Antihypertensives/vasodilators Flashcards
Hypertensive urgency
Severe asymptomatic hypertension >180/>120
Without acute end organ injury
Hypertensive Emergency
Severe hypertension >180/>120
With acute end organ injury
Vasodilators
Drugs that dilate vasculature
Subdivided: arterial vs venous
Differentiate between antihypertensives and vasodilators
All systemic vasodilators are antihypertensives
BUT
All antihypertensives are NOT vasodilators
Preop chronic hypertension control
Hypertension associated with increased perioperative adverse events
If inadequately controlled- greater intraop swings in BP may be cause of these adverse events
Organ perfusion in hypertension
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
Intraop complications of hypertension
Bleeding- in specific operations
Trauma to vessel anastomoses
Extension of aortic dissections
Calcium Channel blockers MOA
Disrupt movement of Ca through calcium channels in vascular AND CARDIAC tissues
Classes of CCBs and preferred muscle/tissue
Dihydropyridines- amlodipine. Smooth muscle» cardiac
Phenylalkylamines- verapamil. Cardiac>smooth muscle
Benzothiazepines- diltiazam Smooth muscle> cardiac
Physiology of CCBs
Decrease afterload (via SVR)- can be used to treat arterial vasospasm
Negative inotropic/chronotropic/dromotropic agents
Clinical utility of CCBs
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
CCB adverse effects
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
Note on B1 selectivity
All “selective” beta blockers show B2 blockade at high doses
Chronic beta blocker therapy in the perioperative setting
Should be continued!
Withdrawal is associated with increased morbidity and mortality
Why are Beta blockers helpful in ischemic heart disease?
They decrease myocardial oxygen supply
Explain antihypertensives effect of beta blockers
Decrease CO -negative inotropy
Decrease renin release
Beta blockers in setting of tachyarrhythmias
Some have a membrane stabilizing effect
Inhibit action potential propagation across myocardial membrane
BB in CHF
HFREF EF<40%
Improves survival
Beneficial effect on LV remodeling- improves performance
Beta blocker elimination
Primarily hepatic
Esmolol- red cell cholinesterases
Beta blocker contraindications
2nd and 3rd degree block in absence of pacemaker….
Class IV CHF?
Adverse effects BB
Exacerbates bronchospastic lung disease (nonselective)
Exacerbates LHF and PVD
Masks hypoglycemia symptoms associated with insulin OD
ACE/ARB in perioperative period
Controversial but the only class that can be held 24 hr prior to surgery
-potentially holding lowers risk of death and postoperative vascular events
What do you give in setting of induction hypotension in an ACE/ARB patient that has continued the medication?
Vasopressin
ACE MOA
Block conversion of angiotensin I to angiotensin II
ARAs MOA
Angiotensin receptor ANTAGONIST
Antagonize effect of angiotensin II at AT1 receptors- no impact on ACE
Physiologic effects of ACE/ARAs
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)
ACE/ARA clinical use
Hypertension
Diabetic neuropathy- slows progression of CKD
Chronic CHF- afterload reduction and regression of ventricular remodeling
ACE elimination
Renal
Adverse effects ACE/ARAs
Hypotension- inducing vasoplegia
Hyperkalemia!!!
Cough- ACE specific
Anemia
Angioedema ACE>ARA
Classes of diuretics
Thiazides (chlorthalidone, metolazone)
Loop diuretics (furosemide, bumetanide)
Potassium-sparing diuretics (spironolactone, amiloride)
Loop diuretics clinical utility
Volume overload
Weak antihypertensive effect
Uses for spironolactone
Hypertension associated with hyperaldosteronism
And chronic CHF
Electrolyte abnormality in thiazide diuretics
Hyponatermia
When do you see HYPER kalemia in diuretics use
K-sparing diuretics especially in combination with ACE inhibitors
MOA alpha-1 adrenergic blockers
Inhibition of norepinephrine mediated vaso constriction
Name some alpha blockers
ZOSIN
Doxazosin
Terazosin
Prazosin
Difference between phentolamine and phenoxybenzamine
Phentolamine- binds competitively-short acting
Phenoxybenzamine- binds irreversibly, long acting
GPCRs for A1 and A2
A1- Gq
A2- Gi
WTF is Fenoldopam
Dopamine Agonist
DA-1 receptor
Arteriolar vasodilation with decreased afterload
Increased renal perfusion
Coronary vasodilation
Does not cross BBB
Fenoldopam kinetics/dynamics
Onset- 5 minutes
Duration 30-60
Hepatic metabolism
Adverse effects Fenoldopam
Hypotension….
Increased intraocular pressure
Reflex tachycardia
Hypokalemia
Cutaneous flushing
Action of direct vasodilators
NO on vessel wall
Nitroprusside
Tachyphylaxis with prolonged infusion
Photosensitive
Arterial and venous vasodilation
Nitroprusside Degradation
Reacts with Hb to form Cyanide and NO
3 pathways to cyanide poisoning in nitroprusside and max dose
- Cyanomethemoglobin- disrupts carrying capacity oh O2
- Thiocyanate- consumes thiosulfate B12
3-cytochrome oxidase- disruption of aerobic respiration
<2mcg/kg/min
Nitroglycerin
Tachyphylaxis
Primarily Venous- preload reduction
Reflex tachycardia
Coronary vasodilation- does NOT cause steal
Can relieve opioid induced biliary spasm
Hepatic metabolism
Hydralazine
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
