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Here are a couple of articles that show guidelines for treatment.

Angina pectoris is a symptom of myocardial ischemia or infarction caused by an imbalance between myocardial oxygen supply and demand.


Etiology. Ischemia is secondary to coronary artery disease in 95% of patients. A decreased oxygen supply from anemia, hypotension, vasospasm, or arrhythmias or an increase in oxygen demand secondary to exercise, emotional stress, CHF, hypertension, tachycardia, sepsis, etc., can lead to a worsening of symptoms. Ischemia can occur in patients with normal coronary arteries in the setting of LV hypertrophy, aortic stenosis or insufficiency, hypertrophic cardiomyopathy, coronary vasospasm, or cocaine abuse.

Types of Angina
Stable. Intensity, character, and frequency of episodes can be predicted, and angina occurs in response to a known amount of exercise or other stress.
Unstable. Intensity, frequency, or duration of episodes is changed and can no longer be predicted. Pain is precipitated by less exercise or is of longer duration. This includes angina at rest and new-onset angina.
Variant. Pain, which may occur at rest, is secondary to vasospasm of coronary arteries.

Diagnosis
History. Classically described as substernal chest pressure or heaviness radiating to the left shoulder and arm, neck, or jaw, associated with nausea, diaphoresis, and shortness of breath. It is usually brought on and exacerbated by exercise and stress and alleviated with rest or sublingual nitroglycerin. Typically, the pain lasts 2 to 10 minutes and rarely 30 minutes. Atypical presentations may include epigastric pain, indigestion, right arm pain, light-headedness, nausea, or shortness of breath (anginal equivalents (see also Box 2-1). In the elderly, symptoms such as confusion, pallor, fatigue or dyspnea may be suggestive of ischemia. Ambulatory ECG monitoring reveals that at least 25% of ischemic episodes are silent even in patients with a history of typical angina.
Physical exam. An S4 gallop may be present during an episode. The patient may be dyspneic, diaphoretic, or have a new heart murmur. High-risk features of angina include heart failure and hypotension. A focused physical exam is crucial in making an assessment of risk.
Evaluation of patients with angina.
Which test? In a population of patients with symptomatic disease and no work-up bias, the sensitivity of a graded exercise test (GXT) is about 45% with a specificity of 85%. The sensitivity of SPECT scanning (thallium GXT) and stress echo are both about 86% with a specificity of 64% and 77%, respectively. Stress-echocardiogram is more operator-dependent. In some patients it may be more cost effective to do cardiac angiography as a first step.
ECG. During an episode of pain, the ECG may show ST-segment depression or T-wave inversions, or it may be normal. The absence of ECG changes during an episode of angina does not rule out cardiac ischemia because the circumflex and posterolateral distributions can be electrically silent. Increasing use is being made of echocardiography and nuclear studies (see below) to evaluate patients with continuing symptoms in the absence of ECG changes. CAD is suggested if there is evidence of an old MI.
GXT or treadmill test. The predictive value of a positive test depends on the prevalence of disease in the population being tested. Specificity is high in particular groups of symptomatic individuals but is generally <50% in asymptomatic individuals. Compared with men, women (especially young women) have higher rates of false-positive GXT. Overall, the GXT is less sensitive for CAD than is a nuclear study or stress echocardiogram. An early positive GXT may be indicative of left main disease or three-vessel disease. Absolute contraindications to GXT include acute CHF, acute MI, active myo- carditis, ongoing unstable angina, recent embolism, dissecting aneurysm, acute illness, thrombophlebitis, moderate-to-severe aortic stenosis, and an ECG that cannot be interpreted (e.g., LBBB). Relative contraindications include severe hypertension, mild-to- moderate aortic stenosis, hypertrophic obstructive cardiomyopathy, frequent ectopy, and many other conditions that may increase the risk of a GXT.
Nuclear (thallium or technetium) chemical or exercise stress tests. Nuclear scans can be useful for patients who cannot tolerate the physical demands of the GXT or in whom the diagnosis will be pursued even in the light of a negative GXT (e.g., those considered to have a high clinical risk of disease). During the test, tracer is taken up by viable, well-perfused myocardium. Areas of MI are indicated by fixed perfusion defects with no uptake during rest or exercise. During the nuclear-GXT, areas that are hypoperfused (i.e., ischemic) demonstrate thallium uptake only during the postexercise "resting" images. Adenosine, dipyridamole, and dobutamine may be used to augment the perfusion of normal myocardium and shunt blood flow away from areas of relative ischemia. These agents are used in patients who have a contraindication to exercise or are unlikely to attain target heart rates. More recently, administration of tracer to patients during episodes of angina has been shown to be a sensitive way to detect abnormalities of perfusion when compared to scans done once the patient is rendered pain free. This can be used as a screening method for the detection of previously undiagnosed coronary disease.
Echocardiography. The stress echocardiogram is a widely performed test used to assess patients for coronary disease. Baseline echocardiographic images are obtained at rest. These are used to evaluate left ventricular function and wall motion. Images are then acquired during peak stress (i.e., during a GXT or with dobutamine) and compared with those at rest. Regional wall-motion abnormalities with stress indicate areas of hypoperfusion or ischemia. Echocardiography is now used more commonly to assess CAD in women because of their high false-positive rate on GXT. It is also gaining increased usage among patients with an abnormal baseline ECG (e.g., LBBB), those receiving digoxin, and after CABG or PTCA.
Coronary angiography. Used to identify foci of coronary disease. It is the evaluation of choice in patients with angina that is (1) poorly responsive to medication or (2) unstable. It is also indicated in patients with test results consistent with a high risk for CAD.

