Right coronary artery

• supplies SA and AV nodes
• Gives off: 
• acute marginal artery
• supplies RV
• posterior descending artery (80%)
• supplies posterior septum

Left Coronary Artery

• Gives off:
• Left Anterior Descending artery
• supplies apex and anterior septum
• most common site of occlusion
• Circumflex artery
• supplies posterior left ventricle
• gives off PD artery 20% of time

Enlarged left atrium can lead to...

Most posterior part of the heart!

• dysphagia due to compression of esophageal nerve
• hoarseness due to compression of recurrent laryngeal nerve

CO and MAP equations

CO= SV x HR

Fick principle: CO= rate of O2 consumtion/O2a-O2v

MAP= CO x TPR

MAP= 2/3 diastolic + 1/3 systolic

What causes SV/contractility to inc? Dec?

• Inc SV/contractility
• catecholamines (inc Ca pump in SR)
• inc intracellular Ca
• dec extracellular sodium
• Digitalis (inc intracellular Na-> inc Ca)
• Dec Sv/contractility
• β1 blockade
• CHF
• Acidosis
• Hypoxia/hypercapnia
• non-dihydropyridine Ca channel blockers

Starling curve

Force of cardiac contraction is proportional to end-diastolic length of cardiac muscle fiber (preload)

Ejection fraction

EF=SV/EDV

normally greater than 55%

What the heck are S3 and S4 heart sounds and who has them?

• S3
• heard in early diastole (just after S2)
• assoc with inc filling pressure (dilated CHF or mitral regurg) 
• normal in kids and preggers
• S4
• "atrial kick" heard in late diastole (just before S1)
• associated with ventricular hypertrophy (chronic hypertension)

Jugular Venous Pulse

• a wave- atrial contraction
• c wave- RV contraction (tricuspid bulges into RA)
• x descent- atrial relaxation
• v wave- inc RA pressure due to filling against closed valve
• y descent- blood flow from RA to RV

Wide S2 Splitting

Fixed S2 splitting

S2 splitting is equal and present in both inspiration and expiration due to atrial septal defect

Paradoxical S2 splitting

Opposite of normal S2 splitting- pulmonic valve closes first and on inspiration moves closer to aortic sound (eliminating the split). Due to aortic stenosis or left BBB.

Auscultation: Aortic post

• Systolic murmurs
• aortic stenosis
• flow murmur
• aortic valve sclerosis

Auscultation: Pulmonic post

• Systolic ejection murmur
• pulmonic stenosis
• flow murmur

Auscultation: Left Sternal Border

• Diastolic murmurs
• aortic regurg
• pulmonic regurg
• Systolic murmur
• Hypertrophic cardiomyopathy

Auscultation: Tricuspid post

• Pansystolic murmur
• tricuspid regurg
• ventricular septal defect
• Diastolic murmur
• tricuspid stenosis
• atrial septal defect

Auscultation: Mitral post

• Systolic murmur
• mitral regurg
• Diastolic murmur
• mitral stenosis

Bedside Manuever's for Heart Sounds

Inspiration

Expiration

Hand Grip

Valsalva

Rapid squat 

Inspiration-> inc right heart sounds

Expiration-> inc left heart sounds

Hand Grip-> inc systemic vasc resist, inc mitral regurg, VSD murmurs

Valsalva-> dec venous return, most murmurs dec in intensity, but inc MVP/hypertrophic cardiomyopathy murmurs

Rapid squat-> inc venous return, dec MVP/hypertrophic cardiomyopathy murmurs

Mitral/Tricuspid Regurg murmurs

• Holosystolic, high-pictched "blowing murmur"
• both can be caused by rheumatic fever
• Mitral
• loudest at apex, radiates to the axilla
• enhanced by squatting, hand grip, expiration
• due to ischemic heart ds, mitral valve prolapse, or LV dilation
• Tricuspid
• loudest at tricuspid area, radiates to right sternal border
• enhanced by inspiration
• due to RV dilation or endocarditis

