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