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Chapter 16 : 

Chapter 16 Electrolyte and Drug Effects

Introduction : 

Introduction  Electrolytes are found in extracellular and intracellular fluid of most cells.  Most important electrolytes are sodium, potassium, calcium, and magnesium.  Flow of these electrolytes into and out of cells creates energy for depolarization and repolarization, and allows contractile mechanisms to function.  Levels of electrolytes affect currents and appearance of complexes on ECG.

The Two Main Electrolytes : 

The Two Main Electrolytes The two main electrolytes that cause diagnostic and recognizable changes on ECG: Potassium Calcium It’s important to correlate ECG findings with possible drug effects. We will concentrate on only digoxin because of its association with various changes and arrhythmias.

Hyperkalemia and Its Effects : 

Hyperkalemia and Its Effects Hyperkalemia = most dangerous of all electrolyte changes. Can kill in seconds Prevents response to drugs used in resuscitation It causes: Changes in appearance of QRS complex Any and all arrhythmias Keys to effectively combating complications of hyperkalemia: Immediate recognition and action to stabilize myocardial membrane and reverse pathological processes

Main Changes in Hyperkalemia : 

Main Changes in Hyperkalemia T wave abnormalities, especially tall and peaked T waves Intraventricular conduction delays (IVCDs) P waves missing or of decreased amplitude ST segment changes simulating an injury pattern Cardiac arrhythmias, any and all varieties Concentrate on T waves, remembering any wide rhythm could be due to hyperkalemia.

Spectrum of Hyperkalemia (1 of 2) : 

Spectrum of Hyperkalemia (1 of 2) Hyperkalemia occurs across a spectrum: T waves become tall and sharp. All intervals begin to widen and decrease in amplitude. P wave loses amplitude until it’s not seen. As K+ levels rise, whole morphology of complexes is lost, and you arrive at sine wave. Finally, a straight line.

Spectrum of Hyperkalemia (2 of 2) : 

Spectrum of Hyperkalemia (2 of 2)

T Wave Abnormalities in Hyperkalemia (1 of 2) : 

T Wave Abnormalities in Hyperkalemia (1 of 2) T wave abnormalities = first changes in patient developing hyperkalemia. T wave changes begin to appear when K+ level exceeds 5.5 mEq/L. Most famous T wave change is tall, peaked, narrow T (22%). Other 78% of the time, any combination of tall, peaked, narrow, or wide T waves is found. Important: Morphology can change as K+ level increases; T wave height decreases as T waves widen.

T Wave Abnormalities in Hyperkalemia (2 of 2) : 

T Wave Abnormalities in Hyperkalemia (2 of 2) At 5.5 mEq/L, T waves are tall, peaked, and narrow; normal or slightly prolonged QT. As K+ increases, T waves and PR, QRS, and QT intervals widen. Amplitudes become smaller. Affects appearance of T waves. T wave changes are usually first noted in V2 to V4. * Don’t be fooled into thinking that peaked, narrow T waves that appear only in V2 to V4 are not due to hyperkalemia!

T Waves in Hyperkalemia : 

T Waves in Hyperkalemia T wave changes are earliest sign of hyperkalemia. T wave changes are seen when K+ exceeds 5.5 mEq/L. Classic T waves that are tall, peaked, and narrow occur in only 22% of cases. T wave morphology may be altered as result of IVCD that develops with severe hyperkalemia. T wave changes may be localized to anteroseptal leads, or changes can be diffuse.

ECG 16-4 : 

ECG 16-4

Hyperkalemia: Helpful Notes : 

Hyperkalemia: Helpful Notes In patients with mild hyperkalemia and end-stage renal disease, aggressively treat K+ abnormalities, not Ca++ imbalances! Excessive Ca++ will cause crystallization of soft tissues, because calcium + phosphate = calcium phosphate.

Review of IVCD and Hyperkalemia (1 of 3) : 

Review of IVCD and Hyperkalemia (1 of 3) IVCD exists when QRS width is more than 0.12 sec and ECG does not meet criteria for LBBB or RBBB. Most common presentation of IVCD: V1 looks like LBBB with monomorphic S wave or rS complex. Leads I and V6 look like RBBB with typical slurred S wave. Whenever you see IVCD, think of hyperkalemia first! Widening of complexes usually begins when K+ concentration is at 6.5 mEq/L or greater.

