Ch. 13 Part 1

Question 1

Patients with serious cardiac diseases such as acute MI, heart failure, and cardiomyopathy are at risk for the development of BBBs, complex ectopy, and wide complex tachycardias.
need to be monitored with lead V1, because it documents interventricular conduction changes.
Leads I and aVF are selected to detect a sudden change in ventricular axis. If ST segment monitoring is required, the lead is selected according to the area of ischemia. If the ischemic area is known, leads V3 and III are recommended to detect ST segment ischemia. In inferior wall injury, leads II, III, and aVF are chosen; if lateral ischemia is present, lead I or aVL should be selected.

Answer 1

Continuous Dysrhythmia Monitoring

Question 2

key responsibility of the critical care nurse is monitoring for myocardial ischemia via ECG changes.
ST segment changes may be accompanied by classic symptoms such as chest pain, or they may be “silent,” without any clinical symptoms except ST segment depression or elevation seen on the ECG monitor. Risk of progression from silent ischemia to overt cardiac events has been documented in patients with diabetes mellitus.
Patients at risk for silent ischemia include patients experiencing an ACS even if treated with fibrinolytics, nitrates, or anticoagulation therapy. Patients undergoing a PCI are at risk for coronary artery repeat occlusion or spasm, reflected by ST segment changes similar to those seen during PCI balloon inflation. Any patient with a history of prior MI, angina, diabetes, or kidney failure is a candidate for ST segment monitoring. ST segment deviation can have nonischemic causes and can create a false-positive alarm. Common culprits include hyperkalemia, pericarditis, hypokalemia, hypomagnesemia, hypothermia, ventricular aneurysm, hypothyroidism, pulmonary infarction, and medications such as quinidine and digitalis. Patients with subarachnoid hemorrhage often demonstrate ST segment changes believed to be caused by excess release of norepinephrine from the myocardial sympathetic nerves.
When setting ST segment alarm parameters, the patient’s condition is always considered. The alarm may be set at 1 mm above and below the baseline ST segment level in patients at high risk for ischemia. In stable, low-risk patients and patients who are more active, the suggested setting is 2 mm above or
below the isoelectric line.
Some ECG patterns do not lend themselves to ST segment monitoring, particularly rhythms that are associated with a wide QRS complex or distortion of the ST segment. This includes LBBB and RBBB, paced rhythms, and idioventricular rhythms. Other rhythms that make ST segment monitoring challenging include erratic atrial fibrillation or atrial flutter that obscures the isoelectric baseline.

Answer 2

Continuous ST segment monitoring

Question 3

can be detected from the 12-lead ECG, because muscle size and shape influences the ECG tracing. may be identified by the size and shape of the P waves and are usually most obvious in lead II. Wide, m-shaped P waves are classically seen in left atrial enlargement Tall, peaked P waves are seen with right atrial enlargement
ECG is not considered definitive in the identification of atrial hypertrophy. The less specific term atrial abnormality is suggested for P wave abnormalities when the underlying pathology is unknown.

Answer 3

Atrial enlargement

Question 4

Ventricular hypertrophy describes an increase in the size and muscle mass of one or both ventricles increased muscle mass results in increased QRS complex voltages, particularly in the precordial leads.
Upright QRS complexes become taller, and negative QRS complexes become even more negative. The QRS complex often becomes slightly wider, because it takes longer to depolarize a larger muscle.
12-lead ECG can suggest hypertrophy, the echocardiogram is the most reliable diagnostic device, because it can visualize ventricular wall thickness and motion.

