Cardiovascular pathophysiology 2 Flashcards

(51 cards)

1
Q

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

A

d. decreased diastolic filling time

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2
Q

Systemic hypertension is almost always caused by

A

increased SVR

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3
Q

Blood pressure is regulated by a feedback network consisting of

A

the SNS (baroreceptors)
RAAS
antidiuretic hormone

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4
Q

Chronic hypertension impacts

A

nearly every organ system in the body

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5
Q

Complications of chronic hypertension include

A

LVH
CAD
CHF
stroke
arterial aneurysm
renal disease

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6
Q

The cerebral autoregulation curve shifts ______________ to protect the brain from a higher blood pressure.

A

to the right
It ends up causing a chronic rightward shift where they do not tolerate a lower blood pressure

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7
Q

Classic teaching recommends maintaining MAP within _________

A

20% of the patient’s preoperative value

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8
Q

In the patient on ACEI/ARB therapy, hypotension that’s not responsive to conventional first-line therapy should be treated with

A

vasopressin, terlipressin, and methylene blue

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9
Q

Patients on a beta-blocker should ________________ throughout the perioperative period

A

continue therapy

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10
Q

Starting beta-blocker therapy on the day of surgery

A

increases the risk of hypotension, bradycardia, stroke, and death

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11
Q

Hypertension is classified as

A

primary or secondary

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12
Q

Primary hypertension has

A

no identifiable cause and accounts for 95% of all HTN cases

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13
Q

For the patient with hypertension, anticipate that the patient will have an

A

exaggerated hypotensive response to anesthetic induction, followed by an exaggerated hypertensive response to intubation and extubation

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14
Q

Hypertensive patients are

A

volume contracted–> adequate hydration before induction helps promote hemodynamic stability

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15
Q

What preoperative blood pressure merits delaying an elective surgical procedure?

A

SBP >180 mmHg
DBP >110 mmHg

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16
Q

Hypertensive crisis occurs when the blood pressure exceeds

A

180/120

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17
Q

A hypertensive emergency is declared when there’s evidence of

A

end-organ injury (otherwise we call it a hypertensive urgency)

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18
Q

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

A

c. renal artery stenosis

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19
Q

Causes of secondary hypertension include

A

coarctation of the aorta
renovascular disease
Cushing’s syndrome
Conn’s disease
pheochromocytoma
pregnancy-induced hypertension

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20
Q

What should not be given to patients with bilateral renal artery stenosis?

A

do not give an ACEI b/c it will significantly reduce GFR and precipitate renal failure

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21
Q

What drug classes target the sympathetic nervous system?

A

alpha 1 antagonists
alpha 2 agonists
cardio-selective beta 1 antagonists
mixed alpha 1/beta 1 & 2 antagonists

22
Q

Give a _______________________ to a patient in hypertensive crisis can precipitate heart failure.

A

non-selective beta-blocker (without the alpha-1 antagonist component)

23
Q

What is the role of alpha 1 antagonists?

A

reduce afterload by causing vasodilation

24
Q

What is the role of alpha-2 agonists?

A

reduce sympathetic outflow

25
What is the role of cardio-selective beta-1 antagonists?
reduce inotropy, chronotropy, dromotropy, and renin release
26
What is the role of mixed alpha-1/beta-1 and -2 antagonists?
give the added benefit of systemic vasodilation
27
What drug classes target the myocardium and vascular smooth muscle?
calcium channel blockers vasodilators
28
Vasodilators promote vasodilation by
increasing nitric oxide
29
Hydralazine reduces
afterload
30
Nitroglycerine reduces
preload
31
Sodium nitroprusside reduces
preload and afterload
32
Drug classes that target the kidney include
ACE inhibitors ARBs Diuretics aldosterone antagonists
33
How do ace-I and ARBs work?
inhibits angiotensin 2 mediated vasoconstriction and aldosterone release
34
How do diuretics work?
decreased BP by reducing intravascular volume
35
How do aldosterone antagonists work?
block aldosterone at mineralocorticoid receptors
36
The suffix of ACE-inhibitors is
pril
37
The suffix of ARBs is
-sartan
38
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
39
Calcium channel blockers improve hypertension by
increasing vasodilation and decreasing inotropy, chronotropy, and dromotropy
40
The following are great choices to reduce heart rate in the patient with tachycardia, atrial fibrillation, or atrial flutter.
verapamil & diltiazem
41
CCBs impair contractility in the following order (ranked highest to lowest):
verapamil> nifedipine> diltiazem > nicardipine
42
______________ is the only CCB proven to reduce morbidity and mortality from cerebral vasospasm.
Nimodipine
43
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
44
Which CCBs target vasodilation & reduce SVR primarily?
nifedipine, nicardipine, nimodipine, amlodipine, clevidipine
45
Which CCBs target mostly the myocardium (chronotropy, inotropy, dromotropy)?
verapamil diltiazem
46
_____________ is useful as a coronary antispasmodic.
Nicardipine
47
What does clevidipine contain that can cause allergic reactions?
EDTA preservative
48
Clevidipine should be discarded after
12 hours d/t risk of bacterial contamination d/t lipid emulsion
49
Contraindications to clevidipine include
allergy to eggs, soybeans, and soy products impaired lipid metabolism: pathologic hyperlipidemia, lipoid nephrosis, acute pancreatitis severe aortic stenosis
50
How is clevidipine metabolized?
plasma & tissue esterases
51
What is the dose of clevidipine?
1-2 mg/hr (max dose 16 mg/hr)