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CRS > Lecture 15+16 > Flashcards

Lecture 15+16 Flashcards

1
Q

hypertensive emergency

A

Severe hypertension with signs of damage to target
organs

need immediate BP reduction through IV

210/150 in healthy person
DBP higher than 120 in someone with preexisting conditions

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2
Q

hypertensive urgency

A

Very high BP without target-organ damage. Acute
complications unlikely so immediate BP reduction not
required

be started on 2-drug oral combination &
close evaluation continued on an outpatient basis

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3
Q

causes of hypertensive emergency

A

Essential hypertension
Renal parenchymal disease
Renovascular disease
Pregnancy (eclampsia)

endocrine: cushing, pheocyto, renin tumor
drugs. . cocaine

drug withdrawal.. clonidine

CNS disorder.. stroke

autonomic hyperreactivity

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4
Q

the management of hypertensive emergency

A

admit to ICU.. IV drugs

lower BP by short-acting IV drug

avoid abrupt drops in BP! can lead to stroke, MI
lower BP no more than 25% per hour

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5
Q

hypertensive emergency drugs

A

• Sodium nitroprusside • Labetalol • Fenoldopam • Nicardipine • Nitroglycerin • Diazoxide • Phentolamine • Esmolol • Hydralazine

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6
Q

sodium nitroprusside

A

always given IV
Prompt vasodilation & reflex tachycardia

Causes peripheral vasodilation by direct effects on
arterial & venous smooth muscle

half life is 1-2 min.. continuous infusion

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7
Q

AE of sodium nitroprusside

A

hypotension if overdose

goose bumps, abdominal cramping, nausea, vomiting, headache

cyanide toxicity in rare instances

Nitroprusside metabolism → cyanide ion

Can be treated with sodium thiosulfate infusion →
nontoxic thiocyanate

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8
Q

labetalol

A

combined alpha and beta blocker
can infuse during HTN emergency

does not cause reflex tachy
commonly used in pregnancy

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9
Q

contraindications of labetalol

A

Asthma, COPD, patients with 2nd or 3rd-degree AV

block or bradycardia

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10
Q

fenoldopam

A

peripheral dopamine receptor agonist

evokes arterial dilation
Maintains or increases renal perfusion as lowers BP
Promotes naturesis

IV infuse during hypertensive emergency

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11
Q

contraindications of fenoldopam

A

glaucoma

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12
Q

Nicardipine

A

Ca channel blocker
IV infuse during HTN emergency
evokes relax tachy

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13
Q

nitroglycerine

A

vasodilator

Drug of choice for hypertensive emergencies in
patients with cardiac ischemia or angina, or after
cardiac bypass surgery

hypotension is most serious SE

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14
Q

Diazoxide

A 
arterial dilator (IV in HTN emergency) 
Prevents vascular smooth muscle contraction by opening K+ channels and stabilizing membrane potential
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15
Q

AE of diazoxide

A

Hypotension, reflex tachycardia, Na+ & H20
retention

Inhibits insulin release and can be used to treat
hypoglycemia secondary to insulinoma

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16
Q

phentolamine

A

Drug of choice for patients with catecholaminerelated emergencies

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17
Q

esmolol

A

Often used for aortic dissection or postoperative

hypertension

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18
Q

Hydralazine

A

Drug of choice in treating hypertensive emergencies

in pregnancy related to eclampsia

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19
Q

HF

A

When cardiac output is inadequate to provide O2
needed by the body

Symptoms:
Tachycardia, decreased exercise tolerance dyspnea, peripheral & pulmonary edema,
cardiomegaly

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20
Q

risk factors of HF

A 
hypertension
coronary artery disease 
MI 
DM
obesity
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21
Q

HFrEF (Systolic failure)

A

Mechanical pumping action (contractility) and the

ejection fraction of the heart are reduced

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22
Q

HFpEF (Diastolic failure)

A

Stiffening and loss of adequate relaxation →
abnormal ventricular filling, resulting in a reduction in
cardiac output (ejection fraction may be normal)

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23
Q

Congestive Heart Failure (CHF)

A

Abnormal increases in blood volume & interstitial
fluid.

Symptoms include dyspnea from pulmonary
congestion in left HF, and peripheral edema in right
HF

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24
Q

Role of Physiologic Compensatory Mechanisms in HF

A

Chronic activation of SNS & renin-angiotensin aldosterone pathway is associated with cardiac tissue remodeling. This prompts additional
neurohumoral activation → vicious cycle → death

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25
Q

compensatory mechanisms for HF

A

increased force, rate, preload, and afterload

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26
Q

preload and HF

A

forced stretched of the ventricles

preload is high bc of volume overload and poor contractility

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27
Q

management of chronic HF

A 
light exercise 
low sodium intake
stop smoking 
ideal weight 
2L fluid restriction