Ventricular septal defect murmur

• holosystolic, harsh sounding
• loudest at tricuspid area

Mitral prolapse murmur

• late systolic crescendo murmur with midsystolic click 
• most frequent valvular lesion
• loudest at S2
• usually benign, but can predispose to endocarditis
• caused by myxomatous degeneration, rheumatic fever, or chordae rupture
• enhanced by standing/valsalva

Aortic Regurg murmur

• immediate high-pitched "blowing" diastolic murmur
• wide pulse pressure
• can present with bounding pulses, head bobbing
• due to aortic root dilation, bicuspid aortic valve, or rheumatic fever
• vasodilators decrease intensity

Mitral stenosis murmur

• late diastolic murmur
• Follows opening snap after S2
• LA>>LV pressure during diastole
• secondary to rheumatic fever
• can lead to LA dilation
• enhanced by expiration

Patent ductus arteriosus murmur

• continuous machine-like murmur
• loudest at S2
• due to congenital rubella or premie

Cardiac action potential stages

• Phase 0
• rapid upstroke
• voltage gated Na channels open
• Phase 1
• initial repolarization
• inactivation of volt gated Na channels, volt gated K channels begin to open
• Phase 2
• Plateau
• Ca influx thru volt gated channels balances K efflux
• Ca influx triggers SR Ca release/myocyte contraction
• Phase 3
• rapid repolarization
• massive K efflux thru volt-gated slow K channels
• closure of volt gated Ca channels
• Phase 4
• resting potential (-85mV)
• high K permeability

Pacemaker potential

• Phase 0
• no volt gated Na channels open because resting voltage is too high
• opening of volt gated Ca channels causes slow upstroke
• Phase 2
• no plateau
• Phase 3
• activation of K channels
• inactivation of Ca channels
• Phase 4
• slow diastolic depolarization
• accounts for automaticity of SA/AV nodes
• slope determines HR
• inc by catecholamines
• dec by ACh/adenosine

Atrial natriuretic peptide

• released from atria in response to inc blood volume and atrial pressure
• causes vascular relaxation
• contricts renal efferent arterioles and dilates afferent arterioles (promotes diuresis) 

Baroreceptors vs Chemoreceptors

• Baroreceptors
• Aortic arch 
• transmits via vagus to medulla
• responds only to inc BP
• Carotid sinus
• carotid transmits via CNIX to solitary nucleus of medulla
• responds to inc and dec in BP
• Chemoreceptors
• Peripheral
• Carotid and aortic bodies respond to:
• dec PO2
• inc PCO2
• dec pH
• Central
• responds to changes in pH and PCO2 (doesnt directly respond to PO2)
• responsible for Cushing Rxn

Cushing Reflex

Inc. ICP-> cerebral ischemia-> hypertension and reflex bradycardia

NOTE: Cushing triad= HTN, bradycardia, respiratory depression

Pulmonary capillary wedge pressure

• good approx of LA pressure
• in mitral stenosis, PCWP>LV diastolic pressure
• measured with Swan-Ganz catheter

Pulmonary blood flow autoregulation

• hypoxia causes vasoconstriction (opposite of other organs)
• this allows well perfused areas to received blood flow preferentially

Physiologic causes of Edema

• inc capillary hydrostatic pressure (CHF)
• dec plasma oncotic pressure (nephrotic syndrome, liver failure)
• inc capillary permeability (toxins, infxns, burns)
• inc interstitial oncotic pressure (lymphatic blockage)

Five causes of early cyanosis in neonates

The 5 T's

• Tetralogy of Fallot
• Transposition of the great vessels
• Truncus arteriosus
• Tricuspid atresia
• absence of tricuspid valve and hypoplastic right ventricle 
• Total anomalous pulmonary venous return
• pulmonary vein drains into right heart

Three causes of late cyanosis in babies

VSD>ASD>PDA

Eisenmenger's Syndrome

• uncorrected VSD/ASD/PDA
• causes compensatory pulmonary vascular hypertrophy-> progressive pulmonary HTN
• as pulm resistance inc-> shunt reverses from L-R to R-L causing late cyanosis

