Cardiovascular pathophysiology 2 Flashcards
Pathophysiologic complications related to chronic systemic hypertension include all of the following EXCEPT:
a. left ventricular hypertrophy
b. increased myocardial oxygen consumption
c. dysrhythmias
d. decreased diastolic filling time
d. decreased diastolic filling time
Systemic hypertension is almost always caused by
increased SVR
Blood pressure is regulated by a feedback network consisting of
the SNS (baroreceptors)
RAAS
antidiuretic hormone
Chronic hypertension impacts
nearly every organ system in the body
Complications of chronic hypertension include
LVH
CAD
CHF
stroke
arterial aneurysm
renal disease
The cerebral autoregulation curve shifts ______________ to protect the brain from a higher blood pressure.
to the right
It ends up causing a chronic rightward shift where they do not tolerate a lower blood pressure
Classic teaching recommends maintaining MAP within _________
20% of the patient’s preoperative value
In the patient on ACEI/ARB therapy, hypotension that’s not responsive to conventional first-line therapy should be treated with
vasopressin, terlipressin, and methylene blue
Patients on a beta-blocker should ________________ throughout the perioperative period
continue therapy
Starting beta-blocker therapy on the day of surgery
increases the risk of hypotension, bradycardia, stroke, and death
Hypertension is classified as
primary or secondary
Primary hypertension has
no identifiable cause and accounts for 95% of all HTN cases
For the patient with hypertension, anticipate that the patient will have an
exaggerated hypotensive response to anesthetic induction, followed by an exaggerated hypertensive response to intubation and extubation
Hypertensive patients are
volume contracted–> adequate hydration before induction helps promote hemodynamic stability
What preoperative blood pressure merits delaying an elective surgical procedure?
SBP >180 mmHg
DBP >110 mmHg
Hypertensive crisis occurs when the blood pressure exceeds
180/120
A hypertensive emergency is declared when there’s evidence of
end-organ injury (otherwise we call it a hypertensive urgency)
What is the most common cause of secondary hypertension?
a. pregnancy-induced hypertension
b. coarctation of the aorta
c. renal artery stenosis
d. cigarette smoking
c. renal artery stenosis
Causes of secondary hypertension include
coarctation of the aorta
renovascular disease
Cushing’s syndrome
Conn’s disease
pheochromocytoma
pregnancy-induced hypertension
What should not be given to patients with bilateral renal artery stenosis?
do not give an ACEI b/c it will significantly reduce GFR and precipitate renal failure
What drug classes target the sympathetic nervous system?
alpha 1 antagonists
alpha 2 agonists
cardio-selective beta 1 antagonists
mixed alpha 1/beta 1 & 2 antagonists
Give a _______________________ to a patient in hypertensive crisis can precipitate heart failure.
non-selective beta-blocker (without the alpha-1 antagonist component)
What is the role of alpha 1 antagonists?
reduce afterload by causing vasodilation
What is the role of alpha-2 agonists?
reduce sympathetic outflow
What is the role of cardio-selective beta-1 antagonists?
reduce inotropy, chronotropy, dromotropy, and renin release
What is the role of mixed alpha-1/beta-1 and -2 antagonists?
give the added benefit of systemic vasodilation
What drug classes target the myocardium and vascular smooth muscle?
calcium channel blockers
vasodilators
Vasodilators promote vasodilation by
increasing nitric oxide
Hydralazine reduces
afterload
Nitroglycerine reduces
preload
Sodium nitroprusside reduces
preload and afterload
Drug classes that target the kidney include
ACE inhibitors
ARBs
Diuretics
aldosterone antagonists
How do ace-I and ARBs work?
inhibits angiotensin 2 mediated vasoconstriction and aldosterone release
How do diuretics work?
decreased BP by reducing intravascular volume
How do aldosterone antagonists work?
block aldosterone at mineralocorticoid receptors
The suffix of ACE-inhibitors is
pril
The suffix of ARBs is
-sartan
A patient has a history of coronary artery disease with an EF of 35%. She develops atrial fibrillation with a RVR. Select the BEST treatment for this patient.
a. verapamil
b. diltiazem
c. nifedipine
d. nicardipine
b. diltiazem
Calcium channel blockers improve hypertension by
increasing vasodilation and decreasing inotropy, chronotropy, and dromotropy
The following are great choices to reduce heart rate in the patient with tachycardia, atrial fibrillation, or atrial flutter.
verapamil & diltiazem
CCBs impair contractility in the following order (ranked highest to lowest):
verapamil> nifedipine> diltiazem > nicardipine
______________ is the only CCB proven to reduce morbidity and mortality from cerebral vasospasm.
Nimodipine
What are the three types of voltage-gated calcium channels?
L-type= long-lasting or slow channel
N-type= neutral
T-type= transient
clinically used CCBs bind to the L-type channel
Which CCBs target vasodilation & reduce SVR primarily?
nifedipine, nicardipine, nimodipine, amlodipine, clevidipine
Which CCBs target mostly the myocardium (chronotropy, inotropy, dromotropy)?
verapamil
diltiazem
_____________ is useful as a coronary antispasmodic.
Nicardipine
What does clevidipine contain that can cause allergic reactions?
EDTA preservative
Clevidipine should be discarded after
12 hours d/t risk of bacterial contamination d/t lipid emulsion
Contraindications to clevidipine include
allergy to eggs, soybeans, and soy products
impaired lipid metabolism: pathologic hyperlipidemia, lipoid nephrosis, acute pancreatitis
severe aortic stenosis
How is clevidipine metabolized?
plasma & tissue esterases
What is the dose of clevidipine?
1-2 mg/hr (max dose 16 mg/hr)