Outpatient Treatment of Stable Angina

Medical. May use two- or three-drug combination to maximize benefit while minimizing side effects.
Aspirin. Daily aspirin (325 mg) unless contraindicated to inhibit platelet aggregation. For those unable to tolerate aspirin an alternative is clopidogrel (75 mg QD).
Beta-blockers. Decrease myocardial oxygen demand by decreasing heart rate, systolic blood pressure, and contractility. Because they prolong diastole, beta-blockers also increase O2 supply by increasing myocardial perfusion time. Some beta-blockers (those without intrinsic sympathomimetic activity [ISA] activity), especially lipophilic ones (timolol, metoprolol, and propranolol) prolong life when given for the first year after an MI. This benefit extends into subsequent years in those with a complicated course. They are also useful in patients whose angina is regularly provoked by exercise, although beta-blockers may limit exercise tolerance. Start with a low dose and increase until symptoms are controlled or the resting heart rate is 50 to 60 beats/min. Side effects can include bradycardia, bronchospasm, fatigue, GI upset, symptoms of LV failure, and orthostatic hypotension. Impotence, depression, and Raynaudís phenomenon can occur. Do not discontinue beta-blockers abruptly, since rebound tachycardia can occur. Diabetes and class I and II stable CHF are no longer considered to be contraindication to beta-blocker use.
Calcium-channel blockers (verapamil, diltiazem, amlodipine, and others). These drugs act by blocking the influx of calcium through slow channels into vascular smooth muscle and myocardial cells. They promote peripheral arterial vasodilatation, which decreases oxygen demand by decreasing afterload. Calcium-channel blockers also decrease coronary vasospasm and improve collateral flow. Diastolic relaxation of the LV is enhanced, and coronary perfusion is increased with those agents that slow heart rate. Verapamil and diltiazem decrease conduction through the AV node. Heart block or asystole can develop in patients with AV node or sinus node disease. First-generation calcium-channel blockers have negative inotropic effects, which can lead to CHF in patients with impaired LV function. Other common side effects of calcium-channel blockers include headache, ankle swelling, GI upset, increased risk of GI bleeding and bleeding after surgery, and constipation. Diltiazem and verapamil are relatively contraindicated after MI in those with CHF and should be avoided. Nifedipine increases heart rate and may increase mortality in some patients. The incidence of these side effects is reported to be less with the newer agents (amlodipine, felodipine).
Nitrates (nitropaste, nitropatches, isosorbide dinitrate, others). Effects include venous and arteriolar vasodilatation, which decreases oxy-gen demand. The resulting coronary artery vasodilatation increases coronary oxygen supply. Tolerance can develop but can be overcome by providing an 8-hour nitrate-free interval each day. Preparations include oral, transdermal patches, ointment, sublingual tablets, or spray. A common side effect is headache, which usually responds to aspirin or acetaminophen and tends to improve with continued use. Sublingual nitroglycerin tablets (0.4 mg PRN) or spray are used for acute episodes of angina and may be repeated at 5-minute intervals for up to 3 doses. Patients should be instructed to go to the emergency department if angina is not relieved after 3 doses of nitroglycerin.
ACE inhibitors. Recently, ramipril has been shown to have a beneficial effect on the incidence of MI, congestive heart failure and stroke in patients with coronary artery disease and in those with diabetes and one other risk factor for CAD. This is likely to be a class specific effect of ACE inhibitors. It is unclear if this benefit is provided by angiotensin receptor blockers (ARB).