Tetralogy of Fallot

PROVe

1. Pulmonary Stenosis *most important
2. RVH
3. Overriding Aorta
4. VSD

• early cyanosis
• boot shaped heart on CXR
• symptoms improve with squatting (inc TPR reduces R-L shunt)

Transposition of Great Vessels

• pulmonary and systemic circ is completely separated
• not compatible with life unless theres a shunt (VSD/PDA/patent foramen ovale)

Coarctation of the aorta

• Infantile type
• stenosis proximal to insertion of DA
• assoc with Turner's syndrome
• Adult type
• stenosis distal to ligamentum arteriosum
• assoc with notching of the ribs
• HTN in upper extremities, weak pulses in lower
• can lead to aortic regurg

What drug can correct a patent ductus arteriosus? What can keep it open?

• ENDomethacin (indomethacin) ends patency of PDA
• PGE keeps it open (may be necessary to sustain life in conditions like transposition of great vessels)
• will hear a "machine like murmur"

Congenital heart defect associations:

• 22q11 syndrome
• Down syndrome
• Congenital rubella
• Turner syndrome 
• Marfan's Syndrome
• Maternal diabetes

• 22q11 syndrome
• Truncus arteriosus, tetralogy of Fallot
• Down syndrome
• ASD/VSD/AV septal defect
• Congenital rubella
• septal defects, PDA, pulm artery stenosis
• Turner syndrome
• Coarctation of the aorta
• Marfan's Syndrome
• aortic insufficiency
• Maternal diabetes
• transposition of great vessels

Hyperlipidemia signs

• atheromas (plaques in BV walls)
• xanthomas (eyelids and tendons)
• corneal arcus (lipid deposit in cornea)

Monckeberg arteriosclerosis

• calcification in the tunica media (esp radial and ulnar)
• usually benign
• "pipestem" arteries
• does not obstruct flow, intima not involved

Arteriolosclerosis

• hyaline thickening of small arteries
• in essential HTN, diabetes
• hyperplastic "onion skinning"= malignant HTN

Atherosclerosis

• ds of elastic arteries and large/med muscular arteries
• Risk factors: smoking, HTN, diabetes, hyperlipidemia, family hx
• Progression: endothelial cell dysfxn-> macrophage and LDL accum-> foam cell formation-> fatty steaks-> smooth m cell migration-> fibrous plaque-> complex atheroma
• Complications: aneurysms, ischemia, infarcts, peripheral vascular ds, thrombus, emboli
• Location: abdom aorta>coronary arteries>popliteal artery>carotid artery
• Sx: angina, claudication, can be asymp

Aortic Dissection

• longitudinal intraluminal tear forming a false lumen
• assoc with HTN or cystic medial necrosis (Marfan's)
• presents with tearing chest pain radiating to the back
• CXR shows medistinal widening
• can rupture-> death

Angina

• Stable
• secondary to atherosclerosis
• ST depression 
• pain with exertion, goes away
• Prinzmetal's variant
• secondary to coronary artery vasospasm
• ST elevation
• Unstable/Crescendo
• thrombosis no necrosis
• ST depression
• pain at rest

Coronary Steal syndrome

• vasodilator aggrevates ischemia by shunting blood from area of stenosis to an area of higher perfusion

Evolution of MI: 0-4 hrs

No gross/micro changes

risk of arrhythmia already (continues thru out)

Evolution of MI: 4-12 hrs

• Gross: dark mottling of infarcted tissue
• Micro: early coag necrosis, edema, hemorrhage, wavy fibers

Evolution of MI: 12-24 hrs

• Gross: dark mottling of infarcted tissue
• Micro: contraction bands, release of necrotic cell contents, neutrophils 

Evolution of MI: 2-4 days

• Gross: hyperemia
• Micro: extensive coag necrosis, acute inflammation, more neutrophils

Evolution of MI: 5-10 days

• Gross: hyperemic border, central yellow-brown softening
• Micro: granulation tissue at margins
• Risk: Rupture! 

