Ecg Dysrhythmias

Front 1

Dysrhythmias result from

Back 1

disorders of impulse formation, conduction of impulses or both

Front 2

Sinus bradycardia

Back 2

the conduction pathway is the same as in sinus rhythm, but the SA node fires at a rate of less than 60 beats/ min and is inadequate for the patient's condition, causing pt to experience symptoms

Front 3

Clinical associations of sinus bradycardia

Back 3

May be normal during sleep and in trained athletes

-occurs in response to carotid sinus massafe, valsalva maneuver, hypothermia, increased IOP, vagal stimulation, admin of CCBs, Beta adrenergic blockers

- Disease states associated w/ are hypothyroidism, increased ICP, hypoglycemia, inferior MI

Front 4

Sinus bradycardia ECG characteristics

Back 4

HR is less than 60 beats/min and rhythm is regular

-The P wave precedes each QRS complex and has a normal shape and duration

-The PR interval is normal and the QRS complex has a normal shape and duration

Front 5

Signs of symptomatic bradycardia include

Back 5

Clinical significance depends on how pt tolerates it

-Pale, cool skin

-Hypotension

-weakness

-Angina

-dizziness / syncope

-SOB, confusion, disorientation

Front 6

TX of sinus bradycardia

Back 6

Admin of atropine (Anticholinergic)

- Pacemaker

-Stop offending drugs

Front 7

Sinus tachycardia

Back 7

The conduction pathway is the same as normal sinus rhythm

- The discharge rate from the sinus node increases because of vagal inhibition or sympathetic stimulation

-The sinus rate is 101 - 200 beats/minute

Front 8

Clinical associations of sinus tachycardia

Back 8

Physiologic and psychologic stressors (exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, MI, HF, hyperthyrodism. anxiety, fear

-epinephrine, norepinephrine, atropine, caffeine, sudaphed, theophulline, hydralazine

Front 9

ECG characteristics

Back 9

HR is 101-200 beats/minute and rhythm is regular

P wave normal, precedes each QRS complex and has normal shape and duration

-PR interval is normal and the QRS complex has a normals shape and duration

Front 10

Clinical significance

Back 10

Depends on pt's tolerance to increased HR

-dizziness, dyspnea, hypotension because of decreased CO

-Increased myocardial oxygen consumption is associated w/ an increased HR

-Angina or an increased in infraction size may accompany sinus tachy in CAD or acute MI

Front 11

Treatment

Back 11

underlying cause of tachycardia guides tx

-treat pain

-vagal maneuvers

-beta adrenergic blockers can be given to reduce HR and decrease o2 consumption

Front 12

Atrial Fibrillation

Back 12

Stroke is the biggest risk

Older and underlying heart disease are most at risk

Atrial fibrillation results in a decrease in CO because ofineffective atrial contractions (loss of atrial kick) and/or a rapidventricular response. Thrombi (clots) form in the atria because of bloodstasis. An embolized clot may develop and pass to the brain, causing a stroke.Atrial fibrillation accounts for as many as 17% of all strokes.

Front 13

TX of A-fib

Back 13

Meds to control ventricular rate and/or convert (CBC, B-adrenergic, digoxin)

Cardioversion

Anticoagulation (Coumadin)

Ablation

Front 14

Ventricular tachycardia associated w/

Back 14

MI

CAD

significant electrolyte imbalances

cardiomyopathy

mitral valve prolapse

long QT syndrome

drug toxicity

central nervoussystem disorders.

This dysrhythmia can be seen in patients who have no evidenceof cardiac disease.

Front 15

Stable v. unstable

& Treatments of these

Back 15

Stable - pulse

Tx: antidysrhythmics, cardioversion

unstable - pulseless

Tx: CPR, Rapid defibrillation

Front 16

Result of a sustained VT?

Back 16

Severe decrease in CO - hypotension, pulmonary edema, decreased cerebral perfusion, cardiopulmonary arrest

VT is an ominous sign because of decreased CO and possible development of v-fib

Front 17

What do you do if the monitor shows VT?

Back 17

1) assess the patient : stable or unstable

2) call a code and start CPR

Front 18

Ventricular fibrillation associate w/

Back 18

MI, ischemia, disease states, procedures

Front 19

Pt is likely to be

Back 19

unresponsive, pulseless, apneic

Front 20

Treatment:

Back 20

CPR and ACLS

-defibrillation

-Drug therapy (epic, vasopressin)

untreated = death

Front 21

Monitor shows V-fib:

Back 21

1) assess

2) start CPR and call a code

Front 22

Atrial flutter caused by:

Back 22

Diseases: CAD, HTN, mitral valve disorders, PE, chronic lung disease, cor pulmonale, cardiomyopathy, hyperthyrodism,

Drugs: digoxin, quinidine, epinephrine

Stroke risk because of the risk of thrombus formation in the atria from the stasisof blood. Warfarin (Coumadin) is given to prevent stroke in patients who haveatrial flutter.

Front 23

Treatment:

Back 23

Meds

Cardioversion

Ablation

•Slow ventricularresponse with calcium channel blockers and β-adrenergic blockers. •Convert withantidysrhythmics - ibutilide [Corvert])•Maintain sinusrhythm (e.g., amiodarone, flecainide [Tambocor], dronedarone [Multaq]).•Cardioversion inan emergency (i.e., the patient is hemodynamically unstable) and electively. •Ablation -treatment of choice for atrial flutter. Tissue is ablated(or destroyed), the dysrhythmia is ended, and normal sinus rhythm is restored.

Front 24

Pacemakers indications

Back 24

Permanent pacemakers are used for chronic heart problems inwhich heart beats too slowly to adequately support perfusion (i.e., AV heartblocks, sick sinus syndrome, atrial fibrillation with slow ventricularresponse, severe heart failure, cardiomyopathy, bundle branch block).