Antihypertensives/vasodilators

Question 1

Hypertensive urgency

Answer 1

Severe asymptomatic hypertension >180/>120

Without acute end organ injury

Question 2

Hypertensive Emergency

Answer 2

Severe hypertension >180/>120

With acute end organ injury

Question 3

Vasodilators

Answer 3

Drugs that dilate vasculature

Subdivided: arterial vs venous

Question 4

Differentiate between antihypertensives and vasodilators

Answer 4

All systemic vasodilators are antihypertensives

BUT

All antihypertensives are NOT vasodilators

Question 5

Preop chronic hypertension control

Answer 5

Hypertension associated with increased perioperative adverse events

If inadequately controlled- greater intraop swings in BP may be cause of these adverse events

Question 6

Organ perfusion in hypertension

Answer 6

Auto regulation is right shifted

=organ hypoperfusion at higher BPs

the heart is also working harder-consuming more O2= increase in LV dysfunction and MIs

Question 7

Intraop complications of hypertension

Answer 7

Bleeding- in specific operations

Trauma to vessel anastomoses

Extension of aortic dissections

Question 8

Calcium Channel blockers MOA

Answer 8

Disrupt movement of Ca through calcium channels in vascular AND CARDIAC tissues

Question 9

Classes of CCBs and preferred muscle/tissue

Answer 9

Dihydropyridines- amlodipine. Smooth muscle» cardiac

Phenylalkylamines- verapamil. Cardiac>smooth muscle

Benzothiazepines- diltiazam Smooth muscle> cardiac

Question 10

Physiology of CCBs

Answer 10

Decrease afterload (via SVR)- can be used to treat arterial vasospasm

Negative inotropic/chronotropic/dromotropic agents

Question 11

Clinical utility of CCBs

Answer 11

Ischemic heart disease

Acute hypertensive events

Aortic dissection

Cerebral and coronary vasospasm (nimodipine)

Antiarrhythmics- depress electrical impulses in SA and AV nodes- useful in atrial tachycardias

Question 12

CCB adverse effects

Answer 12

Prolong Neuromuscular blockade

Dihydropyridines- reflex tachycardia

Non-dihydropyridines heart block when combined with Beta blockers

Flushing/ankle edema?

Decreased hepatic clearance related to decreased CO

Question 13

Note on B1 selectivity

Answer 13

All “selective” beta blockers show B2 blockade at high doses

Question 14

Chronic beta blocker therapy in the perioperative setting

Answer 14

Should be continued!

Withdrawal is associated with increased morbidity and mortality

Question 15

Why are Beta blockers helpful in ischemic heart disease?

Answer 15

They decrease myocardial oxygen supply

Question 16

Explain antihypertensives effect of beta blockers

Answer 16

Decrease CO -negative inotropy

Decrease renin release

Question 17

Beta blockers in setting of tachyarrhythmias

Answer 17

Some have a membrane stabilizing effect

Inhibit action potential propagation across myocardial membrane

Question 18

BB in CHF

Answer 18

HFREF EF<40%
Improves survival

Beneficial effect on LV remodeling- improves performance

Question 19

Beta blocker elimination

Answer 19

Primarily hepatic

Esmolol- red cell cholinesterases

Question 20

Beta blocker contraindications

Answer 20

2nd and 3rd degree block in absence of pacemaker….

Class IV CHF?

Question 21

Adverse effects BB

Answer 21

Exacerbates bronchospastic lung disease (nonselective)
Exacerbates LHF and PVD

Masks hypoglycemia symptoms associated with insulin OD

Question 22

ACE/ARB in perioperative period

Answer 22

Controversial but the only class that can be held 24 hr prior to surgery

-potentially holding lowers risk of death and postoperative vascular events

Question 23

What do you give in setting of induction hypotension in an ACE/ARB patient that has continued the medication?

Answer 23

Vasopressin

Question 24

ACE MOA

Answer 24

Block conversion of angiotensin I to angiotensin II

Question 25

ARAs MOA

Answer 25

Angiotensin receptor ANTAGONIST Antagonize effect of angiotensin II at AT1 receptors- no impact on ACE

Question 26

Physiologic effects of ACE/ARAs

Answer 26

Mitigate effect of angiotensin II on VSM Increase parasympathetic tone Decrease impact of aldosterone on distal convoluted tubule= Na/water loss Inhibit ACE mediated breakdown of kinins =enhanced vasodilation (ACE only)

Question 27

ACE/ARA clinical use

Answer 27

Hypertension Diabetic neuropathy- slows progression of CKD Chronic CHF- afterload reduction and regression of ventricular remodeling

Question 28

ACE elimination

Answer 28

Renal

Question 29

Adverse effects ACE/ARAs

Answer 29

Hypotension- inducing vasoplegia Hyperkalemia!!! Cough- ACE specific Anemia Angioedema ACE>ARA

Question 30

Classes of diuretics

Answer 30

Thiazides (chlorthalidone, metolazone) Loop diuretics (furosemide, bumetanide) Potassium-sparing diuretics (spironolactone, amiloride)

Question 31

Loop diuretics clinical utility

Answer 31

Volume overload Weak antihypertensive effect

Question 32

Uses for spironolactone

Answer 32

Hypertension associated with hyperaldosteronism And chronic CHF

Question 33

Electrolyte abnormality in thiazide diuretics

Answer 33

Hyponatermia

Question 34

When do you see HYPER kalemia in diuretics use

Answer 34

K-sparing diuretics especially in combination with ACE inhibitors

Question 35

MOA alpha-1 adrenergic blockers

Answer 35

Inhibition of norepinephrine mediated vaso constriction

Question 36

Name some alpha blockers

Answer 36

ZOSIN Doxazosin Terazosin Prazosin

Question 37

Difference between phentolamine and phenoxybenzamine

Answer 37

Phentolamine- binds competitively-short acting Phenoxybenzamine- binds irreversibly, long acting

Question 38

GPCRs for A1 and A2

Answer 38

A1- Gq A2- Gi

Question 39

WTF is Fenoldopam

Answer 39

Dopamine Agonist DA-1 receptor Arteriolar vasodilation with decreased afterload Increased renal perfusion Coronary vasodilation Does not cross BBB

Question 40

Fenoldopam kinetics/dynamics

Answer 40

Onset- 5 minutes Duration 30-60 Hepatic metabolism

Question 41

Adverse effects Fenoldopam

Answer 41

Hypotension…. Increased intraocular pressure Reflex tachycardia Hypokalemia Cutaneous flushing

Question 42

Action of direct vasodilators

Answer 42

NO on vessel wall

Question 43

Nitroprusside

Answer 43

Tachyphylaxis with prolonged infusion Photosensitive Arterial and venous vasodilation

Question 44

Nitroprusside Degradation

Answer 44

Reacts with Hb to form Cyanide and NO

Question 45

3 pathways to cyanide poisoning in nitroprusside and max dose

Answer 45

1. Cyanomethemoglobin- disrupts carrying capacity oh O2 2. Thiocyanate- consumes thiosulfate B12 3-cytochrome oxidase- disruption of aerobic respiration <2mcg/kg/min

Question 46

Nitroglycerin

Answer 46

Tachyphylaxis Primarily Venous- preload reduction Reflex tachycardia Coronary vasodilation- does NOT cause steal Can relieve opioid induced biliary spasm Hepatic metabolism

Question 47

Hydralazine

Answer 47

Arterial vasodilation Hypertension in pregnancy CHF with reduced EF Variable IV onset Hepatic via acetylation- some patients see reduced acetylation which can lead to lupus like symptoms