exam2 Flashcards
normal sinus rhythm
SA node at rate of 60 to 100 per minute and follows the normal conduction pattern of the cardiac cycle
sinus bradycardia
sinus rhythm at a rate less than 60 beats/min
clinical associations for sinus bradycardia
may be normal in trained atheletes and other individuals during sleep. Can occur as response to carotid sinus message, Valsalva maneuver, hypothermia, increased intracranial pressure, hypoglycemia, and inferior wall MI
ECG characteristics of sinus bradycardia
HR less than 60, rhythm regular, p wave before each QRS, and has a normal shape and duration. PR interval is normal, QRS complex is normal shape and duration
clinical significance of sinus bradycardia
depends on the patient. S/S can include pale, cool skin, HypoTN, weakness, angina, dizziness or syncope, confusion or disorientation, SOB
TX for sinus bradycardia
may require atropine for pt with symptoms. Pacemaker may be necessary, discontinue/hold drugs that cause bradycardia and dose may need to be adjusted
sinus tachycardia
normal sinus rhythm tthat is 101 to 200 beats/min
clinical associations for sinus tachycardia
stressors: exercise, fever, pain, hypoTN, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, HF, hyperthyroidism, anxiety and fear. DRUGS: epi, norepi, atropine, caffeine, theophylline, nifedipine, or hydralazine. OTC cold remedies (pseudoephedrine)
ECG characteristics of sinus tachycardia
HR: 101 to 200. P wave: normal, before every QRS and normal shape and duration. PR: normal, QRS: normal shape and duration
clinical significance of sinus tachycardia
depends on pt tolerance of increased HR. S/S dizziness, dyspnea, hypoTN due to decreased CO. increased myocardial oxygen consumption is associated with increased HR. anginia or increase in infarction size may accompany in pt with CAD or MI
Tx for sinus tachycardia
treat underlying cause (Pain management, hypovolemia), for clinically stable pt: vagal maneuvers,
drugs for sinus tachycardia
beta adrenergic blockers can be given to reduce HR and decrease myocardial oxygen consumption
Premature Atrial Contraction
contraction orgininating from an ectopic focus in the atrium.
clinical associations for PAC
emotional stress or physical fatigue, use of caffeine, tobacco, ETOH. Hypoxia, Elyte imbalances, hyperthyroidism, chronic obstructive pulmonary dz, heart dz (CAD, and valvular dz)
ECG characteristics of PAC
HR varies with underlying rate, frequency of PAC and rhythm is irregular. P: different shape from a P wave from the SA. May be notched or downward, may be hidden in a T wave. PRI: shorter or longer than PR orginating from SA node, however WNL. QRS: normal, if QRS is greater than or equal to 0.12 sec abnormal conduction through the ventricles is present
clinical significance of PAC
in healthy hearts not significant. “skipped a beat” . Persons with heart dz: frequent PACs may indicate enhanced automaticity of the atria, reentry mechanisms. May be a warning of initiate more serious dysrhythmias (supraventricular tachycardia)
Tx for PAC
depends on symptoms. Withdrawl stimulation sucha as caffiene or sympathomimetic drugs may be warrented. Beta adrenergic blockers used to decrease PACs
Paroxysmal supraventricular tachycardia
dysrthythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His. (Id of ectopic focus is often difficult even with a 12 lead ECG, as it requires recording the dysrhythmia as it is initiated
PSVT occurs because
reentrant phenonmenon (reexcitation of the atria when there is a one- way block) Usually a PAC triggers a run of repeated premature beats. Paroxysmal refers to an abrupt onset and termination
clincal associations of PSVT
overexertion, emotional stress, deep inspiration and stimulates such as caffine and tobacco. Rheumatic heart dz, dig toxicity, CAD, and corpulmonale
ECG characteristics of PSVT
HR: 150-220 beats/min. Rhythm: regular or slightly irregular. P: often hidden in preceding T wave, if its seen it may have an abnormal shape. PRI: shortened or normal. QRS: normal
clinical significance of PSVT
depends on symptoms. Prolonged episode and HR greater than 180 beats/min may precipitate a decreased CO due to reduced stroke volume. HypoTN, dyspnea, angina
Tx for PSVT
vagal stimulation (coughing and Valsalva) and drug therapy- 1st choice: IV adenosine (Adenocard), IV beta adrenergic blockers and calcium channel blockers and amiodarone can be used
Tx for PSVT if drugs/vagal stimulation are ineffective and pt becomes hemodynamically unstable
direct current cardioversion
