6. Labs: troponin q8-12h x 2 or alternatively CK&MB q8h x 3, basic labs including PT/PTT, cholesterol panel if no previous workup, and HgA₁C if diabetic.

7. Enteric coated ASA 325 mg PO QD. Have patient chew and swallow first dose for rapid absorption.

8. NTP q6h to chest wall according to sliding scale; after 24 hours, wipe off q night 12am-6am. (See Sliding Scales: Nitropaste).

9. Beta–blocker: use if there are no contraindications as numerous trials have shown a mortality benefit. Typical starting dose is metoprolol 25 mg PO BID or atenolol 25 mg PO QD. Alternatively, a trial of metoprolol 5 mg IV q 5 min x 3 can be given initially. If this IV dose is tolerated you can usually start 25 mg PO bid, but be sure to write hold parameters. Goal HR 50-60’s.

10. Colace 250 mg PO bid – hold for loose stools

11. Chest pain protocol: VS, ECG, NTG 0.4 mg SL q5 minutes x 3, call MD. When seeing patient for persistent chest pain, can give morphine in 1–2 mg boluses. If ever in doubt, call for back-up.

ACUTE CORONARY SYNDROME: ST-SEGMENT ELEVATION OR NEW LBBB

1. Diagnostic criteria:

· ST-segment elevation ³ 1 mm in 2 or more contiguous leads (remember RV: use V₄R and V₅R).

· New or presumably new LBBB and history suggesting acute MI.

2. Admit to CCU:

· Primary Angioplasty vs. Thrombolysis

- Early treatment can limit infarct size, preserve LV function, and reduce mortality. Best performed within first 12 hours after onset of pain.

- Primary Angioplasty: preferable to thrombolysis when available (GUSTO IIb), especially if thrombolysis contraindicated, cardiogenic shock, anterior MI, or s/p CABG. Aim for balloon dilatation within 90 ± 30 minutes of diagnosis of acute MI.

- Fibrinolysis: use when percutaneous coronary intervention (PCI) is unavailable. Contraindications: see Cardiology: Contraindications to anticoagulation

° t-PA accelerated regimen: 15 mg IV bolus, then 0.75 mg/kg (maximum 50 mg) over 30 minutes, then 0.5 mg/kg (maximum 35 mg) over 60 minutes.

° Most serious complication is intracerebral hemorrhage (0.5%). If suspect bleed discontinue all anticoagulation, get a head CT, and call neurosurgery.

° Consider PCI if reperfusion not evident in 90 minutes or cardiogenic shock.

· Aspirin: all patients should chew 325 mg aspirin in the ED.

· Clopidogrel: 300 mg PO, in anticipation of stent placement. Continue at 75 mg PO QD at least 30 days post-stent. Contraindications: high risk for GI bleed, known allergy, or low platelets.

· Heparin: 5000 U IV bolus (no continuous infusion).

· Nitroglycerin: gtt (infusion) for persistent chest pain or pulmonary edema. Start at 10 mcg/min and titrate to pain, not to exceed 200 mcg/min. Watch for hypotension! After 24 hours, give 6h holiday to prevent tolerance and consider switch to PO nitrates or nitropaste.

· Beta-blockers: Metoprolol 5 mg IV q5 min x 3 in ED, then switch to PO dosing. Target HR < 60. Contraindications: AV block, SBP < 100, moderate or severe CHF, active wheezing.

· Consider IV amiodarone for patients with resuscitated sudden cardiac death. 150 mg IV over 10 minutes followed by 1 mg/min drip x 6 hours, then 0.5 mg/min x 18 hours. Further dosing dictated by clinical course.

· ACE-inhibitor: Start within first 24 hours with Captopril 6.25 mg PO TID and increase dose as BP allows. Write hold parameters for BP.

· Morphine: can be used for pain (1-2 mg IV boluses PRN).

· If ST-elevation is in inferior distribution (II, III, aVF) rule out right ventricular MI. Obtain right-sided leads and look for ST elevation in V₄R. The RV is preload dependent, and extra IV fluids may be required to maintain cardiac output. Avoid nitrates in RV infarct.

· Complications include cardiogenic shock, LV/RV failure, arrhythmias (VT, VF, various AV blocks within 24 hours), infarct extension (in 48 hours), mural thrombus, pericarditis (early and late), and other mechanical complications such as papillary muscle rupture, ventricular rupture, ventricular aneurysm and VSD in 4-7 days.

A clinical trial comparing primary coronary angioplasty with tissue plasminogen activator for acute myocardial infarction. The (GUSTO IIb) Angioplasty Substudy Investigators. N Engl J Med. 1997 Jun 5;336(23):1621-8.

ACUTE CORONARY SYNDROME: UNSTABLE ANGINA / NSTEMI

1. Definitions:

· Unstable angina: negative enzymes.

· Non-Q wave MI: non-ST elevation or ST depression, positive enzymes.

· Myocardial necrosis: positive enzymes or new wall motion abnormality on echo but no coronary disease (seen in sepsis).

2. Categorize according to overall clinical risk: all patients are assumed to have a clinically evident acute coronary syndrome.

· Critically unstable: persistent severe symptoms, hemodynamic compromise, or cardiogenic shock.

· High risk: clinically evident acute coronary syndrome, and > 1 of the following high risk features:

- Ongoing ischemic symptoms despite initial medical therapy.

- High risk ECG finding: ST depression > 1 mm in two contiguous leads, minimal ST elevation (< 1 mm in two contiguous leads) lasting less than 20 minutes, or deep T-wave inversions in contiguous leads of > 3 mm or more in > 3 limb leads or > 4 precordial leads, excluding V₁.

- Elevation of troponin.

- TIMI Risk Score (see below) > 2.

· Low risk: patients with “real” unstable angina but don’t meet the criteria above.

3. TIMI Risk Score: assign one (1) point to each of the following, if present:

· Age > 65.

· > 3 cardiac risk factors.

· Prior coronary stenosis (as determined by angiography) > 50%.

· ST segment depression.

· > 2 anginal episodes in last 24 hours.

· Received aspirin within the last 7 days.

· Elevated troponin I.

4. Management – critically unstable patients: these patients should be referred urgently for cardiac catheterization. If catheterization is unavailable and the patient does not meet criteria for thrombolysis, the patient should be transferred immediately to a facility with catheterization facilities.

· Intra-aortic balloon pump (IABP) may be an option as temporary bridge for cardiogenic shock or refractory/recurrent ACS. Placement performed by cardiology only. Patient must be on heparin. Complications include infection, hemolysis, rupture (manifests as ischemic lower extremity).

5. Management – high risk patients:

· Admit to telemetry, step-down unit, or CCU depending on clinical severity; rule out MI, as above.

· Aspirin: 325 mg chewed in ED.

· Clopidogrel: 300 mg PO load then 75 mg QD for > 9 months. Don’t give at all (or discontinue 5-7 days prior to surgery) if acute coronary bypass a possibility. Contraindications: high risk for GI bleed, known allergy, or low platelets.

· Enoxaparin: 1 mg/kg SQ q12h. Avoid if Cr > 2.5 mg/dl, CrCl < 30 ml/min, or weight > 150 kg. If unable to give enoxaparin, give unfractionated heparin infusion. See Sliding scales: heparin.