Revascularization.
Coronary artery bypass grafting (CABG). Primary indication is angina refractory to medical therapy or lesions that are more amenable to surgery than to angioplasty. CABG has been shown to prolong survival in patients with left main disease (50% luminal narrowing) and in three-vessel CAD with LV dysfunction (ejection fraction <50%). Surgery may prolong survival in three-vessel disease with normal LV function and in two-vessel disease with significant proximal stenosis of LAD (if not anatomically suited for PTCA). Surgical advances such as minimally invasive surgery, transcutaneous myocardial revascularization (TMR), and selected single vessel bypass have made surgical therapy an option for patients who previously would not have been considered surgical candidates secondary to significant co-morbidity or poor target vessels.
Contraindications to CABG. Advanced age with pronounced debility, absence of ischemia, or ungraftable coronary arteries. Advanced age in and of itself is not a contraindication. In one sample of patients 80 years and older, coronary revascularization by either CABG or PTCA (see below) was associated with a high likelihood of attaining a good or excellent quality of life and of a patient being able to care for himself or herself subsequent to an MI.
Intracoronary stenting. The current standard for interventional cardiology involves the use of intracoronary stents combined with anti-platelet agents (aspirin and clopidogrel). The indications for the different therapeutic modalities in interventional cardiology are beyond the scope of this text. Choice of intervention versus surgery, type of intervention, and medical therapy should be made in consultation with a cardiologist. It has been recently established that the use of g2,3b platelet aggregation receptor inhibitors (abciximab, tirofiban) in conjunction with primary coronary intervention (PCI) is superior to medical therapy alone, or the use of such interventions without those inhibitors. Percutaneous transluminal coronary angioplasty (PTCA) still has uses and indications. Several controlled clinical trials have shown that PTCA can be used as an alternative to CABG in two- and three-vessel CAD when lesions are amenable to PTCA. There was general agreement among these trials that the procedures provide equal improvement in angina. The PTCA groups generally have a higher frequency of antianginal use after 1 year and are more likely to require additional intervention (CABG or repeat PTCA) compared to patients who undergo CABG. PTCA or stenting is an acceptable alternative to repeat CABG if lesions are amenable to dilatation (single-vessel stenosis, or easily accessible two-vessel stenoses). Diabetics have a worse long-term result with PTCA than does the non-diabetic population. Consequently, intracoronary stenting is preferred in these patients.
Vascular endothelial growth factor (VEG-F) has been used to increase the vascular supply of the heart in those who are not candidates for bypass or PTCA. Although short-term studies are favorable, long-term outcomes are not known.
Transmyocardial revascularization uses a laser to create channels through the myocardium. It clearly reduces anginal pain, but it is not clear if this is just a result of nerve destruction (i.e., the patient can no longer feel anginal pain) or because of revascularization. There are no long-term outcome studies and this is currently considered experimental.
Inpatient Treatment of Angina and MI
See chapter 2 for treatment of acute chest pain. Inpatient treatment is indicated for (1) unstable angina, (2) prolonged anginal episode, which might represent an infarction, and (3) MI.