Use of ACE-inhibitors, diuretics, b-blockers &
inotropic agents

NSAIDS, alcohol, Ca2+-channel blockers should be
avoided if possible

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28
Q

drugs used to treat systolic HF

A
  • Diuretics
  • Spironolactone
  • Inhibitors of angiotensin (ACE-inhibitors / ARBs)
  • Direct vasodilators
  • b-adrenoceptor antagonists (b-blockers)
  • Inotropic agents
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29
Q

drugs to treat diastolic HF

A
  • Diuretics
  • ACEI /ARBs
  • b-adrenoceptor antagonists (b-blockers)
  • Calcium-channel antagonists
30
Q

ARNI drugs (Angiotensin receptor-neprilysin inhibitor)

A

Sacubitril/Valsartan

new drug approved for the treatment of systolic HF

31
Q

clinical app of ARNI drugs

A

patients with systolic HF

32
Q

MOA of sacubitril and valsartan

A

Sacubitril blocks the action of neprilysin, thus preventing the breakdown of natriuretic peptides

This leads to a prolonged duration of the favorable effects of these peptides

Because neprilysin breaks down angiotensin II, inhibiting neprilysin will result in accumulation of angiotensin II

33
Q

ARNI AE

A 
• Hypotension
• Hyperkalemia
• Angioedema
• Teratogenic (Valsartan)
• Worsening in renal function when combined with
NSAIDs
34
Q

contraindications of ARNI’s

A

history of angioedema with ACEI or ARB’s due to accumulation of bradykinin

In diabetic patients receiving aliskiren due to an increased risk of hypotension, hyperkalemia, and renal impairment.

35
Q

ACEi’s (HF)

A

one of the drugs of choice for HF

decrease vascular resistance & BP → increase cardiac output (afterload)

decrease salt & H20 retention ( preload)

decrease long-term remodeling of the heart

36
Q

ACEi’s clinical app. in HF

A

recommended:
symptomatic HF and asymptomatic HF (past MI / decreased LVEF)

Suggested for patients:

at high risk of developing heart failure due to
atherosclerotic disease, obesity, diabetes mellitus or hypertension

37
Q

ACEi’s AE

A 
• Hypotension,
• Persistent dry cough
• Hyperkalemia
• Angioedema
• Acute renal failure (patients with bilateral renal artery
stenosis)
• Teratogenic
38
Q

ARBs

A

Candesartan / Valsartan

do not effect bradykinin levels
use in those that cannot tolerate ACEi’s

AE:
teratogenic
no cough

39
Q

Beta blocker clinical app for HF

A

Recommended in addition to an ACEI for patients with:
symptomatic heart failure
asymptomatic patients with a decreased LVEF
or history of MI

USE CAUTIOUSLY in decompensated HF and are
contraindicated in cardiogenic shock

40
Q

spironolactone uses in HF

A

+ ACE inhibitors are shown to decrease
morbidity & mortality in patients with severe
heart failure

AE: hyperkalemia, GI, lethargy, endocrine

41
Q

direct vasodilators clinical app. in HF

A

Concurrent use of hydralazine & isosorbide dinitrate
recommended for use in patients:

who cannot tolerate ACEI or ARB
or
in African American patients with advanced
heart failure as an adjunct to standard therapy

42
Q

SGLT2 inhibitors

A

Dapagliflozin

reduce risk of hospitalization for HF by patients with DM2

no DM still reduced risk for HF or CV death

AE = hypoglycemia

43
Q

If channel inhibitor

A

Ivabradine

decrease HR by inhibition of cardiac pacemaker If current

Used as an adjunct to lower heart rate which is directly
related to improved outcomes

Before initiating ivabradine, the dose of beta-blocker
should be optimized

44
Q

AE of Ivabradine

A
  • Bradycardia
  • Atrial fibrillation
  • Sinus arrest
  • QT prolongation
  • Torsade de pointes
45
Q

contraindications of Ivabradine

A 
• HFpEF/decompensated HF (diastolic HF) 
• Arrhythmia
• Heart block,
• BP<90/50 mmHg / HR<90
• Severe liver failure
• Concomitant use of CYP3A4 inhibitors (verapamil,
diltiazem)
46
Q

digoxin

A

inotropic agent
widely used for treatment of HF with atrial fibrillation

Digoxin can decrease the symptoms of heart failure,
increase exercise tolerance and decrease rate of
hospitalization, but DOES NOT increase survival

47
Q

MOA of digoxin

A

MOA:
increase force
decrease HR

increase cytoplasmic Ca2+ concentration
that enhances contractility of cardiac muscle and →
increases cardiac output

enhances vagal tone = decrease in HR

48
Q

AE of digoxin

A

cardiac effects = arrhythmia

GI- nausea and vomiting
CNS - headache, fatigue

hypokalemia
can have toxicity

49
Q

digoxin toxicity predispositions

A 
K depleting diuretics' ( increased activity of drug) 
corticosteroids 
hypothyroidism
hypoxia 
renal failure 
myocarditis
50
Q

drugs that can lead to digoxin toxicity

A

• Quinidine, verapamil & amiodarone

they all increase digoxin levels due to drug displacement and competition for renal secretion

