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Dysrhythmias > Chapter 36 > Flashcards

Chapter 36 Flashcards

0
Q

Automaticity, excitability, conductivity, and contractility enable the conduction system to perform what?

A

Initiate an electrical impulse, transmit it through the cardiac tissue and stimulate muscle contraction.

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1
Q

What are the four properties of cardiac cells?

A

Automaticity, excitability, conductivity, and contractility

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2
Q

Automaticity

A

Ability to initiate an impulse spontaneously and continuously.

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3
Q

Electrocardiogram

A

A graphic tracing of the electrical impulses produced in the heart.

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4
Q

Changes in a 12-lead ECG may occur with damage such as?

A

Ischemia or infarction, electrolyte imbalance, dysrhythmias, enlarged cardiac chambers, or drug toxicity.

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5
Q

The process of a normal cardiac impulse

A

Begins in the upper right atrium at the SA node, spreads via intra-atrial pathways and intermodal pathways causing atrial contraction, the impulse then travels to the AV node, through the bundle of His, down the left and right bundle branches, and ends in the Purkinje fibers transmitting the impulse to the ventricles.

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6
Q

Excitability

A

Ability to be electrically stimulated

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7
Q

Conductivity

A

Ability to transmit an impulse along a membrane in an orderly manner

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8
Q

Contractility

A

Ability to respond mechanically to an impulse

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9
Q

Autonomic Nervous System Roles of the Heart

A

Rate of impulse formation, speed of conduction, and the strength of cardiac contraction.

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10
Q

Components of the ANS affecting the heart

A

Vagus nerve fibers of the PNS and nerve fibers of the SNS

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11
Q

Most common ECG leads used for patient monitoring

A

ECG Leads II, V1and MCL 1

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12
Q

Telemetry Monitoring observes patient’s

A

Heart rate and rhythm which provides a rapid diagnosis of dysrhythmias, ischemia and infarction.

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13
Q

P wave

A

Represents time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction).

Normal duration: 0.6-0.12 sec

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14
Q

P-R interval

A

Represents time taken for impulse to spread through the atria, AV node and bundle of His, bundle branches, and Purkinje fibers, to a point preceding ventricular contraction.

Normal duration: 0.12-0.20 sec

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15
Q

QRS interval

A

Represents time taken for depolarization (contraction) of both ventricles (systole).

Normal duration: <0.12 sec

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16
Q

ST segment

A

Represents the time between ventricular depolarization and repolarization (diastole).

Normal duration: 0.12 sec

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17
Q

T wave

A

Represents time for ventricular depolarization.

Normal duration: 0.16 sec

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18
Q

QT interval

A

Represents time taken for entire electrical depolarization and repolarization of the ventricles.

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19
Q

Source of possible variation in P wave

A

Disturbance in conduction within atria.

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20
Q

Source of possible variation in P-R interval

A

Disturbance in conduction usually in AV node, bundle of His, or bundle branches, but can be in atria.

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21
Q

Source of possible variation in QRS interval

A

Disturbance in conduction in bundle branches or in ventricles.

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22
Q

Source of possible variation in ST segment

A

Disturbances usually caused by ischemia, injury or infarction.

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23
Q

Source of possible variation in T wave

A

Disturbances usually caused by electrolyte imbalances, ischemia or infarction.

24
Q

Source of possible variation in QT interval

A

Disturbances usually affecting repolarization more than depolarization and caused by drugs, electrolyte imbalances, and changes in heart rate.

25
Q

Intrinsic rate of the SA node

A

60-100 times/min.

26
Q

Intrinsic rate of the AV node

A

40-60 times/min

27
Q

Intrinsic rate of the bundle of His, Purkinje fibers

A

20-40 times/min

28
Q

Common cardiac causes of dysrhythmias

A

Accessory pathways, cardiomyopathy, conduction defects, heart failure, myocardial ischemia, infarction, valve disease.

29
Q

Other common conditions causing dysrhythmias

A

Acid base imbalance, alcohol, caffeine, tobacco, connective tissue disorders, drug toxicity, electric shock, hypokalemia and hypocalcemia, emotional crisis, herbal supplements, hypoxia, metabolic conditions, near-drowning, poisoning, sepsis, shock

30
Q

Atrial fibrillation definition

A

Is characterized by a total disorganization of atrial activity due to multiple ectopic foci resulting in loss of effective atrial contraction.

31
Q

Clinical associations of Atrial Fibrillation

A

CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, heart failure, and pericarditis.

32
Q

ECG characteristics of Atrial Fibrillation

A

Atrial rate: 350-600 bpm, P waves are replaced by fibrillatory waves, R-R intervals (rhythm) is irregular, P-R interval is not measurable, and the QRS complex normal shape and duration.

33
Q

Clinical significance of Atrial Fibrillation

A

Results in a decrease in CO, increasing a risk for CVA due to clot formation in the atria.

34
Q

Treatment for a patient with Atrial Fibrillation for less than 48 hours

A

Calcium channel blockers or electrical conversion of Atrial Fibrillation to a normal sinus rhythm may be consideration.

35
Q

Treatment for a patient that is in Atrial fibrillation more than 48 hours

A

Anticoagulation therapy with warfarin (Coumadin) is needed for 3 weeks before the cardioversion and 4 weeks after successful cardioversion.

Patients INR is monitored for therapeutic levels.

36
Q

Treatment for patients with drug refractory atrial fibrillation

A

Radiofrequency catheter ablation is done to restore normal sinus rhythm.

