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Step 1 Subjects > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Wolf-Parkinson White

A

Accessory pathway in heart bypassing AV node

  • -> ventricular pre-excitation
  • -> shortened PR, delta wave, widened QRS
  • Re-entrant tachycardia= narrowed QRS
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2
Q

Mitral regurgitation

A

Blowing holosystolic murmur over 5th LICS, midclavicular line
Radiates to axilla
- Can lead to CHF, pulmonary edema

Prevent by decreasing LV afterload
–> decreased systolic pressure driving blood into LA, increased forward stroke volume

Treat with arterial vasodilators

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3
Q

Isoproterenol

A

Beta agonist

  • Increases cardiac contractility (B1)
  • Decreases peripheral resistance (B2)
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4
Q

Phentolamine

A

Alpha receptor blocker

  • -> subcutaneous vasodilation
  • Used in NE-induced tissue necrosis (reverse effects of alpha agonist)
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5
Q

Tetralogy of Fallot

A

Abnormal neural crest cell migration featuring:

  • VSD
  • Overriding aorta
  • Pulmonary stenosis
  • R ventricular hypertrophy

Features:

  • Blue baby
  • Squat–> increase systemic pressure–> decrease R-> L shunt–> more blood to lungs

**Seen in 22q11 syndromes

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6
Q

Truncus arteriosis

A

Abnormal migration of neural crest cells
- Doesn’t divide into pulmonary trunk and aorta (only partial septum formation)

** seen in 22q11 syndromes

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7
Q

Transposition of great vessels

A

abnormal migration of neural crest cells

  • RV–> aorta
  • LV–> pulmonary artery

Symptoms:

  • Irritable
  • Machine-like murmur between scapulae (PDA)
  • Severe cyanosis
    • only survives with shunt (PDA, Atrial shunt)
    • seen in infant of diabetic mother
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8
Q

Endocardial cushion defect

A

Membranous septal defect= AV septum defect–> L to R shunt–> pulmonary HTN–> Eisenmenger syndrome

Eisenmengers= blood reverses to R–> L shunt
- Cyanosis, clubbing, polycythemia

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9
Q

Patent foramen ovale

A

Failure of septum primum and secundum to fuse after birth

  • Fusion driven by increase in pulmonary blood flow (decreased resistance)–> increased L atrial presssure–> pushes flap of septum primum closed over foramen ovale
  • Normally develops into fossa ovalis

Patent foramen ovale–> increased risk of venous clots causing stroke (bypass pulmonary system)

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10
Q

Umbilical vein

A

Carries oxygenated blood from placenta–> ductus venosus–> IVC–> heart

  • After birth: ligamentum teres hepaticus (within falciform ligament)

** Vitelline veins–> portal venous system

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11
Q

Umbilical arteries

A

Two: Connect internal iliac arteries (carrying fetal venous blood)–> to placenta
- become medial umbilical ligaments after birth

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12
Q

Ductus arteriosus

A

Connects pulmonary artery (RV) and aorta (LV)

  • Patency ensures oxygenated blood reaches aorta
  • At birth–> baby breathes O2–> decrease in prostaglandins–> ductus arteriosus closes–> ligamentum arteriosum

PDA= patent ductus arteriosus

  • Maintained by indomethacin (essential to have PDA in babies with transposition of great vessels until surgical correction)
  • See in congenital rubella infection
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13
Q

Ductus venosus

A

Carries oxygenated blood from umbilical vein–> IVC

After birth: ligamentum venosum

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14
Q

Notochord

A

Becomes nucleus pulposus of IV disc

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15
Q

Bulbus cordis

A

Base of Truncus arteriosus

Becomes smooth parts (outflow tracts) of L and R ventricle

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16
Q

Left horn of sinus venosus

A

Between SVC and IVC in early heart

Becomes coronary sinus

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17
Q

Right horn of sinus venosus

A

Between SVC and IVC in early heart

Becomes smooth part of R atrium

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18
Q

Right common cardinal vein, R anterior cardinal vein

A

Drain into sinus venosus

Become SVC

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19
Q

Wide split S2

A

Conditions delaying RV emptying:
- Pulmonic stenosis
- RBBB
Exaggerrated normal splitting

