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115 Cards in this Set

  • Front
  • Back
What is the definition of coronary artery disease?
-myocardial ischemia secondary to increased myocardial work and/or decreased myocardial oxygen supply
-reversible myocardial ischemia the produces disturbances in myocardial function w/o causing myocardial necrosis
Name the 5 clinical syndromes of reversible ischemia. Which 3 are acute coronary syndromes?
-stable angina pectoris
-variant or Prinzmetal's angina
-Silent myocardial ischemia
-Syndrome X
-Unstable angina

ACS= unstable angina, non-STEMI and STEMI
What is the pathophysiology of stable angina pectoris?
large single- to multi- vessel atherosclerotic CAD, coronary artery vasospasm or both

->75% atherosclerotic reduction causes sx
What factors affect myocardial oxygen demand?
-basal O2 requirements
-ventricular wall stress
-HR
-contractility

O2 demand=HR x SBP
What factors affect myocardial oxygen supply?
Coronary blood flow
-Vascular resistance (metabolic control, compressive forces, autoregulation, neural factors, humoral factors)
-diastolic phase duration

O2 carrying capacity
What is the definition of stable angina pectoris?
discomfort in the chest or adjacent areas caused by myocardial ischemia

-anginal episodes quality, frequency, severity, duration of sx, time of day, etc have not changed over the past 2 months
How is stable angina subclassified?
-Fixed threshold
-Variable threshold
-Mixed angina
What is the clinical presentation of stable angina? (PQRST)
P: precipitating factors and palliative measures
-exercise, weather changes, large meal, stress/ fear/anger, coitus
-pain relieved with nitroglycerin
Q: quality of pain
-heavy weight on chest, SOB w/ feeling of constriction, burning/tightness/crushing feeling, gradual inc in intensity then gradual dec
R: region and radiation
-over sternum between epigastrium and pharynx, lower jaw, lower cervical or upper thoracic spine, L interscapular or suprascapular area
-radiates to L arm and shoulder, jaw, right arm (maybe)
S: severity of pain
T:timing and temporal pattern
-duration 0.5-30 min
Explain the New York Heart Association's Functional Classification of angina pectoris
-Class I: sx occur w/ unusual activity; minimal to no functional impairment

-Class II: sx occur w/ prolonged or slightly more than usual activity; mild functional impairment

-Class III: sx occur with usual ADL; moderate functional impairment

-Class IV: sx occur at rest; severe functional impairment
What is the definition of Variant (Prinzmetal's) angina?
syndrome of cardiac pain that occurs exclusively at rest

shows ECG ST-segment elevation
What causes variant (Prinzmetal's) angina?
-coronary artery spasm
-reduction in myocardial oxygen supply (inc HR, BP)
What are the clinical characteristics of variant (Prinzmetal's) angina?
-similar to stable angina, but pain occurs at rest and is more intense
-occurs more in early morning hours
What is the definition of silent myocardial ischemia?
-objective documentation of MI through exercise ECG testing that happens w/o angina
How is silent myocardial ischemia classified?
-Class I: pts w/ ischemia that is totally asymptomatic
-Class II: pts who have both symptomatic and unsymptomatic episodes
What causes silent MI and what it the lack of pain due to?
-Unknown: possibly secondary to dec myocardial oxygen supply or inc. myocardial oxygen demand or both

-lack of pain: defects in pain perception, altered physiologic response to ischemia, or less ischemia than symptomatic episodes
What is the definition of syndrome X?
-microvascular angina
-occurence of effort angina and exercise-induced ECG changes despite no coronary artery stenosis or coronary artery spasm
-angina with ST-segment depression
How is ischemic heart disease diagnosed?
-ECG: ST segment depression, T wave inversion, ST segment elevation in Prinzmetal's
-Exercise tolerance testing:BP and HR response
-Exercise Electrocardiography: determine risk stratification and assess need for surgical/medical treatment; determine LVEF
-Cardiac imaging: stress testing w/ thallium 201 myocardial perfusion screening; radionuclide angiocardiography (Technetium-99m), electron beam computerized tomography)
-Cardiac catheterization and coronary angiography: only definitive dx
What are the goals of therapy for stable angina?
-minimize the frequency and severity of angina and increase functional capacity
-reduce cardiovascular morbidity and mortality
What are the guidelines for management of stable angina (ABCDE)?
A: aspirin and antianginals
B: Beta Blocker and Blood Pressure
C: Cholesterol and Cigarettes
D: Diet and Diabetes
E: Education and Exercise
What effect do nitrates, BB, nifedipine, verapamil, and diltiazem have on HR, contractility, SBP, and LV volume?
HR
-inc.: nitrates, nifedipine
-dec: BB, verapamil, diltiazem (to lesser extent)