Answer 4

Ventricular hypertrophy

Question 5

Ischemia is by nature a transient process; when the balance of supply versus demand is restored, the cardiac muscle tissue recovers.
Infarction refers to the death and disintegration of muscle cells and their eventual replacement by fibrotic scar tissue. After infarction has occurred, the process cannot be reversed. Thus careful ECG monitoring and swift intervention to restore myocardial perfusion before infarction can take place is critically important.
ECG changes indicating ischemia and infarction
Infarct location by 12-Lead ECG
Infarction progression on ECG

Answer 5

Ischemia and infarction

Question 6

ST segment elevation is seen when the positive electrode lies directly over an area of transmural (full-wall thickness) injury
The ST segment changes on the surface ECG are caused by differences in voltage gradients between ischemic and healthy myocardium, referred to as injury currents. This represents a preinfarction state, and interventions to unblock the occluded coronary artery must be initiated to prevent death of myocardium.
ST segment depression occurs when the reduction of blood flow is limited to the endocardium and some normal muscle tissue remains between the ischemic area and the positive electrode
T waves most commonly flatten or become inverted.Infarction involves necrosis (death) of muscle cells with eventual formation of scar tissue. These cells can no longer be depolarized when an impulse reaches them.
STEMI is typically associated with a Q wave infarction. Conversely, NSTEMI is more likely to result in a non Q wave infarction

Answer 6

ECG changes indicating ischemia and infarction

Question 7

The location of the infarction can be roughly determined by noting the specific leads in which the ST segment and T wave changes are seen on the 12-lead ECG.
Right ventricular infarction and posterior wall infarction are particularly difficult to identify on a standard 12-lead ECG, because none of the standard leads directly view these areas. Nitrates and other vasodilatory agents, commonly administered in acute infarction of the left ventricle, can cause profound hypotension with negative effect on preload and CO when the infarcted area is in the right ventricle.
A posterior wall infarction may be suspected in a patient with an acute inferior wall MI when there is ST segment depression in leads V1, V2, and V3 on the standard 12-lead ECG. Tall, upright R waves may also be present.
Posterior wall involvement can be verified by adding posterior precordial leads V7, V8, and V9

Answer 7

Infarct location by 12-Lead ECG

Question 8

On the ECG tracing, this process is illustrated as follows: Within minutes of the onset of infarction, ST segment elevation occurs in the leads directly overlying the affected heart wall. This ST segment elevation persists for a period of hours to 1 day, gradually becoming less severe. Within the first few hours, T waves may become tall and symmetric. They are known as hyperacute T waves, and they indicate acute ischemia. Meanwhile, usually within 4 to 24 hours from the onset of the infarction, abnormal Q waves begin to develop in the affected leads, and T waves begin to invert.
Sometimes, instead of Q waves developing, the R waves become smaller.
The ST segments become isoelectric again in a few days, and the T wave becomes symmetric and deeply inverted in the affected leads.
The T waves usually return to normal within several days. The Q waves may persist for the remainder of the patient’s life, or they may get smaller over time and disappear altogether in some individuals.

Answer 8

Infarction progression on ECG

Question 9

A dysrhythmia is any disturbance in the normal cardiac conduction pathway. Dysrhythmias can be detected on a 12-lead ECG, but they often occur only sporadically.
Dysrhythmias occur frequently in cardiac and noncardiac critically ill patients.
HR determination
Rhythm determination
P wave evaluation
PR interval evaluation
QRS complex eval
QT evaluation

Answer 9

Dysrhythmia interpretation

Question 10

first thing to assess when evaluating a rhythm strip is the ventricular rate. Regardless of the dysrhythmia involved, the ventricular rate and blood pressure are key to whether the a patient can tolerate the dysrhythmia
Once the patient can no longer tolerate the dysrhythmia, often a ventricular rate greater than 200 or less than 30, emergency measures must be started to correct the condition.
The three methods for calculating rate are as follows:
1. Number of R-R intervals in 6 seconds times 10 (ECG paper is usually marked at the top in 3-second increments, making a 6-second interval easy to identify).
2. Number of large boxes between QRS complexes divided into 300
3. Number of small boxes between QRS complexes divided into 1500
To find the atrial rate, the P-P interval, instead of the R-R interval, is used in one of the three methods listed for determining rate.
The choice of method for calculating the HR depends on the regularity of the rhythm. If the rhythm is irregular, the first method (R-R intervals in 6 seconds times 10) is the only method that can be used. If the rhythm is regular, any method can be used.

