CV

Question 1

Stage 1 HTN

Answer 1

130/80 to 139/89

Question 2

Stage 2 HTN

Answer 2

> or = 140/90

Question 3

Most common form of HTN with no clear pathophysiology

Answer 3

Essential (primary) HTN

Question 4

The presence of __________ properties results in less bradycardia & negative inotropic effects compared with “pure” beta blockers. (Carvedilol, labetalol) However these properties may result in __________

Answer 4

Alpha blocking; orhtostatic hypotension

Question 5

Prazosin, terazosin, & doxazosin are oral selective _________ resulting in vasodilating effects on ______ vaculature

Answer 5

Postsynaptic a1 antagonists; BOTH arterial and venous

Question 6

Why are a1 antagonists unlikely to elicit reflex increses in CO and renin release?

Answer 6

They do not block a2 receptors which leaves intact the normal inhibitory effect on NorEpi release from nerve endings

Question 7

______ & _______ are non-selective a blockers used almost exclusively in the management of pheochromocytoma

Answer 7

Phenoxybenzamine; phentolamine

Question 8

Used to relieve vasospasm of Raynaud’s phenomenon and preop in preparation of pts with pheochromocytoma

Answer 8

Prazosin

Question 9

Nearly completely metabolized with < 60% bioavailability after oral admin which suggest first-pass hepatic metabolism. This makes this drug suitible for pts with renal failure

Answer 9

Prazosin

Question 10

If a pt taking prazosin exhibits hypotension during epidural anesthesia preventing compensatory vasoconstriction, what would be the best choice to increase SVR?

Answer 10

Epinephrine

Question 11

How does clonidine work in neuraxial placement?

Answer 11

Inhibits substance P release and nociceptive neuron firing produced by noxious stimulation

Question 12

When does clonidine peak? Half time? Duration?

Answer 12

Peak plasma: 60 -90 min;
H/t: 9-12 hrs (50% m liver, 50% unchanged in urine);
D of hypotensive effect: 8 hrs

Question 13

Clonidine’s effect on postsynaptic a2 receptors in CNS affects anesthesia how?

Answer 13

A 50% decrease in anesthetic requirements for inhaled anesthetics and injected drugs in pts pretreated with clonidine

Question 14

What causes rebound htn with abrupt discontinuation of clonidine?

Answer 14

> 100% increase in circulating concentrations of catecholamines and intense peripheral vasoconstriction

Question 15

ACE inhibitors are most effective in treating which type of HTN?

Answer 15

Systemic HTN secondary to increased renin production

Question 16

First line therapy for systemic htn, CHF, and MR. also more effective/safer in diabetics.

Answer 16

ACE inhibitors

Question 17

ACE inhibitors decrease ______ & ______ which leads to?

Answer 17

Angiotensin II & plasma aldosterone;

Reduced vasoconstricion and reduction of Na and water retention

Question 18

ACE inhibitors block the breakdown of ________, an endogenous vasodilator substance which contributes to the antihypertenzive effects of these drugs

Answer 18

Bradykinin

Question 19

If respiratory distress develops d/t ACE/ARB inhibitors, what should be given?

Answer 19

Epi 0.3 - 0.5 ml of a 1:1,000 dilution SQ

Question 20

_________ is possible with ACE/ARBs d/t decreased production of aldosterone

Answer 20

Hyperkalemia

Question 21

Can ACE inhibitors be used in renal pts?

Answer 21

Caution with preexisitng renal dysfunciton, C/I in renal artery stenosis (⬇️ glomerular filtration rate)

Question 22

Exaggerated hypotension attributed to continued ACE inhibitor therapy has been responsive to?

Answer 22

Crystalloids and/or admin of catecholamine or vasopressin (works on NO) infuison

Question 23

CCB inhibit Ca influx through voltage-sensitive ______ Ca channels in vascular smooth muscle. Do they work on arteries, veins, or both?

Answer 23

L-type; arterial specific

Question 24

_____ & ______ are less potent vasodilators & have (-) inotropic & chronotropic activity limiting their use in pts with cardiac dz.

More used for antiarrhythmic action

Answer 24

Verapamil & diltiazem

Question 25

The _________ CCB are potent vasodilators and are relatively safe to use in pts with heart failure & cardiac conduction defects, EXCEPT large doses of short-acting ________. Why?