contractility
-dec: BB, verapamil, nifedipine/diltiazem (to lesser extent)

SBP
-dec: all

LV volume:
-inc: BB
-Dec: nitrates, CCB (to lesser extent)
What is the mechanism of action of nitrates?
-vasodilation
-enhance collateral blood flow
-reverse coronary artery spasm
-antiplatelet activity?
Explain nitrate tolerance.
-dec response in presence of continuously or frequently admin nitrates
-due to depletion of sulfhydryl donors impairing the intracellular formation of nitric oxide and S-nitrosothiols, resulting in dec. formation of cGMP

-Require nitrate free period of at least 10-12 hours
What are the adverse effects of nitrates?
-HA (throbbing or pulsating)- take OTC analgesics
-hypotension, dizziness, lightheadedness, facial flushing (not w/ SL)
-reflex tachycardia
When is nitrate therapy contraindicated?
-When phosphodiesterase inhibitors have been used 24 hours (viagra) and 36-48 hours (cialis) prior
-Causes fatal hypertensive events (significant BP dec)
What are the monitoring parameters of nitrates?
-BP
-HR
-# chest pain episodes
-# SL tablets needed
What is the mechanism of action of beta blockers?
-competitively inhibit binding of catecholamines to B adrenergic receptor
-dec HR
-enhance diastolic filling
-dec. contractility: (-) iontrope
-dec. AV nodal conductance: (-) dronotrope
What factors do you look at to determine which beta blocker to use?
-cardioselectivity: atenolol and metoprolol
-intrinsic sympathomimetic activity: do not use in post-MI pt
-lipophilicity: high-propanolol low-atenolol

Know carvedilol, metoprolol, metoprolol XL, and atenolol
What are the adverse effects of beta blockers?
-cardiac: sinus bradycardia, sinus arrest, AV block, reduced LVEF
-bronchoconstriction
-fatigue, depression
-nightmares
-sexual dysfunction
-intensification of insulin-induced hypoglycemia and peripheral vascular complications

-Withdrawal syndrome: dec. dose gradually over 1-2 week period
What are the monitoring parameters of beta blockers?
-BP
-HR goal 50-60bpm (<100bpm for exercise)
What is the mechanism of action of CCBs?
-block the transmembrane flux of calcium into cardiac and vascular smooth muscle-> reduces the excitation-contraction-coupling mechanism responsible for myocardial and smooth muscle contraction
-DHPs: similar effects to nitrates (primarily vascular effects)
-non-DHPs: similar effects to beta blockers and some vasodilator effects
What are the adverse effects of CCBs?
DHPs: hypotension, HA, ankle edema
-nifedipine, nicardipine, isradipine: reflex tachycardia, flushing, dizziness

non-DHPs: bradycardia, AV nodal conduction disturbances, HF, hypotension, HA, dizziness, edema
-verapamil: constipation
What are the monitoring parameters of CCBs?
-HR <60bpm at rest + <100bpm exercise
-BP <140/<90
-ankle edema in DHPs
What is the mechanism of action, indication, ADR, and drug interactions of ranolazine (Ranexa)?
MOA: unknown; inh. late inward Na+ channel
Indication: chronic angina w/ inadequate response to other antianginals
ADR: QT prolongation, constipation, HA, dizziness, nausea
DI: substrate of CYP 3A4, 2D6, and p-gp
What are the therapeutic goals and treatment strategies for CV risk reduction?
Dyslipidemia: LDL<70-100mg/dl
-statins, plant sterols/stanols, Omega 3 FA