Evolution of MI: 7 wks

• Gross: recanalized artery, grey-white tissue
• Micro: contracted scar complete
• Risk: ventricular aneurysm

MI diagnosis: Cardiac Enzymes

• First 6 hrs: EKG is gold standard
• Cardiac Troponin I
• rises after 4hrs
• elevate for 7-10 days
• more specific than other enzymes
• CK-MB
• peaks 24 hrs post MI, then rapidly declines
• useful in diagnosing a reinfarction on top of acute ME
• also release from skeletal m
• AST
• nonspecific (also found in liver, skeletal m)

MI complications

• arrhythmia- common cause of death on way to hospital
• LV failure/pulmonary edema
• Cardiogenic shock
• Ventricular free wall rupture-> cardiac tamponade
• Papillary m rupture-> severe mitral regurg
• IV septal rupture-> VSD
• Aneurysm
• Postinfarction fibrinous pericarditis
• Dressler's syndrome- autoimmune phenom resulting in fibrinous pericarditis 

Dilated cardiomyopathy

• most common cardiomyopathy
• Findings:
• S3 heart sound, dilated heart on ultrasound, balloon appearance on CXR
• systolic dysfxn
• Causes (ABCCCD)
• Alcohol abuse
• wet Beriberi
• Coxsackie B
• Cocaine
• Chagas ds
• Doxorubicin toxicity
• hemochromotosis
• peripartum cardiomyopathy

Hypertrophic Cardiomyopathy

• Hypertrophied IV septum leads to mitral outflow tract obstruction (diastolic dysfxn)
• half of cases are familial
• assoc with Friedrich's Ataxia
• cause of sudden death in athletes
• normal sized heart, S4, systolic murmur
• Tx: β-blocker, non-dihydropyridine calcium channel blocker (verapamil)

Restrictive Cardiomyopathy

• Major Causes: 
• sarcoidosis
• amyloidosis
• postradiation fibrosis
• endocardial fibroelastosis
• Loffler's Syndrome
• Hemochromatosis
• Diastolic dysfxn ensues

Bacterial Endocarditis

• Symptoms: FROM JANE
• Fever
• Roth's spots (on retina)
• Osler's nodes (on fingers/toes)
• Murmur 
• Janeway lesions (palms/soles)
• Anemia
• Nail-bed/splinter hemorrhages
• Emboli
• Location: mitral>aortic>tricuspid (IV drugs)
• Causes:
• acute, rapid onset-> S. aureus
• insidious, sequela of dental procedure-> Strep viridans
• IV drugs-> s. aureus, pseudomonas, candida
• Colon cancer-> S. bovis
• Prosthetic valves-> S. epidermidis
• Complications: 
• chordae rupture
• glomerulonephritis
• suppurative pericarditis
• emboli

Rheumatic Fever

• consequence of URTI with group A, β-hemolytic strep
• early death due to myocarditis
• late sequelae: 
• Rheumatic heart ds
• Mitral>aortic>>tricuspid
• early sign is mitral valve prolapse
• late lesion is mitral stenosis
• Aschoff bodies (granuloma with giant cells)
• Anitschkow's cells (activated histiocytes)
• anti-streptolysin O titers inc.
• Immune mediated (type II hypersens)
• FEVERSS
• fever
• erythema marginatum (pink rings on trunk/arms)
• valvular damage
• ESR elevated
• Red-hot joints (migratory polyarthritis)
• Subcut nodules
• St. Vitus' dance (chorea)

Acute pericarditis

• presents with sharp pain, aggravated by inspiration, relieved by leaning forward
• Fibrinous
• most common
• Dressler's syndrome
• uremia
• radiation
• presents with loud friction rub
• Serous
• noninfectious inflammatory ds (SLE, RF)
• Suppurative/purulent
• caused by infectious agents (duh)

Cardiac Tamponade

• compression of heart by fluid in pericardium leading to dec CO
• Findings: hypotension, JVD, quiet heart sounds, inc HR, pulsus paradoxus (dec systolic BP during inspiration)

Syphilitic Heart Disease

• tertiary syphilis-> disrupts vasa vasorum of the aorta with consequent dilation of the aorta and valve ring
• "tree bark" appearance of aorta due to calcification
• can result in aneurysm of ascending aorta/arch and aortic valve incompetence

Heart Tumors

Most common heart tumor?

