E4 Concepts Flashcards
Depolarization
Causes mechanical contraction
Sodium enters the cardiac cell changing it from - to +
Repolarization
Cardiac muscles relax
Potassium moves out and calcium enters the cell to change it to -
Refractory period
No action potential can occur
Cells resist depolarization until full recovery
Automaticity
Self-excitation
Ability of a group of cells to generate spontaneous electrical impulse (SA node)
Excitability
Capability of the cardiac cell to depolarize in response to electrical stimulation
Conductivity
Ability of the cardiac cells to transmit an electrical impulse
Contractility
Ability of cardiac muscle to contract in response to electrical stimuli
You are working in the ER when a patient with palpitations and shortness of breath arrives.
What are some baseline assessments you will want to do?
General Survey: Color, distress, fatigue?
Respiratory Assessment: Oxygenation? Rate, rhythm, effort, SOB?
Cardiovascular Assessment: Distress, Pain? Color, diaphoresis, clutching chest?
- EKG, Mental status (awake, alert, orientated), Health history, Medications
PAC - what is it and treatment
Electrical impulse that comes from the atrium before the next sinus impulse from SA
Tx: reduce stimulants, limit caffeine, tabacco should also hydrate
Treatment of a flutter
Anticoagulation, cardioversion, ablations, controlling the rate and rhythma
treatment of a fib
beta blockers, calcium channel blockers, digoxin and class III antidysrhythmics (amiodarone, sotalol and ibutilide) prevent clots with anticoags, attempt to restore NSR with cardioversion or ablation
PSVT
paroxysmal supraventricular tachycardia (PSVT) starts in part of the heart above the ventricles, does not significantly reduce cardiac output
PVC
premature ventricular complexes, beat originates from site in the ventricle before the sinus beat is conducted
treatment: stop caffeine and stimulant’s, hydrate and beta blockers
v-tach
repeated firing of the ventricles, always assess ABC’s if persistent cardioversion is treatment of choice
emergency treatment: amiodarone + lidocaine
if unconscious or in respiratory arrest begin CPR
v-fib
rapid firing of the ventricles from multiple different ectopic places, most serious arrhythmia there is no perfusion and the patient cannot survive if it persists
Class 1 antidysrhythmics
Sodium channel blockers, results in decreased conduction
Quinidine, procainamide, disopyramide phosphate (norpace)
IV lidocaine label
‘lidocaine for dysrhythmias’ or ‘lidocaine without preservatives’
Antidysrhythmic hospital teaching to patient who says: ‘they aren’t doing anything for me’
When giving IV medications and stabilizing pts require continuous monitoring even if it seems like
- Rise slowly and sit or lie down if feeling faint
How do anticoagulants work?
Ex - heparin and warfarin
Work to prevent thrombosis in the VEINS (DVT, PE) can also work in arteries (MI, CVA, valves)
Reduces the formation of fibrins by inhibiting clotting factors
Anticoagulants, how do they work? (Arteries)
Primarily prevent arterial thrombosis, prevent platelet aggregations (clumping of platelets that form a vlot)
Thrombolytics, how do they work
attack and dissolve blood clots that have already formed
promotes conversion of plasminogen to plasmin which digests the fibrin to degrade the clot
How does a clot form?
Decreased circulation (stasis) platelet aggregation and blood coagulation
Arterial: platelets initiate, fibrin formation occurs, RBCS are trapped in fibrin mesh
Venous: platelet aggregation and fibrin attaches to RBCS
Antiplatelets
Prevents thrombosis primarily in arteries, prophylactic for use in MI/CVA and prevention for stroke (TIA) patients
Thrombolytic indication: MI
Must be administered within 4 hours of symptoms (time-frame is expanding)