5. Management – high risk patients (continued):

· Eptifibatide: (Integrilin) 180 mcg/kg IV single bolus over 1-2 minutes, followed by drip at 2 mcg/kg/min if Cr < 2.0 mg/dl, 1 mcg/kg/min if Cr 2.0-4.0 mg/dl. Maximum weight for dosing is 120 kg. If Cr > 4.0 mg/dl, give abciximab (Reopro®). Contraindications: see Cardiology: Contraindications to anticoagulation. First dose must be given early (in ED or at presentation) for patient to derive a benefit. Continue infusion for 18 hours post-PCI. (12 hours if using Reopro®).

· Beta-blockers: Metoprolol 5 mg IV q5 min x 3 in ED, then switch to PO dosing. Target HR < 60. Contraindications: AV block, SBP < 100, moderate or severe CHF, active wheezing.

· ACE-inhibitor: Start within first 24 hours with Captopril 6.25 mg PO TID and increase dose as BP allows. Write hold parameters for BP.

· Morphine: can be used for pain (1-2 mg IV boluses PRN).

· Nitrates: either IV NTG or Nitropaste to keep chest pain free.

· In general, these patients should be managed with an early interventional approach.

6. Management – low risk patients:

· Admit to telemetry or step-down unit depending on clinical severity; rule out MI, as above.

· Aspirin: 325 mg chewed in ED.

· Enoxaparin: 1 mg/kg SQ q12h. Avoid if Cr > 2.5 mg/dl, CrCl < 30 ml/min, or weight > 150 kg. If unable to give enoxaparin, give unfractionated heparin infusion. See Sliding scales: heparin.

· Beta-blockers: Metoprolol 5 mg IV q5 min x 3 in ED, then switch to PO dosing. Target HR < 60. Contraindications: AV block, SBP < 100, moderate or severe CHF, active wheezing.

· ACE-inhibitor: Start within first 24 hours with Captopril 6.25 mg PO TID and increase dose as BP allows. Write hold parameters for BP.

· Morphine: can be used for pain (1-2 mg IV boluses PRN).

· Nitrates: either IV NTG or Nitropaste to keep chest pain free.

· In general, these patients should be managed with an early conservative approach, which includes stress testing either as an inpatient or as an outpatient, depending on patient stability.

· The patient should be referred for cardiac catheterization if any of the following features are present:

- Persistent or recurrent ischemia.

- Positive stress test (perform catheterization prior to discharge).

- CHF or LV dysfunction (EF < 50%).

- Prior PTCA or CABG.

- Malignant ventricular arrhythmias.

Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA 2000; 284:835-42.

Boden WE, O'Rourke RA, et al. Outcomes in patients with acute NQWMI randomly assigned to an invasive as compared with a conservative management strategy. (VANQWISH) Trial. N Engl J Med 1998; 338:1785-92.

Braunwald E, Antman EM, et al. ACC/AHA 2002 guideline update for the management of patients with UA/NSTEMI: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). 2002. Available at: http://www.acc.org/clinical/guidelines/unstable/incorporated/index.htm.

Cannon CP, Weintraub WS, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the GP IIb/IIIa inhibitor tirofiban. (TARGET) N Engl J Med 2001; 344:1879-87.

Cohen M, Demers C, et al. A comparison of low-molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. (ESSENSE) Study Group. N Engl J Med 1997; 337:447-52.

Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. (CURE) N Engl J Med 2001; 345:494-502.

ACUTE CORONARY SYNDROME: RISK FACTOR MODIFICATION

1. Smoking: all ACS patients who smoke should be counseled to quit smoking. Document this in the medical record.

2. Diet: all ACS patients should be counseled on a diet low in saturated fat and cholesterol. Provide the patient with educational materials if available.

3. Lipid management:

· All ACS patients should have a fasting lipid panel within 24 hours of presentation.

· Patients with an LDL > 100 mg/dl should be started on a statin. If they are already on a statin, the dose should be increased.

4. Always contact the primary care physician to ensure adequate follow-up care.

The above sections are based on: Fung G, Kayser S, Michaels A, Thompson C, Zaroff J. UCSF Guidelines for management of acute coronary syndromes. Revised June 23, 2002.

CONTRAINDICATIONS TO ANTICOAGULATION

1. The following criteria apply mainly to thrombolytics (e.g. tPA) and GP IIB/IIIa inhibitors (e.g. tirofiban, integrilin, etc). However, it is well worth looking over these contraindications for all forms of anticoagulation(e.g. heparin, enoxaparin, etc). You must weigh the risks and benefits of anticoagulation in all patients individually.

2. Absolute contraindications:

· Any active internal bleeding.

· Any abnormal bleeding within the previous 30 days.

· History of CVA or head trauma within 30 days; within one year if using tPA.

· Any history of hemorrhagic stroke.

· Suspected aortic dissection.

· Intracranial tumor or pathology.

3. Relative contraindications:

· Presence or history of bleeding diathesis.

· INR > 2.0.

· Platelets < 100,000.

· Uncontrolled hypertension (SBP > 200 mmHg, DBP > 110 mmHg).

· Major surgery or trauma within past 6 weeks.

· Known hypersensitivity to any component of the anticoagulant.

· Prolonged CPR.

· Age > 75 or weight < 67 kg (higher risk of bleeding).

· Pregnancy.

· Active peptic ulcer disease.

COCAINE CHEST PAIN

1. Cocaine can and does (not infrequently) cause real myocardial ischemia and infarction in young healthy people. Always remember to take a detailed cocaine/crack history in patients with chest pain, especially young patients.

2. Pathophysiology: prevention of norepinephrine and dopamine reuptake leading to alpha-1 activation; increased myocardial demand (increased HR and afterload); coronary and peripheral vasoconstriction; promotes in situ thrombus formation; can lead to premature atherosclerosis and LVH.

3. History: chest pain usually 30 minutes to 4 hours after use, but can occur up to 24 hours after use or even longer with withdrawal (up to 2 weeks).

4. ECG: criteria for lysis often present; abnormal in >50% of patients; many with J point elevation or LVH with repolarization abnormality; may be normal in many patients with MI.

5. Most patients should be admitted; 6% of patients with cocaine-associated chest pain have MI.

6. Management: (no randomized controlled trials) benzodiazepines, aspirin, oxygen, NTG for persistent pain, calcium channel blocker, thrombolysis vs angioplasty. The conventional wisdom is that beta-blockers should be avoided in cocaine chest pain, since they can lead to unopposed alpha-stimulation and thus, theoretically, worsening of the underlying pathophysiology. Labetalol may be of use in this situation since it is a combined alpha-1 and beta blocker.

Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med 2001; 345:351-8.

CONGESTIVE HEART FAILURE

1. Etiologies of exacerbation: myocardial ischemia, non-compliance with diet/drugs, inadequate drug therapy, hypertension, arrhythmia, valvular heart disease, fluid overload, PE, infection (pulmonary or systemic), pericardial constriction or tamponade, thyrotoxicosis, physical or emotional stress.

2. Determine if left-sided, right-sided, or both:

Left-sided	Right-sided
Tachypnea	Elevated JVP
Rales	Hepatojugular reflex, RUQ tenderness, congestive hepatopathy
Left-sided S3	Ascites, peripheral edema

3. Diagnosis with BNP: if available at your hospital, this test can be helpful in distinguishing CHF from other causes of dyspneic patients who present to the ER.

BNP has a sensitivity of 90% and a specificity of 74% overall.
The level of BNP correlates to the severity of heart failure.
In a recent study on BNP for the diagnosis of CHF, the initial (clinical) diagnostic uncertainty was 43%; BNP reduced this uncertainty to 11%.