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20
Q

Fixed S2 splitting

A

Seen in ASD (patent foramen ovale)
ASD–> L–>R shunt
–> RA, RV volume increased
–> increased flow thru pulmonic valve

–> Eisenmenger if untreated (increased pulmonary vascular resistance)–> permanent damage–> shunt reverses R–>L

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21
Q

Paradoxixcal S2 splitting

A 
Conditions delaying LV emptying:
- Aortic stenosis
- LBBB
P2 sound occurs before A2
- On inspiration, splitting "paradoxically" eliminates as P2 delayed--> closer to A2
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22
Q

Hand grip maneuver

A

Increases systemic vascular resistance

  • Increases: MR, AR, VSD, MVP
  • Decreases: AS, HOCM
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23
Q

Valsalva, standing from sitting

A

Decreases venous return (less blood in LV)

  • Increases MVP, HOCM
  • Decreases most other murmurs
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24
Q

Rapid squatting

A

Increases venous return, preload (afterload with prolonged squatting)
- Decreases MVP, HOCM

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25
Q

Ventricular AP

A

Occurs in bundle of his, Purkinje fibers as well

Phase 0= rapid upstroke
- Na+ channels open;

Phase 1= initial repolarization
- inactivate voltage-gated Na+ channels, K+ channels begin to open

Phase 2= plateau

  • Ca+2 influx (depolarizing) through voltage-gated Ca+ channels balances K+ efflux
  • Ca+2 influx–> Ca+2 release from SR–> myocyte contraction
  • (different from skeletal muscle= electrical depolar–> dihydropyridine R–> RyR–> Ca+2 release)

Phase 3= repolarization

  • K+ efflux through slow K+ channels
  • Closure of voltage-gated Ca+2 channels

Phase 4= Resting potential
- High K+ permeability

** Cardiac myocytes electrically coupled via gap junctions

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26
Q

Pacemaker action porential

A

SA and AV nodes

Phase 0= upstroke

  • Opening of voltage-gated Ca+2 channels–> slow conduction velocity (prolong transmission from A–> V (allow for ventricular filling))
  • Permanent inactivation of fast Na+ channels d/t more positive resting voltage of nodal cells

Phase 3= Repolarization

  • inactivation of Ca+2 channels
  • Increased activation of K+ channels

Phase 4= Diastolic depolarization

  • membrane depolarizes by action of “funny” Na+ channels (slow)
  • Funny channels allow for automaticity in SA/AV nodes
  • Slope of depolarization= HR
  • Catecholamines increase slope–> inc HR
  • ACh/adenosine decrease slope–> dec HR
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27
Q

P wave

A

Atrial depolarization

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28
Q

PR interval

A

Conduction through AV node

  • Delayed by Ca+2 channels slow depolarization
  • Normal < 200 ms
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29
Q

QRS complex

A

Ventricular depolarization

- Normal < 120 ms

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30
Q

T wave

A

Ventricular repolarization

- Inversion= recent MI; repolarization occurring away from dead tissue toward tissue

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31
Q

ST segment

A

Isoelectric period; ventricles completely depolarized

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32
Q

U wave

A

bradycardia, hypokalemia

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33
Q

Pacemakers in heart

A
  1. SAN (Crista terminalis)- (60-120 BPM)
  2. AVN (45-60 BPM)
  3. His-Purkinje-Ventricular (<40 BPM)
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34
Q

Speed of conduction

A
  1. Purkinje (fastest)
  2. Atria
  3. Ventricles
  4. AV node (slowest d/t Ca+2 channel depolarization–> ventricular filling)
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35
Q

QT interval

A

Mechanical contraction of ventricles
- Prolongation–> Torsades de Pointes
—> Vfib
Tx: Magnesium sulfate

Prolonged in congenital long QT:

  • Defects in cardiac Na+ or K+ channels
  • Romano-Ward syndrome (autosomal dominant)
  • Jervell Lange-Nelson syndrome: autosomal recessive; May have congenital sensorineural deafness
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36
Q

Atrial fibrillation

A

Irregularly irregular
- Can cause atrial stasis–> stroke

Associated with:

  • Valvular heart disease–> atrial enlargement
  • Atherosclerosis
  • Cardiomyopathy
  • Sick sinus syndrome

