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myocardial infarction

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irreversible necrosis of heart muscle secondary to prolonged ischemia.

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acetylsalicylic acid

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antiplatelet agent, nonnarcotic analgesic, antipyretic

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angina pectoris

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chest discomfort when the heart does not receive enough oxygen.

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stable angina

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remains constant and predictable in terms of severity, signs and symptoms, precipitating events, and response to treatment.

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unstable angina

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symptoms occur at rest and usually last more than twenty minutes. Symptoms that are severe and or new onset within the last two months. Symptoms that are increasing in intensity, duration, and or frequency in a patient with a history of stable angina.

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Cerebral vascular accident

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stroke or brain attack. A sudden change in neurological function caused by an alteration in cerebral blood flow.

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ischemic stroke

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80% of all strokes. Blood flow in one of the arteries in the brain is blocked.

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hemorrhagic stroke

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20% of strokes. Blood vessel in brain ruptures.

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TIA

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The reversible episode of localized neurologic dysfunction that typically lasts a few minutes to a few hours, resolving within 24 hours.

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sputum

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matter expectorated from the lungs and respiratory passages

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Coronary circulation physiology

answer

The major vessels of the coronary circulation. The left main coronary divides into the left anterior descending and circumflex branches. The right coronary artery supplies blood to the right atrium, the right ventricle, the bottom portion of the left ventricle and back of the septum.

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Cardiac action potential phases

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phase 0 - rapid depolarization - sodium moves into cell. The cell becomes positive. phase 1- initial repolarization. sodium channels close, potassium channels open, potassium moves out of cell. phase 2 - the plateau phase of repolarization. The ST segment on the ECG. calcium moves into cell while potassium moves out. phase 3 - rapid repolarization. Fast potassium moves out of cell. the T wave on the ecg. phase 4- returning to resting state

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CPAP indications

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respiratory distress secondary to chf

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moa of adenosine

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slow the conduction of impulses at the AV node

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moa of amiodarone

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delay repolarization and increase the duration of the action potential.

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moa of ACE inhibitors

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blocks the enzyme responsible for production of angiotensin two.

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moa of asprin

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prevents the formation of thromboxane A

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moa of atenolol

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inhibits strength of hearts contraction

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atenolol indications

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acs, hypertension, SVT, atrial flutter, A Fib

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moa of atropine

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competes reversibly with acetylcholine

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atropine indications

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symptomatic bradycardia, asystole, pea, nerve agent exposure, organophosphate poisioning

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moa of clopidogrel

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blocks platelet aggregation

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clopidogrel indications

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acs, ischemic stroke, chronic coronary and vascular disease

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moa of digoxin

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inhibits sodium potassium pump, which causes an increase in the force of contraction

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digoxin indications

answer

chf, to control ventricular rate in chronic AF and A flutter, narrow PSVT

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moa diltiazem

answer

blocks calcium channels which prolongs electrical impulses thru the AV node

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diltiazem indications

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stable narrow QRS tachycardia,

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moa of dobutamine

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beta one agonist, increases myocardial contractility and stroke volume. increases cardiac output

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dobutamine indications

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chf, cardiogenic shock

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moa of dopamine

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stimulates alpha and beta, inotropy and increased cardiac output

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dopamine indications

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hypotension, bradycardia unresponsive to atropine

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moa of epinephrine

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binds with alpha and beta, increased heart rate, blood pressure, bronchdilation

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epinephrine indications

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bronchspasm, cardiac arrest, allergic reactions

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moa of lasix

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decreased absorption of water and increased urine production

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lasix indications

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pulmonary edema, chf, hypertensive emergency

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moa of labetalol

answer

binds with alpha 1, beta 1 and 2 receptors, inhibits strength of contraction and heart rate

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labetalol indications

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acs, svt, severe hypertension

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moa of lidocaine

answer

blocks sodium channels, suppresses automaticity in the HIS purkinje system and depolarization in the ventricles

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lidocaine indications

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ventricular arrhythmias, VF and VT cardiac arrest, stable monomorphic V tach