4. General considerations:

· Look for prior records, echo, or catheterization report to determine ejection fraction and presence of systolic versus diastolic dysfunction.

· Consider rule-out MI if ischemic heart disease is a consideration

· All patients should be on a 2 g sodium-restricted diet and may even need to be fluid restricted (particularly if hyponatremic).

· Oxygen via NC or face mask to relieve dyspnea.

· Morphine 0.5-2 mg IV q4h can be given to relieve dyspnea.

· If severe exacerbation, may need to admit to CCU for Dopamine/Dobutamine therapy, NTG gtt, nitroprusside. General goals are RA 7, PCWP 15, SVR 1000-1200, CI>2.5.

5. Systolic dysfunction:

· Diuretics: acutely used to reduce symptoms of pulmonary edema.

- Furosemide 0.5-1.0 mg/kg IV. If inadequate response, double the dose. Monitor for hypotension!

- Convert IV furosemide to PO by doubling dose. Furosemide is effective for approximately six hours.

- If inadequate diuresis with furosemide alone, try adding thiazide such as HCTZ 25 mg PO qd or metolazone 5-20 mg PO qd (give 30 min before furosemide) or consider furosemide drip.

- Watch serum electrolytes (especially K⁺) carefully and replete as necessary

· Nitrates: also useful in acute setting to reduce pulmonary edema by decreasing preload.

- Sublingual, nitropaste, or IV nitroglycerin (start at 10-20 mcg/min and titrate as BP allows). When stable, can convert to PO nitrate (eg. start with Isordil 10 mg PO tid).

· ACE inhibitor: proven mortality benefit

- Captopril 6.25 mg PO tid and increase dose as BP allows. If one dose is well tolerated, increase next dose immediately; it’s not necessary to wait 24 hours. Watch K⁺, Cr.

- Once stable, switch to equivalent dose of once-daily ACE-I. Rough conversion:

Captopril	Enalapril	Benazapril, Fosinopril, Lisinopril
6.25 mg PO tid	n/a	5 mg qd
12.5 mg PO tid	5 mg bid	10 mg qd
25 mg PO tid	10 mg bid	20 mg qd
50 mg PO tid	20 mg bid	40 mg qd

- If ACE-I not tolerated, can try ARB (angiotensin II receptor blocker) e.g. Losartan.

- Another alternative is hydralazine + nitrates, especially if concomitant renal insufficiency or hyperkalemia.

· Spironolactone:

- Demonstrated mortality benefit in Class III-IV CHF

- Dose is 25 mg PO QD. Contraindicated if Cr > 2.5 or K⁺ > 5.0. Follow K⁺ closely after spironolactone started, especially as usually used in combination with ACE inhibitor.

· Beta-blockers:

- Also shown to have mortality benefit. However, you should not start beta-blockers in the acute setting; you may even wish to hold beta-blockers in acute CHF exacerbations due to systolic dysfunction.

- Start with Metoprolol 25 mg PO bid or Carvedilol 3.125 mg PO bid and titrate up as HR and BP allow. Target doses: Toprol XL 200 mg qd, Carvedilol 25 mg bid (50 mg bid if > 85 kg).

· B-type Natriueretic Peptide (BNP, Nesiritide®):

- Can be considered in severe heart failure requiring ICU stay; may provide additional improvement in clinical status and symptoms.

- Dose: IV bolus of 2 µg/kg followed by a continuous infusion of 0.01 µg/kg/min. Increase q 3 hour by 0.005 µg/kg/min, preceded by a bolus of 1 µg/kg, up to a maximum of 0.03 µg/kg/min. If hypotension occurs, the infusion should be discontinued and restarted when the blood pressure has stabilized, at a 30 percent lower dose without a repeat bolus.

6. Diastolic dysfunction: improve ventricular relaxation, decrease heart rate, maintain sinus rhythm

· Beta-blockers: Metoprolol, Atenolol titrated up as heart rate and BP allow.

· Ca-blockers: Start with Diltiazem 30 mg PO QID or Verapamil 40 mg PO TID; titrate up as BP tolerates and then change to once-daily formulation.

Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002; 347:161-7.

McMurray J, Pfeffer MA. New therapeutic options in congestive heart failure: Part I. Circulation 2002; 105:2099-106.

McMurray J, Pfeffer MA. New therapeutic options in congestive heart failure: Part II. Circulation 2002; 105:2223-8.

Colucci WS, Elkayam U, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated

congestive heart failure. Nesiritide Study Group. N Engl J Med. 2000 Jul 27;343(4):246-53.

ATRIAL FIBRILLATION

1. If symptomatic or unstable (CP, SOB, CHF, SBP < 90, ischemia), proceed directly to cardioversion. If relatively stable, control rate, anticoagulate, and then proceed to cardioversion.

2. Etiologies:

· Cardiac: CAD, ischemia, CHF, HTN, valvular heart disease, pericarditis, myocarditis, cardiomyopathy, congenital heart disease, cardiomyopathy, changes in myocardial wall stress.

· Pulmonary: pneumonia, PE, lung cancer, chronic lung disease.

· Other: fever, pain, surgery (up to 1/3 of patients go into a-fib after cardiopulmonary bypass, post-valve replacement), HTN, alcohol (holiday heart), thyrotoxicosis, severe infection, diabetes.

· Lone A-fib: A-fib in patients less than 60 years old without clinical heart disease, HTN, DM, or other risk factors for A-fib. CVA risk appears to be much lower than other a-fib subgroups.

3. Rate control (b-blockers and Ca-blocker together can cause excessive AV nodal blockade):

· b-blocker:

- Contraindicated if active wheezing or in uncompensated heart failure.

- Metoprolol: 5 mg IV q5 minutes x 3.

- Esmolol: good for potentially unstable patient (e.g. ICU patient) because half-life only 9 min. Bolus 500 mcg/kg, drip 25-300 mcg/kg/minute.

· Calcium channel blocker:

- Contraindications: VT, 2^nd degree or 3^rd degree AV block without pacemaker, severe hypotension, cardiogenic shock, bypass tracts, close administration with IV beta-blockers.

- Diltiazem 0.25 mg/kg or 20 mg IV over 2 min. Watch for hypotension! Rebolus in 15 min PRN with 0.35 mg/kg or 25 mg. Drip: 5-15 mg/hr if unable to control rate.

- Verapamil: 0.1 to 0.3 mg/kg (up to 5 to 10 mg) IV over 2 minutes. Repeat 5-10 mg IV in 15-30 minutes PRN. Drip: 5-20 mg/hour.

· Amiodarone: good for controlling ventricular rate in critically-ill patients due to short-term Ca-channel blocking and sympatholytic effects. Load 150 mg IV over 10 minutes. Drip 1 mg/min x 6 hrs, then 0.5 mg/min x 18 hrs.

· Digoxin: Lower incidence of hypotension. Controls ventricular rate at rest, but not during exercise. Slower onset of action than Ca-blockers and b-blockers. Load 0.5 mg IV once, then in 6 hours 0.25 mg IV q6h x 2. Start maintenance dose at 0.125-0.25 mg PO/IV QD.

Daily dose will need to be adjusted in presence of renal failure, amiodarone, etc. Usually used as adjunctive therapy – rate will not be controlled immediately if only digoxin is given!