Tx: Diltiazem, Verapamil, cardio-selective Beta-blockers, Warfarin, cardioversion, ablation
- Or digoxin–> vagus stim–> parasympathetic tone increases–> decreased AVN conduction

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37
Q

Atrial flutter

A

Circuit in R atrium (CCW) around tricuspid annulus (isthmus between tricuspid and IVC)
- Depolarization waves–> sawtooth appearance

Tx:

  • Class IA, IC, III antiarrhythmics (Na and K channel blockers)
  • Rate control: Diltiazem, verapamil, Beta-blocker
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38
Q

Ventricular fibrillation

A

Completely erratic rhythm (no identifiable waves)

- Fatal without immediate CPR, defibrillation

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39
Q

1st Degree AVN block

A

PR interval prolongation

  • > 200 msec
  • Asymptomatic
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40
Q

2nd degree Mobitz Type I (Wenckebach)

A

Lengthening of PR interval until beat “dropped” (P wave without QRS)
- Asymptomatic (usually)

Seen in athletes, sleep

AVN conduction slowed by:

  • Beta blockers, diltiazem/verapamil
  • Digitalis
  • MI–> AVN ischemia
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41
Q

2nd degree Mobitz Type II

A

Dropped beat (QRS complex) with no preceding change in PR interval length

  • Block below AVN
  • Often 2:1 conduction block (2 p waves–> 1 QRS)
  • May progress to 3rd degree block

Tx: pacemaker

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42
Q

3rd degree AVN block (complete)

A

Atria and ventricles beat independently of one another

  • P and QRS present, but bear no relationship to one another
  • P (atrial rate) faster than ventricular rate

Causes:

  • Lyme disease
  • Congenital/acquired defects
  • Primary conduction system disease
  • Cardiomyopathy, infiltrative heart disease
  • myocarditis
  • MI: inferior–> reflex vagal action (reversible); anterior–> his-purkinje necrosis (irreversible)
  • Drugs

Tx: Pacemaker

43
Q

ANP

A

Atrial natiuretic peptide:
Released from myocytes in response to increased blood volume, atrial P
- Vascular relaxation
- decreased collecting tubule Na reabsorption (counteracts aldosterone)
- constricts efferent arterioles, dilates afferents (via cGMP)–> diuresis

44
Q

Aortic arch baroreceptor

A

Increased BP–> vagus–> solitary nucleus of medulla

45
Q

Carotid sinus

A

Change in BP–> glossopharyngeal–> solitary nucleus of medulla

46
Q

Baroreceptors

A

Hypotension–> decreased atrial pressure/stretch–> decreased afferent baroreceptor–> increased sympathetic efferent (decrease parasymp)–> vasoconstriction, increased HR, contractility, BP
* Seen in severe hemorrhage

Carotid massage–> increased pressure/stretch–> increased afferent firing–> decreased HR

47
Q

Cushing’s triad

A

Increased intracranial P (ICP)–> constricted arterioles–> cerebral ischemia

  • -> HTN to increase perfusion–> stretch
  • -> reflex baroreceptor-induced bradycardia (decrease HR)
48
Q

Autoregulation of perfusion (by tissue type)

A

Heart: local metabolites (CO2, adenosine, NO)–> vasodilate

Brain: local metabolites (CO2, pH)–> vasodilate (central chemoreceptors)

Kidneys: myogenic, tubuloglomerular feedback

Lungs: Hypoxia–> vasoCONSTRICTION

Skeletal muscle: local metabolites (adenosine, lactate, K+)–> vasodilation

Skin: Sympathetic stimulation–> vasoconstriction (keep in body heat)
- Buildup of metabolites–> forced vasodilation (hence white then red in cold)

** Peripheral chemoreceptors= carotid, aortic bodies stimulated by decreased PO2 (< 60 mmHg), increased PCO2, decreased pH

49
Q

Tricuspid atresia

A

Absence of tricuspid valve
Hypoplastic R ventricle
- Requires ASD and VSD for viability

50
Q

Total anomalous pulmonary venous return (TAPVR)

A

Pulmonary veins drain into R heart circulation (SVC, coronary sinus)

  • Associated with ASD, PDA to maintain R–> L shunt, maintain CO
  • Similar to transpostion of great vessels
51
Q

Down syndrome cardiac defects

A

ASD, VSD, AV septal defect (endocardial cushion defects)

