Technicians aren't all destined to be cardiologists. But all technicians should understand what a normal cardiac rhythm looks like and how it's generated.
Technicians aren't all destined to be cardiologists. But all technicians should understand what a normal cardiac rhythm looks like and how it's generated. When we started working in a referral clinic, our first cardiac lesson was from a cardiologist who asked us to let him know if we saw anything "wide and bizarre" on the electrocardiograph monitor. He was planting the seed to help us understand why a cardiologist would be concerned about the electrocardiogram (ECG) pattern for a patient with gastric dilatation-volvulus (GDV). We wondered what the heart had to do with the stomach. We also wondered what "wide and bizarre" meant.
Our cardiologist questions and consults didn't end there. Concern also arose with other patients including cats with urinary obstructions. How does the inability to urinate cause problems with heart function?
We were fortunate to work with a team that wanted to educate us on the relationship between heart function and many common veterinary emergencies. We hope to do the same for you in this article.
In order to understand what causes the heart to produce an abnormal rhythm, you must first recognize and appreciate a normal sinus rhythm. To do that, you need some background on the circulatory system. This system transports nutrients, water, and oxygen throughout the entire body and carries away wastes such as carbon dioxide. The circulatory system also oxygenates red blood cells and delivers them to all parts of the body. If there is a breakdown of oxygen delivery, cells will die, organs will fail, and the body will eventually shut down.
This cardiac cycle plays the most significant role in the circulatory system. The cycle describes the flow of blood as it enters the heart, is pumped to the lungs, travels back to the heart, and is pumped out to the rest of the body. In order to cycle the blood, the heart has a contractility phase (systole) for pushing blood out and a relaxing phase (diastole) for filling up the heart. Anatomy, electricity, and volume all contribute to the synchronicity of these systolic and diastolic phases.
The heart is divided in half by a partition (the septum), and the halves are further divided into four chambers (two atria and two ventricles), with a series of valves controlling blood flow. Muscle makes up most of the walls of the atria and ventricles, and a fluid-filled sac called the pericardium surrounds the heart. The cells of the myocardium, or cardiac muscle, can conduct electricity. These specialized myocytes, or cardiac "beating" cells, are interconnected by intercalated disks that have low electrical resistance.1 The disks allow the electrical impulse to easily spread through the atria, down the septum, and up the free walls of the ventricles. This coordination of cardiac muscle cells facilitates heart contraction to propel blood from the atria to the ventricles and out to the lungs and blood vessels of the circulatory system (Figure 1).
1. An illustration of the cardiac cycle.
The path of electricity begins with the pacemaker of the heart—the sinoatrial (SA) node. The SA node fires in the right atrium, causing the atria to contract. Unoxygenated blood from the right atrium is pushed through the open tricuspid valve into the right ventricle. When the left atrium contracts, oxygen-rich blood is pushed through the open mitral valve into the left ventricle. This process is atrial systole, and it represents the P wave of the ECG. Note: When the P wave is missing, there may be a dysfunction of the right atrium, the SA node, or both.
The electrical impulse is then conducted to the atrioventricular (AV) node. The AV node sends electricity through the interventricular septum, causing the ventricles to contract. Blood is forced out of the right ventricle through the pulmonary semilunar valve. The valve opens to the pulmonary artery, which transports blood to the lungs to be oxygenated. With ventricular contraction, oxygenated blood in the left ventricle passes through the aortic semilunar valve into the aorta and then to all parts of the body. This is ventricular systole and represents the interval between the closing of the AV valves (i.e. tricuspid and mitral) and the opening of the semilunar valves (i.e. aortic and pulmonary). Electrically, it is the interval between the start of the QRS complex on the ECG and the end of the T wave (QT interval) (Figures 2A & 2B).
2A. A normal sinus rhythm: The P wave, QRS complex, and T wave are consistent and present with each heartbeat.
Diastole is the period of time when the heart fills with blood after systole (i.e. contraction). For the blood to return to the heart, the left and right atria need to be at rest. This phase is called atrial diastole. Unoxygenated blood travels from the body via the vena cava into the right atrium. The left atrium accepts oxygen-rich blood from the lungs via the pulmonary vein. At this point in the cycle, the ventricles also need to be at rest for the blood to be received from the atria during the atrial systolic phase. This is a period of repolarization of the heart known as ventricular diastole. It represents the T wave on the ECG. Even though the atria do systole together, and both ventricles do systole together, the atria do systole before the ventricles. However, all four chambers do diastole at the same time (i.e. cardiac diastole).
2B. An illustration of a normal sinus rhythm showing the P wave, QRS complex, and T wave.
In order for the process to go smoothly and to achieve adequate tissue perfusion, all parts must be functioning correctly, and there must be enough fluid volume to pump to all parts of the body.1 The body's hemodynamic status needs to be normal or the cardiac cycle will be compromised. Many factors can influence hemodynamics, such as changes in circulating fluid volume (e.g. hydration status, bleeding, vomiting), respiration, vascular diameter and resistance, and blood viscosity (e.g. anemia). Each of these can be influenced by other factors, such as disease or medications. For example, in response to hypovolemia, or low blood volume, the systolic pressure decreases and the heart beats at a faster rate in an attempt to maintain perfusion to the core organs (the heart, brain, and kidneys). This results in tachycardia, diminished blood pressure, and decreased tissue perfusion, which may be seen as increased capillary refill time.