4. Anticoagulation:

· If in atrial fibrillation for longer than 48 hours, will need to be anticoagulated for 2-4 weeks before cardioversion to decrease risk of acute thromboembolism. Continue anticoagulation for 3-4 weeks after cardioversion due to sluggish atrial mechanical recovery. Alternatively, if no evidence of atrial thrombus on early transesophageal echocardiogram (TEE), the patient can safely be cardioverted followed by anticoagulation for 3-4 weeks.

· In the hospital setting, anticoagulate with unfractionated heparin or enoxaparin and overlap with warfarin until therapeutic INR of 2-3 is obtained.

· If anticoagulation is not feasible or contraindicated (e.g. GI bleed), transesophageal echocardiogram may be used to rule out left atrial thrombus prior to cardioversion.

· Long-term anticoagulation: warfarin, with goal INR 2-3, has been proven to reduce risk of embolic stroke in patients with chronic and paroxysmal A-fib by 68%. Highest risk of stroke is in patient with valvular disease, older age, previous stroke/TIA, HTN, and DM.

5. Cardioversion:

· Electrical: Useful for symptomatic patients; start with 100 J. Predictors of success: short duration of A-fib, normal left atrial size. Pre-treatment with Ibutilide (1 mg IV) may increase the likelihood of cardioversion. QTc should be monitored if using ibutilide. 80% success rate.

· Chemical: sinus rhythm can be achieved in 30-40% of patients with class Ia (procainamide), class Ic (propafenone), or class III (amiodarone, sotalol, ibutilide) agents. Patient who have been in A-fib for greater than one year, or with enlarged left atria, are less likely to convert.

· Maintenance of sinus rhythm: due to high rates of recurrent A-fib, many patients are started on maintenance anti-arrhythmic therapy after cardioversion. Most common effective agent used at is amiodarone (see antiarrythmics section).

6. Rate control vs. rhythm control: recent findings demonstrate that rate control is equal to and may be better than rhythm control in the management of a-fib in elderly patients (not lone a-fib).

· The results of the AFFIRM trial showed that there was no difference in all-cause mortality between patients who are treated conservatively (rate control + anticoagulation) vs. those treated more aggressively (antiarrhytmics, cardioversion). Disabling stroke, hospitalizations, and new arrhythmias were less in the rate control group and at 2 years of follow up, the survival curve was slightly better for the rate control group.

· The results of the RACE trial showed that patients in the rate control group were less likely to experience thromboembolic complications, heart failure, and adverse drug effects.

Falk RH. Atrial fibrillation. N Engl J Med 2001; 344:1067-78.

Baseline characteristics of patients with atrial fibrillation: the AFFIRM Study. Am Heart J. 2002 Jun;143(6):991-1001.

PULMONARY HYPERTENSION

1. Definition: mean PAP > 25 mmHg or PASP > 40 mmHg at rest or >30 mmHg with exercise. PVR/SVR > 0.7.

2. Etiologies:

· Pre-capillary/capillary (high PAP, high PVR, normal PCWP): primary pulmonary HTN, Eisenmenger’s Syndrome, COPD, interstitial lung disease, pulmonary emboli, obstructive sleep apnea, high altitude, cirrhosis, chronic hypoxia, thyrotoxicosis, collagen vascular disease, HIV, drugs (cocaine, amphetamines, heroin, appetite suppressants).

· Post-capillary (high PAP, ± high PVR, PCWP>15): Left heart failure, mitral regurgitation, mitral stenosis, aortic insufficiency, aortic stenosis, pulmonary veno-occlusive disease (PCWP may be normal), cardiomyopathy, atrial myxoma, cor triatriatum, tumor compressing pulmonary veins, chronic HTN, pericardial disease.

3. Evaluation:

· Echo with doppler and bubble study: congenital heart disease, valvular disease, LV failure, cardiomyopathy, intra-cardiac shunt.

· V/Q scan: pulmonary veno-occlusive disease, chronic PE.

· PFT: obstructive or restrictive pulmonary disease, decreased diffusion capacity.

· ABG: hypoxemia.

· Serologic studies: collagen vascular disease.

· High resolution chest CT: interstitial lung disease.

· Cardiac catheterization with O2 sat: evaluate hemodynamics to distinguish pre-capillary versus post-capillary etiologies, look for evidence of shunt.

· Sleep study: obstructive sleep apnea.

4. Treatment

· Vasodilators: Cannot predict response from hemodynamic characteristics. Initial response to vasodilator challenge predicts response to long-term therapy. Perform vasodilator challenge in CCU, with PA line in place. Monitor for ¯PAP, CO (which may systemic arterial P)

- Epoprostanol (Prostacyclin, Flolan®). Works by vasodilation, inhibition of platelet aggregation, and vascular remodeling. Given by continuous IV infusion with portable pump due to short half-life (3-5 minutes). Monitor for headache, jaw pain, cutaneous erythema, diarrhea, arthralgias, catheter-related infections and thrombosis.

- Ca-channel blocker: Nifedipine, Diltiazem (Verapamil ineffective because of negative inotropic effects). Usually use higher doses than for systemic HTN.

- Nitric Oxide: Inhaled, specific to pulmonary vascular bed so less problems with systemic hypotension. Used for short-term therapy at 5-80 ppm. Currently limited to research.

- Bosentan: oral endothelin antagonist recently shown to increase functional capacity and improve pulmonary hemodynamics.

· Anticoagulation: recommended due to increased risk of thrombosis and in-situ thrombosis due to slugging pulmonary blood flow. Use warfarin to achieve INR of approximately 2.0

· Transplant: combined heart/lung.

· Other supportive measures: oxygen, diuretics (especially if left heart failure).

Channick RN, Simonneau G, et al. Effects of the dual endothelin-receptor antagonist bosentan in patients with

pulmonary hypertension: a randomised placebo-controlled study. Lancet. 2001 Oct 6;358(9288):1119-23.

Rubin LJ. Primary pulmonary hypertension. N Engl J Med 1997; 336:111-7.

SYNCOPE

Defined as transient loss of consciousness and postural tone with spontaneous recovery.

Causes	Characteristics	Prevalence range (%)	Examples
Cardiac
· Organic Heart Disease	chest pain, dyspnea, exertional, postoperative	1–8	AS, HCM, PE, Pulm HTN, myxoma, MI, coronary spasm, tamponade, aortic dissection
· Arrhythmias	sudden syncope, injury	4–38	Bradycardia: sinus node disease, 2° or 3° heart block, pacemaker malfunction, drug-induced Tachycardia: VT, torsades, SVT (palpitations characteristic)
Reflex–mediated
· Vasovagal	warmth, nausea	8–37
· Situational	occurs after daily activity	1–8	cough, micturation, defecation, swallow
· Neurocardiogenic	provacable stimulus	2-3
· Other	after neck pressure or head turning	0–4	carotid sinus, neuralgia
Neurologic	HA, diplopia, hemiparesis	3–32	migraines, TIA, subclavian steal
Orthostatic hypotension	Symptomatic upon standing	4–10
Medications	Symptoms with drug use	1–7
Psychiatric	frequent symptoms, lack of injury	1–7
Unknown	negative workup	13–41

1. Guidelines for hospital admission with syncope: worried about MI, stroke, arrhythmia

· Defnitely admit:

- HPI: chest pain

- PMH: CAD, CHF, ventricular arrhythmia

- PEX: CHF, valvular disease, focal neurologic deficit or disorder

- ECG: ischemia, arrhythmia, bundle branch block, prolonged QT

· Strongly consider admission:

- HPI: age > 70, exertional syncope, frequent syncope, cardiac disease suspected

- PEX: tachycardia, moderate to severe orthostasis, injury

2. Indications for Holter monitoring (telemetry for admitted patients):

· Symptoms that suggest arrhythmia: cluster of spells, sudden loss of consciousness, palpitations, use of meds associated with arrhythmia.