52
Q

Congenital rubella cardiac defects

A

Septal defects, PDA, pulmonary artery stenosis

53
Q

Monckeberg Arteriosclerosis

A

Calcification in media of arterias (radial or ulnar)

  • Benign
  • Pipestem arteries
  • NO obstruction of blood flow
  • No intimal involvement
54
Q

Hyaline arteriosclerosis

A

Thickening of small arteries (intima and media) due to essential hypertension, DM–> narrrowed lumen

  • DM–> non-enzymatic glycosylation of proteins–> hyalinization
55
Q

Hyperplastic arteriosclerosis

A

“Onion skinning” of arterioles d/t malignant HTN (diastolic > 120)
- Most common in kidneys, intestine, retina)

56
Q

Abdominal aortic aneurysm

A

Associated with atherosclerosis
- Male smokers with HTN, 50+ years

  • Most common location of atherosclerosis followed by coronary arteries > popliteal artery > carotid artery
57
Q

Thoracic aortic aneurysm

A

Associated with HTN, cystic medial necrosis (Marfans) and tertiary syphillis

Cystic medial degeneration= myxomatous change in media of large arteries

  • Elastic tissue fragmented, separation of elastic and fibromusclular components–> fill with ECM
  • Seen in Marfan (fibrillin-1 defect)
  • Defect in lysyl oxidase (d/t copper deficiency or beta-aminopropionitrile= sweet peas)–> can’t cross link elastin and collagen–> angioathryrism)
58
Q

Angina subtypes

A

Symptomatic with > 75% lumen narrowing, no myocyte necrosis

Stable= secondary to atherosclerosis

  • ST depression
  • Retrosternal chest pain on exertion

Prinzmetal’s variant=

  • ST elevation
  • Occurs at rest secondary to vasospasm

Unstable/crescendo= thrombosis with incomplete occlusion

  • ST depression
  • Worsening chest pain at rest or minimal exertion

** In MI, see ST depression–> ST elevation with increased ischemia and transmural necrosis

Treatment: Decrease myocardial O2 consumption:

  • nitrates (lower preload)
  • beta-blockers (decrease afterload)
    • pindolol and acebutolol= beta blockers contraindicated in angina)
59
Q

Evolution of MI

A

0-4 hours: no changes
- risk of arrhythmia, CHF exacerbation, cardiogenic shock

4-12 hours: early coagulation necrosis
- risk of arrhythmia

12-24 hours: contraction bands (reperfusion injury), necrotic cells release contents, neutrophils migrate
- risk of arrhythmia

1-3 days: Coagulation necrosis, tissue inflammation around infarct–>
- Fibrinous pericarditis (d/t inflammation)

3-14 days: Macrophages, granulation tissue

  • yellow and soft tissue by 10 days, hyperemic border
  • Risk of free wall rupture–> tamponade
  • Papillary muscle rupture
  • Ventricular aneurysm–> arrhythmia, thrombi
  • IV septum rupture–> VSD

2 weeks +: scarring complete, contracted

  • Risk of Dressler’s syndrome= autoimmune problems d/t fibrinous pericarditis
  • Fever, pleuritic pain, pericardial effusion
60
Q

Diagnosis of MI

A
  1. ECG in first 6 hours
  2. Cardiac troponin I (most specific enzyme)= 4 hours to 7 days

CK-MB: seen in cardiac and skeletal muscle
- Used to diagnose reinfarction (as levels normalize 48 hours after first infarct)

ECG changes:

  • ST elevation= transmural (widespread= pericarditis from Dressler’s)
  • ST depression= subendocardial
  • Pathologic Q waves= transmural
  • PR depression= pericarditis
61
Q

Dilated (congestive) cardiomyopathy

A 
Most common cardiomyopathy; due to ECCENTRIC HYPERTROPHY (sarcomeres added in series)
Causes:
- Idiopathic
- Genetic: x-linked dilated cardiomyopathy= mutation in cardiac cytoskeleton or mitochondrial enzymes (ex: dystrophin)
- Alcohol abuse
- wet Beriberi
- Coxsackie B
- Chronic cocaine use
- Chagas disease
- Doxorubicin tox
- Hemochromatosis
- Peripartum cardiomyopathy

Findings:

  • S3 (volume overload)
  • Dilated appearance
  • L Atrial enlargement can compress esopagus (dysphagia)

Tx:

  • Na+ restriction
  • ACE-I
  • Diuretics
  • Digoxin
  • Heart transplant
62
Q

Hypertrophic cardiomyopathy

A

CONCENTRIC HYPERTROPHY (sarcomeres added in parallel)

Hypertrophied IV septum: too close to mitral valve leaflet–> outflow tract obstruction

  • Familial, AD
  • cause: beta-myosin heavy chain mutation (35-50%), myosin binding protein C (15-25%), cardiac troponin C (15-20%), tropomyosin (< 5%)
  • associated with Friederich’s ataxia
  • Sudden death in young athletes

Findings:

  • S4 (pressure overload)
  • Normal heart
  • Apical impulses (triple ripple)
  • Bifid pulse
  • Systolic murmur

Treatment:

  • Beta-blocker
  • non-dihydropyridine Ca+ channel blocker (Verapamil)
63
Q

Restrictive/obliterative cardiomyopathy

A

Diastolic dysfunction due to:

  • Sarcoidosis
  • Amyloidosis (senile cardiac amyloidosis in atria due to deposition of beta-folded ANP)
  • Post-radiation
  • Endocardial fibroelastosis (young children)
  • Loeffler’s syndrome (eosinophilic infiltrate)
  • Hemochromatosis
64
Q

Chronic constrictive pericarditis

A

Infiltration of pericardium

  • Most common cause= TB
  • Restricted ventricular filling, Low CO, R-sided heart failure resistant to meds
  • Kussmaul’s sign= rise in JVP with inspiration (normally falls): increased venous return to restricted heart–> blood goes up!)
65
Q

Treatment of CHF

A

Reduced mortality:

  • ACE-I (inhibits remodeling/left ventricular hypertrophy)
  • Beta-blockers (except in acute decompensated HF)
  • Angiotensin receptor antagonists (ARB)
  • Spironolactone (blocks aldosterone neurohormonal stimulation–> prevents cardiac fibrosis)
  • Hydralazine with nitrate (symptoms and mortality)

Reduced symptoms:
- Thiazide/loop diuretics

66
Q

Bacterial endocarditis

A
  • Roth’s spots= white spots on retina with surrounding hemorrhage
  • Osler’s nodes
  • Janeway lesions
  • Splinter hemorrhages on nail bed

Acute causes: S. aureus
- Large vegtations on previously normal valves

Subacute causes: S. viridans

  • Small vegetations on congenitally abnL or diseased valves
  • Seen in dental procedures
  • S. epidermis on prosthetic valves
  • S. bovis d/t colon cancer

IV drug use–> tricuspid valve endocarditis
- S. aureus, pseudomonas, candida

Nonbacterial:

  • Malignancy, hypercoagulable state
  • Lupus (marantic/thrombotic endocarditis)

Complications:
- Chordae rupture, glomerulonephritis, suppurative pericarditis, emboli

67
Q

Rheumatic fever

A

** Antibodies to M protein (antiphagocytic)–> type II hypersensitivity reaction (NOT reaction to bacteria)

group A beta-hemolytic strep (strep pyogenes)
- Mitral > aortic&raquo_space; tricuspid

Associated with:

  • Aschoff bodies= granuloma in giant cells
  • Anitschokow’s cells (activated histiocytes)
  • Elevated ASO titers

Symptoms:

  • Fevers
  • Erythema marginatum
  • Valvular damage
  • ESR increase
  • Red-hot joints (migratory polyarthritis)
  • Subcutaenous nodules
  • St. Vitus’ dance (Syndeham’s chorea)
68
Q

Cardiac tamponade

A

Equilibration of diastolic P in all 4 chambers
- Hypotension, increased venous pressure (JVD), distant heart sounds, increased HR, pulsus paradoxus)

Pulsus paradoxus= decrease in systolic BP > 10 on inspiration
- d/t cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup

69
Q

Polyarteritis nodosa

A

Young adults

  • Hep B seropositive in 30%
  • Constitutional symptoms, melena, abdominal pain
  • HTN, neurologic dysfunction, renal damage

Path:

  • Renal, visceral vessels (not pulmonary)
  • Immune-complex mediated (type III)
  • Transmural inflammation of arterial wall, fibrinoid necrosis