Maintaining the correct hemoglobin concentration and the balance of electrolytes in the body is also necessary for normal organ function. Hemoglobin is the oxygen-carrying molecule of the red blood cell and is crucial for oxygen delivery to the body. If a patient has an anemia, or lack of red blood cells, then it also has a reduced amount of hemoglobin. Electrolytes are substances that can acquire the capacity to conduct electricity. Maintaining the balance of electrolytes in the body is essential for normal function of cells and organs. Common electrolytes measured include sodium, potassium, chloride, and bicarbonate. If there is an abundance or deficiency of an electrolyte in the blood, then the function of the heart muscle can be compromised.
Now that you understand a normal sinus rhythm, we can move on to the first question at hand: Why should we be concerned about a cardiac arrhythmia in a patient with GDV? To make it easier to understand why, consider what is happening internally. With GDV, the stomach fills up with air and, in many cases, twists, eventually leading to a state of circulatory shock. The distended stomach can compress the abdominal caudal vena cava, which results in decreased venous return to the heart. If less fluid volume is returned, cardiac output will decrease. Abdominal pressure also restricts diaphragm movement, resulting in reduced oxygen consumption through respiration. In an attempt to preserve perfusion of the core organs, systolic blood pressure drops and peripheral vasoconstriction occurs. This disrupts the cardiac cycle. Oxygen-rich blood cannot circulate to all cells, which causes ischemia and necrosis. The decrease of venous return and oxygen to the heart can damage the myocardial muscle.2
The most common arrhythmia that occurs is ventricular premature contractions (VPCs), marked by absent P waves, followed by "wide and bizarre" QRS morphology (Figure 3). These "extra" ventricular beats are generated from electrical impulses in the tissue of the ventricles. Therefore, the highly coordinated electrical pathways that make up the cardiac cycle are disrupted. Myocytes of the ventricles may spontaneously fire before the SA node generates the next impulse. This can result in an absent P wave. Communication from the AV node to the SA node is nonexistent, so no PR interval is present. The QRS complex is exaggerated because of slow conduction of electricity through the damaged myocardial muscle of the ventricles.
3. Absent P waves followed by "wide and bizarre" QRS morphology indicate VPCs, the most common arrhythmia that occurs in patients with GDV.
Arrhythmias usually develop 12 to 36 hours after the inception of GDV and may not appear until after the stomach is decompressed. Treating patients with GDV postoperatively with oxygen supplementation, fluid volume replacement, and electrolyte correction usually resolves the arrhythmia. Treatment with antiarrhythmic medications is reserved for persistent ventricular tachycardia.3
Just like GDV and ECGs can be related, so can ECGs and urinary problems. All cats and dogs are susceptible to urethra blockage resulting from trauma, neoplasia, stricture, calculi, or urethral plugs. However, male cats, with their long narrow urethras, are at highest risk for becoming obstructed by a urethral plug composed of crystalline and cellular material. The most common life-threatening problems for these cats are poor tissue perfusion and severe electrolyte and acid-base changes, specifically hyperkalemia and metabolic acidosis.
Here's why: Potassium plays an important role in cell excitability, nerve impulse conduction, muscle contraction, and myocardial membrane responsiveness. As serum potassium concentrations increase, neuromuscular and cardiac functions are impaired. The electrolytes' physiological effect on the myocardial cells compromises the heart's electrical conduction.4 Elevated potassium concentrations (> 5.5 mEq/L) accelerate the repolarization of the heart, seen on an ECG as tall tented T waves (Figure 4). At higher concentrations (> 6.5 mEq/L), conduction between cardiac myocytes is depressed, demonstrated by prolonged PR and QRS intervals. With rising potassium concentrations (> 7 mEq/L), the atrial myocytes are also affected, which may produce a flattening effect of the P wave. If potassium concentrations continue upward, the patient can develop ventricular fibrillation and eventually cardiac arrest.5
4. An ECG from a 6-year-old castrated male domestic shorthaired cat that came in for urinary blockage with a potassium concentration of 7.23 mmol/L. The P wave is present; in some cases of severe hyperkalemia, the P wave amplitude can be reduced or lost. The R wave amplitude is decreased consistently in this example. The most prominent distinction is the tall tented T wave present in each heartbeat.
The goal of treatment is to relieve the obstruction and bring down the potassium concentrations through fluid therapy. If potassium concentrations are extremely high (> 8 mEq/L), treatment with intravenous calcium gluconate, sodium bicarbonate and/or insulin, and dextrose can be initiated.6
We hope this review helps you better understand the relationship between the heart and all body systems and how cardiac abnormalities illustrated on ECGs can help you assist the veterinarian in pinpointing disease.
Kerr and Gottlieb are the founders of Four Paws Consulting, a veterinary consulting firm in Cedar Grove, N.J., with the mission to encourage excellence in technicians through continuing education.
1. Tighe MM, Brown M. Animal anatomy and physiology. In: Mosby's comprehensive review for veterinary technicians. 2nd ed. St. Louis, Mo: Mosby, 2003;2-22.
2. Murtaugh RJ, Kaplan PM. Surgical emergencies: gastric dilatation-volvulus, intervertebral disc disease, spinal trauma, and fracture management. In: Veterinary emergency and critical care medicine. St. Louis, Mo: Mosby Year Book, 1992;122-144.
3. Fox PR, Sisson D, Moise S. Cardiac manifestations of systemic and metabolic disease. Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia, Pa: WB Saunders, 1999;757-780.
4. Cahill M. When potassium tips the balance. In: Fluids and electrolytes made incredibly easy. North Wales, Pa: Springhouse Corporation, 1997;95-110.
5. Chew HC, Lim SH. Electrocardiographical case. A tale of tall T's. Singapore Med J 2005;46(8):429-432.
6. Murtaugh RJ. Critical care: quick look series in veterinary medicine. Jackson, Wyo: Teton Media, 2002;9.
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