The cardiovascular system is a circuit with two hydraulic pumps placed in series. The pumps (right and left heart) provide the energy for the blood to circulate through the system. This is a rather complex system with several properties:

Because of passive filling, mean cardiovascular pressure is dependent upon volume and compliance. In addition, the pumping action of the heart provides the blood with a significant amount of kinetic energy while consuming vastly different amounts of chemical energy.

The physics of the circulatory system in its most basic elements can be described by Ohm’s Law, which mathematically relates flow, resistance and pressure. As applied to the flow of electricity it is generally expressed as:

where V is the voltage, or electromotive force, I is the current, and R is the resistance. In physiologic terms, the voltage is equivalent to the mean intravascular hydrostatic pressure (P) and the current is the flow (Q), with R as the expression of vascular resistance.

Therefore, if there is no pressure differential along the circuit, there is no flow, and if there is a high resistance without increase in pressure, there is little flow. In practical terms, the pressure (P) is either the systemic mean arterial pressure (MAP) or mean pulmonary artery pressure (MPAP), with the flow (Q) as cardiac output and the resistance (R) as either systemic vascular resistance (SVR) or pulmonary vascular resistance (PVR).

Much of the basic research into the physiology of the heart was performed a century ago by German physiologist, Otto Frank, and English physiologist, Ernest Starling. More recently, extensive work has been done by Kiichi Sagawa et al. at Johns Hopkins.

Otto Frank appreciated the necessity of applying physics to the study of biology. He also recognized the need for measurement systems, which could respond with speed and precision. Frank’s work, Zur Dynamik des
Herzmuskels, published in 1895,¹ begins with observations of the heart under the “simplest mechanical conditions”: Isolated isometric contraction, isotonic contraction, then variables added singly. The pressure-volume loop is derived from his work and is redrawn in Figure 19.1.

During each cardiac cycle, pressure is related to volume in a reproducible fashion. Frank’s¹ and Sagawa’s² work delineated the keys of the end-diastolic pressure-volume relation (EDPVR), end-systolic pressure-volume relation (ESPVR), and effective arterial elastance (EAE). The EDPVR is a measure of how easily the ventricular wall stretches with volume loading, and is frequently referred to as the compliance, characterizing the diastolic or lusitropic function of the heart. The ESPVR is a measure of how easily the ventricular wall contracts at a given volume, and is frequently referred to as the contractility, thereby depicting the systolic or inotropic function of the heart. The EAE is actually the arterial pressure-volume relation and is related to the arterial resistance or impedance to ventricular ejection, and therefore related to afterload, for example, the cardiac ventricular wall tension during ejection. The x-intercept of the EAE reflects preload or ventricular end-diastolic volume (VEDV). The intercept of the EAE and ESPVR is the pressure-volume at which the aortic valve closes, and is the volume at end-systole (ESV). The area within the loop is cardiac work, and the distance between the two limbs of the loop (upward = isovolumic contraction, downward = isovolumic relaxation) is the stroke volume (SV). Figure 19.2 demonstrates the pressure-volume loop with the inclusion of controlling parameters.

Ernest Henry Starling spent a great deal of his professional career defining the relation of the heart and its function.³ He examined methods to vary blood volume and measure ventricular filling pressure and cardiac output. He showed that initial muscle fiber length was the prime determinant of work done during the next contraction. Systemic resistance was not considered in Starling’s in vitro studies.⁴ A plot of preload or VEDV vs. ventricular output or SV at different levels of contractility are generally called Starling or ventricular function curves, as depicted in Figure 19.3. Starling, although recognizing that the ventricular volume at end-diastole was the critical factor influencing cardiac output, measured mean right atrial pressure as his index for preload. Clinicians also often rely on the pressure correlates of VEDV using surrogates for ventricular end-diastolic pressure (VEDP), such as central venous pressure (CVP) for the right ventricle and pulmonary artery wedge
(PAWP) or pulmonary artery occlusive pressure (PAOP) for the left ventricle. This, which will be further discussed in the subsequent text, creates difficulty when examining the role of ventricular compliance and diastolic function on cardiac performance using Starling curves.

For each heart, there is typically a “family” of curves, rather than a single curve. This family, then, allows for variations in contractility: “Higher” curves typically indicate higher contractility, with a higher SV for a given VEDV. Because Starling did not believe that vascular resistance had any negative impact on ventricular function, changes in resistance and afterload cannot be characterized by the Starling curves.

Shock, and its manifestations, can be defined as a syndrome of failure of the heart to pump volume in sufficient quantity and under sufficient pressure, to maintain the pressure-flow relation for adequate tissue perfusion and the maintenance of aerobic metabolism. Traditional teaching includes three primary categories of shock: (i) Hypovolemic, (ii) cardiogenic, and (iii) septic. This classification fails to recognize other etiologies, including anaphylactic, inflammatory, obstructive, and neurogenic. Whereas obstructive shock results in a decrease in preload leading to a low cardiac output and high resistance, the others mentioned exhibit a similar pathophysiology to septic shock; that is, a low resistance and elevated cardiac output. This has led to the use of the term, hyperdynamic, which is used to characterize any shock state manifested by vasodilation with a compensatory increase in cardiac output. A simplistic approach to any given clinical syndrome of hypoperfusion often leads to a single pathophysiologic diagnosis and treatment related to a single form of shock. However, a better understanding of the pathophysiology shows that frequently, there are mixed shock states, with coexisting components of hypovolemic, cardiogenic, and hyperdynamic shock. A prime example are patients suffering from the systemic inflammatory response syndrome (SIRS).⁵ These patients frequently exhibit manifestations of hypovolemia (increased capillary permeability and vasodilation). They are also in a hyperdynamic state (vasodilation from microbial toxins and circulating cytokines) and suffer cardiogenic depression (negative inotropic effects of cytokines, microbial toxins, and coronary hypoperfusion).

Tachycardia is the most common dysrhythmia in all forms of shock, with the obvious exception of bradydysrhythmias that can occur with cardiogenic shock (e.g., third degree A-V block). Compensatory tachycardia is associated with increased myocardial oxygen demand and decreased supply. The decrease in myocardial oxygen delivery to the myocardium is caused by a decrease in diastolic time. With 70% of coronary perfusion occurring during diastole (predominantly to the left ventricle), shortening of the diastolic time may prove critical and
result in mismatch of myocardial oxygen supply/demand, with resultant coronary ischemia and cardiac failure. However, treatment directed primarily towards reducing heart rate with negative chronotropic agents (β-blockers or Ca⁺⁺ channel antagonists) will often not be tolerated due their coexisting negative inotropic effects. Instead, efforts should always be predominantly directed towards eradication of the underlying process and improvement of SV.