Pacemaker Identification Codes



Bojar, R. M. (2016). Manual of perioperative care in adult cardiac surgery (5th ed.). West Sussex, UK: Wiley-Blackwell



Cardiac Rhythm Series: Second Degree AV Block, Mobitz Type I

Click here to review First Degree AV block before reading this post.

In a Mobitz I (Wenckebach) block, the PR interval becomes progressively longer with each cardiac cycle until a P-wave appears with no QRS to match1, 2. This occurs when the cardiac conduction system delays or blocks an atrial impulse traveling through the AV node and/or bundle of His3. If you look closely at an ECG, you will see the atrial rhythm (P-P interval) is regular but the ventricular rhythm (R-R interval) is irregular2. The P-wave is not moving, but the QRS complex is.

Mobitz I

Characteristics: PR interval progressively widens until a QRS is ‘dropped’; QRS less than 0.12 seconds; regular atrial rhythm but the ventricular rhythm is irregular.

Wenckebach has many possible causes:

  • Cardiac surgery: AV node conduction is affected in approximately 25% of CABG patients1.
  • Digitalis toxicity: Digoxin increase the refractory time of the AV node which slows conduction.
  • Myocardial ischemia/infarction: The AV node is perfused by the right coronary artery in 90% of individuals and the left circumflex coronary artery in the remaining 10%2.

“Longer, longer, longer, DROP– now you have a Wenckebach”

Treatment is not usually required unless the ventricular rate is slow1. Atropine or chronotrope infusion (dopamine or epinephrine) may be administered if cardiac output is inadequate2. The patient may experience symptoms related to decreased cardiac output– lightheadedness, dizziness, or syncope2. If symptomatic, AV pacing (DVI mode) at a slightly faster rate is recommended. If the atrial rate is too fast to overdrive, it can be treated by pacing in DDD mode1.

  1. Bojar, R. M. (2016). Manual of perioperative care in adult cardiac surgery (5th ed.). West Sussex, UK: Wiley-Blackwell
  2. University of Maryland Medical Center Office of Clinical Practice and Professional Development. (2014). Introduction to cardiac rhythm interpretation (6th ed.).

Cardiac Rhythm Series: First Degree AV Block

In first degree AV block, the sinoatrial (SA) impulse is delayed longer than normal at the AV node before being transmitted to the ventricles causing a prolonged PR interval1, 2. As a reminder, the PR interval represents the time needed for an electrical impulse to travel from the SA node throughout the cardiac conduction system to the Purkinje fibers2.


Characteristics: P waves present and uniform with one per QRS, PR interval greater than 0.2 seconds and consistent, QRS less than 0.12 seconds, regular rate and rhythm.

First degree AV block has a number of possible causes:

  • AV node ischemia: The AV node’s blood supply comes from the right coronary artery in 90% of individuals and the left circumflex coronary artery in the remaining 10%2, 3.
  • Enhanced vagal tone: Well-trained athletes can develop first-degree AV block due to an increased vagal tone3.
  • Acute myocardial infarction: First-degree AV block occurs in just under 15% of patients with acute MI (particularly of the inferior wall) admitted to coronary care units3.
  • Drugs: Digoxin, amiodarone, beta-blockers, and calcium-channel blockers increase the refractory time of the AV node which slows conduction. These drugs are not completely contraindicated, but their use increases the risk of developing a higher degree of AV block3.
  • Infective endocarditis or rheumatic fever2, 3.

“If the R is far from the P, then you have a first degree.”

First degree AV block is typically considered benign and usually does not progress to higher degrees of AV block2. If asymptomatic, no treatment is needed2. The patient should be monitored for progression to higher degrees of AV block2.

  1. Bojar, R. M. (2016). Manual of perioperative care in adult cardiac surgery (5th ed.). West Sussex, UK: Wiley-Blackwell
  2. University of Maryland Medical Center Office of Clinical Practice and Professional Development. (2014). Introduction to cardiac rhythm interpretation (6th ed.).

For the next post of this series, click here: second degree AV block, Mobitz type I (Wenckebach).



3 Easy Steps for Interpreting ABGs

Arterial blood gases (ABGs) are used to monitor patients on ventilators, monitor critically ill non-ventilator patients, establish preoperative baseline parameters and regulate electrolyte therapy. They provide valuable information for assessing and managing a patient’s respiratory and metabolic acid-base balance.

