Chronic HTN releases what in the vessels? Which causes what?
Inflammatory mediators to cause thickened endothelium and increase in permeability to water and electrolytes > coronary artery occlusion and MI

Etiology of primary HTN
1. Increased SNS activity
2. Increased activity of RAS
3. Altered natriuretic activity (inhibits ADH) of ANF
4. Decrease synthesis OR increased breakdown of NO

What is the first-line therapy for HTN?
1. Diuretics
2. ARBs
3. ACEi
4. CCBs

Anesthetic considerations with pt on BP meds
1. Mono- vs poly-therapy
2. Is pt at max dose
3. Check algorithm

What is the reason NOT to use B-blockers?
Blocks “fight or flight” which may need to happen during anesthesia

What are the A1 receptor antagonists?

What are B1 receptor antagonists?
Atenolol, metoprolol, esmolol, nebivolol, acebutolol

What are B1&2 receptor antagonists?
Propranolol, Nadolol, Timolol

What are B1&2 and A1 receptor antagonists?
Labetalol, carvedilol

Sodium nitroprusside MOA
NO production > increase cGMP > decreases Ca in vascular sm musc > increase Ca mvmt into ER > vasodilation

Sodium nitroprusside side effects
1. Tachycardia and increased CO d/t decrease in BP
2. Coronary steal > increase damage from MI
3. Cerebral vasodilation > increase ICP
4. Counteracts Hypoxic Pulm Vasoconstriction > overrides (body’s) shunt away from under ventilated area in lungs > decreases PaO2
5. Inhibition of platelet aggregation (good for perfusion)

What is the mechanism of cyanide toxicity?
1. Cyanide is formed
2. Reacts with methemoglobin
3. Prevents oxidative phosphorylation > tissue anoxia and aneaerobic metabolism

Sodium nitroprusside onset
30 seconds

Sodium nitroprusside DOA
3 minutes

Sodium nitroprusside dose
0.25 mcg/kg/min

Sodium nitroprusside considerations
Hypotension potentiated by IA, B-blockers, clonidine

Nitroglycerin MOA
NO production > cGMP formation > inhibits Ca mobilization > direct dilation of vasc sm muscle > VENOdilation > reduction in LVEDP and secondary arteriodilation

NTG action in coronary arteries
Preferentially diverts blood flow to ischemic subendocardial areas > decrease area of damage of MI

NTG side effects
1. Increases ICP
2. Attenuates HPV
3. Tachycardia (with profound hypotension)

NTG dose
0.25-5 mcg/kg/min

What is the difference between NTG and Na NP?
NTG is gentler on myocardium

What can you do for refractory hypotension?
1. Catecholamine agonists (NE, Epi, Vaso)
2. Methylene blue

Methylene blue MOA
Inhibits guanylate cyclase > opposes NO dilation > increases BP and SVR

What is arteriosclerosis?
Chronic, abnormal thickening and hardening of vessel wall

What is atherosclerosis?
Fat and fibrin in vessels hardens to a clot, can break off and cause ischemia

Causes of atherosclerosis
1. HTN
2. Low HDL, high LDL
3. Aging

What is the difference between ischemia and infarction?
Ischemia is temporary deprivation of blood supply, infarction is complete occlusion and persistent ischemia

What is the pathophysiology of an MI?
1. Atherosclerosis deprives myocardium of O2
2. Thrombus is caused by plaque, platelets
3. Platelet agg > thromboxane A2 > vasoconstriction > further platelet agg

What is the difference between a Q wave MI and a non-Q wave MI?
Presence of a Q-wave indicates a deeper (i.e. larger) area of infarction > lower EF

What can you do if you see ST elevation and low BP?
1. NTG (depending on where BP is, fluids)
2. Titrate down IA (depends on case)

What are signs of ACS in the OR?
1. Change in HR, BP
2. Perspiration
3. ST elevation/depression, Q-waves
4. PVCs

What affects O2 supply to the heart?
1. Hemodynamics
2. HR/diastolic filling time
3. Anemia
4. Shock

What affects O2 demand of the heart?
1. High SBP
2. Increased ventricular volume
3. Increased myocardial thickness
4. Increased HR

What is angina?
Ischemia > anaerobic metabolism > lactic acid > substernal pain

What is unstable angina?
1. Increase in intensity and frequency of angina
2. Severe chest pain
3. 3rd or 4th heart sounds

Management of angina
1. Serial enzyme labs
2. Heparin, MONA
3. Angiograms/plasty/CABG

