Cardiology

Pete A. Gutierrez MD, MMS, PA-C Miami 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.

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Cardiology

by Miami Dade on Dec 05, 2008

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Cardiology — Presentation Transcript