Most common primary heart tumor?

Most common primary in children?

• Most common= metastasis from melanoma/lymphoma
• Most common primary= myxomas
• 90% in LA
• "ball valve" obstruction-> syncopal episodes
• Most common primary in children= rhabdomyoma 
• assoc with tuberous sclerosis

Large vessel vasculitis: Temporal Arteritis

• old ladies
• unilateral HA, jaw claudication
• may lead to irreversible blindness due to ophthalmic artery occlusion 
• focal granulomatous inflammation
• inc ESR
• Treat with high-dose steroids
• assoc with polymyalgia rheumatica

Large vessel vasculitis: Takayasu's arteritis

• asian females <40 yo
• pulseless disease
• weak UE pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
• granulomatous thickening of aortic arch, prox great vessels
• inc ESR

Medium vessel vasculitis: Polyarteritis nodosa

• young adults, Hep B seropos in 30%
• Symptoms (due to ischemia):
• fever, weight loss, malaise, HA
• Abdominal pain, melena
• HTN, neuro dysfxn, cutaneous eruptions
• involves renal and visceral vessels (NOT pulmonary arteries)
• immune complex mediated
• mult aneurysms and constrictions
• Tx- steriods, cyclophosphamide

Medium vessel vasculitis: Kawasaki Disease

• asian babies
• fever, LAD, conjunctivitis, "strawberry tongue", hand/foot erythema, desquamation
• may develop coronary aneurysms
• treat with IV immunoglobulin and aspirin

Medium vessel vasculitis: Buerger's Ds

• thromboangitis obliterans
• heavy smokers
• males >40
• claudication may lead gangrene/amputation
• Raynaud's phenomenom
• segmental thrombosing vasculitis
• Tx: stop smoking

Small vessel vasculitis: Microscopic polyangiitis

• pauci-immune (minimal evidence of hypersens) glomerulanephritis, palpable purpura
• no granulomas
• p-ANCA (perinuclear antineutrophil cytoplasmic antibodies)

Small vessel vasculitis: Wegener Granulomatosis

• TRIAD:
• Focal necrotizing vasculitis
• Necrotizing granulomas in the lung and upper airway
• Necrotizing glomerulonephritis
• Presentation:
• URT: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
• LRT: hemoptysis, cough, dyspnea
• Renal: hematuria, red clast cells
• c-ANCA (cytoplasmic anti-neutrophil cytoplasmic antibodies)
• large nodular densities on CXR
• Tx: cyclophosphamide, corticosteroids

Small vessel vasculitis: Churg-Strauss syndrome

• pauci immune granulomatous vasculitiss with eosinophilia
• Presents with:
• asthma
• sinusitus
• palpable purpura
• peripheral neuropathy (wrist/foot drop)
• can also involve the heart, GI, and kidneys
• p ANCA

Small vessel vasculitis: Henoch-Schonlein purpura

• most common form of childhood systemic vasculitis
• follows URTIs
• TRIAD:
• palpable purpura on butt/legs
• arthralgia
• GI: abdom pain, melena, multiple lesions
• IgA immune complexes (cause nephropathy)

Sturge-Weber ds

• congenital vascular disorder that affects capillary-sized BVs
• Port-wine stain (on face), ipsilat leptomeningeal angiomatosis, seizures, early onset glaucoma

Strawberry hemangioma

• benign capillary hemangioma of infancy (first few weeks of life)
• grows rapidly and regresses spontaneously at 5-8 years of age

Cherry hemangioma

• benign capillary hemangioma of old people
• does NOT regress
• freq inc with age

Pyogenic granuloma

• polypoid capillary hemangioma that can ulcerate and bleed
• assoc with trauma and pregnancy

Cystic hygroma

• cavernous lymphangioma of the neck
• assoc with Turner Syndrome

Glomus Tumor

• benign, painful, red-blue tumor under fingernails
• modified smooth m cells of glomus body

