Step 3 Cardiology II

Unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI) are part of the spectrum of ACS and are distinguished by the absence (UA) or presence (NSTEMI) of elevated cardiac biomarkers.

• It is usually made with a combination of symptoms, electrocardiogram (ECG) abnormalities, and elevation in the serum markers of myocardial injury.
• The chest pain or discomfort can often be atypical at presentation, and ECG abnormalities may be absent or nonspecific in patients with baseline ECG abnormalities (eg, left ventricular hypertrophy, paced rhythm, left bundle branch block).
• The initial cardiac enzymes are usually normal; however, it may take up to 6 hours for cardiac troponin levels to become elevated.

It runs laterally in the left atrioventricular groove to supply the lateral and posterolateral parts of the left ventricle.

• The LAD artery runs along the anterior interventricular groove and supplies the anterior wall of the left ventricle.
• Diagonal branches from the LAD artery also run downward to supply the anterolateral wall of the left ventricle

It runs in the right atrioventricular groove to supply the right ventricle and inferoposterior walls of the left ventricle.

• The first step in management is to stabilize the airway and start oxygen.
• The next step is to determine the patient's volume status.
• Volume overload and elevated filling pressures are central to the pathophysiology of most ADHFs. They respond extremely well to intravenous loop diuretics.
• Current guidelines recommend initially treating patients with hypertension and volume overload with intravenous loop diuretics to attempt to relieve symptoms and improve oxygenation.
• Patients who do not respond should then have vasodilator therapy added.

The two most commonly used antihypertensive agents in the management of hypertensive crisis complicated by acute pulmonary edema are IV nitroglycerine and IV nitroprusside.

• Exercise electrocardiogram (ECG) stress testing is the preferred initial modality for the diagnosis of coronary heart disease in most patients with normal baseline ECG and the ability to achieve adequate workload during exercise.
• Pharmacologic myocardial perfusion stress testing with vasodilator stress (eg, adenosine, regadenoson) should be performed as an alternate in patients who are unable to achieve adequate workload during exercise due to osteoarthritis or peripheral vascular disease.

• SVT includes such common entities as AV nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia.
• The term 'paroxysmal SVT' excludes atrial fibrillation and atrial flutter, other common forms of supraventricular arrhythmias.
• ECG:narrow and regular QRS complexes, absent P wave

• WPW Syndrome can be identified in around 0.2% of the population.
• It is characterized by a short PR interval (less than 0.12sec ), a delta wave at the beginning of the QRS complex, QRS duration of 0.12sec or wider, and non specific ST segments or T wave abnormalities.

Initial stabilization measures include full-dose aspirin, oxygen, adequate pain control with morphine and nitroglycerin (contraindicated in hypotension), platelet P2Y12 receptor blocker (eg, clopidogrel, prasugrel, ticagrelor), beta blocker, and anticoagulation.

• Multiple randomized controlled trials have shown improved cardiovascular outcomes with dual antiplatelet therapy with aspirin and platelet P2Y12 receptor blockers rather than aspirin alone.
• The initial loading dose of aspirin is 162-325 mg (chewed so that it enters the bloodstream quickly) followed by 75-100 mg indefinitely.

• Beta blockers are indicated in all acute coronary syndrome (ACS) patients as they decrease myocardial demand, improve diastolic function, and have long term effects on improved mortality.
• Contraindications to beta blocker therapy include severe reactive airway disease, bradycardia, heart failure, and high risk of cardiogenic shock.

Anticoagulation (bivalirudin, low-molecular-weight heparin, or unfractionated heparin) is recommended for all STEMI patients undergoing percutaneous coronary intervention.

• Calcium channel blockers such as immediate-release nifedipine have been shown to increase mortality in ACS patients due to hypotension and subsequent increased sympathetic reflex activity.
• Non-dihydropyridines such as verapamil or diltiazem may be used in ACS patients (with no atrioventricular block or heart failure) with ongoing ischemia.
• They may also be used for short-term management of rapid ventricular response in atrial fibrillation/flutter when beta blockers are contraindicated or ineffective.

Thease includes evidence of active bleeding, adverse intracerebral history (history of hemorrhage, ischemic stroke, or neoplasm), systolic blood pressure greater than 180 mm Hg, recent trauma, or drug allergy.

• If patient presents within 12 (and sometimes 24) hours of symptom onset and if an electrocardiogram demonstrates ST elevations more than 1 mm in two contiguous leads .
• It is important to administer nitroglycerin in these patients before performing the electrocardiogram to rule out coronary vasospasm.
• Additional candidates for thrombolytic therapy include individuals with persistent symptoms of new left bundle branch block.

• It occurs when the R wave in leads V1 through V4 remains the same size or increases very little.
• Common pathologic causes of poor R wave progression include LVH, RVH, COPD, anterior infarction, conduction defects, and cardiomyopathy.

