313 Cardio Flashcards

ECG Monitoring

Graphic tracing of electrical impulses produced by the heart. Waveforms of ECG represent activity of charged ions across membranes of myocardial cells

Telemetry monitoring

Continuous observation of HR and rhythm in real time, may be at a distant site from the patient such as a centralized monitoring system

Lead placement of telemetry

Clouds over grass, smoke over fire, brown in the middle

Patient preparation for telemetry

Clip excessive hair on chest wall, rub skin with dry gauze, may need to use an alcohol wipe on oily skin. Apply electrodes

Artifact

results from leads unsticking, muscle or electrical activity like movement.

How many seconds is one strip on an ECG?

6 seconds

Assessment of cardiac rhythm

Must make accurate interpretation and immediately evaluate consequence of findings for individual patient. Assess the patient not the monitor, assess hemodynamic status

Steps in ECG interpretation

1: Rate

2: Rhythm

3: Are P waves present

4: Is the QRS complex present

5: Are intervals WNL

6: is there a P wave for every QRS

7: Is there a QRS for every P wave

Calculating Heart Rate

The best way to calculate HR is to count the number of QRS complexes in 1 minute

Normal Sinus Rhythm

Sinus node 60-100 BPM, follows normal conduction pattern

Dysthymias

Abnormal cardiac rhythms. Due to disorders of impulse formation or disorders of conduction impulses

Which node is the normal pacemaker of the heart

SA node

Common assessment findings with dysrhythmias

Abnormal rate, irregular rhythm, changes in BP, decreased O2, chest, neck, shoulder, back, jaw pain, dizziness, syncope, anxiety, decreased LOC, feeling of doom, numbness, cold clammy skin, diminished pulses, pallor, palpitations, weakness, N/V

Emergent interventions in dysrhythmias

Ensure ABCs, admin O2, obtain baseline VS and O2 sat, obtain 12 lead EKG, hook up telemetry, identify underlying rate and rhythm, establish IV line

Sinus bradycardia

regular rhythm, rate < 60bpm

Cases of sinus bradycardia

normal rhythm in aerobically trained athletes during sleep, occurs in response to valsalva maneuver, vagal stimulation, hypothermia, admin of certain drugs

S+S of sinus bradycardia

hypotension, pale, cool skin, weakness, angina, dizziness, syncope, confusion, SOB

Treatment of sinus bradycardia

atropine 0.5 mg push, pacemaker may be required

Pacemaker

used to pace the heart when the normal conduction pathway is damaged or diseased, consists of power source, one or more conducting leads, myocardium

Temporary pacemaker

pacemaker used temporarily with a power source outside the body

Transvenous pacemaker

leads threaded transvenously to right atrium and/or right ventricle and attached to external power source. Used as a bridge until permeant pacemaker can be inserted or the bradycardia is resolved

Transcutaneous pacemaker

noninvasive temporary procedure, used until transvenous pacemaker is inserted or definitive therapy is available, power source and rate/voltage control device attaches to 2 electrode pads

Placement of transcutaneous pacemaker

attach one pad to the anterior chest and the other pad on the back between the spine and the left scapula at the level of the heard

pt care of a temporary pacemaker

always use lowest current capable of causing a ventricular contraction to minimize pt discomfort. Tell patient what to expect, reassure patient that it is only temporary, whenever possible provide analgesia and sedation

Permanent pacemaker

pacemaker implanted totally within the body. Power source placed subcutaneously, usually over the pectoral muscle on patients non dominant side. Pacer leads are thread transvenously to the right atrium and attached to power source

failure to capture

electrical charge to myocardium is insufficient to produce atrial or ventricular contraction, can result in serious bradycardia or asystole

Failure to sense

failure to recognize spontaneous atrial or ventricular activity and pacemaker fires inappropriately. Fires during excitable period in cardiac cycle can result in VT

Complications of pacemakers

Infection, hematoma formation, pneumothorax, failure to sense or capture, perforation of atrial or ventricular septum, battery failure

Post insertion care of pacemakers

prophylactic antibiotics, post insertion CXR, close observation of insertion site for infection or bleeding, continuous telemetry, limit arm and shoulder movement

Patient education of pacemakers

regular pacer function checks, report signs of infection, avoid lifting arm on pacer side above shoulder, environmental control

Sinus tachycardia

regular rhythms, rate > 100 bpm

Clinical associations sinus tachycardia

Vagal inhibition or sympathetic stimulation, exercise, fever, pain, anxiety, hypovolemia, drugs, caffeine

S+S sinus tachycardia

Dizziness, Dyspnea, hypotension, increased myocardial O2 consumption, increased HR, angina,

Treatment sinus tachycardia

Determined by underlying cause, treat hypotension, fever, or pain. Vagal maneuvers and carotid massage, beta blockers, CCB

Atrial dysrhythmias

caused by pacemaker cells not firing from the SA node but from somewhere else in the atria

Premature atrial contraction

contraction originating from ectopic focus in the atria and not the SA node

Manifestation of PAC

non life threatening dysrhythmia can be seen in NSR, travals across atria by abnormal pathway and creates a distorted P wave,

Causes of PAC

in normal heart it can result from emotional stress or fatigue, caffeine, tobacco, alcohol

Clinical significance of PAC

isolated PAC are not significant in those with healthy hearts, may be warning of more serious dysrhythmia in those with heart disease

Treatment of PAC

monitor frequency and eliminate cause, Beta blockers

Atrial fibrillation

total disorganization of atrial electrical activity due to multiple ectopic foci, resulting in loss or atrial contraction