· Patients with known heart disease or abnormal ECG.

3. Indications for tilt table testing:

· Normal hearts and relatively infrequent syncope.

· Non-diagnostic Holter monitoring.

· Symptoms that suggest vasovagal spells (warmth, nausea) but no clear-cut precipitating event.

Kapoor WN. Syncope. N Engl J Med 2000; 343:1856-62.

Linzer M, Yang EH, Estes NA, 3rd, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997; 126:989-96.

JUGULAR VENOUS PULSATIONS

<labeled pressure tracing>

1. Waves:

· a wave: rise in right atrial pressure during atrial contraction

· x descent: atrial relaxation + RV contraction (pulls atrium downward)

· c wave: bowing of tricuspid valve into RA during systole

· v wave: right atrial filling, tricuspid valve closed

· y descent: emptying of right atrium after tricuspid valve opens

2. Tips:

· no a wave in atrial fibrillation due to lack of coordinated atrial contraction

· cannon a waves in complete heart block as atrium contracts against closed tricuspid valve

· large v wave in tricuspid regurgitation due to augmented right atrial filling

· y descent diminished in cardiac tamponade

· JVP changes with respiration and angle of bed, can be occluded, increases with hepatic pressure; try palpating opposite carotid pulse to help separate arterial from venous pulsations

HEART MURMURS

1. Aortic stenosis: Crescendo-decrescendo systolic murmur heard best in the aortic area, radiating to the supraclavicular fossa and carotids. Rarely heard at the apex. A2 decreased; paradoxical S2 split (sign of critical AS in absence of LBBB); narrow pulse pressure. Pulsus parvus et tardus, S2 softens, murmur peaks later as aortic stenosis progresses. Gallavardin’s phenomenon is AS murmur heard in mitral area. Aortic sclerosis can mimic AS murmurs very closely.

2. Aortic insufficiency: High-pitched blowing diastolic murmur at left sternal border, 3^rd or 4^th interspace. Heard best with patient sitting, leaning forward, and holding breath at end-expiration. Wide pulse pressure, Quincke’s sign (capillary pulsation in nailbed with gentle pressure), Musset’s sign (head bobbing), Muller’s sign (pulsating uvula), Corrigan’s pulse (bounding, full carotid pulse with rapid downstroke), Hill’s sign (systolic BP in leg at least 30 mmHg higher than in arm). Austin-Flint: diastolic murmur in mitral area due aortic regurgitant flow impinging anterior mitral leaflet.

3. Pulmonic stenosis: Systolic murmur heard in pulmonic area, transmitted to the neck or left shoulder. A2 is decreased, P2 is delayed. RVH with parasternal lift.

4. Pulmonic insufficiency: High pitched decrescendo diastolic murmur heard in pulmonic area; often associated with pulmonary hypertension. Intensity may increase with inspiration.

5. Mitral stenosis: low-pitched rumbling diastolic murmur heard best at apex. Opening snap sometimes present.

6. Mitral insufficiency: loud, high-pitched holosystolic murmur heard best at apex, radiating to the left axilla (when ant leaflet incompetent) or to left sternal border (when pos leaflet incompetent). Soft S1.

7. Tricuspid insufficiency: high-pitched blowing systolic murmur best heard along the lower left sternal border, radiating to the right sternal border. Intensity increases with inspiration.

8. Pericardial friction rub: scratchy, leathery, scraping sound heard best along the left sternal border, 3^rd interspace. 3 components: (1) atrial systole, (2) ventricular systole, (3) ventricular diastole. Usually the first two components are present. Heard best with patient leaning forward at end exhalation.

Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA 1997; 277:564-71.

Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA 1999; 281:2231-8.

ECG READING MADE EASY

This is the thumbnail outline of selected criteria for certain ECG abnormalities.

· Note: height: 0.1 mV = 1 mm, duration: 0.04 seconds = 1 mm

· Rate: 60–100 bpm normal

· QRS Axis: normal axis is –30° to +90°. < -30° is left axis, >90° is right axis.

· Differential diagnosis of axis deviations (in order of likelihood):

Right Axis	Left Axis
1. RVH	1. LAFB
2. Lateral or anterolateral MI	2. Inferior MI
3. WPW with left freewall pathway	3. WPW with posteroseptal pathway
4. LPFB	4. COPD or PE

· Intervals

PR: normal 120 – 200 msec

QRS: normal < 90 msec, abnormal > 120 msec

QTc: normal <0.45 (measured QT/square root of R–R interval)

· Right atrial abnormality (only 1 criteria needed)

lead II P > 0.25 mV or > 25% QRS amplitude

lead V₁ P > 0.15 mV

· Left atrial abnormality (only 1 criteria neede)

lead II P > 120 msec with notches separated by at least 1 small box

lead V₁ P wave has a negative terminal deflection that is 40 msec by 0.1 mV

· Left ventricular hypertrophy: There are numerous criteria; three useful ones are below. All are specific but all are insensitive, so fulfillment of one set is sufficient for LVH (applies to age > 55)

RaVL >11 mm (men), >9 mm (women)

RaVL + SV₃ >20 mm (women) and >25 mm (men)

SV1 + (RV₅ or RV₆)>35 mm

· Right ventricular hypertrophy: the following findings suggest RVH; there are several others.

Right axis deviation

R in V₁ + S in V₆ > 11 mm

R:S ratio > 1 in V₁ (in absence of RBBB or posterior MI)

· RBBB (Right Bundle Branch Block)

QRS > 120 msec

Wide S wave in I, V₅, V₆

Secondary R wave (R’) in right precordial leads with R’ greater than initial R (rsR’ or rSR’).

· LBBB (Left Bundle Branch Block)

QRS > 120 msec, broad R in I and V₆, broad S in V₁ and normal axis or

QRS > 120 msec, broad R wave in I, broad S in V1, RS in V₆, and left axis deviation.

· LAFB (Left Anterior Fascicular Block): There are several sets of criteria for LAFB

Axis is more negative than – 45 degrees

Q in aVL, and time from onset of QRS to peak of R wave is > 0.05 seconds.

Also helpful is QI, SIII pattern

· LPFB (Left Posterior Fascicular Block; must exclude anterolateral MI, RVH, RBBB)

Axis >100 and QIII, SI pattern

· Q Waves: Use the following screening mantra, courtesy of Tom Evans, M.D.  V₁, V₂, V₃: "any, any, any"; V₄, V₅, V₆: "20, 30, 30"; I, II, aVL, aVF: "30, 30, 30, 30"; V₁, V₂: "R > 40, R > 50". Numbers refer to width of Q wave in milliseconds.

DIAGNOSIS OF WIDE-COMPLEX TACHYCARDIA (VT VS. SVT)

1. Is there absence of an RS complex in allof the precordial leads (V₁-V₆)? If yes, diagnosis = VT (stop).

2. Is the R to S interval (beginning of R to nadir of S) > 100 msec in any one of the precordial leads? If yes, diagnosis = VT (stop).