Hypertension: <140/<90 or DM <130/<80
-BB and ACEIs

Diabetes Mellitus: HgB A1C < 7%

Smoking cessation

Diet: <7% saturated fat, <200mg/dl cholesterol

Physical activity: 30-60 min 3-4 days/week
When should ACEI therapy be added to management of chronic stable angina pectoris?
Consider in pts w/ LVEF<40%, HTN, DM, or CKD
-reduces CV events in high risk CAD pts
Ramipril 10mg/day studied
When should anti-platelet therapy be used in pts with stable angina?
Reduces CV events by inh. plt aggregation

Primary prevention
-ASA if pts >50yo with additional risk factor (HTN, DM, FH, etc)

Secondary prevention
-absence of coronary artery stents: ASA 75-162 mg/day or clopidogrel 75mg/day if CI to ASA indefinitely
-presence of drug eluding stent: ASA 75-162mg/day + clopidogrel (min 15 months)
-presence of bare metal stent: ASA 75-162mg/day + clopidogrel (min 12-15 months)
What are the adverse effects of antiplatelet therapy?
-ASA: bleeding
-ticlopidine, clopidogrel, prasugrel: N/D, dyspepsia, anorexia, rash, pruritus, uticaria, ecchymoses, bleeding, NEUTROPENIA, aplastic anemia, thrombocytopenia, cholestasis, hepatitis
What are the monitoring parameters of antiplatelet therapy?
-CBC
-s/sx of bleeding: bruising, occult blood
How should stable angina be treated acutely?
SL nitroglycerin tablets (0.15-0.6mg) or spray (0.4mg/spray)
Which chronic therapy is best for treating stable angina?
-BB reduce CV events- use if no CI (vasospastic angina, conduction disturbances; monitor in pts w/ lung disease, DM, peripheral vascular disease, and depression)

-CCB useful in pts w/ lung disease, DM, peripheral vascular disease
What combinations of antianginals should be used to treat stable angina?
-nitrates and BB
-non-DHPs and nitrates
-DHPs and BB
-triple therapy for severe angina/CAD that doesn't allow for surgical correction
What antianginals are used to treat variant (Prinzmetal's) angina?
-nitrates
-CCBs
-combo nitrate + CCBs

NO BBs!
How should one take SL nitroglycerin tablets?
-Sit down (dec. BP- don't want to faint)
-Tablet under tongue
-in 5 min, if pain not gone, call 911
-take 2nd tablet
-in 5 min if pain not gone, take 3rd tablet
What is the definition of unstable angina?
-Worsening angina or angina lasting >20min
-not relieved or only partially relieved by SL nitroglycerin
What is the definition of acute myocardial infarction?
necrosis of cardiac muscle caused by prolonged dec. in oxygen delivery to the affected muscle
-thrombus formed at site of plaque- totally occludes the artery
What causes acute coronary syndromes? (pathophysiology)
-atherosclerotic CAD- 85%
-severe coronary vasospasm- 15%
(drug-induced: cocaine, triptans, TZDs, amphetamines, oral contraceptives, estrogen-containing products)
cocaine causes vasospasm and atherosclerosis with long-term use

-Tissue death moves like a wave: in 30min goes through the ventricular wall (transmural MI)
-ventricular wall remodeling: aldosterone promotes growth of scar: use BB, ACEI/ARBs, aldosterone inh.
What determines short and long term morbidity and mortality?
-LV function
-age>70
-HTN
-Afib
-infarct size, anterior location
-previous MI
-female sex
-infarct artery patency, cardiac marker conc.
What is the clinical presentation of acute coronary syndromes?
-prolonged (>30min for MI; <30min for unstable angina) substernal chest discomfort
-radiates to neck, throat, jaw, shoulders, arms
-N/V, diaphoresis, SOB, sense of impending doom
What type of patient do silent MIs typically happen to?
-women
-older men
-diabetics
What will a physical examination show on a pt with acute coronary syndrome?
-s/sx of LV or RV dysfunction
-variable HR, low grade fever, inc. RR, SBP 90-100
-abnormal heart sounds: S3 and S4 (LV dysfunction)
-leukocytosis
-signs of severe hyperlipidemia: corneal arcus, xanthelasma, tendon xanthomas
What changes will you see in a 12-lead ECG of a pt with acute coronary syndrome?
-ST depression
-ST elevation: STEMI
-Q wave changes
-T wave changes
What biochemical cardiac markers will you look at for a pt dx with acute coronary syndrome?
-cardiac troponin I (cTnI)/ cardiac troponin (cTnT): elevated (>0.4ng/ml)- higher the conc., worse the MI
-creatinine kinase (CK-MB): elevated