Manifestations of A fib

atrial rate 300-600bpm, irregular rate and rhythm, no P wave, narrow QRS

Rate of a fib with controlled ventricular response

normal (60-100)

rate of a fib with rapid ventricular response

over 100

rate of a fib with slow ventricular rate

under 60

Cause of A fib

often occurs with underlying cardiac disease

Complications of A fib

loss of CO, loss of atrial kick, thrombi formation as a result of blood stasis, may lead to stroke

Treatment of A fib

decrease the ventricular rate to within normal limits, anticoagulation to prevent thrombus, electric cardioversion

drugs for ventricular rate control

Digoxin, Beta blockers, calcium channel blockers

Drugs to improve cardioversion

amiodarone

Radiofrequency catheter ablation

electrode tipped ablation catheter burns areas of conduction system responsible for irregular rhythm. Definitive treatment for tachycardic dysrhythmias

Synchronized cardioversion

considered for a fib after adequate anticoagulation has been attained, synchronized circuit delivers a counter-shock on the R wave of the QRS complex on the ECG

treatment for complex a fib

anticoagulation therapy needed for a fib not responding to cardioversion

atrial flutter

dysrhythmia produced by pacemaker other than the SA node,

manifestations of atrial flutter

atrial rate 250-350 bpm, ventricular rate will vary, no P waves, flutter waves, QRS narrow

causes of atrial flutter

acute MI, severe mitral valve disease, thyrotoxicosis, COPD, patient who have had thoracic surgery, digoxin toxicity

Clinical significane atrial flutter

high ventricular rates and loss of the atrial kick can decrease CO, risk for stroke due to risk of thrombus formation from blood stasis

Treatment of atrial flutter

primary goal is to control the ventricular rate until SA node can take over. Medication therapy, antiarrhythmatic drugs

Medication therapy for A flutter

CCBs, beta blockers, digoxin

Superventricular tachycardia

any narrow QRS complex with a rhythm over 100 BPM, originates above bundle of his, usually PAC triggers a run of repeated premature beats,

manifestations of superventricular tachycardia

rate 150-200 bpm, rhythm is regular or slightly irregular, P wave often hidden in proceeding T wave, PR is shortened, QRS normal

Causes of superventricular tachycardia

overexertion, emotional stress, stimulants(caffeine, tobacco)

Clinical significance of superventricular tachycardia

prolonged episode and increased HR may precipitate decreased CO, palpitations, hypotension, dyspnea, angina

Treatment of superventricular tachycardia

vagal maneuvers, valsalva, cardioversion, drug therapy

medications for superventricular tachycardia

beta blockers, CCBs, amiodarone

Ventricular rhythms

rhythms that originate somewhere in the ventricles. No P wave, wide QRS complex

Premature ventricular contraction

contraction originating in ectopic focus of the ventricles, premature occurrence of wide distorted QRS complex. No P wave because it originates in the ventricle, compensatory pause

manifestations of PVC

rate varies, irregular rhythm, no P wave, distorted QRS

unifocal PVC

all PVCs look the same

multifocal PVC

multiple PVCs that look different

Couplet PVC

PVCs occur in twos

Triplet PVC

PVCs occur in threes

Ventricular bigeminy

PVC occurs every other beat

Ventricular trigeminy

PVC occurs every third beat

Causes of PVC

stimulants(caffeine, alcohol, nicotine, epinephrine,) fever, exercise, recreational drug use

Clinical significance of PVC

is normal heart, usually benign, pulse deficit may exist

Treatment of PVC

based on cause of PVC, O2 therapy, electrolyte replacement, assess hemodynamic status, drug therapy

Medications for PVC

beta blockers, procainamide, amiodarone, lodocaine

Ventricular tachycardia

run of three or more PVCs, considered life threatening because of decreased CO and the possibility of deterioration to V fib, will cause death if prolonged or untreated

Manifestations of V tach

rate > 150 BPM, regular or irregular rhythm, P wave independent of QRS complex, QRS is distorted

Causes of V tach

hypokalemia, hyperkalemia, MI

Treatment of VT with a pulse

Maintain BP and pulse with or without symptoms, amiodarone, replace electrolytes, cardioversion (usually for symptomatic pts)

Treatment pulseless VT

patient is in cardiac arrest, preform CPR and defibrillation

Defibrillation

most effective method of terminating VF and pulseless VT, passage of DC electrical shock through the heat to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker

Clinical significance V tach

treatment for VT must be rapid, may recur is prophylactic treatment is not initiated, V fib may develop

Ventricular fibrillation

Lethal dysrhythmia requiring immediate treatment, most frequent seen rhythm in cardiac arrest occurring outside the hospital, Ventricle has multiple chaotic impulses rapidly firing

manifestation V fib

no effective CO or contraction occurs, no measurable rate, irregular rhythm, no identifiable P waves or QRS complexes, ECG is shaky

Causes of V fib

MI, coronary reperfusion, hypokalemia, hyperkalemia, electric shock

clinical significance

unresponsive, pulseless, apneic state, death will result quickly

treatment for V fib

immediate initiation of CPR and advanced cardiac life support measure with use of defibrillation and drug therapy

Medications for V fib

Vasopressor-epinephrine, amiodarone

Idioventricular rhythm

SA node and AV node fail to function and the rhythm is generated in the ventricle

Agonal rhythm

dying heart, rate under 20 bpm

accelerated idioventricular rhythm

rate between 40-100 bpm,

Causes of idioventricular rhythm

MI, cardiac arrest, mediactions, electrolyte imbalances, myocarditis, congenital heart disease

Treatment of IVR

is patient is symptomatic, correct the cause, pacing, atropine

Asystole

no measurable electrical activity originating from the heart, straight or flat line is seen on cardiac monitor. Should be assessed with second monitor lead

Treatment asystole

compressions should be started immediately, epinephrine, treat cause defibrillation not indicated

Premature Atrial Contraction

Sinus Bradycardia