On a recent night, ambulance No. 32 responds to a shooting, an overdose and a medical emergency.
All these calls have one thing in common, the fact that some form of cardiac assessment is completed.
Many times, the assessment is minimal, while other times require detailed, in-depth cardiac evaluation. The knowledge you apply to components of cardiac function will influence treatment pathways for your patients.
Let’s define cardiac function
Cardiac muscle is almost exclusively an aerobic organ. Thus, there is little capacity to function in anaerobic metabolism to produce energy.
For cardiac muscle to function, nutrients cannot diffuse from the heart’s chambers to supply all layers of the muscle. So, in order to compensate, the myocardium removes about 75% of oxygen available in blood circulating through coronary vessels.
Because the heart cannot diffuse oxygen as other organs, it limits the ability to meet demand by increasing oxygen extraction. The compensation for this is increased coronary blood flow.
Consequently, we often see the result of this flow and oxygen deficit as cardiac ischemia and damage.
When asked about cardiac function, many EMS providers are quick to answer with the most familiar principles. These include preload, contractility, afterload and heart rate.
Detailing each of these components in addition to peripheral vascular resistance and systemic vascular resistance will bring a greater understanding.
All these principles of cardiac function display a degree of interdependence. Thus, a deficiency in one element could be secondary to a problem with one or more of the other components.
Cardiac assessment terms you need to know
A review of these essential functions, based on information from the Cleveland Clinic, can help with your overall comprehensive cardiac assessment:
Preload: The pressure generated in the left ventricle at the end of diastole. It’s the degree of tension on the muscle when it begins to contract. Preload is the most significant contributor to cardiac output. One can increase preload by vasoconstriction, increase in venous return and increasing vascular volume. Reversing these processes can help to decrease preload when needed. The introduction of diuretics may also decrease preload.
Heart rate: Heart rate is the number of times the heart beats in one minute. Adult resting heart rate is 60-100 beats per minute. Importantly, influence comes from many effects, such as exercise, stress, drugs and rest. As the most efficient function of the cardiac muscle, heart rate is dependent on tolerance of rate extremes. All aspects of cardiac function can influence this.
Stroke volume: The volume of blood ejected with each beat during systole. Stroke volume depends on the force of contraction and has three major factors — preload, afterload and contractility. Thus, to increase or decrease stroke volume, influence any of those major elements.
Afterload: This is the resistance to ejection of blood and the load against which the muscle exerts its contractile force. Aortic pressure is an effective index of afterload. A decrease in aortic pressure allows the left ventricle to pump larger volumes. To increase afterload, increase aortic pressure and peripheral vascular resistance, and vasoconstrict. On the other hand, decreasing afterload can reverse this.
Ejection fraction: The percentage of blood ejected from the left ventricle. Stroke volume divided by end diastolic volume equals ejection fraction. Normal ejection fractions are between 60% and 70% — or 70-80 ml — with each heartbeat.
Associated ejection fractions to expect
According to Cleveland Clinic, the following ejection fractions may be associated with these levels of heart function:
55% to 70%: Heart function may be normal or heart failure may be present.
40% to 54%: Pumping ability of the heart is below normal. Less blood gets ejected and a lower than normal amount of oxygen is available to the rest of the body.
35% to 39%: Mild heart failure with reduced ejection fraction. This will cause many patients to display significant signs and symptoms of cardiac compromise.
Less than 35%: Severe decrease of pumping ability during which severe heart failure may be present. Patients may be experiencing life-threatening rhythms as well as desynchronization (right and left ventricles do not pump in unison).
Peripheral vascular resistance: The resistance to left ventricular emptying, causing more workload. Influencing an increase or decrease in peripheral vascular resistance is influenced by arteriolar constriction or dilation.
Systemic vascular resistance: This is the result of peripheral vascular resistance and preload. Influencing both of these in a positive or negative way will cause change in systemic vascular resistance. Remember, this resistance influences the diameter and elasticity of vessels throughout the body, with the exception of the pulmonary system.
Contractility: The force and strength of the heart’s contraction. Increasing contractility can be accomplished by decreasing aortic pressure, decreasing peripheral vascular resistance and sympathetic simulation. Decreasing contractility will be influenced by increasing aortic pressure, parasympathetic stimulation and peripheral vascular resistance. Muscular stretch will respond accordingly. The more forceful the contraction, the greater the stroke volume. Additional influences on contractility include high blood calcium levels, glucagon and thyroid hormones.
Influencing any of these components will have an impact on remaining cardiac functions. By using this knowledge, your patients will benefit from initial stabilization and a treatment pathway that can be continued in-hospital.