Answer 10

HR determination

Question 11

rhythm refers to the regularity with which the P waves or R waves occur.
If the rhythm is regular, the R-R intervals are the same, within 10%. If the rhythm is regularly irregular, the R-R intervals are not the same, but some sort of pattern is involved, which could be grouping, rhythmic speeding up and slowing down, or any other consistent pattern. If the rhythm is irregularly irregular, the R-R intervals are not the same, and no pattern can be found.

Answer 11

Rhythm determination

Question 12

considering whether the P wave is present or absent.
Sometimes, two, three, or four P waves may be in front of every QRS complex. If this pattern is consistent, the P waves and QRS are still associated, although not on a 1:1 basis.

Answer 12

P wave evaluation

Question 13

The duration of the PR interval, which normally is 0.12 to 0.20 second (120 to 200 ms), is measured first. This is measured from the start of a visible P wave to the beginning of the next QRS complex (Fig. 13.55). All PR intervals on the strip are verified to be sure they have the same duration as the original interval

Answer 13

PR interval evaluation

Question 14

entire ECG strip must be evaluated to ascertain that the QRS complexes are consistently the same shape and width. The normal QRS complex duration is 0.06 to 0.10 second (60 to 110 ms). Any QRS longer than 0.10 second is considered abnormal. If more than one QRS shape is visible on the strip, each QRS complex must be measured. The QRS complex is measured from where it leaves the baseline to where it returns to the baseline

Answer 14

QRS complex eval

Question 15

length of the QT interval varies with the HR. The QT interval is shorter when the HR is faster. A QT interval corrected for HR (QTc interval) that is longer than 0.50 second (500 ms) is of concern, as discussed earlier in the section on QT interval.

Answer 15

QT evaluation

Question 16

NSR
Sinus bradycardia
Sinus tachycardia

Answer 16

Sinus rhythms

Question 17

Rate: The intrinsic rate of the sinus node is 60 to 100 beats/min.
External factors such as medications, fever, or exercise can affect the intrinsic rate.
Rhythm: The rhythm must be regular, within 10%.
P wave: P waves must be present, and only one must precede every QRS complex.
PR interval: The PR interval represents the expected delay in the AV node. In normal sinus rhythm, the PR interval is 0.12 to 0.20 second.
QRS complex: All QRS complexes must look alike. However, QRS complex size and shape may vary in sinus rhythms and often depend on lead placement and gain adjustments on the monitor. If conduction through the ventricles is normal, the QRS complex duration is 0.06 to 0.10 second.

Answer 17

NSR

Question 18

meets all the criteria for normal sinus rhythm except that the rate is less than 60 beats/min
usually is not treated unless the patient displays symptoms of hypoperfusion, such as hypotension, dizziness, chest pain, or changes in level of consciousness.

Answer 18

Sinus bradycardia

Question 19

meets all the criteria for normal sinus rhythm except that the rate is greater than 100 beats/min any sinus tachycardia with a rate greater than 150 beats/min should lead to a search for a triggering focus other than the sinus node.
Tachycardia increases heart work and myocardial oxygen demand, while decreasing oxygen supply by decreasing coronary artery filling time.
Several medications are available to decrease the HR if needed. Calcium channel blockers and beta blockers are widely used for this purpose. However, a word of caution is warranted. Both HR and SV contribute to the CO
If an injured heart can no longer maintain an adequate SV, HR can be increased to maintain CO and supply an adequate blood flow to vital body tissues. If a medication is administered to force the sinus node to slow, severe and relatively immediate heart failure can result.

Answer 19

Sinus tachycardia

Question 20

originate from an ectopic focus in the atria somewhere other than the sinus node. The ectopic impulse occurs prematurely, before the normal sinus impulse occurs.
The premature atrial depolarization may initiate a normal QRS complex, an abnormal or aberrant pattern, or an SVT.
Supraventricular tachycardia
Atrial fibrillation

Answer 20

Atrial dysrhytmias

Question 21

describes a varied group of dysrhythmias that originate above the AV node. SVT is not a specific term; it includes sinus tachycardia, atrial tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation, and junctional tachycardia.
SVT may also be described as a narrow complex tachycardia, defined as a QRS complex that is less than 0.12 second (120 ms).
SVT describes a rapid, sustained atrial or junctional tachycardia when the exact mechanism is unknown.
The differentiation of wide complex SVT from VT requires specific knowledge of the relevant ECG criteria
SVT is not always benign.
A baseline 12-lead ECG is helpful, and a 12-lead ECG should be obtained during the palpitations when possible.