Tx:
- Corticosteroids, cyclophosphamide

70
Q

Buerger’s disease

A

Thromboengiitis obliterans

Heavy smokers, males < 40 years

Path:

  • Intermittent claudication–> gangrene, autoamputation, superficial nodular phlebitis
  • Reynaud’s
  • Segmental thrombosing vasculitis

Tx: smoking cessation

71
Q

Microscopic polyangiitis

A

Vasculitis in lung, kidneys, skin

  • Pauci-immune glomerulonephritis
  • Palpapable purpura

NO granulomas
- p-ANCA

Tx: cyclophosphamide, cortiocosteroids

72
Q

Wegener’s granulomatosis

A

Upper respiratory tract problems: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
Lower resp tract: hemoptysis, cough, dyspnea
Renal: hematuria, red cell casts

Triad:

  • Focal necrotizing vasculitis
  • Necrotizing granulomas in lung, upper airway (large nodular densities on x-ray)
  • Necrotizing glomerulonephritis

Granulomas
- c-ANCA

Tx: cyclophosphamide, corticosteroids

73
Q

Churg-Strauss

A

Asthma, sinusitis, palpable purpura, peripheral neuropathy (foot/wrist drop)
- Also heart, GI, kidneys (pauci-immune glomerulonephritis)

Granulomatous necrotizing vasculitis with eosinophilia
- pANCA, elevated IgE

74
Q

Pyogenic granuloma

A

Polypoid capillary hemangioma

  • Can ulcerate and bleed
  • Associated with trauma, pregnancy
75
Q

Cystic hygroma

A

Cavernous lymphangioma of neck

- Associated with Turner’s and Down syndrome

76
Q

Glomus tumor

A

Benign, painful red-blue tumor under fingernails

- Arises from smooth muscle cells of glomus body

77
Q

Bacillary angiomatosis

A

Benign capillary skin papules in AIDS patients

  • Caused by Bartonella henselae infections
  • Mistaken for Kaposi’s sarcoma
78
Q

Angiosarcoma

A

Blood vessel malignancy in head, neck, breast

  • Associated with radiation therapy (breast cancer, Hodgkin’s lymphoma)
  • Aggessive, difficult to resect due to delay in diagnosis
79
Q

Lymphangiosarcoma

A

Lymphatic malignancy associated with persistent lymphedema (post-radical mastectomy, filariasis)

80
Q

Sturge-Weber disease

A

Congenital vascular disorder of capillary-sized blood vessels

  • Port-wine stain
  • Ipsilateral leptomeningeal angiomatosis (intracerebral AVM)–> seizures
  • Early-onset glaucoma
81
Q

Nifedipine, Amlodipine

A

Dihydropyridine Ca+2 channel blocker

  • Blocks voltage-dependent L-type Ca+2 channels of cardiac, smooth muscle
  • Highly effective on vascular smooth muscle
  • Less effective on cardiac tissue

Use:

  • HTN
  • angina (similar effect to nitrates= n for nifedipine)
  • Prinzmetal’s angina, Raynaud’s
  • Post-SAH: lowers M+M d/t vasospasm

Tox:

  • Cardiac depression
  • AV block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
82
Q

Verapamil, Diltiazem

A

Non-dihydropyridine Ca+2 channel blocker

  • Blocks voltage-dependent L-type Ca+2 channels of cardiac, smooth muscle
  • Less effective on vascular smooth muscle
  • Highly effective on cardiac tissue

Use:

  • Arrhythmias
  • angina (similar to beta-blockers)
  • Prinzmetal’s angina, Raynaud’s
  • Post-SAH: lowers M+M d/t vasospasm

Tox:

  • Cardiac depression
  • AV block
  • Peripheral edema
  • Flushing
  • Dizziness
83
Q

Hydralazine

A

MOA: increases cGMP–> smooth m. relaxation–> vasodilation (arterioles > veins)
- reduces afterload

Use: Severe HTN, CHF

  • 1st line in pregnancy for HTN (with methyldopa)
  • Coadministered with Beta-blocker (labetolol) to prevent reflex tachycardia

Tox:

  • Reflex tachycardia (contraindicated in angina/CAD)
  • Fluid retention
  • Nausea
  • H/A
  • Angina
  • Lupus-like syndrome (slow acetylators)
84
Q

