Pete A. Gutierrez MD, MMS, PA-CMiami Dade College

November 2008

Unstable Angina:◦ Causes

Plaque rupture Ulceration Hemorrhage and thrombus formation When to call angina unstable or stable?

New-Onset sometimes considered unstable If it is exertional and responsive to rest and medication,

it does not carry the same poor prognosis.

Diagnosis:◦ EKG exhibits commonly ST segment depression or

T wave flattening or inversion but sometimes and more ominously, ST segmental elevations. Usually during chest pain and involving the left ventricle.

◦ Treatment:◦ Multifaceted and vigorous.

Hospitalization Bed rest Monitoring and Oxygen Sedation or pain medication Nitrates Systolic BP 120-100 and Heart rate slow to >60.

Treatment Continued:◦ Anticoagulation, Antiplatelet, and Thrombolytic

Therapy: Heparin either regular or low molecular (Lovenox) Aspirin 325 mg (Baby aspirin 81 x 4 ) Nitroglycerin sublingual or IV Beta Blockers Calcium Channels Blockers not recommended for

unstable angina Revascularization or PTCA.

Coronary Vasospasm:◦ Can occur spontaneously◦ Be induced by cold weather◦ Emotional Stress◦ Vasoconstriction Medications◦ Occur in both normal and abnormal coronary

arteries.◦ Drugs induced (Cocaine)

Prinzmetal’s (variant) Angina:◦ Chest pain without the usual precipitating factors

and is associated with ST segment elevation rather than depression.

◦ Often affect women under 50 years.◦ Usually in the morning.◦ Involved most often the right coronary artery.◦ Associated with arrhythmias.◦ Need to undergo coronary arteriography studies.

Treatment of Prinzmetal’s Angina:◦ Sublingual Nitrates which reduces both preload

and afterload by decreasing arteriolar and venous tone.

◦ Lowers oxygen demand Doses is 0.3, 0.4, 0.6 mg.◦ Long acting nitrates such as isosorbide

mononitrate 10-40mg daily.◦ Beta blockers which prevent angina by reducing

myocardial oxygen demand.◦ Calcium Channels blockers.◦ Verapamil, Diltiazem prevent angina by reducing

oxygen consumption and inducing coronary and artery vasodilatation.

Cardiac Failure, (CHF):◦ Symptoms:

SOB Exertional Dyspnea at first. Progressing to orthopnea. Nonproductive cough worse in the recumbent position. Fatigue. Exercise intolerance. (Also these patients may experience right upper

quadrant pain due to passive congestion of the liver, loss of appetite, and nausea due to edema in the gut.

Cardiac failure may present acutely in a previous asymptomatic patient.

Causes may included:◦ Myocardial infarction◦ Myocarditis◦ Acute valvular regurgitation due to endocarditic

or other conditions.◦ Patients usually present with SOB and pulmonary

edema.

Signs:◦ At times comfortable at rest.◦ Dyspneic during conversations.◦ Vital signs may be normal.◦ Tachycardia, hypotension and reduce pulse

pressure may be present.◦ Increase sympathetic nervous system activity,

and included cold extremities and diaphoresis.◦ Examination of neck, lungs and abdomen.

Thyroid studies should be always preformed since both Hyperthyroidism, and Hypothyroidism are treatable causes of Heart Failure.◦ Pleural effusions may cause bibasilar dullness to

percussion.◦ Expiratory wheezing.◦ Right side failure severe liver enlargement.◦ Ascites may be present.◦ Cardiac findings: Parasternal lift and indicating

pulmonary hypertension.

Laboratory findings:◦ Anemia◦ Renal insufficiency◦ Pre-renal azotemia◦ Also need to think about amyloidosis.◦ Thyroid function test◦ Electrolytes imbalances

Electrocardiography:◦ Arrthymia◦ Myocardial Infarction◦ Ventricular conduction defects.◦ Ventricular Hypertrophy◦ Chest X-Ray enlarged Heart◦ Echocardiogram.◦ Cardiac Catherization.

Treatment:◦ Correction of reversible causes:◦ Diet and Activity◦ Diuretics (Lasix), (Bumex), (zaroxilyn).◦ Ace inhibitor should be the initial treatment in

most symptomatic patients.◦ Mild fluid retention thiazide diuretics. These are

ineffective when the glomerular filtration rate falls below 30ml/min.

The ACE inhibitors have become standard therapy for heart failure patients because of their beneficial effects which include both vasodilatation and inhibition of increase neurohormonal activity. These agents block the angiotensin II induced vasoconstriction and decreasing sodium retention, by reducing aldosterone secretion.

The most important thing in medicine is to know that you don’t know anything.