-takes 24 hours to get lab results back
What is the initial treatment of all ACS in the ER department?
OMAN
-Oxygenation: mask or nasal cannula (goal O2 sat>90%)
-Morphine sulfate: MS 2-4mg IV every 5-20min in increments of 2-8 mg for pain relief and pt comfort
-Aspirin 162-325mg chewed and swallowed (3 baby or 1 normal)
-Nitrates: SL nitroglycerin every 5 min; evaluate for IV nitrates (do not use if pt took PDE inh 24-36 hrs prior)
What are the goals of therapy for acute coronary syndromes?
-rapid and complete coronary artery reperfusion and minimize infarct size: thrombolytics
-relief of ischemic chest discomfort: nitrates
-prevention of reinfarction:BB, ACEI
-prevention of ventricular remodeling (and reduced systolic dysfunction and LVEF): BB, ACEI/ARBs, aldosterone inh.
-identification and tx of hemodynamically significant dysarhythmias: lidocaine, amiodarone, cardiofibrillator
What medications will be given within the first 24 hours?
Nitrates: IV NTG 5-10mcg/min titrated to 75-100 (max 200) until sx relief or limiting SE
-CI: SBP <90mmHg or >30mmHg from baseline, severe bradycardia (<50bpm) or tachycardia (>100bpm) or suspected RV infarction

Analgesia: MS 2-4 mg IV every 5-30 min in increments of 2-8mg or meperidine
-D/C NSAIDs before STEMI and during hospitalization

Anxiolytics

Stool softeners: 100 mg docusate sodium daily

ASA: 162-325 mg chewed and swallowed; 75-162mg daily if no stent;162-325 mg daily x 30days if bare metal stent, 3-6months for drug eluding stent, then 75-162 mg daily indefinitely

Clopidogrel/ Prasugrel:
Plavix 300mg loading (600 if PCI) then 75mg/day for 14days-1 yr (12-15 months if PCI)
-do not give loading dose in pts >75yo
-D/C 5 days prior to CABG
-Use indef. if ASA allergy
Prasugrel 60mg load followed by 10mg (5mg if wt<60kg) x 12-15 months if primary PCI
-D/C 7 days prior to CABG
Explain the interaction between PPIs and plavix. Does this happen with PPIs and prasugrel?
-Clopidogrel req. conversion to active metabolite mediated by CYP2C19
-Prasugrel has multiple pathways
-Pts taking PPIs or if poor CYP2C19 metabolizers will have reduced formation of the active metabolite and will have higher CV events
What is the key treatment for patients with ACS?
Open artery through reperfusion
-PCI (more effective)
-fibrinolysis
What is the door to procedure time for PCI and fibrinolysis?
-Primary PCI door to balloon time: 90min
-Fibrinolytic door to needle time: 30min
What criteria is used to determine if reperfusion therapy is necessary?
-chest discomfort consistent with MI
-ST-segment elevation
What are the direct fibrinolytic medications? What are the indirect fibrinolytic medications
Direct
-rt-PA
-rscu-PA
-UK

Indirect
-Streptokinase
-APSAC
What is the difference between a hemostatic plug and thrombus?
Composition
-Hemostatic plug has red cells in it as well as plts and fibrin