Answer 21

Supraventricular tachycardia

Question 22

Atrial fibrillation may be classified under the broad category of SVT, because the HR is rapid and many patients have symptoms of hypotension and breathlessness during paroxysmal atrial fibrillation when uncontrolled by medication.
Uncoordinated atrial electrical activity leads to a rapid deterioration in atrial mechanical function. The ECG tracing in atrial fibrillation is notable for an uneven atrial baseline that lacks clearly defined P waves and instead shows rapid oscillations or fibrillation wavelets that vary in size, shape, and frequency. The atrial fibrillation waves are particularly visible in the inferior ECG leads II, III, and AVF.
Atrial fibrillation displays irregular R-R intervals (different timing intervals between the QRS complexes) that do not show any logical pattern.
In atrial fibrillation, the QRS complex shape is usually narrow and normal in appearance as long as the pathway through the ventricles is intact after the impulse leaves the AV node. The AV node acts as a filter to protect the ventricles from the hundreds of atrial impulses that occur each minute, although the AV node does not receive all these atrial impulses.
When the atrial muscle tissue immediately surrounding the AV node is in a refractory state, impulses generated in other areas of the atria cannot reach the AV node, which helps explain the wide variation in R-R intervals during atrial fibrillation
Pathogenesis
Risk factors
Atrial fibrillation management.

Answer 22

Atrial fibrillation management.

Question 23

For a hospitalized patient with new-onset atrial fibrillation with unstable hemodynamic values, the primary focus is generally on rhythm control (conversion to sinus rhythm) using antidysrhythmic medications or electrical cardioversion.
Success is less likely if atrial fibrillation has existed for a long time.

Answer 23

• Atrial fibrillation management.

Question 24

For a hospitalized patient with new-onset atrial fibrillation with unstable hemodynamic values, the primary focus is generally on rhythm control (conversion to sinus rhythm) using antidysrhythmic medications or electrical cardioversion.
Success is less likely if atrial fibrillation has existed for a long time.

Answer 24

Rhythm control - Atrial fibrillation management.

Question 25

Cox-Maze III procedure (typically called the maze procedure) is an open-heart surgical operation.
The surgical maze procedure is now rarely performed, as it has been replaced by catheter-based techniques

Answer 25

Surgical procedures to manage atrial fibrillation. - Atrial fibrillation management.

Question 26

Many factors must be considered before choosing radiofrequency catheter ablation. Type of atrial fibrillation, degree of symptoms, presence of structural heart disease, candidacy for alternative options, candidacy for anticoagulation, and patient preference must all be assessed. The goal of radiofrequency catheter ablation is to reduce clinical symptoms associated with atrial fibrillation

Answer 26

Catheter procedures to manage atrial fibrillation. - Atrial fibrillation management.

Question 27

medications work to slow conduction through the AV node. They have no effect on the fibrillating atria.

Answer 27

Rate control - Atrial fibrillation management.

Question 28

Atrial fibrillation, because of the development of thrombi in the atria, greatly increases the risk of embolic stroke.
Electrical and chemical (medication-induced) forms of cardioversion entail the threat of precipitating emboli into the systemic circulation.
If cardioversion is successful and normal sinus rhythm is restored, the atria again contract forcibly and, if thrombus formation has occurred, may send clots traveling through the pulmonary or systemic circulation.
To prevent embolic stroke, it is important to pay attention to the 48-hour rule. Patients who have been in atrial fibrillation for greater than 48 hours, or unknown, must be adequately anticoagulated with an oral vitamin K antagonist (warfarin) to a goal INR of 2.0 to 3.0, a factor Xa inhibitor, or a direct thrombin inhibitor for at least 3 weeks before elective cardioversion.