Image result for arterial blood gas draw

Before going into interpreting ABG results, let’s first take a look at the components of an ABG:

  • pH is inversely proportional to the actual hydrogen ion concentration of blood. So, as the hydrogen ion concentration decreases, the pH goes up. A pH of 7.35-7.45 is a normal value; greater than 7.45 is considered alkalosis and less than 7.35 is acidosis.
  • PCO₂ is a measure of the partial pressure of CO₂ in the blood. This is the respiratory component in acid-base determination because it is primarily controlled by the lungs. As the CO₂ level increases, pH decreases and vice versa. The faster and more deeply the patient breathes, the more CO₂ is blown off causing PCO₂ levels drop. This can be used as a compensatory mechanism for respiratory acidosis. Alternatively, in metabolic acidosis the respiratory rate may decrease to retain CO2 and decrease pH.
  • HCO₃- (bicarbonate ion) is regulated by the kidneys and used as a measure of the metabolic component of acid-base equilibrium. As HCO₃- increases, the pH also increases- HCO₃- is elevated in metabolic alkalosis and decreased in metabolic acidosis. The kidneys are also used to compensate for respiratory acid-base imbalances. In respiratory acidosis, the kidneys attempt to compensate by retaining excess amounts of HCO₃- and in respiratory alkalosis, the kidneys excrete more HCO₃- out of the body in an attempt to lower the pH.
  • PO₂ is an indirect measure of the O₂ content of the arterial blood. The normal value for PO₂ is 80-100 mmHg. This measure is useful in determining the effectiveness of O₂ therapy.

Now that we covered the basics, here are three easy steps you can use for interpreting the majority of ABGs:

Step 1: Evaluate the pH to determine Acidosis or Alkalosis.


Step 2: Look at the PCO₂ to determine respiratory effect. If the PCO is high in a patient who has acidosis, the patient has respiratory acidosis and if their PCO is low with a high pH, the patient has respiratory alkalosis. If the PCO is low in a patient who has been said to have acidosis, the patient has metabolic acidosis and is compensating by blowing off CO.  If their PCO is high with a high pH, the patient has metabolic alkalosis and is compensating by retaining CO. If that lost you (I got lost a bit just writing it), the chart below simplifies the thought process and is right most of the time.


Step 3: Assume metabolic cause when respiratory is ruled out, but use the HCO₃- to verify metabolic effect (normal is 21-28 mmHg).

PATIENT SAFETY NOTE: After an ABG draw, pressure must be held or applied to the site for 3-5 minutes. The draw puts a patient at risk for excessive bleeding and hematoma formation. If the patient is taking anticoagulants, pressure should be applied for longer- approximately 15 minutes.

References: Pagana, K. D. & Pagana J. P. (2014). Mosby’s Manual of Diagnostic and Laboratory Tests, 5th Edition. [Pageburstl]. Retrieved from


Electrolyte Imbalance and EKG Changes

Typical ECG changes in hyperkalemia begin with tall, “peaked” T waves and a shortened QT interval and progress to the lengthening of the PR interval and loss of P waves. Widening of the QRS complex culminating in a “sine wave” morphology and death may occur if left untreated. (click images to enlarge)

Generally, the amplitude of the T wave goes up and down, proportional to the K+ level. The earliest ECG change seen with hypokalemia is a decrease in the T-wave amplitude. As K+ levels decline further, ST-segment depression and T-wave inversions are seen with prominent U waves.

Hypercalcemia typically causes a shortening of the ST segment and QT interval; the T wave may become widened. In severe hypercalcemia, Osborn waves (J waves) may be seen. This can progress to ventricular irritability and VF arrest if extreme hypercalcemia is left untreated.

The QT interval generally lengthens and shortens opposite to Ca2+ levels. Accordingly, hypocalcemia causes a long ST segment and long QT interval.

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Probably More Than You Wanted to Know About Heart Murmurs

A heart murmur is a swooshing sound that occurs with turbulent blood flow in the heart or great vessels. This may result from congenital heart defects or acquired valve defects. Atherosclerosis, hypertension, heart failure, myocardial infarction, rheumatic fever, and infectious endocarditis may stretch, distort, damage, scar, or cause calcification of the heart valves.