Note: antiarrhythmic drugs may give a false positive diagnosis of VT, under this criteria.

3. Is there AV dissociation or V-A block? If yes, diagnosis = VT (stop).

4. Determine if there is a RBBB- or LBBB-type pattern to the wide complex tachycardia.

RBBB-type QRS pattern: dominant positive in V₁
LBBB-type QRS pattern: dominant negative in V₁

5. Are there morphologic criteria for VT present? If yes, diagnosis = VT (stop).

6. If none of the above criteria are met, the diagnosis = SVT with aberrancy (sensitivity 97%, specificity 99%).

Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991 May;83(5):1649-59.

CARDIAC TESTING

1. Exercise treadmill test (ETT):Good screening test for patients with chest pain concerning for CAD, normal resting ECG, and ability to undergo vigorous exercise testing. Exercise increases myocardial O₂ demand and unmasks hypoperfusion in patients with CAD. ST depression (especially if downsloping) has a very high sensitivity and specificity for detecting CAD if peak HR of 85% of max predicted rate (220-age) is achieved; however, studies have shown a high false positive rate in both women and patients with atypical or no chest pain. There is also a high false negative rate in patients with a history of coronary artery disease.

2. Echocardiography:

· 2-D: Good for looking at anatomic abnormalities of the heart and great vessels, to assess the size and function of cardiac chambers, and to assess valvular function. Hypokinesis and akinesis of the LV wall is highly suggestive of ischemic heart disease, and can be used to determine distribution of culprit coronary artery stenoses. Try adding contrast to obtain higher-quality images in patients with emphysema, chest wall deformities, and obesity.

· Exercise (stress) 2-D: Used to determine regional wall motion abnormalities in patients with normal resting Echo, with signs or symptoms of ischemic heart disease. Difficult to perform due to movement and respiratory artifacts during exercise.

· M(motion)-mode: used as adjunct to 2-D echo to measure size of structures and for resolution of complex cardiac motion patterns.

· Doppler: used to investigate blood flow in the heart and great vessels. Very useful for detecting regurgitant blood flow across the valves and any abnormal communications within the heart. Doppler velocities across a valve can be converted to pressure gradients; cardiac output and pressure gradient data can be used to calculate stenotic valve area.

· Bubble study: uses injection of agitated normal saline to assess for intra-cardiac shunts. For instance, a PFO is unmasked by seeing bubbles flowing directly from the right to left atrium. An intrapulmonary shunt may be suggested by delayed appearance (4-5 rather than 1-2 cardiac cycles) of bubbles in the left atrium.

· Transesophageal (TEE): Small ultrasound probe placed into the esophagus allows for higher resolution images of posterior cardiac structures, detection of left atrial thrombi, small mitral valve vegetations, and thoracic aortic dissection. Patient must be NPO and has no dysphagia.

PARASTERNAL LONG AXIS VIEW

SHORT AXIS VIEW

2. Myocardial perfusion imaging (P-Thal or P-MIBI):

· Functional study looking for presence and distribution of areas of myocardial ischemia.

· Persantine (or adenosine) is used to induce coronary vasodilation, which increases flow to the myocardium perfused by healthy coronary arteries. As ischemic regions are already maximally dilated, this “steals” blood away from diseased segments.

· Thallium is a potassium analog which is extracted from blood by viable myocardial cells. Perfusion images will show defects in areas where blood flow is relatively reduced. If a defect on the initial (stress) imaging disappears on repeat (rest) images after 3-24 hours, the area is presumably still viable. A fixed defect suggests myocardial scar tissue. Redistribution images can be performed after 24 hours to look for additional areas of viable myocardium.

· MIBI can be used in lieu of thallium; its shorter half-life allows for a higher-dose to be given, with higher-quality images. However, since it undergoes less washout after the initial stress study, the follow-up rest study will require a second injection.

3. MUGA: Multiple-gated acquisition angiography. Technetium-99m is used to label patient’s red blood cells and cardiac images are acquired for several hours. A composite cardiac cycle representing 200 heart beats is generated, and is used to assess left ventricular ejection fraction, especially in patients with inadequate echocardiograms.

Tavel ME. Stress testing in cardiac evaluation: current concepts with emphasis on the ECG. Chest 2001; 119:907-25.

Zaret BL, Wackers FJ. Nuclear cardiology (1). N Engl J Med 1993; 329:775-83.

Zaret BL, Wackers FJ. Nuclear cardiology (2). N Engl J Med 1993; 329:855-63.

Popp RL. Echocardiography (1). N Engl J Med 1990; 323:101-9.

Popp RL. Echocardiography (2). N Engl J Med 1990; 323:165-72.

CARDIAC CATHETERIZATION

1. Indications:

· Elective or diagnostic

· Primary: initial reperfusion therapy for acute ST-segment elevation or new LBBB MI

· Rescue: after failed thrombolysis (<50% decrease in ST elevation 90-120 minutes after thrombolysis)

2. Coronary stents:

· Used as primary therapy, for recurrent restenosis, PTCA of saphenous vein grafts, if extensive or threatening dissection, if large thrombus burden, or if poor angiographic result obtained from standard angioplasty; data for brachytherapy mounting, especially with recurrent restenoses

· Post stent care:

- Integrilin® (eptifibatide): continued for 18-24 hours; occasionally ReoPro® (abciximab) used instead

- Plavix 75 mg PO qd x 28 days

- ASA 325 mg PO qd

3. Post-cath care:

· Check groin for oozing, bleeding, hematoma, or bruit.

· Oozing: direct pressure for at least 10 minutes, pressure bandage.

· Bleeding: manual compression ASAP and contact cath team. Consider FemoStop®.

· Hematoma: check Hct, platelets, type and cross. Outline borders in ink, document lower limb neuro exam, follow size, ensure blood bank sample and IV access.

· Transfuse PRBC, FFP, and platelets as indicated. For abciximab, consider platelet transfusions even if platelet count normal. Consider hemodialysis if eptifibatide given. Consider protamine if prolonged PTT secondary to heparin.

· New bruit (systolic suggests pseudoaneurysm, continuous suggests AV fistula): contact cardiology, order ultrasound, consult vascular surgery.

· Check distal pulses. If diminished, check distal strength, sensation, capillary refill, and temperature. If abnormal, consider ischemic limb and consult vascular surgery.

· Check hematocrit. If ¯ then rule out retroperitoneal bleed with non-contrast abdominal CT

· Check creatinine: if then consider contrast-induced acute renal failure versus cholesterol emboli. Consider gentle hydration. See also Renal: Contrast nephropathy.