Treatment of malignant HTN

A 
Nitroprusside
Nicardipine
Clevidipine
Labetolol
Denoldopam
85
Q

Nitroprusside

A

Short acting
MOA: increases cGMP via release of NO

Tox: cyanide release

86
Q

Fenoldopam

A

MOA: Dopamine D1 receptor agonist

  • Coronary, peripheral, renal, splanchnic vasodilation
  • Decreases BP, increases natriuresis
87
Q

Nitroglycerin, isosorbide dinitrate

A

MOA: Vasodilate by releasing NO in smooth muscle–> increased cGMP, smooth m. relaxation

  • Dilates veins&raquo_space; arteries
  • Main effect= decrease cardiac preload via venodilation (retain blood in venous system)

Use: Angina, pulmonary edema

Tox: Reflex tachycardia, hypotension

  • Flushing, headache
  • “Monday disease”= tolerance development–> tachycardia, dizziness, H/A on re-exposure
    • Isosorbide DInitrate= tablet with extensive 1st pass metabolism compared to isosorbide MONOnitrate
    • Nitroglyceride= sublingual
88
Q

Statins

A

MOA: HMG-CoA reductase inhibitors

  • Inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)
  • Increased LDL-R in liver (increase LDL uptake from periphery)

Use:

  • Most effective LDL-lowering therapy
  • Increases HDL
  • Lowers TGs

Side effects:

  • Hepatotoxic (increased LFTs)
  • Rhabdomyolysis
  • Myopathy (greatly increased with Fibrate use–> increased [statin])
89
Q

Niacin

A

Vitamin B3
MOA:
- Inhibits lipolysis in adipose tissue
- Reduces hepatic VLDL secretion

Use:

  • Lowers LDL
  • Most HDL increase
  • lowers TG

Tox:

  • Red, flushed face (pre-dose with aspirin, long term use decreases flusing)–> antihypertensives + niacin–> vasodilation!
  • Hyperglycemia: decreases insulin sensitivity–> acanthosis nigricans)
  • Hyperuricemia (exacerbates gout)
90
Q

Cholestyramine
Colestipol
Colesevelam

A

Bile acid resins
MOA:
- Prevent intestinal reabsorption of bile acids
- Increases LDL-R on liver (so liver can make more cholesterol)

Use:

  • Lowers LDL
  • Slight HDL increase
  • Slight TG increase

Tox:

  • Patients hate taste, causes GI discomfort
  • Decreases absorption of fat-soluble vitamins (Vit A, D, E, K)
  • Decreases statin absorption
  • Cholsterol gallstones (esp with fibrates)
91
Q

Ezetimibe

A

Cholesterol absorption blocker
MOA: prevents cholsterol abs at small intestine brush border

Use:

  • 20-30% decrease in LDL
  • NO change on other profile

Tox:

  • Rare increase in LFTs
  • Diarrhea
  • slight increased risk of myopathy with statins
92
Q

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

A

MOA:
Activate PPAR-alpha–> Upregulate LPL–> increased TG clearance

Use:

  • Slight decrease in LDL
  • Increase HDL
  • Most decrease in TGs

Tox:
- Myositis, hepatotoxicity, cholseterol gallstones (with bile acid resins)

93
Q

Digoxin

A

Cardiac glycoside

MOA:

  • Inihibits Na/K ATPase–> accumulation of Na+ in cell–> inhibition of NCX (Na/Ca exchanger)–> slows Ca+2 efflux
  • Positive inotrope (contractility)
  • Stimulates vagus nerve–> negative chronotrope (decreases HR)

Use:

  • CHF: increased contractility
  • A fib: vagal nerve stimulation–> decreased AVN conduction, depression of SAN

PK:

  • 75% bioavailable
  • 20-40% protein bound
  • t1/2= 40 hours
  • Urinary excretion

Tox:

  • Cholinergic: N/V/D, blurry yellow vision
  • ECG: increased PR interval, decreased QT, ST scooping, T-wave inversion
  • Arrhythmia (d/t increased intracell [Ca+2]–> delayed afterdepolarization)–> ventricular tachyarrhythmias
  • AV block
  • Hyperkalemia (poor prognostic indicator)
  • Predisposed to toxicitiy with: renal failure (decreased excretion), hypokalemia, (binds at Na/K ATPase), quinidine (decreases clearance, displaces from tissues)