Both affected by fibrinolytics
What is the dosing of streptokinase in ACS?
1.5million units in 50ml NS or D5W over 60 min
What is the dosing of t-PA, rt-PA (alteplase, Activase)
-15mg bolus
-0.75mg/kg (max 50mg) over 30 min
-0.5mg/kg (max 35mg) over 60 min
What is the dosing of Reteplase (Retavase)
10units IV, repeat dose in 30 min
What are the ADR of streptokinase?
-antigenicity and allergic reactions
-hypotension
-hemostatic defect
-intracerebral bleeds
What is the dosing of Tenecteplase (TNKase) in ACS?
< or = 60kg: 30mgIV
60-69.9kg: 35mg IV
70-79.9kg: 40mg IV
80-89.9kg: 45mg IV
> or = 90kg: 50mg IV
What are the ADR of direct fibrinolytics?
-hemostatic defect
-intracerebral bleeds
What are absolute CI of fibrinolytic therapy in ACS?
-prior Intracranial hemorrhage
-known structural cerebral vascular lesion or malignant intracranial neoplasm
-ischemic stroke within 3 months
-suspected aortic dissection
-severe active bleeding
-significant closed head or facial trauma within 3 months prior
What are some relative CI of fibrinolytic therapy in ACS?
-poorly controlled HTN (SBP>180mmHg; DBP>110mmHg)
-traumatic or prolonged (10+min) CPR or major surgery in last 3 weeks
-internal bleeding in last 2-4 weeks
-pregnancy
-active peptic ulcer
-current use of anticoagulants
What are the monitoring parameters of thrombolytic use?
-prompt relief of chest pain
-prompt resolution of ECG findings
-reperfusion arrhythmias
-early CK peak
-maintenance or restoration of hemodynamic instability
-s/sx of bleeding: bloody stools, bruising
-baseline CBC, plt count, INR/aPTT, daily CBC
-mental status changes
What is rescue PCI?
-treat in catheter lab, because no changes; already given full thrombolytic

-inc. bleeding risk
What is facilitated PCI?
-give 1/2 dose of thrombolytic agent, then 1 hour later taken to cath lab
-done at academic medical centers

-dissolve some of the clot before going to cath lab
What is the rationale for using BB in ACS?
-limit myocardial damage and/or mortality (dec. myocardial demand)
-reduce risk of reinfarction and/or mortality (reduce Vfib threshold)

-Use within first 12-24 hours
What doses of BB are used in ACS?
-Oral dosing is preferred

Oral (early: lower doses more often)
-Metoprolol: 25-50mg every 6 hours
-Propanolol: 40-80mg every 6-8 hours
-Atenolol: 50-100mg daily
-Carvedilol: 25-50mg BID
What are the monitoring parameters of BB for pts with ACS? How often should these be monitored for oral admin? for IV admin?
-BP, HR, 12 lead ECG, s/sx of heart failure

-Oral: every shift during hospitalization
-IV: every 5 minutes
How long should ACS pts be on anticoagulation?
-48 hrs to 8 days or end of hospitalization
-May or may not stop if PCI

-This is used to prevent extention of clot
What doses of anticoagulants should be used in ACS pts taking fibrinolytics?
-Take simultaneously with fibrinolytics

Heparin
-60units IV/kg bolus (max 4000units)
-12 units/kg/hr (max 1000) infusion

UFH: use infusion if SK (3 hours past)

LMWH:
-enoxaparin 30mg IV bolus + 1mg/kg/hr SC Q12h until discharge
What anticoagulants should be used in pts not receiving thrombolytics or primary PCI?
-prophylaxis therapy
-enoxaparin
What are the three GP IIb/IIIa inhibitors? What are their dosages?
-Abciximab, eptifibitide, tirofiban
-ONLY for PCI

-Abciximab: 0.25mg/kg bolus + 0.125mg/kg/min (max 10mg) up til 12 hours post-PCI

-eptifibitide: 180mcg/kg IV bolus + 2mcg/kg/min infusion; repeat 180mcg/kg bolus 10 min later; continue infusion 12-18hrs post-PCI

-tirofiban:25mcg/kg IV bolus + 0.1mcg/kg/min infusion continued until 18 hrs post-PCI
When should an ACEi be given to a patient with ACS?
-within the first 24 hrs, but after PCI, fibrinolytics, etc

