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Cardiac Flashcards

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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
Ventricular AP
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
26
Pacemaker action porential
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
27
P wave
Atrial depolarization
28
PR interval
Conduction through AV node - Delayed by Ca+2 channels slow depolarization - Normal < 200 ms
29
QRS complex
Ventricular depolarization | - Normal < 120 ms
30
T wave
Ventricular repolarization | - Inversion= recent MI; repolarization occurring away from dead tissue toward tissue
31
ST segment
Isoelectric period; ventricles completely depolarized
32
U wave
bradycardia, hypokalemia
33
Pacemakers in heart
1. SAN (Crista terminalis)- (60-120 BPM) 2. AVN (45-60 BPM) 3. His-Purkinje-Ventricular (<40 BPM)
34
Speed of conduction
1. Purkinje (fastest) 2. Atria 3. Ventricles 4. AV node (slowest d/t Ca+2 channel depolarization--> ventricular filling)
35
QT interval
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
36
Atrial fibrillation
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
37
Atrial flutter
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
38
Ventricular fibrillation
Completely erratic rhythm (no identifiable waves) | - Fatal without immediate CPR, defibrillation
39
1st Degree AVN block
PR interval prolongation - > 200 msec - Asymptomatic
40
2nd degree Mobitz Type I (Wenckebach)
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
41
2nd degree Mobitz Type II
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
42
3rd degree AVN block (complete)
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
ANP
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
Aortic arch baroreceptor
Increased BP--> vagus--> solitary nucleus of medulla
45
Carotid sinus
Change in BP--> glossopharyngeal--> solitary nucleus of medulla
46
Baroreceptors
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
Cushing's triad
Increased intracranial P (ICP)--> constricted arterioles--> cerebral ischemia - -> HTN to increase perfusion--> stretch - -> reflex baroreceptor-induced bradycardia (decrease HR)
48
Autoregulation of perfusion (by tissue type)
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
Tricuspid atresia
Absence of tricuspid valve Hypoplastic R ventricle - Requires ASD and VSD for viability
50
Total anomalous pulmonary venous return (TAPVR)
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
Down syndrome cardiac defects
ASD, VSD, AV septal defect (endocardial cushion defects)
52
Congenital rubella cardiac defects
Septal defects, PDA, pulmonary artery stenosis
53
Monckeberg Arteriosclerosis
Calcification in media of arterias (radial or ulnar) - Benign - Pipestem arteries - NO obstruction of blood flow - No intimal involvement
54
Hyaline arteriosclerosis
Thickening of small arteries (intima and media) due to essential hypertension, DM--> narrrowed lumen - DM--> non-enzymatic glycosylation of proteins--> hyalinization
55
Hyperplastic arteriosclerosis
"Onion skinning" of arterioles d/t malignant HTN (diastolic > 120) - Most common in kidneys, intestine, retina)
56
Abdominal aortic aneurysm
Associated with atherosclerosis - Male smokers with HTN, 50+ years * Most common location of atherosclerosis followed by coronary arteries > popliteal artery > carotid artery
57
Thoracic aortic aneurysm
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
Angina subtypes
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
Evolution of MI
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
Diagnosis of MI
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
Dilated (congestive) cardiomyopathy
``` 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
Hypertrophic cardiomyopathy
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
Restrictive/obliterative cardiomyopathy
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
Chronic constrictive pericarditis
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
Treatment of CHF
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
Bacterial endocarditis
- 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
Rheumatic fever
** Antibodies to M protein (antiphagocytic)--> type II hypersensitivity reaction (NOT reaction to bacteria) group A beta-hemolytic strep (strep pyogenes) - Mitral > aortic >> 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
Cardiac tamponade
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
Polyarteritis nodosa
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
Buerger's disease
Thromboengiitis obliterans Heavy smokers, males < 40 years Path: - Intermittent claudication--> gangrene, autoamputation, superficial nodular phlebitis - Reynaud's - Segmental thrombosing vasculitis Tx: smoking cessation
71
Microscopic polyangiitis
Vasculitis in lung, kidneys, skin - Pauci-immune glomerulonephritis - Palpapable purpura NO granulomas - p-ANCA Tx: cyclophosphamide, cortiocosteroids
72
Wegener's granulomatosis
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
Churg-Strauss
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
Pyogenic granuloma
Polypoid capillary hemangioma - Can ulcerate and bleed - Associated with trauma, pregnancy
75
Cystic hygroma
Cavernous lymphangioma of neck | - Associated with Turner's and Down syndrome
76
Glomus tumor
Benign, painful red-blue tumor under fingernails | - Arises from smooth muscle cells of glomus body
77
Bacillary angiomatosis
Benign capillary skin papules in AIDS patients - Caused by Bartonella henselae infections - Mistaken for Kaposi's sarcoma
78
Angiosarcoma
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
Lymphangiosarcoma
Lymphatic malignancy associated with persistent lymphedema (post-radical mastectomy, filariasis)
80
Sturge-Weber disease
Congenital vascular disorder of capillary-sized blood vessels - Port-wine stain - Ipsilateral leptomeningeal angiomatosis (intracerebral AVM)--> seizures - Early-onset glaucoma
81
Nifedipine, Amlodipine
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
Verapamil, Diltiazem
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
Hydralazine
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
Treatment of malignant HTN
``` Nitroprusside Nicardipine Clevidipine Labetolol Denoldopam ```
85
Nitroprusside
Short acting MOA: increases cGMP via release of NO Tox: cyanide release
86
Fenoldopam
MOA: Dopamine D1 receptor agonist - Coronary, peripheral, renal, splanchnic vasodilation - Decreases BP, increases natriuresis
87
Nitroglycerin, isosorbide dinitrate
MOA: Vasodilate by releasing NO in smooth muscle--> increased cGMP, smooth m. relaxation - Dilates veins >> 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
Statins
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
Niacin
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
Cholestyramine Colestipol Colesevelam
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
Ezetimibe
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
Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)
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
Digoxin
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
Class IA antiarrhythmics
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
Class IB antiarrhythmics
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
Class IC antiarrhythmics
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
Class II antiarrhythmics
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
Class III antiarrhythmics
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
Class IV antiarrhythmics
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
Adenosine
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
Mg+2
Administered in TdP and digoxin toxicity
102
Mitral stenosis
Severity of murmur indicated by A2--> OS (opening snap) interval - Shorter interval= more severe stenosis)
103
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Right ventricle wall replaced by fibrofatty tissue (idiopathic) - May be due to mutation in Ca+2-binding protein of sarcoplasmic reticulum
Step 1 Subjects
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