51
Q

treatment for digoxin toxicity

A

give K supplements

withdraw drug

52
Q

Severe digoxin intoxication

A

Bradyarrhythmias, suppressed automaticity →
temporary cardiac pacemaker

Treat with digitalis antibodies (Digoxine immune
fab, Digibind)

53
Q

contraindications of digoxin

A
  • In patients with diastolic or right-sided HF
  • In presence of uncontrolled hypertension
  • In presence of bradyarrhythmias
  • In non-responders or intolerant patients
54
Q

overview of congenital heart disease

A

abnormalities of the heart or great vessels that are present at birth

occur between weeks 3 through 8

55
Q

Eisenmenger syndrome

A

when a left to right shunt becomes a right to left shunt

cyanotic

56
Q

left to right shunt

A

increased pulmonary blood flow
Normally low volume low resistance side becomes high volume high pressure side

Initially pulmonary artery undergoes fibrotic intimal thickening, medial hypertrophy and vasoconstriction

RV will under go hypertrophy
will have pulmonary HTN

57
Q

right to left shunt

A

pulmonary circulation will be bypassed
poorly oxygenated blood shunts into circulation

hypoxemia and cyanosis occurs

58
Q

atrial septal defect

A

left to right shunt
a murmur is usually heard

abnormal opening between the left and right atria
asymptomatic until adulthood usually

59
Q

the 3 types of atrial septal defects

A

Secundum ASD (90% of all ASDs): result from a deficient septum secundum formation near the center of the atrial septum

Primum anomalies (5% of ASD):occur adjacent to the AV valves and are often associated with AV valve abnormalities and/or a VSD.

Sinus venosus defects (5%): located near the entrance of the superior vena cava

60
Q

ventricular septal defect

A

left to right shunt
most are membranous
most close spontaneously

incomplete closure of the ventricular septum; communication between left and right ventricles

associated with trisomy 21,13,18

61
Q

clinical features of VSD

A

Pulmonary hypertension; CHF, pansystolic
murmur

can lead to shunt reversal; increased risk for paradoxical embolism

62
Q

Patent Ductus Arteriosus

A

L to R shunt
seen more in females and those in mothers who had rubella

allows blood flow from the pulmonary artery to aorta

will have a machine like murmur
no cyanosis
shunt could reverse
close with indomethacin

63
Q

Tetralogy of Fallot

A

right to left shunt

  1. Ventricular septal defect
  2. Obstruction of the right ventricular outflow tract
    (subpulmonic stenosis)
  3. An aorta that overrides the VSD
  4. Right ventricular hypertrophy
associated with down syndrome 
increased risk for IE and systemic emboli 
present by month 6 
most common cyanotic CHD 
dyspnea on exertion
polycythemia
64
Q

Transposition of Great Arteries

A

right to left shunt

Aorta arises from right ventricle and pulmonary artery arises from left ventricle- Ventriculoarterial discordance

incompatible with post-natal life unless a shunt is present

in utero: foramen ovale and ductus arteriosus ensure mixing of blood

after birth: both the foramen ovale and ductus arteriosus close, thus no more mixing of blood and cyanosis

65
Q

Truncus Arteriosus

A

right to left shunt

Failure of partitioning of embryologic truncus into aorta and pulmonary artery
single great artery gets blood from both ventricles
thus mixing of the blood

could lead to pulmonary HTN and difficulty breathing due to.. to much blood flow to the lungs

66
Q

Coarctation of Aorta

A

narrowed aortic lumen
associated with turner’s syndrome
more common in males

67
Q

preductal (infantile) coarctation of the aorta

A

Has PDA
Congestive heart failure.
Selective cyanosis of lower extremities (PDA)

Femoral pulses are weaker than those of the
upper extremities

68
Q

postductal (older children and adult)

A

• No selective cyanosis is seen
• Hypertension of the upper extremities
• Blood pressure is low and pulses are weak in
lower extremities
• Notching of ribs due to collaterals
• Intermittent claudication – arterial insufficiency

69
Q

cardiac neoplasm

A

Sudden onset of severe, rapidly progressive heart failure without apparent cause and/or arrhythmia

Silent till impair function

70
Q

cardiac myxoma

A

most common primary tumor in adults
females are more likely
30-60

Often calcify and at times can be seen on X- ray
90% of myxomas arise in the atria

clinical:
• Most are asymptomatic
• Some may fragment and embolize
• Ball-valve obstruction of atrioventricular valve → syncopal episodes, sudden death

71
Q

histo of cardiac myxoma

A

• Multinucleated stellate cells
• Edematous mucopolysaccharide rich stroma
• Peculiar vessel-like or glandlike structures
are characteristic

can have a gelatinous gross appearance

CRS (16 decks)

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