-Use in pts w/ LVEF<0.4, DM, or CKD
When should an aldosterone antagonist be given to a pt with ACS?
-in addition to ACEi or ARB in pts with LVEF<40% with HF sx or DM

-use eplerenone 25mg initial, then 50mg daily
-spironolactone 12.5mg initial, then 25-50mg daily
When should magnesium be given to a pt with ACS?
-ONLY when LOW magnesium
When should CCBs be used in pts with ACS?
-pts with ischemia who cannot tolerate BB

-only use verapamil or diltiazem
What are the goals of therapy for unstable angina/ non-ST segment elevation MI?
-prevent MI and death by inh. extension of thrombus
-reverse ischemia and relieve chest pain by inc. myocardial O2 supply, dec. myocardial O2 demand or both
-differentiate between UA from non-STEMI
If you don't use PCI in a pt with UA or NSTEMI, how is clopidogrel used
-same dose as STEMI, but continue clopidogrel for at least 9 months
What are the CI of GP IIb/IIIa therapy?
-active internal bleeding
-hx of hemorrhagic stroke
-intracranial neoplasm
-acute pericarditis
-uncontrolled HTN
-THROMBOCYTOPENIA
What are the monitoring parameters of GPIIa/IIIb therapy?
-s/sx of bleeding
-baseline: CBC, plt count, SCr
-daily: CBC, plt count 2-4 hrs post initiation and daily
What are the MP for anticoagulant therapy in UA/NSTEMI?
-Hgb/ Hct daily for 3 days
-plts daily
-s/sx of bleeding
What is the difference in dosing of enoxaparin for STEMI vs. NSTEMI
-give supplemental dose of enoxaparin 0.3mg/kg IV bolus in UA/NSTEMI pts that undergo PCI
How are thrombolytics used in UA/NSTEMI?

How are ACEi/ARBs/ aldosterone antag used in these pts?
-not used!

-ACEi/ ARBs are used the same
-aldosterone antag are not used
Describe the anatomical structure and function of the cardiac conduction system.
•Sinus Node= pacemaker of heart (60-100bpm); found in the high right atrium
•Atrioventricular (AV) node (40-60bpm); found in lower right atrium
•Ventricular tissue (30-40bpm)
oBundles: left divides because left ventricle is larger than the right ventricle (arterial pressure> venous pressure)

•Functions to electrically depolarize cells in waves to generate contractions
Explain PQRST.
•P=atrial depolarization
•PR interval= time for impulse to travel through AV node
•Q=phase 0
•QRS= depolarization time
o Na+ blocker will inc QRS
•T= phase 3 repolarization
•QT= overall ventricular repolarization
o Use this calculation to determine if the relative refractory period is prolonged
Explain what is happening in the different phases of the cardiac action potential. (include ions)
•Phase 0: Depolarization- mediated by movement of Na+ ions into myocytes through fast Na+ channels
•Phase 1: Repolarization-mediated by movement of K+ ions out of myocytes through K+ channels
•Phase 2: Repolarization (plateau)- a balance of movement of K+ ions out of myocytes through K+ channels and movement of Na+ and Ca2+ ions into myocytes through slow Na+ and slow Ca2+ channels
•Phase 3: Repolarization-movement of K+ ions out of myocytes greatly exceeds movement of Na+ and Ca2+ ions into myocytes
Explain the relationship between the cardiac action potential and the electrocardiogram (ECG).
•Q= phase 0
•S=phase 2 (start of plateau)
•T hump=extent of phase 3
What drugs slow the PR interval?

What does this mean?
-non DHP CCBs
-amiodarone
-digoxin
-BB

PR>0.2 sec = primary AV block
What drugs slow the QRS?
-flecainide
-propafenone
-Na+ channel blockers
What drugs slow the QT interval?