Answer 28

Stroke risk assessment and antithrombotic therapy in atrial fibrillation - Atrial fibrillation management.

Question 29

is an easy-to-remember risk assessment tool used to predict stroke risk in atrial fibrillation and to guide antithrombotic therapy. The letters stand for cardiac failure, hypertension, age, diabetes, stroke (double points). The score ranges from 0 to 6.

Answer 29

CHADS2. - Atrial fibrillation management.

Question 30

include acute heart failure, hypertension, age 75 years or older (double points), diabetes, stroke (double points), vascular disease, age 65 to 74 years, and sex (female) demonstrated increased specificity and is more widely used.

Answer 30

CHA2DS2-VASc. - Atrial fibrillation management.

Question 31

result from an ectopic focus in any portion of the ventricular myocardium.
usual conduction pathway through the ventricles is not used, and the wave of depolarization must spread from cell to cell. The QRS complex is prolonged and is always greater than 0.12 second. The width of the QRS complex, not the height, is important in the diagnosis of ventricular ectopy.
ventricular dysrhythmias have more serious implications
Premature ventricular contractions (PVC)
Ventricular fibrillation
Differential Diagnosis of Wide QRS Complex Tachycardia

Answer 31

Ventricular Dysrhythmias - Atrial fibrillation management.

Question 32

single ectopic impulse originating in the ventricles. Some PVCs are very small in height but remain wider than 0.12 second. If there is doubt, a different lead is evaluated.
Because the ectopic focus may be any cell in the ventricle, the QRS complex can manifest in an unlimited number of shapes or patterns. If all the ventricular ectopic beats look the same in a particular lead, they are called unifocal, which means that they probably all result from the same irritable focus
if the ventricular ectopic beats are of various shapes in the same lead, they are called multifocal
A PVC originates in a ventricular cell that has become abnormally permeable to sodium, usually as a result of damage.
Compensatory pause
Describing ventricular ectopy
Premature ventricular contraction timing.
Causes of premature ventricular contractions.
Premature ventricular contraction management.
Ventricular tachycardia.

Answer 32

Premature ventricular contractions (PVC)

Question 33

When the impulse from the sinus node is interrupted by a PVC, a compensatory pause occurs.
If the normal sinus P wave that occurs immediately after the PVC finds the ventricles sufficiently recovered to accept another impulse, a normal QRS complex results, and the PVC is sandwiched between two normal beats - referred to as interpolated
The ventricular impulse occasionally spreads backward across the AV node to depolarize the atria. When this occurs, the sinus node is reset, and no full compensatory pause occurs.

Answer 33

Compensatory pause - Premature ventricular contractions (PVC)

Question 34

PVCs can develop concurrently with any supraventricular dysrhythmia. It is not sufficient to describe a patient’s rhythm as “frequent PVCs” or even “frequent unifocal PVCs.” The underlying rhythm must always be described first

Answer 34

Describing ventricular ectopy - Premature ventricular contractions (PVC)

Question 35

The timing of PVCs can be important. The relative refractory period, represented on the ECG by the last half of the T wave, is a particularly vulnerable time for ectopy to occur, because repolarization is incomplete.

Answer 35

Premature ventricular contraction timing. - Premature ventricular contractions (PVC)

Question 36

Metabolic abnormalities are common causes of PVCs.
Any form of structural heart disease can lead to ventricular ectopy. In these situations, the ectopy usually resolves with removal or advancement of the catheter.
Certain medications can cause ventricular ectopy.

