Physiology, Stroke Volume

Article Author:
Zachary Bruss
Article Editor:
Avais Raja
Updated:
9/19/2019 11:30:45 AM
PubMed Link:
Physiology, Stroke Volume

Introduction

To understand the principles of cardiac stroke volume (SV), it is necessary first to define the concept of cardiac output. Cardiac output (CO) is the blood volume the heart pumps through the systemic circulation over a period measured in liters per minute.[1] There are various parameters utilized to assess cardiac output comprehensively, but one of the more conventional approaches involves multiplying the product of the heart rate (HR) and the stroke volume.[1]

  • CO = SV x HR 

The definition of stroke volume is the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction. This volume may be calculated as the difference between the left ventricular end-diastolic volume and the left ventricular end-systolic volume. The average stroke volume of a 70 kg male is 70 mL.

Critical care physicians employ several variables when monitoring severely ill hypovolemic patients. Utilizing stroke volume as a hemodynamic variable compared to other commonly used parameters is becoming increasingly popular in assessing cardiac pump function and organ perfusion as it is subject to less influence from compensatory mechanisms.[2] Cardiologists' also use stroke volume when assessing cardiac dysfunction in those with congestive heart failure. The computation of left ventricular ejection fraction involves dividing the stroke volume by the end-diastolic volume (EDV) and is considered a central component in the assessment of both systolic and diastolic heart failure.[3]

  • LVEF = SV/EDV 

Issues of Concern

In a healthy person considered to be hemodynamically stable, cardiac output is sustained to reduce a mismatch between oxygen delivery to tissue and organ demand. For example, to meet the oxygen demands that occur during situations of a low-exercise aerobic load (not maximal load) cardiac output increases due to a linearly increasing heart rate and non-linearly increasing stroke volume response.[4] Hemodynamic instability occurs with a mismatch of oxygen delivery. In such a situation, the cardiac output supply does not meet the end-organ oxygen demand. In this case, the risk of decreased organ perfusion increases which in turn leads to eventual organ dysfunction. Both cardiac and extra-cardiac factors are capable of influencing such a mismatch. Examples of this include but are not limited to alterations in effective circulating blood volume, cardiac function, and vascular tone.[5]

Mechanism

The mean arterial pressure (MAP) calculates as the product of cardiac output (CO) and systemic vascular resistance (SVR). These three parameters must co-exist to balance each other accordingly. 

  • MAP = CO x SVR

When cardiac output decreases, for example, during an acute myocardial infarction, systemic vascular resistance must increase to maintain a relatively normal mean arterial pressure. As the cardiac output is the product of heart rate and stroke volume, both these parameters may be manipulated to maintain adequate perfusion and match the bodies global metabolic needs.[6]

There are three variables affecting stroke volume, which include contractility, preload, and afterload.[7] The definition of contractility is the force of myocyte contraction, referred to as the heart's inotropy. Increasing the contractility of the heart which occurs, for example, during exercise generally increases the stroke volume. Preload is the passive ventricular wall stress at the end of diastole and is synonymous with the end-diastolic volume.[6] Generally speaking, an increase in the preload causes an increase in stroke volume.[8] During early pregnancy, for example, the increase in blood volume leads to an increase in preload and turn, an increase in stroke volume and cardiac output. Afterload encompasses the factors that contribute to myocardial wall stress during systolic ejection. An increase in afterload, for example, in individuals with long-standing high blood pressure, generally causes a decrease in stroke volume.[6] In summary, stroke volume may be increased by increasing the contractility or preload or decreasing the afterload.