Unstable Angina (USA)
Management.
The decision to admit is based on the history, since 50% of patients with acute MI will have a nondiagnostic ECG changes and cardiac enzymes will not be positive for up to 6 hours after an infarction. If ECG changes indicate MI, or if enzymes are positive, treat as per MI section below.
Admit to monitored bed. Bed rest with bedside commode, continuous cardiac monitoring, oxygen, and IV access. Obtain screening lab tests, including cardiac enzymes, CBC, glucose, BUN, creatinine, UA, serum electrolytes, including sodium, potassium, chloride, CO2, and magnesium, PT/PTT/INR if planning to anticoagulate.
Obtain serial cardiac enzyme levels. Cardiac troponin I and T are proteins that are highly sensitive and specific for myocardial injury. These markers are now considered the standard. An alternative is creatine phosphokinase (CPK). Obtain an MB isoenzyme level if the total CPK is elevated since CPK can be the result of both cardiac and other muscle breakdown. The CPK is more sensitive than the troponin at hours 4-8 (84% versus 74%) and at 8-12 hours (94% versus 88%). The troponin is essentially 100% sensitive at 12 hours. The troponin may remain elevated for 4 to 7 days. Either troponin or CPK levels should be checked Q8h x 3 (although if the CPK and troponin are negative at 12 hours after pain resolves, an MI is effectively ruled out).
Serial ECGs with intervals depending on circumstances.
Increase anti-anginals. Topical, oral, or SL nitrates, calcium-channel blockers, or beta-blockers. May need IV nitroglycerin. Morphine (2 to 5 mg Q10-20min) may be given for analgesia, preload reduction, and anxiety. Ongoing chest pain that does not respond to standard anti-ischemic regimens (aspirin, heparin, beta-blockers and IV nitroglycerin) is a cardiac emergency and should prompt consideration of referral to a center equipped with a catheterization laboratory.
Other medications. Sedation may be beneficial in certain patients. Acetaminophen and a stool softener may be given for headache and preventing the need to strain, respectively.
Aspirin. With few exceptions, aspirin should be given to anyone with unstable angina or an evolving MI and will reduce the rate of MI and death. Aspirin should be continued indefinitely.
Heparin. Those patients who appear particularly unstable or who have recurrent ischemia are likely to benefit from adding heparin (APTT 1.5 to 2 times normal) to aspirin for the duration of the period of the unstable angina. See Chapter 6 for the details of heparin management. Recently, enoxaparin 1mg/kg SQ BID has been shown to be at least as good and perhaps superior to IV heparin for this indication. However, these data are preliminary and need to be confirmed.
G2,3B platelet inhibitors. Studies have shown benefit from treating the patient with eptifbatide (Integrelin) (180 mg/kg load then 2 mg/kg/min x 72 hours] or tirofiban (Aggrastat) [0.4 mg/kg/min x 30 min, then 0.1 mg/kg/min x 2-4 days as indicated) combined with heparin (dosed to achieve PTT of 2 times control). These drugs are indicated in essentially all patients who are going for other intervention (e.g., PTCA or stent placement). There is still debate about the usefulness of these agents before planned bypass surgery and in those with unstable angina in whom no further intervention is planned. If coronary artery bypass surgery is planned, aspirin should be started preoperatively because it increases postoperative graft-patency rates.
For patients not anticoagulated, heparin 5000 units SQ Q12h should be given for DVT prophylaxis.
If cardiac enzymes become positive, treat the patient for MI. If the patient is ruled out for an MI, the patient will still need some assessment of myocardium at risk (such as GXT on increased medications, a thallium study, or cardiac catheterization).