• The QT interval is considered prolonged if it measures more than half the R-R interval, though measurement of the interval is of little clinical significance if the patient is tachycardic.
• Common causes of QT prolongation include drugs (eg, antiarrhythmic agents and tricyclic antidepressants), electrolyte imbalances (eg, hypokalemia), and CNS catastrophes (eg, stroke, seizure).

• It is often difficult to distinguish between PSVT and the numerous other types of SVT (e.g., sinus tachycardia, AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial fibrillation, and atrial flutter).
• One diagnostic and therapeutic maneuver to distinguish between these entities is to increase vagal tone to the heart by Valsalva or adenosine administration.
• This will slow the heart rate until a rhythm can be recognized. It can also potentially "break" the SVT and return the patient to normal sinus rhythm.

• TCAs inhibit fast sodium channels, which result to slowing of the phase 0 depolarization in His-Purkinje tissue and the myocardium.
• This may lead to QRS prolongation and reentrant arrhythmias, like ventricular tachycardia, ventricular fibrillation, and torsades de pointes.
• Sodium bicarbonate is the most effective agent for the management of TCA-induced cardiotoxic effects.
• Lidocaine is the antiarrhythmic drug of choice for TCA-induced ventricular dysrhythmias.

• It can occur within one to four days as a direct complication of a transmural myocardial infarction. The recurrence of chest pain three days after a myocardial infarction, which gets worse with position changes and deep inspiration, is suggestive of infarction pericarditis.
• EKG changes of pericarditis sinus tachycardia, diffuse ST segment elevations with PR segment depression.
• Infarction pericarditis is seen less frequently in patients with early and complete reperfusion. It is usually a transient episode and does not affect the management of acute myocardial infarction, unless it is complicated by a large pericardial effusion or tamponade.

• A pericardial rub is usually heard over the left sternal border and can be present during any of the phases of the cardiac cycle.
• It is heard as a superficial scratchy or grating sound, which gets more pronounced when the patient leans forward.

• It is a life threatening mechanical complication of an acute myocardial infarction. It usually occurs two to seven days after the infarction and causes acute hemodynamic instability.
• Patients also develop acute pulmonary edema.

• Acute pericarditis occurring after a myocardial infarction is usually transient (lasts for only a few days).
• It should be managed with close clinical observation and adequate pain control.
• Aspirin (anti-inflammatory doses) is effective in alleviating the pain associated with acute pericardial inflammation.
• There are some concerns that other NSAIDs may increase the risk of myocardial rupture after a transmural MI.

• The cause of syncope can be established by careful history taking, physical examination, simple lab tests and ECG in 70% of cases.
• Examples of significant diagnostic clues in the history are preliminary nausea or lightheadedness (neurocardiogenic syncope), convulsions, chest pain, dyspnea, palpitations, etc.
• Physical examination findings that also provide important clues are orthostatic blood pressure changes, abnormal cardiac examination, response to carotid massage, etc.
• ECG helps to reveal brady- or tachyarrhythmias and conduction abnormalities , organic heart disease.

• An aortic valve area of less than 1.0 cm2 is considered severe stenosis.
• The onset of symptoms markedly affects the prognosis in patients with aortic stenosis; therefore, prompt intervention is recommended in patients who have cardinal symptoms of aortic stenosis (dyspnea of heart failure, anginal pain, and syncope).
• Aortic valve replacement is associated with marked reduction in symptoms and mortality in patients with symptomatic aortic stenosis, and is considered the treatment of choice.

• It refers to the separation of the carotid artery wall layers and is seen with trauma, connective tissue disease, smoking, neck manipulation, hypertension, or 3-point restraint seatbelts in motor vehicle accidents.
• Anhidrosis may be absent in internal carotid artery dissection (partial Horner syndrome) because sweat nerve fibers travel along the external carotid artery.

• Imaging of head and neck vasculature must be obtained in the patients. CT angiography is a reasonable first step; if the results are negative but carotid dissection is still suspected, either magnetic resonance angiography or catheter angiography (gold standard) may be performed.
• Management consists primarily of antithrombotic therapy such as antiplatelet agents or anticoagulation.
• Stroke is an important potential complication of carotid artery dissection.

• The main factor that leads to myocardial ischemia is vasospasm, although other mechanisms (e.g., increased oxygen demand) also play a role.
• Cocaine-associated vasospasm may lead to coronary artery thrombosis, which cannot be reversed by vasodilator agents.
• Initial treatment regimen consists of nitrates (or calcium channel blockers), aspirin and benzodiazepines.
• If the patient does not promptly improve with these drugs, immediate coronary angiography should be performed to check for any coronary thrombus.