37
Q

Sinus Bradycardia definition

A

The conduction pathway is the same as that in sinus rhythm but the SA node fires at a less than 60 bpm. Symptomatic bradycardia refers to a HR that is less than 60 bpm and is inadequate for the patient’s condition, causing the patient to experience chest pain, syncope.

38
Q

Clinical associations with Sinus Bradycardia

A

Normal in some athletes and some individuals during sleep. It may occur in carotid sinus massage, valsalva maneuver, hypothermia, increased ocular pressure, Vagal stimulation and certain drugs.

39
Q

ECG characteristics of Sinus Bradycardia

A

HR <60 bpm, rhythm is regular, P wave precedes each QRS complex (normal shape and duration), P-R interval is normal.

40
Q

Clinical significance of Sinus Bradycardia

A

Depends on how the patient tolerates hemodynamically. Signs of symptomatic bradycardia include pale, cool skin; hypotension; weakness; angina;dizziness or syncope; confusion or disorientation; and SOB.

41
Q

Treatment of bradycardia

A

May require administration of Atropine, pacemaker therapy, and if bradycardia is due to drugs, they may need to be held, discontinued, or dosages reduced.

42
Q

Sinus Tachycardia definition

A

The conduction pathway is the same in sinus tachycardia as that in normal sinus rhythm. The discharge rate from the sinus node increases because of Vagal inhibition or sympathetic stimulation.

The sinus rate is 101-200 bpm

43
Q

Clinical associations with sinus Tachycardia

A

Exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure, hyperthyroidism, anxiety and fear.

It can also be an effect of drugs such as epinephrine, norepinephrine (levophed), atropine, caffeine, theophylline, nifedipine, or hydralazine.
Many OTC cold remedies with active ingredient (pseudo ephedrine) can cause tachycardia.

44
Q

ECG characteristics of sinus tachycardia

A

HR: 101-200 bpm, rhythm is regular, P wave is normal, QRS complex has normal shape and duration, PR interval is normal.

45
Q

Treatment for sinus tachycardia

A

If tachycardia is caused from pain (pain management). If caused from hypovolemia ( treat hypovolemia). In stable patients the Vagal maneuver can be attempted.

IV metoprolol (Lopressor) can be given to reduce HR and decrease myocardial oxygen consumption.

46
Q

Ventricular Fibrillation definition

A

A severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude. No cardiac output occurs, a lethal dysrhythmia.

47
Q

Clinical associations of ventricular Fibrillation

A

Acute MI, myocardial ischemia, heart failure, and cardiomyopathy. It may occur during cardiac pacing or cardiac catheterization procedures because of catheter stimulation of the ventricle. Can occur with coronary perfusion after fibrinolytic therapy.

48
Q

ECG characteristics of ventricular fibrillation

A

HR: not measurable, rhythm is irregular and chaotic, P wave is not visible, PR interval and QRS intervals are not measurable.

49
Q

Clinical significance of Ventricular Fibrillation

A

Results in an unresponsive, pulse less, and pandemic state. Patient will die if not treated immediately.

50
Q

Treatment of Ventricular Fibrillation

A

initiate CPR immediately and advanced cardiac life support (ACLS) measures with the use of defibrillation and definitive drug therapy.

51
Q

Ventricular Tachycardia definition

A

A run of three or more PVCs. It occurs when ventricle takes control as the pacemaker.

Decrease in CO and possibility of developing ventricular fibrillation.

52
Q

Monomorphic Ventricular tachycardia

A

QRS complexes are the same in shape, size and direction.

53
Q

Polymorphic Ventricular tachycardia

A

QRS complexes gradually change back and forth from one shape , size, and direction to another over a series of beats.

Torsades de pointers: prolonged QT interval

54
Q

Clinical associations with Ventricular tachycardia

A

MI, CAD, significant electrolyte imbalance, cardiomyopathy, mitral valve prolapse, long QT syndrome, drug toxicity, and CNS disorders.

VT dysrhythmia can be seen in patients who have no evidence of cardiac disease.

55
Q

ECG characteristics of Ventricular Tachycardia

A

Ventricular rate is 150-250 bpm, rhythm may be regular or irregular, AV dissociation may be present, with P waves occurring independently of the QRS complex. The atria may be depolarized by the ventricles in a retrograde fashion. The P wave is usually buried in the QRS complex, and the PR interval is not measurable.

The QRS complex is distorted in appearance, with a duration greater than 0.12 sec and with the ST -T wave in the opposite direction of the QRS complex. The R-R interval may be regular or irregular.

56
Q

Clinical significance of Ventricular Tachycardia

A

VT can be stable (patient has a pulse) or unstable (patient is pulseless). Sustained VT causes a severe decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction. This results in hypotension, pulmonary edema, decreased cerebral blood flow, and cardio pulmonary arrest. The dysrhythmia must be treated quickly, even if it occurs only briefly and stops abruptly. Episodes may recur if prophylactic treatment is not started. Ventricular fibrillation my also develop.

57
Q

Treatment for Ventricular Tachycardia

A

If patient is hemodynamically stable and has preserved left ventricular function, IV lidocaine is administered. Drugs that prolong QT interval are discontinued.

If patient is unstable, CPR and rapid defibrillation are performed followed by the administration of vasopressors (epinephrine) and anti dysrhythmias (amiodarone).

58
Q

VA: Accelerated idioventricular rhythm treatment

A

Atropine can be considered, temporary pacing may be required.

Dysrhythmias (1 decks)

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