What does this mean?
-K+ channel blockers

-QT>0.5 sec = Torsades de Pointe
What is the calculation of a QTc?
QTc= QT / (RR)^1/2
What are the normals values of : PR interval, QRS duration, QT interval, and QTc interval?
PR interval: 0.12-0.2 sec
QRS duration: 0.08-0.12 sec
QT interval: 0.38-0.46 sec
QTc interval: 0.36-0.44 sec
What are the three mechanisms of cardiac arrhythmias?
Abnormal impulse formation
-spontaneous impulse generation in normally latent pacemaker tissue (SA node, AV node, His/Purkinje system, specialized atrial fibers)
-influenced by cholinergic and sympathetic stimulation

Abnormal impulse conduction-Reentry
-two pathways for impulse conduction with an area of unidirectional block; one pathway has slowed impulse conduction

Both changes in automaticity rate with depolarizations happening where they should not be and reentry
What are the 4 classes of the Vaughan Williams classification system?
Some Block Potassium Channels

Class I: Sodium channel blockers
Class II: Beta Blockers
Class III: Potassium channel blockers
Class IV: Calcium channel blockers
Which drugs change automaticity? Which drugs change repolarization? Which drugs change conduction velocity?
Automaticity slowing
-Class I drugs: Procainamide, Lidocaine, Flecainide, Propafenone

Repolarization/ inc. refractory period
-Class III drugs: amiodarone, dofetilide, dronedarone, ibutilide, sotalol
-Class IA: procainamide

Conduction velocity dec.
-Class I drugs: (Flecainide, propafenone>procainamide>lidocaine)
What are examples of supraventricular arrhythmias?
-sinus bradycardia
-AV nodal block
-sinus tachycardia
-atrial fibrillation
-paroxysmal supraventricular tachycardia
What are examples of ventricular arrythmias?
-ventricular premature depolarizations
-ventricular tachycardia
-ventricular fibrillation
Explain sinus bradycardia (features, mechanism, etiologies/ risk factors, sx, and treatment)
Features: HR < 60
Mechanism: Decreased automaticity of SA node
Etiology:
-MI/ischemia
-Abnormal sympathetic/parasympathetic tone
-Hyperkalemia, hypermagnesemia
-Drugs: digoxin, B-blockers, diltiazem, verapamil, amiodarone, dronedarone
Symptoms: Hypotension, dizziness, fainting
Treatment:
-Atropine (AE: tachycardia, urinary retention, blurred vision, dry mouth, mydriasis)
-Pacemaker
Explain atrial fibrillation (features, mechanism, etiologies/ risk factors, sx, and treatment)
Features:no full atrial contractions
HR 120-180 with irregularly irregular rhythm and absent P waves
Mechanism: Abnormal atrial automaticity (via pulmonary vein), re-entry via multiple simultaneous circuits
Mortality: Stroke and development of HF
Etiology: Hypertension, CAD, HF
Valvular heart disease, rheumatic heart disease, hyperthyroidism, post-surgery
-Idiopathic
-Drugs: sympathomimetics, theophylline, alcohol
Symptoms: Palpitations, dizziness, lightheadedness, SOB, angina, hypotension, exacerbations of HF
Treatment:
-based on type of Afib
-goal: HR < 100bpm or reduction by 20% with sx relief
-if hemodynamically unstable (SBP<90, HR>150bpm, loss of consciousness)-> DCC immediately
What is the treatment plan for pts with 1st detected episode or persistent Afib?
Ventricular rate control
-no HF: CCB or BB
-with HF: digoxin or amiodarone

Stroke prevention
-1st episode: heparin
-persistent: warfarin and/or aspirin

Conversion to sinus rhythm
-<48 hrs, DCC
->48hrs, warfarin x 3 weeks then DCC or heparin IV and TEE to r/o atrial clot, then DCC
if DCC unsucessful
-no HF: flecainide, propafenone, ibutilide
-with HF: amiodarone, dofetilide, ibutilide
What is the treatment plan for pts with paroxysmal or permanent Afib?
ventricular rate control
-no HF: CCB or BB, then add digoxin, then only amiodarone
-with HF: BB, BB + digoxin, then only amiodarone