Answer 36

Causes of premature ventricular contractions. - Premature ventricular contractions (PVC)

Question 37

PVCs do not represent an increased risk for sudden death and are considered benign. If the patient complains of palpitations or becomes symptomatic, therapy includes reassurance and correction of any potentially contributing factors

Answer 37

Premature ventricular contraction management. - Premature ventricular contractions (PVC)

Question 38

caused by a ventricular pacing site firing at a rate of 100 times or more per minute, usually maintained by a reentry mechanism within the ventricular tissue
complexes are wide, and the rhythm may be slightly irregular, often accelerating as the tachycardia continues. In most cases, the sinus node is not affected, and it continues to depolarize the atria on schedule.
occurs in the presence of structural cardiac disease, Other triggers include medication toxicities, electrolyte disturbances, and certain antidysrhythmic medications.
Life-threatening dysrhythmia and must be treated quickly.
Clinical management of VT depends on whether the patient is stable or unstable and whether a pulse and adequate blood pressure are present.
Patients with stable or wide complex “slow VT” who have a HR below 150 beats/min, palpable pulse, and stable blood pressure may be treated pharmacologically and/or with synchronized cardioversion as described in the advanced cardiac life support protocols.
After the acute episode is over, patients who have already experienced sustained VT or cardiac arrest continue to be at risk for sudden cardiac death.
Therapy is aimed at preventing a recurrence of sustained VT or VF. It may include treating the underlying cause, administering antidysrhythmic medications, performing ablation of the reentrant pathway within the ventricle, or inserting an implantable cardioverter defibrillator (ICD).

Answer 38

Ventricular tachycardia. - Premature ventricular contractions (PVC)

Question 39

chaotic electrical activity in the ventricles from repetitive, small areas of reentry or a series of rapid discharges from various foci within the ventricular myocardium.
When VF occurs in the setting of an acute ischemic event and is accompanied by a significant amount of myocardial damage, the survival rate is poor. Resuscitation is often unsuccessful; recurrence rates are high for patients who are resuscitated.
As with any cardiac arrest situation, supportive measures such as cardiopulmonary resuscitation, intubation, and correction of metabolic abnormalities are performed concurrently with definitive therapy.

Answer 39

Ventricular fibrillation

Question 40

VT is the most common reason for a sudden-onset wide complex tachycardia; however, an atypical supraventricular wide complex tachycardia with an ectopic atrial or junctional focus arising from an irritable site above the ventricles may also be the cause.
Typical SVT has a narrow QRS complex (less than 0.12 second duration), because the electrical impulse enters the ventricle through the AV node and continues down the normal conduction pathway by means of the bundle branches through the ventricles.
Significance of ventricular tachycardia and supraventricular tachycardia.
Clinical differentiation of ventricular tachycardia from supraventricular tachycardia.

Answer 40

Differential Diagnosis of Wide QRS Complex Tachycardia

Question 41

treated with a variety of medications that work by blocking the AV node conduction pathway: important to be sure of the cause of the tachycardia in individuals who are relatively hemodynamically stable before treatment is initiated.
rapid wide QRS complex tachycardia may not be well tolerated, largely because of the fast HR and decreased CO. Hemodynamic deterioration is evidenced by syncope, severe hypotension, or ischemic symptoms.
If there is a history of VT or sudden cardiac death and the patient is already on antidysrhythmic therapy, a recurrent episode of VT indicates that the current treatment regimen is not effective and the therapy needs to be changed.

Answer 41

Significance of ventricular tachycardia and supraventricular tachycardia. - Differential Diagnosis of Wide QRS Complex Tachycardia

Question 42

The most reliable bedside method of diagnosing a wide QRS complex tachycardia is through careful analysis of the ECG. HR and heart rhythm are evaluated first, although they are not the only diagnostic indicators.
When the sinus node remains in control of the atria and a ventricular ectopic focus is in control of the ventricles, it is likely that at some point the timing will be coordinated, and, by chance, the sinus impulse will conduct through the AV node and begin to depolarize the ventricles just as the ventricular ectopic focus fires. The resulting QRS complex is a fusion beat which resembles a blend of the patient’s normal QRS complex and the wide QRS complex of the ventricular dysrhythmia. The presence of fusion beats also strongly suggests VT.