Bacillary angiomatosis

• benign capillary skin papules found in AIDS pts
• caused by Bartonella henselae 
• freq mistaken for Kaposi's sarcoma

Angiosarcoma

• highly lethal malignancy of the liver
• associated with vinyl chloride, arsenic, and Thorotrast exposure

Lymphangiosarcoma

• Lymphatic malignancy 
• assoc with persistent lymphedema
• eg post-radical mastectomy

Kaposi's Sarcoma

• Endothelial malignancy of the skin
• assoc with HHV-8 and HIV
• frequently mistaken for bacillary angiomatosis

Cardio Pharm

Antihypertensives

• Essential HTN
• diuretics, ACE inhibitors (-pril), ARBs (-sartan), calcium channel blockers (-dipine, etc)
• CHF
• Diuretics, ACE inhibitors/ARBs, β-blockers (in compensated CHF), K sparing diuretics
• Diabetes
• ACE inhibitors (protective against nephropathy)/ARBs, calcium channel blockers, diuretics, β-blockers, α-blockers

Hydralazine

• vasodilates arterioles>veins; dec afterload
• inc cGMP-> smooth m relaxation
• used for severe HTN/CHF and as first-line in HTN in pregnancy (with methyldopa)
• freq coadmin with β-blocker to prevent reflex tach
• TOX: tachycard (C/I in angina/CAD), fluid retention, nausea, HA, angina, Lupus-like syndrome

Calcium channel blockers

Nifedipine, amlodipine, verapamil, diltiazem

• block L-type Ca channels of cardiac and smooth muscle (reduce contractility)
• Vascular smooth muscle: nifedipine>diltiazem>verapamil
• Cardiac smooth muscle: verapamil>diltiazem>nifedipine
• used for HTN, angina, arrhythmia (not nifedipine), Prinzmetal's angina, Raynaud's
• TOX: cardiac depression, AV block, edema, flushing, dizziness, constipation

What 3 drugs are used to treat malignant HTN?

• Nitroprusside
• short acting, inc cGMP via NO release
• can cause CN toxicity
• Fenoldopam
• Dopamine D1 agonist
• relaxes renal vascular smooth muscle
• Diazoxide
• K channel opener
• hyperpolarizes/relaxes vascular smooth muscle
• can cause hyperglycemia

Nitroglycerin, isosorbide dinitrate

• vasodilator, releases NO in smooth muscle
• dilates veins>>arteries
• decreases preload
• used for angina and pulmonary edema (also for boners)
• TOX: reflex tach, hypotension, flushing, HA
• "Monday Ds"
• industrial exposure
• you develop tolerance over work week and then lose it over weekend-> symptoms on Monday

What is the goal of antianginal tx?

• Reduce myocard O2 consumption
• Decrease one or more of the following:
• End-diastolic vol (nitrates)
• BP (nitrates/beta blockers)
• Contractility (beta blockers)
• HR (beta blockers)
• Ejection time (nitrates)
• Nifedipine is similar to Nitrates in effect
• verapamil is similar to beta blockers in effect
• Pindolol/acebutalol are partial agonist beta blockers and are contraindicated in angina

HMG-CoA reductase inhibitors

-statins

• decrease LDL (most of any), inc HDL, dec TRIG
• inhibits cholesterol precursor, mevalonate
• TOX: hepatotox, rhabdomyolysis

Niacin

• dec LDL, inc HDL, dec TRIG
• Inhibits lipolysis in adipocytes
• reduces hepatic VLDL secretion into circ
• TOX: red flushed face (reduced with aspirin), hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbates gout)

Bile acid resins

Cholestyramine, colestipol, colesvelam

• dec LDL, slight inc in HDL, slight inc in TRIG
• prevents reabsorption of bile-> liver must use cholesterol to make more
• patients hate taking this-> GI upset, dec absorption of fat sol vitamins, cholesterol gall stones

Ezetimibe

• prevents cholesterol reabsorption at small intestine brush border
• decreases LDL, no effect on HDL and TRIG