stroke prevention
-warfarin or aspirin

maintenance of sinus rhythm
-treat disease-induced
-with CAD and/or HF: amiodarone, dofetilide, sotalol
-no CAD, no HF: propafenone or flecainide, dofetilide, dronedarone, sotalol
What is the CHADS2 score?
shows risk of bleeding
Chronic heart failure 1 pt
Hypertension 1 pt
Age> or = 75 1 pt
Diabetes mellitus 1 pt
Stroke or TIA hx 2 pts
Explain paroxysmal supraventricular tachycardia (PSVT).
•Features: HR 120-250
-Regular rhythm
-Narrow QRS complex
-Spontaneous initiation and termination
•Mechanism: Re-entry within AV node (single re-entrant circuit)
Other minor mechanisms
•Etiology:
-Heart disease
-Fever, infection
-Electrolyte abnormalities
-Idiopathic
•Symptoms:Palpitations, dizziness, weakness, syncope, angina exacerbation, HF exacerbation
Treatment
oTerminate PSVT, restore sinus rhythm
-Vagal maneuvers (non-PCOL): carotid sinus massage, coughing, Valsalva maneuver
-Adenosine
-Verapamil
-Diltiazem
-Digoxin
-Esmelol
-Propranolol
-Metoprolol
-Amiodarone
oPrevent recurrence
-AV nodal radiofrequency catheter ablation (non-PCOL)
What is the algorithm for termination of hemodynamically stable PSVT?
1) vagal maneuvers
2) adenosine (6,12,12)
no-HF
-diltiazem or verapamil, then BB, digoxin
with HF
-digoxin, then amiodarone
Explain ventricular premature depolarizations (VPD)/ ventricular premature contractions (VPC).
•Features: Ectopic beats from ventricular muscle fibers
-Wide QRS complexes
-Variable frequency (that increases with age)
•Types
oSimple: Single beats
oComplex: Pairs/couplets
-Every second beat/ bigeminy
-Every third beat/ trigeminy
-Every fourth beat/ quadrigeminy
•Mechanism: increased automaticity of ventricular muscle fibers
•Etiology: CAD, MI
-Can occur in normal individuals
-Drugs: sympathomimetics, antiarrhythmics, TCAs
-Anemia
-Hypoxia
-Cardiac surgery
•Symptoms: Often asymptomatic
Palpitations, syncope
•Treatment:Asymptomatic VPDs SHOULD NOT BE TREATED
-Symptomatic VPDs: PO B-blockers, PO amiodarone (2nd line)
Explain ventricular tachycardia.
•Features: HR 100-250
-Regular rhythm
-Wide QRS complexes
-Series of consecutive VPDs
•Types
oNon-sustained: 3 or more consecutive VPDs, lasting < 30 seconds, terminating spontaneously
o Sustained: VT lasting longer than 30 seconds
•Mechanism: Increased automaticity in ventricular tissue
Re-entry within ventricles
•Etiology: CAD, MI, HF (major), Hypokalemia, hypomagnesemia
•Symptoms: May be asymptomatic (non-sustained)
Hypotension, palpitations, syncope
•Implication: May progress to ventricular fibrillation and then death; sudden cardiac death
Treatment
oTerminate VT/restore sinus rhythm
-Lidocaine
-Procainamide
-Amiodarone
oPrevent recurrence of VT
-ICD
-Amiodarone
-Sotalol
oReduce risk of sudden cardiac death: ICD
What is the algorithm for termination of hemodynamically stable VT?

What is used for prevention of recurrence and sudden cardiac death?
With MI
-lidocaine
-then procainamide
-then amiodarone

No MI
-procainamide
-then amiodarone

Prevention:
-ICD
-amiodarone
-sotalol
Explain ventricular fibrillation.
•Features: Irregular, disorganized ventricular rhythm
-No recognizable QRS complexes
•Etiology: MI, HF, cardiomyopathy, CAD
•Symptoms:Syndrome of sudden cardiac death (patient collapses, no HR, no BP)
•Treatment: Defibrillation!
-Drugs to facilitate:epinephrine or Vasopressin, then Amiodarone, then Lidocaine then sodium bicarb