The cardiac cycle is a highly coordinated process that keeps blood moving throughout the body. It is heily dependent on tight choreography of events and any disruption of these events can be detrimental. Some of these problems can occur acutely (electrolyte imbalances) or may take years to develop (heart failure).
Electrolyte imbalanceElectrolytes are important ions found both within cells and in the extracellular fluid. They are particularly important in generating and propagating action potentials. One particularly important ion as it pertains to activation of muscle action potentials is potassium (K+). Potassium ions are important in altering the cells’ resting membrane potential. Significant increase or decrease in the amount of these ions in the extracellular fluid (hyperkalemia and hypokalemia) can be fatal.
HyperkalemiaA build-up of potassium ions in the blood is referred to as hyperkalemia. The presence of more potassium ions outside the cells changes the electrical gradient across the cell membrane. As a result, the cell membrane becomes less negative and is initially more easily excitable. However, as the potassium concentration increases more, fewer sodium ion channels are recruited during depolarization. This results in a decline in the influx of sodium ions into the muscle cells and consequently a slower generation of action potential and eventually a reduction in the conduction of the impulse. Hyperkalemia can also cause nodal block, which impairs the passage of the depolarization we to the ventricles.
Hyperkalemia is most detrimental when it develops over a short period of time. While some patients may remain asymptomatic, others may complain of chest pain, shortness of breath, muscle paralysis, and palpitations. There are classic signs on the ECG tracing that are highly suggestive of hyperkalemia:
The T wes become tall and peaked because of the sudden repolarization The P we widens and becomes flattened due to paralysis of the atria The PR interval widens due to a delay in the conduction from the SAN to the N The QRS complex becomes wider and may eventually blend with the T we. This results from the nodal block.Essentially, the heart becomes flaccid, dilated, and slow. This decreased contractility results in a decrease in the forward movement of blood, which can be fatal.
HypokalemiaA significant fall in the number of potassium ions in the blood is referred to as hypokalemia. Hypokalemia has the opposite effect on the membrane potential than hyperkalemia. The decrease in extracellular potassium causes the cellular membrane to become more negative, resulting in an increase in the electrical gradient across the membrane. While this makes it more difficult for other cells to depolarize, an increased electrical gradient causes faster depolarization of myocardiocytes. This effect is most profound at the Purkinje fibers, which are most sensitive to changes in potassium concentration.
The increased excitability at points other than the pacemaker site predisposes the heart to develop ectopic heartbeats. These may lead to uncoordinated contraction of the ventricles and varying types of ventricular arrhythmias.
Additionally, a dramatic fall in the serum potassium level can also cause inhibition of some potassium ion channels. This impairs the transportation of potassium from the intracellular to the extracellular space. Consequently, ventricular repolarization is impaired and the cell may become depolarized prematurely. This can cause reentrant rhythms and other arrhythmias to occur. These repolarization abnormalities can be appreciated on ECG as:
Flattening and inversion of the T we More prominent U wes Depression of the ST segment Prolonged QT intervalsThe rapid, irregular heart is no longer effective in propelling blood forward through the circulatory system.
Heart failureHeart failure is a syndrome that refers to the inability of the heart to move blood forward through the circulatory system. This is often the common final pathway of many different forms of heart failure. Heart failure may occur as a result of reduced contractility of the ventricles or increased resistance to blood flow. Both these factors are the hallmark features of systolic dysfunction. On the other hand, the ventricles may not relax properly or the walls may be too stiff, thus impairing cardiac filling. These features are typical of diastolic dysfunction.
Heart failure can be further subdivided into right and left heart failure depending on the symptoms and signs present. Patients with left heart failure often he a history of chronic, uncontrolled (or poorly controlled) systemic hypertension, valvular insufficiency, or dilated cardiomyopathy. Patients may experience:
Shortness of breath Paroxysmal nocturnal dyspnea Orthopnea Coughing with or without rusty sputumIn contrast, patients with right heart failure may he a history of pulmonary hypertension, tricuspid insufficiency, pulmonary stenosis, or left heart failure (referred to as left to right heart failure). In the absence of left heart failure, symptoms of right heart failure include:
Peripheral edema Sacral edema Ascites Anasarca Hepatosplenomegaly Weight loss (cardiac cachexia)Although there are many compensatory mechanisms that mitigate the progression of heart failure, the process – once it has begun – cannot be reversed. Patients may continue to compensate for the impaired cardiac function; they may still he acute decompensation following illness or noncompliance with medication or dietary restriction.