The intensity of a murmur is described in terms of six grades:

  • Grade i– Barely audible, heard only in a quiet room with difficulty
  • Grade ii– Clearly audible, but faint
  • Grade iii– Moderately loud, easy to hear
  • Grade iv– Loud, associated with a thrill palpable to the chest wall
  • Grade v– Very loud, heard with one corner of the stethoscope lifted off the chest wall
  • Grade vi– Loudest, heard with entire stethoscope lifted slightly off the chest wall

In addition to grading the murmur, it is important to note the timing of a murmur in relation to the normal heart sounds. S1 is the first heart sound (LUB) caused by the closure of the AV valves signaling the beginning of systole. S2 is the second heart sound (DUB) caused by the closure of the semilunar valves signaling the end of systole. The location is also very meaningful– the point where the murmur is best heard (maximum intensity) should be noted by the valve area or intercostal space.

Let’s take a look at the various types of murmurs and their causes:

Mid-systolic Ejection Murmurs


A mid-systolic ejection murmur results from restricted forward flow through the aortic or pulmonic semilunar valve due to valve calcification. This can be heard as a “LUB-woosh-DUB” upon auscultation with a crescendo-decrescendo effect (increases then decreases in loudness). A murmur resulting from aortic stenosis will be loudest at the second right intercostal space. This will often be accompanied by low blood pressure and a slow, diminished radial pulse and may cause left ventricular hypertrophy as the heart is required to work more to maintain adequate cardiac output. A murmur resulting from pulmonic stenosis will be best heard at the second left intercostal space.  Right ventricular hypertrophy commonly develops due to the increased workload on the right ventricle.

Pansystolic Regurgitant Murmurs


A pansystolic regurgitant murmur results from the backward flow of blood from an area of higher pressure to one of lower pressure. This again will be heard as a “LUB-woosh-DUB” upon auscultation except the “woosh” extends steadily from S1 to S2. Mitral regurgitation results from a stream of blood flowing back through an incompetent mitral valve into the left atrium during systole. This murmur is best heard at the apex of the heart and may result in left ventricular dilation and hypertrophy. Tricuspid regurgitation results from the back-flow of blood through an incompetent tricuspid valve– it is best heard at the left lower sternal border. The back-up of pressure may cause engorged, pulsating neck veins and liver enlargement; the extra strain on the right ventricle may cause hypertrophy, as well.

Diastolic Rumbles of AV Valves


Diastolic rumbles of the AV valves are due to filling murmurs at low pressures. This is best heard by lightly touching the bell of the stethoscope against the skin. Mitral stenosis results from a calcified mitral valve not opening properly. This impedes the forward flow of blood into the left ventricle during diastole causing increased left atrial pressure, left atrial hypertrophy, and pulmonary edema. This creates a low-pitched diastolic rumble best heard at the heart’s apex while the person is in a left lateral position. Tricuspid stenosis results from a calcified tricuspid valve impeding forward flow into the right ventricle during diastole. The rumble is best heard at the left lower sternal border.

Early Diastolic Murmurs


An early diastolic murmur results from semilunar valve incompetence. Aortic regurgitation causes a stream of blood to flow back through an incompetent aortic valve into the left ventricle during diastole. The murmur is best heard at the left third intercostal space (base of the heart) as the person sits up and leans forward. A soft high pitched, decrescendo sound begins simultaneously with S2 (“LUB-DUB-woosh”). Left ventricular dilation and hypertrophy develop due to increased LV stroke volume. Pulmonic regurgitation is caused by a back-flow of blood through an incompetent pulmonic valve from the pulmonary artery to the right ventricle. The timing and characteristics are similar to that of aortic regurgitation and are difficult to distinguish upon physical assessment.

Reference: Jarvis, C. (2012). Physical Examination and Health Assessment, 6th Edition. [Pageburstl]. Retrieved from


Auscultatory Areas of the Heart

Above, you can see the auscultatory areas of the heart. There are four traditional valve areas noted– these are not the actual anatomical locations of the valves, but where they are heard the best. The sound is projected in the direction of blood flow. Understanding the valve areas allows for more accurate assessment of heart murmurs.

The valve areas are:

  • Aortic valve area– 2nd right intercostal space
  • Pulmonic valve area– 2nd left intercostal space
  • Tricuspid valve area– left lower sternal border
  • Mitral valve area– 5th intercostal space at approximately the left midclavicular line

Sounds produced by the valves may also be heard over the precordium (area directly over the great the heart and great vessels). It is recommended to inch your stethoscope in a rough ‘Z’ pattern from the base of the heart, across and down, then over to the apex.

Jarvis, C. (2012). Physical Examination and Health Assessment, 6th Edition. [Pageburstl]. Retrieved from