Answer 42

Clinical differentiation of ventricular tachycardia from supraventricular tachycardia. - Differential Diagnosis of Wide QRS Complex Tachycardia

Question 43

On the ECG, the ability of the AV node to conduct is evaluated by measuring the PR interval and the relationship of P waves to QRS complexes. The normal PR interval, measured from the beginning of the P wave to the beginning of the QRS complex, ranges from 0.12 to 0.20 second. When the normal conduction of the AV node is impaired, the PR interval will be greater than 0.2 second, resulting in a heart block.
First-Degree Atrioventricular Block
Second-Degree Atrioventricular Block
Third-Degree Atrioventricular Block
Management of Atrioventricular Block

Answer 43

Atrioventricular Blocks

Question 44

When all atrial impulses are conducted to the ventricles and the PR interval is greater than 0.20 second, a condition known as irst-degree AV block exists
First-degree AV block can be chronic or acute, and it may be caused by a multitude of conditions. Chronic first-degree block may occur related to fibrosis and sclerosis of the conduction system, lack of blood supply to the conduction system secondary to coronary artery disease (CAD), valvular heart disease, myocarditis, and various cardiomyopathies. First-degree heart block that develops acutely is of much greater concern. Causes include medication toxicity related to digoxin, beta blockers, or amiodarone administration; acute myocardial ischemia or MI; hyperkalemia; edema after valvular heart surgery; and increased vagal tone. If the associated QRS complex is narrow, it is likely that the only conduction abnormality is in the AV node. However, if the associated QRS complex is widened, it is likely that there is also damage to the bundle branches as a result of sclerosis, ischemia, or infarction.

Answer 44

First-Degree Atrioventricular Block

Question 45

a condition in which some atrial impulses are conducted to the ventricles, but others are “blocked” at the AV node. This description of intermittent AV conduction covers two patterns with markedly different clinical significance: Second-degree AV block is divided into Mobitz type I (also known as Wenckebach block) and Mobitz type II.
Mobitz type I.
Mobitz type II

Answer 45

Second-Degree Atrioventricular Block

Question 46

the AV conduction times progressively lengthen until a P wave is not conducted.
the QRS complex is generally of normal width and appearance.
The sinus node is functional and generates impulses that conduct to the AV node at a constant rate. On the ECG, the measured P-P interval is regular.
each successive atrial impulse arrives earlier into the relative refractory period of the impaired AV node, more time is needed to conduct the impulse. On the ECG, this is seen as an incremental increase in the length of each PR interval. The R-R interval usually becomes shorter with each beat.
The PR interval is shortest in the first beat.
final P wave of the group is not conducted. The atrial impulse arrives during the absolute refractory period of the AV node and is not conducted. This is seen on the ECG by a P wave that is not followed by a QRS complex
The expected groups are 3:2, 4:3, or 5:4.
does not generally cause significant hemody- namic compromise as long as the ventricular HR is maintained.

Answer 46

Mobitz type I. - Second-Degree Atrioventricular Block

Question 47

always anatomically located below the AV node in the bundle of His, in the bundle branches, or in the Purkinje fibers. This results in an all-or-nothing situation with respect to AV conduction.
When conduction does occur, all PR intervals are the same. Because of the anatomic location of the block, the PR interval is constant and the QRS complexes are wide on the ECG may progress to complete AV block.
the QRS complex is usually wide, and the PR interval is usually normal

Answer 47

Mobitz type II - Second-Degree Atrioventricular Block

Question 48

complete, AV block is a condition in which no atrial impulses can conduct from the atria to the ventricles.
Pacemaker support is often necessary to maintain an adequate CO.
On the ECG, P waves are present and usually occur at regular intervals.
If a ventricular focus is pacing the heart, the QRS complex is wide and unrelated to the P waves

Answer 48

Third-Degree Atrioventricular Block

Question 49

consequences of AV block range from benign to life-threatening. First-degree AV block is seldom of immediate concern but requires close observation for progression of the conduction disturbance. Second-degree Mobitz I (Wenckebach) is usually benign as long as the patient is not bradycardic. If hemodynamic compromise is present or deemed likely, a temporary pacemaker can be inserted prophylactically. Second-degree Mobitz II is more serious and often precedes complete AV block. Use of a temporary pacemaker is recommended
Complete heart block causes AV dissociation and is associated with a low CO that requires use of a pacemaker.