Acute MI (AMI)
Modalities begun for acute angina should be continued (see Chapter 2). Thrombolysis should be used as if the patient meets ECG criteria and is within the first 12 hours by symptoms.
Defined by ECG changes or serum cardiac enzyme changes; 50% of patients with an acute MI will have a nondiagnostic initial ECG, and so the decision to admit should be made on the basis of the history.
ECG patterns.
Ischemia is indicated by ST-segment depression, nonspecific ST-T-segment changes, and T-wave inversion. These may also accompany a non-Q wave infarction.
Injury indicated by ST-segment elevation. Tall peaked T waves (10 mV) are suggestive of hyperacute injury.
Infarct indicated by the development of Q waves.
Infarct location by ECG (Table 3-1).
Management. See acute management of chest pain in Chapter 2.
Orders similar to unstable angina. Unless contraindication, all patients should have aspirin.
Hypokalemia and hypomagnesemia are risk factors for arrhythmias and should be corrected if present.
Studies are currently underway to assess the efficacy of MAGIK (magnesium, glucose, insulin and potassium) in acute MI. At this point, these cannot be recommended for routine use.
Percutaneous coronary intervention (PCI). In the era of intracoronary stents with antiplatelet agents, this has clearly become the preferred modality for the treatment of AMI. If care is rendered at a facility where PCI can be performed in a timely fashion, it is recom- mended that this be done. Otherwise, treat as per thrombolytics section.
Thrombolytics. It is recommended that every patient with an evolving MI be considered for thrombolytic therapy, which reduces both in-hospital and 1-year mortality by 25%. Evolving MI is defined as at least 30 minutes of ischemic cardiac pain and at least 1 mm of ST-segment elevation in at least two adjacent limb leads or at least 1 to 2 mm of ST-segment elevation in at least two adjacent precordial leads. (These criteria indicate a high likelihood of evolving MI.) The presence of a new complete bundle branch block in addition to characteristic pain also indicates the patient will benefit from thrombolysis. Patients with only ST-segment depression or normal ECGs, even with symptoms, do not benefit. There is evidence that patients who receive thrombolytics from 6 to 12 hours after onset of acute MI may still benefit, although the benefit is less than that for patients who present less than 6 hours after onset of pain.
Absolute contraindications to thrombolytic therapy include recent (<6 weeks) surgery or biopsy of a noncompressible site, recent stroke, any history of hemorrhagic stroke, intracranial neoplasm, recent head trauma, pregnancy, or prolonged or traumatic CPR, aortic dissection, acute pericarditis, active bleeding, and antibodies to streptokinase (substitute tissue-type plasminogen activator [TPA] if the patient has antibodies to streptokinase). If there has been a previous allergic reaction to streptokinase, use of TPA is indicated.
Dosing and administration. TPA may provide a greater decrease in mortality than does streptokinase. In general, if there are no contraindications, streptokinase is preferred by some because of its lower cost.
Streptokinase 1.5 million IU given IV over 1 hour or
TPA 100 mg of single-chain preparation. The accelerated dose regimen is preferred and consists of giving 60 mg during the first half-hour and the second 40 mg over an additional hour. Concurrent heparin infusion to achieve PTT 2 times normal (see Chapter 6 for management of anticoagulation) or
Reteplase 10.8 units over 2 minutes; repeat in 30 minutes. Concurrent heparin infusion.
Heparin and aspirin. It is recommended that every patient who receives thrombolytic therapy be considered for adjuvant anticoagulation therapy for approximately 48 hours (heparin to keep APTT 1.5 to 2 times control, see Chapter 6 for management of anticoagulation). Discontinuing heparin after 72 hours or so may result in rebound angina because of a relatively hypercoagulable state from antithrombin III deficiency. Long-term aspirin therapy (160 to 325 mg QD) should be considered for all patients unless specifically contraindicated.
Beta-blockers are indicated for most patients early (within 6 or 7 hours) during the evolution of an MI and those with persistent or recurrent pain or tachyarrhythmias. A beta-blocker such as metoprolol 15 mg can be given in 5 mg aliquots Q5min. This should be followed by oral beta-blocker therapy to reduce long-term mortality. Patients who are seen in the first 4 to 6 hours of onset of an MI or who present with hypertension or sinus tachycardia and are not in heart failure are considered to be good candidates for beta-blockade.
Some of the relative contraindications to beta-blocker use include: lengthening of the PR interval 0.24 second, second- or third-degree AV block, bradycardia with pulse <50, systolic blood pressure <90 mm Hg, pulmonary artery wedge pressure greater than a range of 20 to 24 mm Hg, rales audible in greater than one-third of the lung fields, wheezing or history of asthma or bronchospasm, and recent use of IV calcium-channel blockers.
Angiotensin-converting enzyme (ACE) inhibitors. There are several large prospective controlled clinical trials demonstrating the efficacy of ACE inhibitors both acutely and chronically in patients who have sustained an MI. Starting an ACE inhibitor within 24 hours of an MI (enalapril 2.5 mg PO BID titrated to 10 mg PO BID) reduces mortality. Additionally, ACE inhibitors (captopril titrated to 50 mg PO TID or ramipril given at a dose of 5 mg PO BID) continued after an MI in those with CHF or an ejection fraction <45% will decrease mortality (including sudden death), increase exercise capacity, reduce CHF, enable ventricular remodeling, and control hypertension.
Angiography. Post-MI coronary angiography and revascularization are indicated for patients with continuing ischemia. Asymptomatic patients with uncomplicated MI and without any inducible angina generally do not require angiography.
Ambulatory monitoring. Ambulatory monitoring after an MI adds information and may be an alternative to stress testing in determining which patient continues to have asymptomatic ischemia.
Prophylactic lidocaine is no longer routinely used for patients with suspected acute MI but is still the drug of choice for the treatment of malignant ventricular arrhythmias. Many patients with ventricular tachycardias or ventricular fibrillation will not have a warning arrhythmia.
Complications of Acute MI