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indications of mag sulfate

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torsades de pointes

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moa of metoprolol

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inhibits strength of contraction

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metoprolol indications

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acs, hypertension, svt, atrial flutter, A Fib

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moa of morphine

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reduces heart rate, cardiac work, oxygen consumption

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morphine indications

answer

moderate to severe pain, chf, pulmonary edema

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moa of nitroglycerin

answer

relaxes vascular smooth muscle, decreases preload and afterload

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indications for nitroglycerin

answer

angina, hypertension, chest discomfort

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moa of norepinephrine

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alpha mediated peripheral vasoconstriction, increase blood pressure and coronary blood flow

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norepinephrine indications

answer

cardiogenic shock, septic shock, severe hypotension

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moa of procainamide

answer

suppresses atrial and ventricular arrhythmias by slowing conduction

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procainamide indications

answer

A Fib with rapid rate in WPW, stable monomorphic V tach

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moa of propranolol

answer

beta antagonist, inhibits heart rate and hearts strength of contraction

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propranolol indications

answer

angina, narrow complex tachycardia reentry SVT, junctional, ectopic, multifocal tachycardia uncontrolled by vagal maneuvers or adenosine. hypertension, migraines.

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moa of vasopressin

answer

vasoconstriction independent of adrenergic receptors

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vasopressin indications

answer

adult shock - refractory VF and pulseless VT, Asystole, PEA, vasodilatory shock

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moa of verapamil

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blocks calcium, prolongs conduction of electrical impulses thru the AV node. Dilates arteries

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verapamil indications

answer

atrial fib, hypertension, psvt,

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effects of vagal nerve stimulation

answer

release acetylcholine to slow conduction through the AV node slowing the heart rate.

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examples of vagal stimulation

answer

coughing, squatting, breath holding, cold stimulus to the face, valsalvas maneuver

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pharmacology therapy for cardiogenic shock

answer

dopamine, norepinephrine, epinephrine, titrate to achieve a minimum systolic blood pressure of 90 mm hg.

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frank starlings law

answer

within physiologic limits, the greater the stretch of the cardiac muscle, the greater the resulting contraction.

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effects of intrathoracic pressure on cardiac output

answer

increased external pressure on the heart and thoracic blood vessels

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signs and symptoms of a stroke

answer

dysarthria is unclear articulation of speech. dysphagia is difficulty in swallowing. inappropriate emotions. ataxia is loss of full control of bodily movements hemiparesis paresthesia aphasia is a speech disorder caused by damage to the brain. dysphasia is difficulty generating speech

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signs and symptoms of a stroke

answer

headache, confusion, altered mental status, coma, vertigo, facial droop, nausea and vomiting, nystagmus is involuntary eye movement

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how to treat a beta blocker overdose

answer

administer glucagon which is indicated for beta blocker overdose. Dose is 2 - 5 mg IV over one minute. follow with a second dose of 10 mg IV if the symptoms of bradycardia and hypotension recur.

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signs and symptoms of beta blocker overdose

answer

hypotension, bradycardia, cardiac dysrhythmias. Shortness of breath, fatigue, dizziness

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hemodynamically unstable

answer

perfusion that is not adequate to support normal organ function. An abnormal or unstable blood pressure.

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systolic heart failure

answer

the left ventricle loses some of its ability to contract.

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diastolic heart failure

answer

the left ventricle is not able to fill properly with blood

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pneumonia

answer

pleuritic chest pain, lethargy, tachycardia, tachypnea, chest, side, back pain. Fever, chills, cough with sputum, crackles.

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pulmonary embolus

answer

acute onset of dyspnea, pleuritic chest pain at onset. anxiety, tachypnea, fever, cough, chills, mucus production, tachypnea. Skin may be cool, pale, diaphoretic, cyanotic,

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pulmonary embolus ECG changes

answer

Abnormally large S waves in lead one, abnormally large Q waves in lead three, absent or very small T wave in lead three.

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