4. Complications:

· Distal microembolization

· Vessel perforation or dissection

· Acute re-stenosis: 75% within minutes of angioplasty, 25% within 24 hours. Usually due to dissection or thrombosis; 1/3 have major ischemic complications requiring emergent revascularization

· Subacute thrombotic occlusion of coronary stent (4%) within 2-14 days; often results in MI or death

· Gradual re-stenosis: 50% narrowing of luminal diameter within 1-6 months

CORONARY ARTERY ANATOMY – LEFT CORONARY ARTERY

LEFT ANTERIOR OBLIQUE (LAO) – CRANIAL VIEW

LEFT ANTERIOR OBLIQUE (LAO) VIEW

RIGHT ANTERIOR OBLIQUE (RAO) VIEW

CORONARY ARTERY ANATOMY – RIGHT CORONARY ARTERY

RIGHT ANTERIOR OBLIQUE (RAO) VIEW

LEFT ANTERIOR OBLIQUE (LAO) VIEW

PA LINES

1. Indications:

· Diagnostic:

- Differentiation of shock/hypotension (example: increased CI, decreased SVR in septic shock versus decreased CI, increased SVR in cardiogenic shock)

- Differentiation of pulmonary edema (cardiogenic versus increased permeability)

- Evaluation of ventricular function

- Titration of medications during severe CHF exacerbation

- Pericardial tamponade

- Acute mitral regurgitation or ventricular septal rupture

- Pulmonary hypertension

- Assessment of oxygen transport

· Monitoring response to therapy:

- Manipulations of intravascular volume, effects of pressors and inotropes, afterload reduction, and vasodilator therapy

- Optimizing oxygen transport

· Therapeutic: ventricular pacing via RV pacing port

2. Relative contraindications:

· Severe coagulopathy

· Significant thrombocytopenia

· Severe pulmonary hypertension

· Ventricular arrhythmia

· Left bundle branch block (3% chance of inducing RBBB and thus complete heart block)

· Severe vascular disease or infection at proposed site

· Prosthetic right heart valve

3. PA line hardware: 5 ports

· Distal PA (accessed via yellow hub)

· Thermistor (accessed via specialized connector on separate yellow hub)

· Balloon (accessed via red hub to inflate and measure PCWP)

· Proximal injection (accessed via blue hub, to inject thermal indicator)

· Proximal infusion (accessed via white hub)

4. Measurements:

· PCWP: PAP and PCWP should be measured during end-expiration, regardless of whether patient is breathing spontaneously or on mechanical ventilator, because intra-thoracic pressure will be closest to zero. This corresponds to the “low” point of the wedge tracing in a vented patient and the “high” point of the tracing in a spontaneously breathing patient.

· CO: Measured using thermodilution method. A known volume of indicator fluid (often chilled) is injected into the proximal injection port (in right atrium) and change in blood temperature is measured at the thermistor (at the main pulmonary artery). Cardiac output is then calculated based on the temperature change. Note that tricuspid regurgitation and intracardiac shunts will cause errors in this calculation.

· SVR = MAP (mmHg) – mean RAP (mmHg) x 80 (normal usually 800-1200)

CO (L/min)

· Oxygen content (CaO₂) = (1.2 x hemoglobin x SaO₂) + (0.003 x PaO₂). Where SaO₂ is the arterial oxygen saturation percentage expressed as a decimal.

5. Waveforms

· RA waveform (see jugular venous pulsations section, above).

· RV waveform: normal systolic pressure between 15-30 mm Hg, normal diastolic pressure between 0-4 mm Hg.

· PA waveform: You know you’ve entered the PA when you see the diastolic step-up. Normal PA systolic pressure 15-30 mmHg, normal PA diastolic pressure 6-12 mm Hg, normal PA mean < 20 mm Hg

· PCW wave form: similar to RA wave form, but dampened; comparable a and v waves should be visible, with x and y descents.

STANDARD PA CATHETER PRESSURE TRACING

6. Findings in specific disorders

· Mitral regurgitation: large v waves transmitted to PCW and PA tracings, resulting in markedly asymmetric PA wave form. Mean PCWP may be artifactually higher than PA end-diastolic pressure.

· Tricuspid regurgitation: Accentuated RA v wave with steep y descent and elevated mean RA pressure. Inadequate CO measurement via thermodilution.

· RV infarction: elevated RA pressure relative to PCWP. Prominent x and y descents due to dilated, non-compliant RV.

· Cardiac tamponade: elevation and equalization of RA, PA diastolic, and PCW pressures, dominant x descent, attenuated y descent, decreased or unchanged RA pressure with inspiration.

· Ventricular septal defect: acute RV volume overload with elevated RA, PA, and PCW pressures. Step-up in O2 saturation from RA to PA. Measure O₂ sat in SVC and PA blood samples: greater than 7% difference is suspicious for shunt.

· PEEP: typically correct PCWP by subtracting ½ of PEEP. For PEEP<10, PCWP is proportional to LVEDP. For PEEP>10, RAP is proportional to LVEDP.

Matthay MA. Invasive hemodynamic monitoring in critically ill patients. Clin Chest Med 1983; 4:233-49.

PACEMAKERS

1. When evaluating a patient that you think needs a pacemaker (sinus node dysfunction, AV block, bi- or trifascicular block, neurogenic syncope, severe cardiomyopathy), consider the following:

· What is the absolute indication for pacing?

· Is there a clear relationship between symptoms and bradycardia or AV dyssynchrony?

· If not, have other causes for the patient's symptoms been investigated?

· If bradycardia is truly causing the patient's symptoms, is there a reversible cause such as recent MI, ischemia-induced bradycardia, meds, or hypothyroidism?

2. Temporary cardiac pacing:

· Common indications:

- Treatment of symptomatic bradycardia (until permanent pacemaker can be implanted or underlying condition reversed).

- Restoration of AV synchrony in acute MI (especially inferior MI, right ventricular MI), CHF, hypertrophic cardiomyopathy.

- Prophylaxis for potential bradycardia which may produce symptoms or hemodynamic instability in acute MI.

- Prophylaxis, to prevent pause-dependent ventricular tachycardias.

· Suspect rupture of the intraventricular septum by the temporary pacer wire if any one of the following occur: chest pain, pericarditis (friction rub), transition from LBBB ® RBBB pattern on ECG (except in temporary biventricular pacing).

3. Generic pacemaker codes for permanent pacemakers:

Chamber paced	Chamber sensed	Response to sensed beat
O – none	O – none	O – none
A – atrium	A – atrium	T – triggered
V – ventricle	V – ventricle	I – inhibited
D – both	D – both	D – triggered and initiated

4. Pacing modes:

· VVI – ventricular pacing on demand; output inhibited by sensed QRS events. Inexpensive. Indicated in patients with A-fib with complete AV block or symptomatic bradycardia. VVIR pacers can increase and decrease in response to sensor input, up to a programmed level, and are used for those with A-fib who do not mount a heart rate during exercise. Don't use in patients with sinus rhythm because of the loss of AV synchrony during pacing; in addition, retrograde atrial activation can induce atrial fibrillation in these patients.

· AAI – atrial pacing is inhibited by sensed P-wave events. Also inexpensive. Indicated for sick sinus syndrome with intact AV node condutions. Use AAIR in patients with chronotropic incompetence. Do not use in patients with extensive conduction system disease and those with atrial flutter or fibrillation.

· DDD – the generator can sense and pace both atria and ventricles. During sinus bradycardia, atrial and if necessary, ventricular pacing occurs. During AV block, ventricular pacing occurs following either a spontaneous or paced atrial impulse. Indicated for AV block with intact sinus node function. Use DDDR in patients with chronotropic incompetence. Rapid ventricular response can occur during atrial tachycardias—this is prevented by setting an upper rate limit or using a mode-switching device.

· DDI – similar to DDD but during atrial tachycardias, the device effectively operates in VVI mode as the atrial impulse is inhibited. Indicated in sick sinus syndrome, hypersensitive carotid sinus syndrome, malignant vasovagal syndrome. The disadvantage is that this DDI cannot maintain AV synchrony during AV block.

· VDD – newer devices with a single ventricular lead but also have sensing electrodes in the right atrium that allow tracking of atrial rhythm. Implantation is simpler than for dual-chamber devices, with less risk of lead displacement and implantation-associated trauma. Indicated for high-grade AV block with intact sinus node function.

