Antihypertensives Flashcards
1st line anti HTN for surgery
There is none but there are general recommendations
Different for all diseases
Common options: clevidipine, hydralazine, cardene, nitroglycerin, esmolol, labetalol, phentolamines
Prevalence of perioperative HTN
80% cardiac surgery
25% noncardiac surgery patients
Does NOT have to have previous diagnosis of HTN
What causes idiopathic HTN
Over reactivity of ANS and RAAS
Related to sodium and volume factors
Causes of perioperative HTN
Light anesthesia
Airway manipulation/ Pain
Hypoxia Hypercarbia
Medications
Aortic Cross clamp
Hypervolemia
Hypothermia
Type of procedure
Pre exhisting diseases that can lead to perioperative HTN
Pheocromocytoma
Hyperthyroid
Autonomic hyperreflexia
MH
Intracranial HTN
Renal disease
Poorly controlled HTN
Primary cause of perioperative HTN
Increased sympathetic discharge with systemic vasoconstriction
Complications of perioperative HTN
CVA MI Ischemia LV dysfunciton arrhythmias
Increased suture tension/ hemmorhage
Pulmonary edema
Cognitive dysfunction
What to do when intraoperative HTN happens
Check depth of anesthesia
Administer analgesia
R/O during intraoperative HTN
Hypoxia / hypercarbia
Distended bladder
Thyroid storm
MH
Hyperthermia
A1 blockers
SIN to take A1 blocker
oral except labetalol
Prazosin
terazosin
doxazosin
tamsulosin
Labetalol
A2 agonist
Clonidine
alpha-methyldopa
How do vasodilators effect systemic circulation (arteries vs venous)
Pure arterial dilation with minimal effect on preload
Pure venodilators are not available bc its big size, although NTG is closest
SE of vasodilator
Reflex tachycardia
Why NTG for hearts?
Improves collateral circulation
Others cause coronary steal
What governs myocardial oxygen perfusion?
Aortic diastolic pressure
90% of coronary artery perfusion is during diastole
When are collaterals maximally dilated?
Ischemic heart disease
Coronary arteries are largely pressure dependent
What is coronary steal?
Narrowed arteries are always maximally dilated,so when a med comes in and dilates good arteries, it takes away from ischemic areas
“The rich get richer, the poor get poorer”
Hydralazine Pharmacodynamics
Direct arterial vasodilator
Alters calcium and movement
Increases HR, contracticlity, renin, fluid retention, CO, and SV
Decreases BP (diastolic more) and thus SVR
Hydralazine SE
CNS headache, dizziness, tremor, caution inICP
CV Palpiatations, angina, tachycardia, flushing, increases o2 demand and ischemia, caution in CAD
GI anorexia, N/V/ abpn, paralytic ileus
Other: Anemia, agranulocytosis, nasal congestion, muscle cramps, SLE
Hydralazine pharmacokinetics and dose
Onset 30 min
Peak 30-60 min
Duration 4-6 hours
Metabolized liver and kidney excretes
Protein bound? highly
Dose 10-20mg q4-6h
NO MOA
Synthesizes cGMP to cause smooth muscle relaxation
NTG
Veins> arteries
Decreases PVR, venous return, myocardial o2 consumption
Relaxes coronary vessels and relives spasms
Non cardiac effects of NTG
Dilates meningeal vessels (caution ICP)
Decreases renal blood flow as decrease in BP
Dilates pulmonary vessels
Used in ACS and acute pulmonary edema
Dont use in volume depleted patients
NTG pharmacokinetics
onset 1 minute
duration 3-5 min
half life 1-4 min
Dose- start at 0.5mcg/kg/min titrate 3-5 min up to 20mcg/kg/min
NTG Metabolism
Glutathion nitrate in the liver
Oxidizes HGB to methoglobin
Tolerance in arterial vessels can occur but not in veins
NTG Side effects and CX
CNS headache, apprehension, blurred vision, vertigo, dizzy, faintness
CV postural hypotension, palpitations, increased heart rate, syncope
GI n/v/abpn, dry mouth
Other methemoglobinemia, flushing, rash, anaphylaxis, conjuctival edema
CX: PDE5 inhibitors, narrow angle glycoma, head trauma/ hemorrhage, anemia, hypotension
NTG pros/cons ???? SNP??
Pros: rapid onset, short diration, coronary vasodilates, decreases o2 consumption, no toxicities, reduced PVR
Cons: Decreases DBP, reflex tachycardia, HOTN, tachyphylaxis, methemoglobinemia
SNP effects
Directly vasodilates arteries and veins
Decrease BP with slight increase in HR
Increases cereberal blood flow and ICP
Slight reduction BP to renal
Reduction in Myocardial O2 demand
With abrupt stop can cause reflex tachycardia and HTN
SNP pharmacokinetics
onset less than 1 min
peak 2 minutes
duration 5-10 min
half life 3-7 days
Dose- 0.5-10 mcg/kg/min
SNP CX
Hypovolemia
Increased ICP
Severe renal/ liver impairement
Major SE in SNP
Cyanide toxicity (thiocyanite)
Presentation: hypotension, blurred vision, fatigue, metabolic acidosis, pink skin, no reflexes, feint heart sounds,
Risk increases over 4mcg/kg/min for over 2 days