Organic nitrates MOA
1. Increase O2 content
2. Increase coronary blood flow from dilation
3. Alter HR to improve filling time
4. Decrease after load
5. Decrease initial fiber length > decrease contractile state

Isosorbide dinitrate (Isordil) MOA
Same as NTG

Effect of B-blocker as anti-anginal
Decrease HR, BP, contractility > Decrease O2 demand

Nicorandil MOA
K/ATP channel activator > vasodilation

Block L-type channels >
1. Decrease transmembrane Ca current > Vasorelaxation
2. Decreases contractility and SA rate and AV conduction velocity > vasodilation > increased coronary blood flow

Statins MOA
Inhibits HMG-CoA reductase > inhibits synthesis of cholesterol

What happens when ANP and BNP are elevated?
Diuresis due to stretch; decrease SVR and CVP

Causes of left heart failure
1. Increased preload
2. Increased after load
3. Neurohormonal (RAS, catechols, vasopressin)

S/Sx left heart failure
1. Pulm congestion, dyspnea
2. Fatigue
3. Edema
4. Fluid overload

Management of left heart failure
Interrupt cycle of decreased contractility
Nitrates, morphine, diuretics, ACEi, etc

Causes of right heart failure
1. Left heart failure
2. Pulmonary HTN/disease

CHF pathophysiology
1. Initial reduction of contractility
2. Frank-Starling compensation to increase SV (dependent on sarcomere length)
3. Balance between fluid and contraction

1. Decrease SNS activity
2. Interrupt RAAS

Omapatrilat MOA
ACE and endopeptidase inhibitor (keeps ANP, BNP, CNP around) > diuresis, vasodilation

Direct Beta stimulated:
1. Positive inotrope: increase CO, SV
2. Decrease ventricular filling pressure
3. May have slight increase in TPR from alpha stimulation

Dobutamine onset

Dobutamine DOA
2 minutes

Dopamine MOA
Immediate precursor to NE and epi
Dopamine receptors > increase cAMP > vasodilation

Carvedilol MOA
1. B and A blocker > depress LV function and reduce after load
2. Use in LV dysfunction following MI, CHF

Carvedilol SE
Pulm edema, heart block

Digoxin MOA
1. Inhibits Na/K pump > more intracellular Na > stimulates Na/Ca pump to get more Ca inside cell > increase force of contraction
2. Decreases sensitivity of SA and AV nodes > decrease HR

Digoxin side effects
1. ECG: long PR, short QT, ST depression
2. Anorexia
3. NV
4. Scotomatas

Treatment of Dig toxicity
Digibind, temporary PM

Amrinon (Inocor), Milrinone (Primacor) MOA
Inhibit phosphodiesterase > increase cAMP > increase Ca

Nesiritide (Natrecor)
Synthetic BNP > diuresis > reduce PCWP in acute CHF

Coenzyme Q10 MOA
Improves O2 and contractility

Thiazide MOA
Block Na and water reabsorption in ALH and DT

Thiazide Use
Primary tx of HTN (chronic)

Thiazide side effects
Electrolyte disturbance > weakness, cramps

Bendroflumethiazides MOA
Inhibits Na reabsorption at beginning of DCT, water comes in and gets excreted

Mannitol MOA
1. Increases osmotic pressure in glomerulus > decreases reabsorption of water > diuresis
2. Increases osmotic pressure to move fluid from extravascular to bloodstream for diuresis

Mannitol use
1. Decrease ICP
2. Increases kidney perfusion

Mannitol side effects
1. Exacerbates CHF (increased IV volume)
2. Pulmonary congestion
3. Tachycardia

Loop diuretics (Bumex, Lasix) MOA
Inhibits Cl reabsorption in ALH > decreases reabsorption of water

Loop diuretic uses
1. CHF, pulmonary edema
2. HTN
3. Nephrotic syndrome

Loop diuretic side effects
1. Hypokalemia
2. Ototoxicity (Lasix)

Spironolactone MOA
Blocks aldosterone receptors to promote Na excretion/K reabsorption

Amiloride MOA
Inhibits Na reabsorption in DT/promotes K reabsorption

Diamox MOA
Inhibits carbonic anhydrase > prevents H secretion > increased HCO3, K, Na excreted

Diamox use
1. Glaucoma (weak diuresis only)
2. Epilepsy (unknown why)
2. Altitude sickness due to metabolic alkalosis

Anesthetic considerations of diuretics
1. Altered electrolytes
2. Fluid volume decrease > increased Hct, BUN
3. Decreased atrial filling pressures
4. Do not withhold for surgery

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