fisdap cardiology study guide

myocardial infarction
irreversible necrosis of heart muscle secondary to prolonged ischemia.

acetylsalicylic acid
antiplatelet agent, nonnarcotic analgesic, antipyretic

angina pectoris
chest discomfort when the heart does not receive enough oxygen.

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

unstable angina
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.

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

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

hemorrhagic stroke
20% of strokes. Blood vessel in brain ruptures.

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

sputum
matter expectorated from the lungs and respiratory passages

Coronary circulation physiology
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.

Cardiac action potential phases
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

CPAP indications
respiratory distress secondary to chf

moa of adenosine
slow the conduction of impulses at the AV node

moa of amiodarone
delay repolarization and increase the duration of the action potential.

moa of ACE inhibitors
blocks the enzyme responsible for production of angiotensin two.

moa of asprin
prevents the formation of thromboxane A

moa of atenolol
inhibits strength of hearts contraction

atenolol indications
acs, hypertension, SVT, atrial flutter, A Fib

moa of atropine
competes reversibly with acetylcholine

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

moa of clopidogrel
blocks platelet aggregation

clopidogrel indications
acs, ischemic stroke, chronic coronary and vascular disease

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

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

moa diltiazem
blocks calcium channels which prolongs electrical impulses thru the AV node

diltiazem indications
stable narrow QRS tachycardia,

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

dobutamine indications
chf, cardiogenic shock

moa of dopamine
stimulates alpha and beta, inotropy and increased cardiac output

dopamine indications
hypotension, bradycardia unresponsive to atropine

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

epinephrine indications
bronchspasm, cardiac arrest, allergic reactions

moa of lasix
decreased absorption of water and increased urine production

lasix indications
pulmonary edema, chf, hypertensive emergency

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

labetalol indications
acs, svt, severe hypertension

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

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

indications of mag sulfate
torsades de pointes

moa of metoprolol
inhibits strength of contraction

metoprolol indications
acs, hypertension, svt, atrial flutter, A Fib

moa of morphine
reduces heart rate, cardiac work, oxygen consumption

morphine indications
moderate to severe pain, chf, pulmonary edema

moa of nitroglycerin
relaxes vascular smooth muscle, decreases preload and afterload

indications for nitroglycerin
angina, hypertension, chest discomfort

moa of norepinephrine
alpha mediated peripheral vasoconstriction, increase blood pressure and coronary blood flow

norepinephrine indications
cardiogenic shock, septic shock, severe hypotension

moa of procainamide
suppresses atrial and ventricular arrhythmias by slowing conduction

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

moa of propranolol
beta antagonist, inhibits heart rate and hearts strength of contraction

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

moa of vasopressin
vasoconstriction independent of adrenergic receptors

vasopressin indications
adult shock – refractory VF and pulseless VT, Asystole, PEA, vasodilatory shock

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

verapamil indications
atrial fib, hypertension, psvt,

effects of vagal nerve stimulation
release acetylcholine to slow conduction through the AV node slowing the heart rate.

examples of vagal stimulation
coughing, squatting, breath holding, cold stimulus to the face, valsalvas maneuver

pharmacology therapy for cardiogenic shock
dopamine, norepinephrine, epinephrine,
titrate to achieve a minimum systolic blood pressure of 90 mm hg.

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

effects of intrathoracic pressure on cardiac output
increased external pressure on the heart and thoracic blood vessels

signs and symptoms of a stroke
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

signs and symptoms of a stroke
headache, confusion, altered mental status, coma, vertigo, facial droop, nausea and vomiting,
nystagmus is involuntary eye movement

how to treat a beta blocker overdose
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.

signs and symptoms of beta blocker overdose
hypotension, bradycardia, cardiac dysrhythmias. Shortness of breath, fatigue, dizziness

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

systolic heart failure
the left ventricle loses some of its ability to contract.

diastolic heart failure
the left ventricle is not able to fill properly with blood

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

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

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