Left Ventricular Dysfunction. See section on congestive failure for long term management of CHF.
The extent of LV dysfunction in the days after an acute MI provides prognostic information.
Treatment of LV dysfunction (CHF) depends on severity but may include:
Avoiding medications that exacerbate heart failure. 2) A low-sodium diet and a diuretic to prevent fluid overload (such as furosemide). 3) Increase FiO2 and provide ventilatory support if required.
If the patient is in cardiogenic shock, IV inotropic agents such as dopamine 2 to 20 mg/kg/min or dobutamine 2.5 to 15 mg/kg/min may help to improve LV function. Hemodynamic monitoring and a urinary catheter maybe required to manage fluid status. A PCWP <10 mm Hg is suggestive of the need for additional fluid volume, whereas a PCWP 20-25 mm Hg is suggestive of fluid overload.
If the cardiogenic shock is secondary to ischemic "stunned" myocardium, intra-aortic balloon counterpulsation, cardiac catheterization, or emergency revascularization may be warranted.

Right Ventricular Dysfunction
Especially prominent with an inferior wall MI secondary to right ventricular infarction. Pronounced hypotension in response to nitrates should be suggestive of this diagnosis.
The triad of clear lung fields, hypotension, and jugular venous distension (JVD) in a patient with an inferior infarction is highly suggestive of a right ventricular infarction. JVD has a sensitivity of 88% and a specificity of 69% for right ventricular infarction. Kussmaulís venous sign (distension of the jugular vein during inspiration) is also highly suggestive. There may also be tricuspid regurgitation, right ventricular gallops, and atrioventricular dissociation.
An ECG with right-sided chest leads can confirm right ventricular MI (RVMI). A 1-mm ST-segment elevation in the right precordial lead CR4R is highly predictive for an RVMI (sensitivity 70%, specificity 100%). Other ECG findings include right bundle branch block and complete heart block.
Echocardiography may reveal right ventricular wall dyskinesia and dilatation. There may be abnormal interventricular septal motion because of a reversal in the transseptal pressure gradient secondary to increased right ventricular end-diastolic pressure.
In addition to conduction deficits, patients with RVMI may develop right ventricular mural thrombi (placing them at high risk for pulmonary embolism), tricuspid regurgitation, and pericarditis.
The following are important components of a treatment regimen for right ventricular infarction:
Maintain right ventricular preload with volume loading as indicated. An infusion of IV normal saline frequently corrects hypotension and increases cardiac output. The use of nitrates, diuretics, and morphine sulfate are all relatively contraindicated, since these medications decrease preload.
Reduce right ventricular afterload if there is concomitant left ventricular dysfunction (e.g., treat left-sided CHF).
Initiate inotropic support with dobutamine if the patient is not stabilized hemodynamically with a saline infusion.
Begin sequential atrioventricular pacing if the patient develops complete heart block.
Initiate thrombolytic therapy or perform angioplasty as indicated.
Among patients who survive a right ventricular infarction, right ventricular function returns to nearly normal levels over time.

Arrhythmias Complicating Acute MI
Premature ventricular complexes (PVCs).
Common in first 72 hours after an MI and may not have an antecedent arrhythmias.
Usually do not require treatment unless they are:
Frequent (10/min).
Multiform.
Occurring close to preceding T-wave (R-on-T phenomenon), or
Occurring in pairs, triplets, or short runs.
Usually treated with a lidocaine bolus followed by infusion. See ACLS protocol in Chapter 1.
Ventricular tachycardia or fibrillation. See protocol in Chapter 1.
Supraventricular tachycardias including PSVT and atrial fibrillation or flutter. See protocol in Chapter 1.
Tachycardia increases O2 demand; so treat promptly.
Rule out reversible underlying causes (such as hypokalemia, hypomagnesemia and hypoxia).