• In patients with WPW syndrome, there is an extra conduction pathway (also known as bypass tract or accessory pathway) that directly connects the atria to the ventricles, bypassing the AV junction.
• The accessory pathway conducts faster than the AV node and excites the ventricles prematurely, manifesting as a short PR interval with characteristic delta wave on EKG. QRS complex is prolonged (more than 0.12 sec).

• Although patients with WPW pattern on EKG can be completely asymptomatic, some develop tachyarrhythmias.
• Paroxysmal supraventricular tachycardia is the most common arrhythmia; it is usually a regular, narrow complex tachycardia.
• If patients with ventricular preexcitation develop atrial fibrillation, they can conduct down the accessory pathway from the atria to the ventricles at a very fast rate; therefore, syncope and collapse are common.
• Progression to life-threatening ventricular arrhythmias may sometimes lead to sudden death.

• Catheter-ablation therapy is the recommended therapy in symptomatic patients with WPW syndrome. Catheter-ablation therapy has a nearly 90% efficacy rate and a less than 5% risk of complications, replacing surgical ablation as the preferred treatment for accessory pathways.
• The incidence of sudden cardiac death in patients with WPW pattern on electrocardiogram (EKG) is generally low (less than 1 %), but this risk is increased in patients with previous episodes of tachyarrhythmia.
• Atrial fibrillation is especially dangerous because impulses can conduct from the atria to the ventricles at a very fast rate and it might eventually degenerate to ventricular fibrillation.

Women, patients with diabetes, and elderly individuals may have an atypical presentation (eg, nausea, abdominal pain, dyspnea, weakness, or syncope) and nonspecific or normal electrocardiogram (ECG).

• Supplemental oxygen should be administered, pulse oximetry readings obtained, and intravenous access established.
• Ideally, 325 mg of aspirin should be chewed en route to the hospital.
• Nitroglycerin is typically given next, unless contraindications exist (e.g., hypotension or recent usage of sildenafil).

• It is associated with prodromal symptoms of nausea, lightheadedness, pallor and diaphoresis.
• It usually occurs when the patient is erect, and recovery occurs in the supine position.
• Patients are usually young and otherwise healthy. Precipitating events include prolonged standing, exertion, venipuncture, or a painful stimulus.

• A seizure may mimic syncope; however, patients usually have a history of tonic-clonic movements, urinary or fecal incontinence, and a postictal state.
• Jerky movements similar to tonic-clonic movements can occur in any patient with syncope, but the postictal confusion is very unlikely with other conditions except seizures.

• Recent myocardial infarction and atrial fibrillation are two most common causes of arterial thromboembolism.
• The single most important step in the early management of the patients with acute arterial occlusion diagnosed by history and physical examination is immediate IV heparin therapy followed by continuous heparin infusion.
• Heparin therapy will prevent further propagation of thrombus, and inhibit thrombosis distally in the arterial and venous systems due to low flow and stasis.

• An acute coronary event should be ruled out with serial cardiac enzymes, and an echocardiogram is needed to evaluate left ventricular function.
• Coronary revascularization is needed if evidence of coronary ischemia exists.
• Patients with multiple risk factors for developing cardiac arrhythmias need proper evaluation for possible implantable cardiac defibrillator placement to prevent sudden cardiac death.

• • Rapid onset of severe pain in the affected extremity that is out of proportion with physical examination findings
• • Pain exacerbated by passive stretch of the muscles in the affected compartment
• • Exquisite tenderness and tense swelling
• • Paresthesias
• • Diminished distal pulses
• • Nerve & muscle injury that can result in permanent loss of extremity function

• Measurement of tissue pressures is diagnostic: Compartment pressure more than 30 mm Hg or delta pressure (diastolic blood pressure - compartment pressure) less than 20-30 mm Hg indicates significant CS.
• If compartment pressures are improving, patients may be observed closely. However, patients with elevated compartment pressures that do not improve rapidly require fasciotomy to avoid long-term complications.

• It is defined as the presence of an organized electrocardiographic rhythm without sufficient cardiac output to produce a palpable pulse or measurable blood pressure.
• The absence of a palpable pulse also means that the brain is not being appropriately perfused; therefore, cardiopulmonary resuscitation (CPR) is necessary despite the presence of an organized rhythm.
• The airway should also be secured, but the 2010 ACLS guidelines place a greater importance on circulation than on airway and breathing.

• In unstable tachycardia, the patient has hypotension, ischemic chest pain, altered mental status, or heart failure, but a pulse is present.
• Cardioversion would be the best choice for patient eith unstable tachycardia.
• However, defibrillation and cardioversion are not a component of ACLS guidelines for PEA management.

Defibrillation is only effective if there is a shockable rhythm, such as ventricular fibrillation or pulseless ventricular tachycardia.