Pathophysiology

In a hypovolemic state, an immediate decrease in venous return, and in turn, preload, initially causes a rapid decline in cardiac stroke volume.[7] At the same time, low-pressure stretch receptors located in the atria and arterial baroreceptors in the aorta and carotid artery also detect this hypovolemia. The compensatory mechanism that follows includes a rise in catecholamine production and an increase in renin release leading to an elevation in heart rate and systemic vasoconstriction in attempts to maintain mean arterial blood pressure.[9] It is only following 15 to 30% of total blood volume loss that tachycardia is observed and only after 30 to 40% of total blood volume loss that systolic blood pressure begins to decline in a healthy set of individuals.[10][11] In response to this hypovolemia, there is a surge of catecholamines, which cause selective vasoconstriction to conserve blood supply to vital organs following which we begin to switch from aerobic to anaerobic respiration.[12]

Clinical Significance

Hypovolemia results in inadequate left ventricular filling volume.[7] Hypovolemic shock is the clinical state where the loss of plasma volume causes inadequate tissue perfusion.[10] The most common cause of hypovolemic shock includes massive hemorrhaging secondary to traumatic injury. Other common causes are related to severe dehydration and include gastrointestinal losses, renal losses, skin losses, and third space sequestration. As shock progresses, decreased intravascular volume will eventually lead to cardiovascular compromise.[11]

For critically ill patients in hypovolemic shock, stroke volume optimization algorithms are increasingly becoming utilized to monitor for early signs of hypovolemia. Critical care specialists currently use several physical examination findings during their clinical assessment to monitor a patient's volume status. Some of these include assessing axillary hydration status, mucous membrane color, sunken eyes, capillary refill time, and mentation status.[13] Some techniques and devices employed to assess hemodynamic stability have limitations of cost or risk to the patient, and other methods may be misleading or confounded by physiological compensatory mechanisms. Examples include the invasive utilization of a pulmonary artery catheter to assess for central venous pressure or the use of heart rate, urine output, and orthostatic blood pressure to evaluate volume status.[7]

There are several new methods of measuring stroke volume that are efficient and becoming increasingly accessible. External Doppler imaging is considered the most popular and can be performed using an ultrasound probe placed along the chest wall cavity. This method is less commonly performed in critically ill patients as it is technically difficult, and the required serial measurements are impractical. In sedated patients such as those in the operating room or intensive care unit, esophageal Doppler imaging may be obtained by placing a probe in the esophagus and collecting Doppler signaling data from the descending aorta. In intubated patients, endotracheal bioimpedance can obtain the stroke volume and cardiac output from measuring the impedance signal from the ascending aorta. Some several other techniques and devices may be implemented to continuously assess for stroke volume using electrodes that will not receive coverage in this article.[7]

Heart failure is among the most prevalent chronic conditions in the elderly population and is the fastest-growing clinical cardiac disease.[14] There are more than 6.5 million people in the US with heart failure, a consequence of various underlying etiologies that result in structural and functional impairment in the heart.[15] This dysfunction may cause impaired filling of the heart during diastole or inadequate ejection of blood from the heart during systole and is commonly classified into diastolic (HFpEF) or systolic (HFrEF) dysfunction.[11] Common causes of systolic dysfunction include coronary vessel disease, dilated cardiomyopathy, and valvular disease. Causes of diastolic dysfunction include valvular diseases, long-standing hypertension, restrictive cardiomyopathy, and hypertrophic obstructive cardiomyopathy.

HFpEF is clinical signs of HF with LVEF over 50% whereas HFrEF is having clinical signs of HF with LVEF below 40%. As described above, the computation of LVEF involves dividing the cardiac stroke volume by the end-diastolic volume.[3] Echocardiography is the most commonly utilized technique in measuring LVEF as its use is readily available and non-invasive. The advent of monitoring LVEF through echocardiography has enabled cardiologists to administer appropriate therapeutic interventions to deter the cardiac remodeling process that occurs in the hearts of those suffering from this disease.[16] The consequence of decreased stroke volume in patients with severely decompensated heart failure includes certain tell-tale signs and symptoms. Symptoms include dyspnea (on exertion, nocturnal), orthopnea, swelling, and weight gain. Signs include elevated jugular venous pressure, tachycardia, abnormal heart sounds or murmurs, edema, ascites, and cachexia.[17]


References

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