Fibrates

gemfibrozil, clofibrate, bezafibrate

• dec TRIG, dec LDL, inc HDL
• upregulates LPL-> inc TRIG clearance
• TOX: myositis, hepatotox, cholesterol gallstones

Digoxin

• cardiac glycoside
• half life= 40 hrs
• Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca antiport-> inc Ca
• positive inotropy
• stimulates vagus nerve
• used in CHF (inc contractility), a fib (slower conduction at AV node)
• TOX:
• cholinergic (N/V, diarrhea, blurry yellow vision)
• EKG (inc PR, dec QT, scooping, T wave inversion, arrhythmia, hyperkalemia
• worsened with renal failure, hypokalemia, quinidine
• ANTIDOTE: slowly normalize K, lidocaine, pacer, Mg

Nesiritide

• Recomb B-type natriuretic peptide
• causes inc cGMP and vasodilation
• used in acute decompensated heart failure
• TOX: hypotension

Class I Antiarrhythmics

Na channel blockers

• local anesthetics, slow/block conduction
• dec slope of phase 0 depolarization 
• inc threshold for firing in abnormal pacemaker cells
• state dependent (selectively depress tissue that is freaking out)
• Class IA
• quinidine, procainamide, disopryramide
• inc AP duration/refractory period/QT interval
• esp good for SVT and ventricular tach
• TOX: cinchonism- HA/tinnitus (quinidine), thrombocytopenia, Tosades de Pointes, reversible SLE-like syndrome (procainamide)

Class IA Antiarrhythmics

quinidine, procainamide, disopryramide

• inc AP duration/refractory period/QT interval
• esp good for SVT and ventricular tach
• TOX: cinchonism- HA/tinnitus (quinidine), thrombocytopenia, Tosades de Pointes, reversible SLE-like syndrome (procainamide)

Class IB Antiarrhythmics

Lidocaine, Mexiletine, Tocainide

• dec AP duration
• preferentially affect ischemic or depolarized Purkinje and ventricular tissue
• useful in acute ventricular arrhythmias (especially post-MI)
• also digitalis-induced arrhythmias
• TOX: local anesthetic, CNS stim/depress, CV depress

Class IC Antiarrhythmias

Flecainide, propafenone

• NO EFFECT on AP duration
• useful in V-tach that progresses to V-fib and intractable SVT
• LAST RESORT
• contraindicated post-MI
• TOX: proarrhythmic, significantly prolongs refractory period in AV node

Class II Antiarrhythmics

Beta blockers (-olol)

• propranolol, esmolol, metoprolol, atenolol, timolol
• suppress abnormal pacemakers by dec slope of phase 4 
• dec cAMP, dec Ca currents, inc PR interval
• used for V-tach, SVT, and slowing ventricular rate in A-fib/flutter
• TOX: impotence, exacerbation of asthma, CV (bradycard, AV block, CHF), CNS depression, may mask hypoglycemia
• metoprolol can cause dyslipidemia
• Tx overdose with glucagon

Class III Antiarrhythmics

K channel blockers

• K IS BAD= Ibutilide, Sotalol, Bretylium, Amiodarone, Dofetilide
• Inc AP duration, inc refractory period, inc QT
• used when others fail
• TOX:
• Sotalol: TdP, excessive beta block
• Ibutilide: TdP
• Bretylium: new arrhythmias, hypotension
• Amiodarone- pulmonary fibrosis, hepatotox, thyroid problems, corneal deposits, photodermatitis, neuro effects, constipation, CV effects
• alters lipid membrane

Class IV Antiarrhythmics

Ca channel blockers

• Verapamil, diltiazem
• dec conduction velocity, inc refractory period, inc PR interval
• prevention of nodal arrythmias (eg SVT)
• TOX: constipation, flushing, edema, CV effects

Adenosine

• inc K out of cells-> hyperpolarization
• drug of choice in SVT
• short acting (15 sec)
• TOX: flushing, hypotension, chest pain
• effects blocked by theophylline

Mg

• effective in TdP and digoxin toxicity