5. Pacemaker emergencies:

· Post-implantation complications:

- Early: pneumothorax, tamponade, myocardial perforation.

- Late: subclavian vein thrombosis, SVC syndrome, lead thrombus or fracture, PE, infection.

· Failure to sense, capture, or output.

· Inappropriate changes in pacemaker rate.

Kusumoto FM, Goldschlager N. Cardiac pacing. N Engl J Med 1996; 334:89-97.

DEFIBRILLATORS

1. AICDs are used for the treatment of ventricular arrhythmias. Their functions are arrhythmia recognition, overdrive pacing, cardioversion/defibrillation, anti-bradycardia pacing, and event memory. Class I indications for their placement are as follows:

· Cardiac arrest due to VF or VT, transient or reversible causes excluded.

· Spontaneous, sustained VT without a reversible cause.

· Syncope with sustained VT/VF during EP study where drug treatment not possible or ineffective.

· NSVT with prior MI, LV dysfunction and inducible VF or sustained VT during EP study that is not suppressible by antiarrhythmics.

2. Some recent AICD trials support prophylactic use of AICDs rather than anti-arrhythmics for patients at higher risk for sudden cardiac death (post-MI, low ejection fraction):

- MADIT: AICD vs. any medical treatmentin high-risk patients (malignant arrhythmias).

- MADIT-II: AICD vs. any medical treatment in all patients with low EF, s/p MI.

- AVID: AICD vs. amiodarone.

3. Contraindications: VT or VF with reversible cause, incessant or very frequent VT (will deliver shocks repeatedly), prognosis markedly limited by co-morbidity.

4. Causes of inappropriate AICD shock: SVT or sinus tachycardia with rate within VT detection zone and over-sensing.

A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The (AVID) Investigators. N Engl J Med 1997; 337:1576-83.

Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. (MADIT-I). N Engl J Med 1996; 335:1933-40.

Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. (MADIT-II). N Engl J Med 2002; 346:877-83.

ANTIARRHYTHMICS

1. Amiodarone

· Used in a wide variety of atrial and ventricular tachyarrhythmias, and for rate control of rapid atrial fibrillation and atrial flutter, especially in patients with impaired LV function.

· Contraindications: thyrotoxicosis, cirrhosis, severe pulmonary disease. Use with caution in patients with sinus or AV node dysfunction.

· Typical IV loading dose: 150 mg IV over 10 min, followed by 1 mg/min x 6 hours, then 0.5 mg/min x 18 hours. Can repeat 150 mg IV over 10-30 minutes for recurrent arrhythmias.

· Typical PO loading dose:

- VT (10 grams): 1200 mg/d (divided doses) x 10d, 800 mg/d x 2-4 weeks, 600 mg/d x 2-4 weeks, then 400 mg/d maintenance.

- SVT or CHF (4 grams): 800 mg/d x 5 days, then 200 mg/d maintenance.

· Switching from IV to PO therapy: If on IV therapy for >2-3 weeks, start with maintenance PO dose. If on IV therapy < 1 week, give full PO load, then continue with maintenance PO dose.

· If a patient on long-term oral therapy has recurrent arrhythmias, assume inadequate myocardial drug concentrations and repeat IV load.

· Dosing of digoxin and warfarin may need to be adjusted in patients treated with amiodarone.

· Short-term adverse effects: vasodilation, hypotension, negative inotropic effects, prolonged QT (although rarely causes torsades)

· Long-term adverse effects (dose-related): photophobia, visual blurring, halo vision, blue skin discoloration, photosensitivity, cough (interstitial pneumonitis), nausea, anorexia, constipation, increased AST and ALT, hypothyroidism (can also cause hyperthyroidism), ataxia, paresthesias, peripheral neuropathy, bradycardia, AV block.

2. Procainamide

· Usually load 1 gram IV over 1 hour (750 mg if elderly) then start Procan SR 750 mg PO qid.

· Monitor for QTc prolongation, prolongation of QRS >50%, hypotension.

· Follow levels of procainamide + NAPA (therapeutic range=10-20).

3. Adenosine

· Used to assess underlying rhythm and/or to break SVT.

· Use 6-12 mg rapid IVP if through peripheral line; 3-6 mg IVP through central line.

4. Lidocaine

· Used for VF/VT arrest, stable VT, and wide complex tachycardia of unknown type.

· 1.0-1.5 mg/kg IV, then maintenance gtt at 1-4 mg/min.

Desai AD, Chun S, Sung RJ. The role of intravenous amiodarone in the management of cardiac arrhythmias. Ann Intern Med 1997; 127:294-303.

PRESSORS AND CARDIAC DRIPS

Name	Receptors	Dose	Action	Side effects
Phenylephrine	a1	10-200 mcg/min	pure vasoconstrictor	vasospasm, ARF
Norepinephrine	a1, b1	1-30 mcg/min	vasoconstrictor, positive inotropy	arrhythmias, ARF, vasospasm
Dopamine	D1	1-2 mcg/kg/min	splanchnic vasodilation
	b1	2-10 mcg/kg/min	positive inotropy	arrhythmias, tachycardia
	a1	10-20 mcg/kg/min	vasoconstriction	arrhythmias, tachycardia
Dobutamine	b1, b2	1-20 mcg/kg/min	positive inotropy and chronotropy	hypotension
Epinephrine	a1, a2, b1, b2	0.25-4 mcg/min	positive inotropy, chronotropy, and vasoconstriction	arrhythmias, tachycardia
Amiodarone	K⁺-, Na⁺- channel blocker, b-blocker, Ca-blocker	150 mg over 10 min, then 1 mg/min x 6 hr, then 0.5 mg/min x 18 hr	anti-arrhythmic, rate control	AV block, hypotension
Procainamide	Na channel blocker	1 g over 20 min, then 1-4 mg/min	anti-arrhythmic	hypotension, prolonged QT
Lidocaine	Na channel blocker	1-1.5 mg/kg, then 1-4 mg/min	anti-arrhythmic	seizures, AMS
Esmolol	b1>b2 blocker	500 mcg/kg then 25-300 mcg/kg/min	rate control, anti-hypertensive	hypotension, CHF, bronchospasm
Propranolol	b-blocker	0.5-2.0 mg, then 1-10 mg/hr	rate control, anti-hypertensive	hypotension, CHF, bronchospasm
Labetalol	a1, b1, b2 blocker	2.5-10 mg, then 10-120 mg/hr	anti-hypertensive	hypotension, CHF, bronchospasm
Diltiazem	Ca-channel blocker	0.25 mg/kg over 2 min, reload 0.35 mg/kg q15 min. prn, then 10-15 mg/hr	rate-control	hypotension, AV block
Verapamil	Ca-channel blocker	2.5-5 mg, then 5-20 mg/hr	rate control	hypotension, AV block
Hydralazine	direct vasodilator	2.5-20 mg q3 min, up to 400 mg, then 5-20 mg q6h	anti-hypertensive	hypotension, angina

CHEST PAIN / BRADYCARDIA / TACHYCARDIA

Enalapril

Benazapril, Fosinopril, Lisinopril

Cardiac

Reflex–mediated

Matthay MA. Invasive hemodynamic monitoring in critically ill patients. Clin Chest Med 1983; 4:233-49.

PRESSORS AND CARDIAC DRIPS

Name

Receptors