Cardiovascular pathophysiology 2 Flashcards

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
Q

What is the role of cardio-selective beta-1 antagonists?

A

reduce inotropy, chronotropy, dromotropy, and renin release

26
Q

What is the role of mixed alpha-1/beta-1 and -2 antagonists?

A

give the added benefit of systemic vasodilation

27
Q

What drug classes target the myocardium and vascular smooth muscle?

A

calcium channel blockers
vasodilators

28
Q

Vasodilators promote vasodilation by

A

increasing nitric oxide

29
Q

Hydralazine reduces

A

afterload

30
Q

Nitroglycerine reduces

A

preload

31
Q

Sodium nitroprusside reduces

A

preload and afterload

32
Q

Drug classes that target the kidney include

A

ACE inhibitors
ARBs
Diuretics
aldosterone antagonists

33
Q

How do ace-I and ARBs work?

A

inhibits angiotensin 2 mediated vasoconstriction and aldosterone release

34
Q

How do diuretics work?

A

decreased BP by reducing intravascular volume

35
Q

How do aldosterone antagonists work?

A

block aldosterone at mineralocorticoid receptors

36
Q

The suffix of ACE-inhibitors is

A

pril

37
Q

The suffix of ARBs is

A

-sartan

38
Q

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

A

b. diltiazem

39
Q

Calcium channel blockers improve hypertension by

A

increasing vasodilation and decreasing inotropy, chronotropy, and dromotropy

40
Q

The following are great choices to reduce heart rate in the patient with tachycardia, atrial fibrillation, or atrial flutter.

A

verapamil & diltiazem

41
Q

CCBs impair contractility in the following order (ranked highest to lowest):

A

verapamil> nifedipine> diltiazem > nicardipine

42
Q

______________ is the only CCB proven to reduce morbidity and mortality from cerebral vasospasm.

A

Nimodipine

43
Q

What are the three types of voltage-gated calcium channels?

A

L-type= long-lasting or slow channel
N-type= neutral
T-type= transient
clinically used CCBs bind to the L-type channel

44
Q

Which CCBs target vasodilation & reduce SVR primarily?

A

nifedipine, nicardipine, nimodipine, amlodipine, clevidipine

45
Q

Which CCBs target mostly the myocardium (chronotropy, inotropy, dromotropy)?

A

verapamil
diltiazem

46
Q

_____________ is useful as a coronary antispasmodic.

A

Nicardipine

47
Q

What does clevidipine contain that can cause allergic reactions?

A

EDTA preservative

48
Q

Clevidipine should be discarded after

A

12 hours d/t risk of bacterial contamination d/t lipid emulsion

49
Q

Contraindications to clevidipine include

A

allergy to eggs, soybeans, and soy products
impaired lipid metabolism: pathologic hyperlipidemia, lipoid nephrosis, acute pancreatitis
severe aortic stenosis

50
Q

How is clevidipine metabolized?

A

plasma & tissue esterases

51
Q

What is the dose of clevidipine?

A

1-2 mg/hr (max dose 16 mg/hr)