Antidote= slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg+2 (KLAM)

94
Q

Class IA antiarrhythmics

A

Na-channel blockers:

  • Quinidine
  • Procainamide
  • Disopyramide

MOA:

  • Increase AP duration, effective refractory period
  • Increase QT interval

Use:

  • Atrial, ventricular arrhythmias
  • Especially reentrant, ectopic supraventicular, ventricular tachycardia

Tox:

  • Quinidine= cinchonism (H/A, tinnitus)
  • Procainamide= Reversible SLE
  • Disopyramidine= heart failure
  • ALL= Thrombocytopenia, TdP due to increased QT interval
95
Q

Class IB antiarrhythmics

A

Na channel blockers:

  • Lidocaine
  • Mexiletine
  • Tocainamide

MOA:
- Decreased AP duration

Use:

  • Ischemic or depolarized Purkinje, ventricular tissue
  • Acute ventricular arrhythmias (post-MI= Best!)
  • Digitalis-induced arrhythmias

Tox:

  • Local anesthetic
  • CNS stim/depression
  • CV depression
96
Q

Class IC antiarrhythmics

A

Na channel blockers

  • Flecainide
  • Propafenone

MOA:
- No effect on AP duration

Use:

  • Useful in Ventricular tachycardias–> Vfib, intractable supra-ventricular tachycardia
  • Last resort in refractory tacharrhythmias

Tox:

  • Proarrhythmic
  • Contraindicated post-MI
  • Prolongs refractory period in AVN
97
Q

Class II antiarrhythmics

A

Beta-blockers:

  • Metoprolol
  • Propanolol
  • Esmolol
  • Atenolol
  • Timolol

MOA:

  • Decreases cAMP, Ca+2 currents–> decreased SA and AV node activity
  • Decrease slope of phase 4 (suppressing abnormal pacemakers
  • Works best on AVN–> increased PR interval

Use:

  • Ventricular tacchycardia
  • Supraventricular tacchycardia
  • Slowing ventricular rate during Afib, Aflutter

Tox:

  • Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF)
  • CNS effects: sedation, sleep alterations
  • May mask signs of hypoglycemia
  • Metoprolol= dyslipidemia
  • treat overdose with glucagon

*Propanolol= exacerbate vasospasm in Prinzmetal’s angina

98
Q

Class III antiarrhythmics

A

K+ channel blockers

  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol

MOA:

  • Increases AP duration
  • Increased effective refractory period (ERP)
  • Increases QT interval

Tox:

  • Sotalol= TdP, excessive beta-block
  • Ibutilide= TdP
  • Amiodarone= pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism (40% iodine), corneal deposits, skin deposits (blue/gray)–> photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF): check PFTs, LFTs, TFTs
  • BUT, Amiodarone has class I, II, III, and IV effects due to alteration of lipid membrane
    • Amiodarone decreases CytP450 activity–> increase in Warfarin (commonly given in atrial fibrillation)
99
Q

Class IV antiarrhythmics

A

Non-dihydropyridine Ca+2 channel blockers:

  • Verapamil
  • Diltiazem

MOA:

  • Slow AVN conduction by increasing phase 0, 4 of depolarization (increase PR interval)
  • Increase ERP

Use:
- Nodal arrhythmias: supraventricular arrhythmias

Tox:

  • Constipation
  • Flushing
  • Edema
  • CV effects: CHF, AVN block, sinus node depression
100
Q

Adenosine

A

MOA:
-Increases K+ flux out of cells–> hyperpolarizes the cell and decreases Ca+2 influx

Use:
Supraventricular tachycardia
- Short-acting

Tox:

  • Flushing, hypotension, chest pain
  • Sense of doom
  • Administer with theophylline, caffeine to offset effects
101
Q

Mg+2

A

Administered in TdP and digoxin toxicity

102
Q

Mitral stenosis

A

Severity of murmur indicated by A2–> OS (opening snap) interval
- Shorter interval= more severe stenosis)

103
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

Right ventricle wall replaced by fibrofatty tissue (idiopathic)
- May be due to mutation in Ca+2-binding protein of sarcoplasmic reticulum

Step 1 Subjects (26 decks)

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