Answer 25

Dihydropyridines; Nifedipine; It may acutely lower the BP and cause myocardial ischemia

Question 26

Inhibition of PDE prevents the breakdown of?

Answer 26

cAMP & cGMP

Question 27

What is the effect of PDE inhibition?

Answer 27

Vascular smooth muscle relaxation & for PDE3 inhibitors positive inotropy from intracellular Ca mobilization

Question 28

NO is administered by inhalation to produce?

Answer 28

Relaxation of the pulmonary arterial vasculature

Question 29

Does inhaled NO affect systemic circulation? Why?

Answer 29

Pulmonary circulation not systemic d/t its extremely rapid uptake by hemoglobin (half life < 5 sec)

Question 30

How does NO improve oxygenation?

Answer 30

By dilating vessels in alveoli where it is locally delivered, it improves oxygenation by improving ventilation-perfusion matching

Question 31

What can happen if NO is given in the presence of left heart dysfuntion?

Answer 31

The increased pulmonary blood flow can precipitate acute left heart failure and pulmonary edema

Question 32

SNP is a direct-acting nonselective peripheral vasodialtor that causes relaxation where?

Answer 32

Arterial and venous vascular smooth muscle only

Question 33

Onset & duration of SNP

Answer 33

O: almost immediate D: transiet requiring continuous IV administration

Question 34

MOA of SNP

Answer 34

SNP interacts with oxyhemoglobin, dissociating immediately & forming methemoglobin while releasing cyanide and NO. NO activates guanylate cyclase increasing cGMP. cGMP inhibits Ca entry into vascular smooth muscle & increases Ca uptake by smooth ER to produce vasodilation. (Prodrug)

Question 35

The SNP infusion rates greater than ________ per minute IV result in dose-dependent accumulation of cyanide and the risk of CN toxicity myst be considered

Answer 35

2mcg/kg

Question 36

Thiocyanate is ____ less toxic than cyanide

Answer 36

100-fold

Question 37

________ can produce pulmonary vasodilation equivalent to the degree of systemic arterial vasodilation

Answer 37

Nitroglycerin

Question 38

MOA of hydralazine

Answer 38

Direct systemic arterial vasodilator which both hyperpolarizes smooth muscle cells and activates guanylate cyclase to produce vasorelaxation

Question 39

Why is hydralazine not recommended for pts with myocardial ischemia or CAD?

Answer 39

The arterial vasodilation produces a reflex SNS stimulation with resulitng increases in HR and contractility

Question 40

A dopamine type 1 receptor agonist that causes systemic arterial dilaiton through increasing cAMP

Answer 40

Fenoldopam

Question 41

The _______ state occurs during the upstroke of the AP and the _______ state occurs during the plateau phase of repolarization

Answer 41

Active; inactivated

Question 42

Drug-induced torsades de pointes is often a/w?

Answer 42

Bradycardia bc QTc interval is longer at slower HR

Question 43

________ is thought to reflect a reentrant tachycardia and easily degenerates to v fib

Answer 43

Wide complex ventricular rhythm

Question 44

Slows phase 0 depolarization in ventricular muscle fibers

Answer 44

IA (Na channel blocker)

Question 45

Shortens Phase 3 repolarization in ventricular muscle fibers

Answer 45

IB (Na channel blockers)

Question 46

Markedly slows Phase 0 depolarization in ventricular muscle fibers

Answer 46

IC (Na channel blockers)

Question 47

Inhibits Phase 4 depolarization in SA and AV nodes

Answer 47

II (B blockers)

Question 48

Prolongs Phase 3 repolarization in ventricular muscle fibers

Answer 48

III (K channel blocker)

Question 49

Inhibits action potential in SA and AV nodes

Answer 49

IV (CCB)

Question 50

Which drugs increase the duration of action potential?

Answer 50

``` Class IA, class III. Class II & IV increase PR interval ```

Question 51

MOA of adenosine in heart

Answer 51

Binds to A1 receptor (Gi protein) > opens K channesl > hyperpolarization. Also ⬇️ cAMP in cardiac cells > ⬇️Ca entry > slow HR & conduction

Question 52

MOA of adenosine in vascular smooth muscle

Answer 52

Binds with A2 receptor (Gs protein) causing ⬆️ cAMP > vasodilaiton

Question 53

______ antagonize adenosine; _______ potentiates it

Answer 53

Xanthines (caffeine); dipyridamole (adenosine uptake inhibitor)