Atrioventricular Block
Mobitz I (Wenckebach).
Common in acute inferior infarction.
See ACLS protocol in Chapter 1.
A permanent pacemaker is rarely required, since Wenckebach block usually resolves within days.
Mobitz II.
Usually occurs in patients with acute anterior Mis.
In the setting of an acute MI, with Mobitz II AV block, a temporary pacemaker should be placed. Often the block is permanent, and a permanent pacemaker should be placed if the block persists for 1 week or more.
Third-degree AV block.
Third-degree AV block is often transient in the setting of an acute inferior MI.
When associated with an anterior MI, it often represents necrosis of the conducting tissue below the AV node and may be permanent, requiring permanent pacemaker implantation.
Bundle branch block.
A left bundle branch block is the most common bundle branch block seen with an MI. The combination of a right bundle branch block and a left anterior hemiblock is also frequently seen.
When a bundle branch block occurs, the site of the infarction is usually anteroseptal, and the infarct is often large.
If the patient is known to have an old bundle branch or fascic- ular block a temporary pacemaker is not necessarily indicated unless dictated by the patientís symptoms and hemodynamic status.
If the patient has a new left bundle branch block or bifascicular block associated with an MI, a temporary pacemaker may be indicated. A bifascicular block is defined as the combination of a right BBB and a left anterior posterior hemiblock.

Left Ventricular Aneurysm
Incidence 7% to 15%, suggested by persistent ST elevations weeks to months after an MI.
May lead to CHF, systemic emboli (caused by mural thrombus formation), and recurrent arrhythmias.
Can be demonstrated on echocardiogram or radionuclide ventriculogram.
Some authors recommend long-term anticoagulation to reduce the risk of embolization. Surgical resection may be indicated for refractory LV failure, recurrent emboli despite anticoagulation, or medically refractory ventricular arrhythmias if electrophysiology studies indicate that the aneurysm maybe the focus of the arrhythmia.

Recurrent Chest Pain
Extension of MI.
Occurs in 10% to 15%.
Characterized by reelevation of cardiac enzymes and additional ECG changes.
Patients with non-Q wave infarcts are at higher risk of extension of infarct in the 12 months after an MI than patients with transmural infarcts.
Angina. For treatment and diagnosis, see section above. If post-MI angina is refractory to medical therapy, cardiac catheterization may be indicated to define anatomy and suitability for revascularization or to perform PTCA.
Pericarditis. May occur after an MI or as the result of a viral infection (especially coxsackie virus), or secondary to uremia. In the setting of an infarction, pericarditis usually occurs after a large transmural infarct.
Physical exam may reveal an audible friction rub.
Pleuritic pain, exacerbated by lying supine, relieved by sitting forward, may be present; tends to radiate to shoulder and be worse on inspiration.
ECG may show diffuse ST-segment elevations, and echocardiogram frequently reveals the presence of a pericardial effusion. However, the ECG may be false negative in up to 20%.
Treatment. NSAIDs, especially indomethacin. Steroids may be used for viral pericarditis but should be avoided in an acute MI. Avoid anticoagulation because of the risk of converting the effusion into a hemorrhagic one with risk of cardiac tamponade.
Pulmonary embolism. If not on IV heparin, post-MI patients should be maintained on prophylactic doses of SQ heparin (5000 units Q12h) until fully mobile. See Chapter 4 for the work-up and treatment of pulmonary embolism.
Pneumonia.

Dresslerís Syndrome
Cause. Pleuropericarditis occurring usually 2 to 4 weeks after an MI. Possibly represents an autoimmune inflammatory reaction.
Symptoms. Pericardial and pleural pain.
Signs. Fever, pericardial friction rub (may be intermittent), and perhaps decreased breath sounds at lung bases and a pleural rub. Chest radiograph may show enlarged cardiac silhouette because of pericardial effusion. ECG may show diffuse ST-segment elevations, decreased R-wave voltage, and occasionally electrical alternans. An echocardiogram may show pericardial effusion.
Treatment. Usually self-limited. NSAIDs; glucocorticoids if NSAIDs not effective. Avoid anticoagulation for reasons stated above.

