP

53
Q

Class 1 antiarrhythmics are most likely to effect which phase(s) of the action potential?

A

Phase 0 and 4

54
Q

What are some side effects of amiodarone?

A

Pulmonary toxicity

Hypo or hyperthyroidism

55
Q

Which phases of the standard cardiac myocyte action potential are caused by outflow of potassium into the extracellular space?

A

Repolarization

  • myocyte = phases 1 through 3
  • pacemaker cells = phase 3
56
Q

List the progression of EKG changes that occur with progressive hyperkalemia.

A 
6-7 --> peaked T-waves
Prolonged PR
Widened QRS
Dec P-wave amplitude and disappearance
Shortened ST
VF or asystole
57
Q

List the EKG changes seen with hypokalemia.

A 
Inc amplitude and width of P-wave
Prolonged PR
T-wave flattening or inversion
ST depression
Prominent U-waves (precordial leads)
SVT, AF, Aflutter, VT, VF
58
Q

Describe the major effect Ca2+ has on global myocardial function.

A

excitation-contraction coupling

changes in Ca2+ movement or binding can affect both inotropy (contractility) and lusitropy (relaxation).

59
Q

How does hypocalcemia affect the cardiovascular system?

A

Dec ionotropy
Hypotension d/t dec tone
QT prolongation

60
Q

What EKG changes occur in hypercalcemia?

A

Short QT
Short PR
Osborn (J-waves)
VF

61
Q

How does Mg2+ regulate cardiovascular smooth muscle function?

A

Ca antagonist and regulates entry into cell –> normal vascular tone, prevention of vasospasm, prevention of Ca overload

62
Q

What are three major cardiovascular consequences of hypomagnesemia?

A

Torsades de Pointes –> VT
Dilated cardiomyopathy
Ionotrope requirement

63
Q

What are the major effects of hypermagnesemia on the vasculature?

A

Vasodilation - direct SM relaxation, enhanced NO release, inhibits catecholamine release

Bradycardia
Hypotension

5-10mg/dl –> AV block, prolonged QT –> cardiac arrest

64
Q

What primary role does phosphorus play in the function of cardiac myocytes?

A

ATP - stores and releases energy via high-energy PO43- bonds.

65
Q

What are the major consequences of hypo- and hyperphosphatemia?

A

Hypo - if severe –> muscle weakness, cardiomyopathy and arrhythmias

Hyper - hypoCa –> dec ionotropy, heart block

Anesthesia (25 decks)

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