Answer 49

Management of Atrioventricular Block

Question 50

Laboratory studies of blood serum are performed to assess the following:
1. Electrolyte levels that can alter cardiac muscle contraction
2. Cardiac biomarkers that reflect myocardial cellular integrity
or infarction
3. Hematologic status to evaluate risk of anemia and infection
4. Coagulation times
5. Serum lipid levels
6. Status of other organ systems that can secondarily affect cardiac function
Electrolytes

Answer 50

Lab tests

Question 51

Potassium
Calcium
Magnesium

Answer 51

Electrolytes

Question 52

During depolarization and repolarization of nerve and muscle fiber, potassium and sodium exchange occurs intracellularly and extracellularly.
Hyperkalemia.
Hypokalemia.

Answer 52

Potassium

Question 53

Elevated serum potassium (higher than 4.5mEq/L), called hyperkalemia, can be caused by various conditions, including excess potassium administration, extensive skeletal muscle destruction (rhabdomyolysis), tumor lysis syndrome, and kidney failure. Some medications may induce hyperkalemia, decreases AV conduction velocity, slows ventricular depolarization, and accelerates repolarization.

Answer 53

Hyperkalemia.

Question 54

(less than 3.5 mEq/L) caused by diuretic therapy with insufficient replacement, gastrointestinal losses, and some medications.85 Hypokalemia is also reflected by changes on the ECG. The earliest ECG change is often PVCs, which can deteriorate into VT or VF without appropriate potassium replacement.
impairs myocardial conduction and prolongs ventricular repolarization; this can be seen by a prominent U wave (a positive deflection after the T wave on the ECG). The U wave is not totally unique to hypokalemia, but its presence is a signal for the clinician to check the serum potassium level.

Answer 54

Hypokalemia.

Question 55

Calcium is an important mediator of many cardiovascular functions because of its effect on vascular tone, myocardial contractility, and cardiac excitability.
Hypercalcemia.
Hypocalcemia.

Answer 55

Calcium

Question 56

defined as increased amounts of ionized calcium (greater than 4.8 mg/dL or 1.30 mmol/L) or increased amounts of total serum calcium (greater than 10.5 mg/dL or 2.60 mmol/L).
Cardiovascular effects of elevated serum calcium include strengthening contractility and shortening ventricular repolarization, demonstrated on the ECG by a shortened Q-Tc interval. Rhythm disturbances may include bradycardia; first-degree, second-degree, and third-degree heart block; and BBB.
Hypercalcemia can potentiate the effects of digitalis and cause hypertension.
Management of symptomatic hypercalcemia involves promotion of calcium excretion

Answer 56

Hypercalcemia.

Question 57

defined as an ionized calcium level below normal (less than 1.05 mmol/L) or a low total serum calcium level.
The cardiovascular effects of hypocalcemia include decreased myocardial contractility, decreased CO, and hypotension. Rhythm disturbances with severe hypocalcemia are variable, ranging from bradycardia to VT and asystole.
When ionized calcium is low, the ECG may show a prolonged QTc interval (Fig. 13.82). A prolonged QTc predisposes a patient to torsades de pointes.

Answer 57

Hypocalcemia.

Question 58

is essential for many enzyme, protein, lipid, and carbohydrate functions in the body and is critical for the production and use of energy.
The normal serum range is 1.5 to 2 mEq/L, 1.8 to 2.4 mg/dL, or 0.7 to 1.1 mmol/L.
Hypermagnesemia.
Hypomagnesemia.

Answer 58

Magnesium

Question 59

rare in critical care patients. It results from kidney failure, tumor lysis syndrome, or iatrogenic overtreatment.

Answer 59

Hypermagnesemia.

Question 60

defined as a total serum magnesium concentration less than 1.5 mEq/L.
ECG changes are similar to changes seen with hypokalemia and hypocalcemia: prolonged PR and QTc intervals, presence of U waves, T wave flattening, and widened QRS complex. Cardiac dysrhythmias may be supraventricular or ventricular and include the polymorphic ventricular rhythm torsades de pointes.

Answer 60

Hypomagnesemia.