This one is for arrhythmia

For outpatient assessment, an "event monitor" worn for a prolonged period and activated when patient has symptoms is more sensitive than a 24- to 48-hour "Holter" monitor and is the preferred modality for intermittent or sporadic arrhythmias.


Atrial fibrillation (A fib) results in the loss of atrial contraction and an irregular ventricular rate. Clinically recognized by an irregularly irregular heart rate. Some causes include hypertension, hyperthyroidism, acute pulmonary embolism, CHF, valvular disease (especially mitral valve), acute alcohol use ("holiday heart"), and postoperative state, especially, thoracotomy.
See protocol in Chapter 1 for acute management of A fib with a rapid ventricular response.
Rate control. Long-term therapy must control ventricular rate with agents that increase the refractory period of the AV node (digoxin, verapamil, diltiazem, or beta-blockers). The ventricular rate should be decreased to a range of 80 to 100 beats/min. Generally, beta-blockers are the drugs of choice. Digoxin is useful in rate control in those with CHF or at bed rest but may not be sufficient in those who are ambulatory. Additionally, digoxin is proarrhythmic.
Long-term anticoagulation with warfarin (INR 2.0 to 3.0) is indicated for those in A fib who are older than 60 years of age or have valvular disease, underlying heart disease, hypertension, diabetes, or previous evidence of embolism (CVA, TIA). Those with "lone" A fib (age less than <60, none of the above risk factors, and no cardiovascular disease) have a low incidence of complications and need not be anticoagulated. Aspirin is second best and should be reserved for those not able to take warfarin (e.g., because of high risk of falls).
Many of those with A fib will convert back to sinus rhythm spontaneously. May attempt to convert back to a sinus rhythm with either class III drugs (amiodarone or sotalol) or class I drugs (quinidine or procainamide), flecainide, or cardioversion. However, these patients should be anticoagulated for 3 weeks before cardioversion if A fib has been present for more than 48 hours. Anticoagulation should be continued for 2 weeks after conversion. Ibutilide has been used to convert atrial fibrillation but is falling out of favor.

Paroxysmal supraventricular tachycardia. Most commonly caused by atrioventricular node reentry with 1:1 atrioventricular conduction, although may also be caused by sinus node reentry, atrial ectopy, or an accessory pathway. Commonly associated with Wolff-Parkinson-White syndrome.
Must be distinguished from a ventricular tachycardia.
See protocol in Chapter 1 for acute management.
Chronically may be suppressed with calcium-channel blockers (verap-amil and diltiazem). However, radioablation of the accessory pathway is both safe and effective.

Ventricular tachycardia. Ventricular rate is generally 150 to 180 beats/min. Rhythm tends to be regular, and AV dissociation is a common feature. By definition, it is characterized by three or more consecutive complexes arising inferior to the bifurcation of the bundle of His at a rate that exceeds 100 beats/min.
May be caused by heart disease, electrolyte imbalances, hypoxia, and drug toxicity. The most frequent cause of sustained ventricular tachycardia is reentry along the margin of old infarcted myocardium.
See protocol in Chapter 1 for acute treatment.
Since recurrence rates are high, long-term antiarrhythmic therapy or the implantation of a cardioverter-defibrillator may be indicated for those with sustained or symptomatic ventricular tachycardia. Overall, implantable defibrillators seem to have the best outcomes. Traditional antiarrhythmic agents (e.g., flecainide/encainide) actually increase mortality 2- to 3-fold. Sotalol and amiodarone are showing promise in the treatment of these patients. Beta-blockers (such as metoprolol, propranolol) also may be useful. Generally, a cardiology consult should be obtained to determine the best approach to chronic suppression of this arrhythmia.

Sick sinus syndrome.
Episodes of bradycardia interspersed with episodic tachycardia from sinus tachycardia or atrial fibrillation. May cause syncope.
Generally a disease of the elderly.
Treatment generally requires pacemaker to prevent bradycardia as well as medications such as digoxin or verapamil to control tachycardia.

I hope this helps.






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