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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
compensatory mechanisms for HF
increased force, rate, preload, and afterload
26
preload and HF
forced stretched of the ventricles preload is high bc of volume overload and poor contractility
27
management of chronic HF
``` 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
28
drugs used to treat systolic HF
* Diuretics * Spironolactone * Inhibitors of angiotensin (ACE-inhibitors / ARBs) * Direct vasodilators * b-adrenoceptor antagonists (b-blockers) * Inotropic agents
29
drugs to treat diastolic HF
* Diuretics * ACEI /ARBs * b-adrenoceptor antagonists (b-blockers) * Calcium-channel antagonists
30
ARNI drugs (Angiotensin receptor-neprilysin inhibitor)
Sacubitril/Valsartan new drug approved for the treatment of systolic HF
31
clinical app of ARNI drugs
patients with systolic HF
32
MOA of sacubitril and valsartan
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
ARNI AE
``` • Hypotension • Hyperkalemia • Angioedema • Teratogenic (Valsartan) • Worsening in renal function when combined with NSAIDs ```
34
contraindications of ARNI's
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
ACEi's (HF)
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
ACEi's clinical app. in HF
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
ACEi's AE
``` • Hypotension, • Persistent dry cough • Hyperkalemia • Angioedema • Acute renal failure (patients with bilateral renal artery stenosis) • Teratogenic ```
38
ARBs
Candesartan / Valsartan do not effect bradykinin levels use in those that cannot tolerate ACEi's AE: teratogenic no cough
39
Beta blocker clinical app for HF
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
spironolactone uses in HF
+ ACE inhibitors are shown to decrease morbidity & mortality in patients with severe heart failure AE: hyperkalemia, GI, lethargy, endocrine
41
direct vasodilators clinical app. in HF
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
SGLT2 inhibitors
Dapagliflozin reduce risk of hospitalization for HF by patients with DM2 no DM still reduced risk for HF or CV death AE = hypoglycemia
43
If channel inhibitor
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
AE of Ivabradine
* Bradycardia * Atrial fibrillation * Sinus arrest * QT prolongation * Torsade de pointes
45
contraindications of Ivabradine
``` • 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
digoxin
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
MOA of digoxin
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
AE of digoxin
cardiac effects = arrhythmia GI- nausea and vomiting CNS - headache, fatigue hypokalemia can have toxicity
49
digoxin toxicity predispositions
``` K depleting diuretics' ( increased activity of drug) corticosteroids hypothyroidism hypoxia renal failure myocarditis ```
50
drugs that can lead to digoxin toxicity
• Quinidine, verapamil & amiodarone they all increase digoxin levels due to drug displacement and competition for renal secretion
51
treatment for digoxin toxicity
give K supplements | withdraw drug
52
Severe digoxin intoxication
Bradyarrhythmias, suppressed automaticity → temporary cardiac pacemaker Treat with digitalis antibodies (Digoxine immune fab, Digibind)
53
contraindications of digoxin
* In patients with diastolic or right-sided HF * In presence of uncontrolled hypertension * In presence of bradyarrhythmias * In non-responders or intolerant patients
54
overview of congenital heart disease
abnormalities of the heart or great vessels that are present at birth occur between weeks 3 through 8
55
Eisenmenger syndrome
when a left to right shunt becomes a right to left shunt cyanotic
56
left to right shunt
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
right to left shunt
pulmonary circulation will be bypassed poorly oxygenated blood shunts into circulation hypoxemia and cyanosis occurs
58
atrial septal defect
left to right shunt a murmur is usually heard abnormal opening between the left and right atria asymptomatic until adulthood usually
59
the 3 types of atrial septal defects
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
ventricular septal defect
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
clinical features of VSD
Pulmonary hypertension; CHF, pansystolic murmur can lead to shunt reversal; increased risk for paradoxical embolism
62
Patent Ductus Arteriosus
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
Tetralogy of Fallot
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
Transposition of Great Arteries
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
Truncus Arteriosus
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
Coarctation of Aorta
narrowed aortic lumen associated with turner's syndrome more common in males
67
preductal (infantile) coarctation of the aorta
Has PDA Congestive heart failure. Selective cyanosis of lower extremities (PDA) Femoral pulses are weaker than those of the upper extremities
68
postductal (older children and adult)
• 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
cardiac neoplasm
Sudden onset of severe, rapidly progressive heart failure without apparent cause and/or arrhythmia Silent till impair function
70
cardiac myxoma
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
histo of cardiac myxoma
• 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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