Review of IVCD and Hyperkalemia(2 of 3) : 

Review of IVCD and Hyperkalemia(2 of 3) As K+ levels increase, QRS complex widens. Height of waves slowly decreases as complexes continue to widen. Prominent S waves form in leads I and V6. Formation of sine wave pattern can occur at any time. T waves of IVCD will be peaked, but smaller than those found at lower K+ levels—usually peaked, symmetrical, and wide.

Review of IVCD and Hyperkalemia(3 of 3) : 

Review of IVCD and Hyperkalemia(3 of 3) The ECG axis can change to RAD or LAD. You can see a new LBBB or RBBB pattern instead of IVCD. Every conceivable arrhythmia can develop at this point.

P Waves and Hyperkalemia : 

P Waves and Hyperkalemia As K+ level increases above 7.0 mEq/L, PR interval increases, P wave amplitude decreases. Eventually, you won’t be able to see P waves. Why? As K+ level increases, atrial myocardial cells stop depolarizing. SA node and special conduction system of atria continue to function, but myocardial cells will NOT. Atrial myocardium creates atrial vectors picked up on ECG as P waves; no atrial activity will be seen on ECG.

ECG 16-9 : 

ECG 16-9

Hypokalemia (1 of 2) : 

Hypokalemia (1 of 2) Hypokalemic changes on ECG aren’t very dramatic. There are nonspecific changes: Mild ST segment depression Mild decreased amplitude of T waves Minimal prolongation of QRS interval Prominent U wave (most common) Small wave that occurs immediately after T wave Usually less than 1/10 height of T wave Can be caused by many different processes

Hypokalemia (2 of 2) : 

Hypokalemia (2 of 2) Differential diagnosis of U waves: Hypokalemia Bradycardia Left ventricular hypertrophy CNS events Drug use: digoxin, Class I antiarrhythmics, phenothiazines Probability of developing an arrhythmia because of hypokalemia is low. Real danger lies in a patient taking digoxin who is also hypokalemic.

The U Wave : 

The U Wave

Hypercalcemia : 

Hypercalcemia Hypercalcemic changes on ECG are also minimal. Main change is shortening of ST segment. In turn presents as shortened QT interval (or shortened QTc). QTc is QT interval for heart rate. Cardiac arrhythmias are rare.

Hypocalcemia : 

Hypocalcemia Main ECG change caused by low calcium level = prolongation of ST segment that produces an apparent lengthening of QTc interval Notice: This is opposite effect of hypercalcemia. “Hyper” means fast, so movements appear shorter. “Hypo” means slow, so it takes time for T wave to develop. Cardiac arrhythmias are rare. Danger of QT prolongation, from any source, is development of torsade de pointes, which can cause sudden death.

Differential Diagnosis for Prolonged QT Interval : 

Differential Diagnosis for Prolonged QT Interval AMI and ischemia Hypocalcemia Drugs: Class Ia antiarrhythmics, amiodarone, phenothiazines, tricyclic antidepressants CNS events Hypothermia Hypothyroidism Congenital or idiopathic prolonged-QT syndromes

Drug Effects and Digoxin : 

Drug Effects and Digoxin Pharmaceutical agents affect function of cells and channels. Alter how cells depolarize, repolarize, and innervate surrounding tissues Alter vectors, and then appearance of ECG Digoxin Causes tremendous problems and deaths Overuse/overdose can cause any and all arrhythmias. Most commonly discussed is paroxysmal atrial tachycardia (PAT) with block Escape rhythm can be either junctional or ventricular

Digoxin : 

Digoxin On ECG, digoxin causes unique scooping of ST segment. T waves have shorter amplitude and can be biphasic. QT interval is usually shorter than expected. U waves are more prominent. Remember that hypokalemia will exacerbate effects of digitalis glycosides. This increases arrhythmogenic and toxic effects. Any digoxin level may be toxic in this case!

Scooped-Out Appearance of ST Segment : 

Scooped-Out Appearance of ST Segment

ECG 16-19 : 

ECG 16-19

Common Toxic Drug Effects (1 of 2) : 

Common Toxic Drug Effects (1 of 2)

Common Toxic Drug Effects (2 of 2) : 

Common Toxic Drug Effects (2 of 2)

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