Heart failure can be classified as acute or chronic, compensated or decompensated, and combinations of these variables. History and physical examination skills are paramount to diagnosis in patients presenting with heart failure and their correlation to invasive hemodynamic alterations. Since the results from the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial, the routine use of the invasive pulmonary artery catheter has largely fallen out of favor. Although the trial demonstrated no changes in primary endpoint with the routine utilization of right heart catheterization, there were correlations in the accuracy of jugular venous pressure (JVP) and right atrial pressure. An elevation of left ventricular filling pressures was associated with the findings of orthopnea and increased JVP. Discharge assessment of fluid status via elevated JVP and orthopnea (“wet”) or decreased cardiac output with reduced perfusion (“cold”) correlated with a 50 % increase in risk of death or re-hospitalization at 6 months [3, 4]. Invasive pulmonary artery catheter hemodynamic assessment is utilized to aid in the understanding and diagnosis of pathophysiology in patients that do not respond to typical initial treatments (Fig. 2.1) [2]. Recognition of these hemodynamic characteristics can lead to alteration in therapeutic decision making.

A decrease in EF due to ischemia or infarction results in primary pump failure. Acutely depressed LV function results in depressed cardiac output and venous congestion.

As the heart suffers a decrease in pump capacity there is an increase in the pressures of the venous system. The increase in venous pressure is a result of the inability of the heart to adequately accept the blood returning to the heart. Right and left atrial pressures increase. These hemodynamic alterations from a decrease in cardiac output occur within a few seconds. With the inability of a low cardiac output to provide adequate systemic perfusion, there is a response in the compensatory mechanism that results in an increase in sympathetic nervous tone.

Sympathetic stimulation results from a complex system of neurohormonal feedback. A decrease in pump function results in lower systemic arterial pressure that in turn activates the baroreceptor reflex mechanism. Ischemic heart responses, intracardiac reflexes, and other components of this feedback system contribute to sympathetic nervous system activation. Parasympathetic inhibition and sympathetic stimulation occurs within a few seconds to compensate for the acute fall in cardiac output. As sympathetic simulation occurs, the target and main effects are to the peripheral vasculature and the heart. An increase in cardiac function occurs with sympathetic stimulation to increase the recruitment of cardiac reserves within the normal and the remaining partially functional damaged myocardium. If there is diffuse damage to the ventricular myocardium during an ischemic insult, there is strengthening in the remaining functional myocytes via sympathetic stimulation. If there is no function of a portion of the ventricle, sympathetic stimulation results in the stimulation of the remaining normal myocardium. The normal myocardium attempts to compensate for the shortcomings of the damaged myocardium.

In addition to increasing myocardial muscle function, sympathetic stimulation leads to changes in the peripheral vasculature. This increase in tone in the peripheral vessels, leads to an increase in venous return. The mean systemic filling pressures are elevated increasing the flow from the venous system to the heart. The increased flow leads to increased filling of the damaged heart that in turn leads to increase in priming the heart to aid in pump function. Less than a minute in needed for the sympathetic nervous system to be completely activated (Fig. 2.2) [5, 6].

The ischemic insult is followed by no, partial, or full recovery over weeks to months. In addition to ventricular myocardial recovery, fluid retention via renal mechanisms also occurs to compensate for this new cardiac pump status and alters the normal physiologic hemodynamics found in invasive assessments (Table 2.2) [7]. Renal function is extremely sensitive to alterations in perfusion. A low cardiac output state can lead to a decline in renal function manifested to the point of anuria. The decrease in urine output can persist until there is normalization in systemic blood pressure and cardiac output.

Blood volume is altered via renal mechanisms to affect cardiac function. Initially, moderate retention of fluid results in an increase in blood volume that is beneficial to the diminished pumping function of the heart. The increase in fluid retention increases venous return, thereby increasing blood flow to the heart.

As the damaged heart receives the increased venous return, there is a gain of cardiac function. If cardiac output becomes too low, the kidneys respond with the inability to excrete adequate amounts of sodium and water. Excess fluid retention is no longer beneficial to myocardial function, and only serves to increase cardiac workload in the damaged heart and manifests as edema.

Extravasation of fluid from the pulmonary vasculature leading to hypoxia from pulmonary edema, and systemic edema develops in various organs and contributes to their dysfunction. Myocardial functional recovery can range from full to none. After partial recovery there is fluid retention that occurs to establish a new hemodynamic state. The increase in blood volume results in an increase in venous return that provides assistance in the pumping function of the heart. The elevated venous pressure persists as the cardiac output improves. As this new steady state is established and this resting cardiac output improves, the sympathetic tone progressively abates over several weeks following an acute ischemic insult. Altered renal function that results in fluid retention persists in this new hemodynamic state. As the pumping function of the heart compensates, the sympathetic tone begins to gradually decrease transitioning from an acute phase to a chronic heart failure state.

As partial recovery of the ventricular myocardial function occurs, the resting pump output from the heart normalizes with the help of an increase in atrial pressure. This increased filling pressure helps in recruitment of myocardium and improved output in the resting state. As a patient begins to exercise, the already maximized heart lacks reserve and symptoms of heart failure return. The lack of cardiac reserve is a common occurrence in heart failure patients as they achieve a resting compensated state and attempt to demand more cardiac output with exercise or systemically stressed state.

In severe cardiac failure, de-compensation occurs as a consequence of the inability of the heart to provide additional cardiac output when there are increased systemic demands. Neither sympathetic stimulation nor fluid retention can increase cardiac output to normal. Fluid retention results as the heart is unable to provide sufficient blood flow to the kidneys to excrete sodium and water.

Correlation of cardiac output on the y axis and the atrial filling pressures on the x axis is represented in Fig. 2.3 [8]. As a poorly functional ventricle responds to gradually increasing filling pressures, the cardiac output rises. After a certain point of maximal myocardial stretch, cardiac output falls and higher filling pressures no longer provide additional aid in cardiac function. A progressive increase in fluid retention increases filling pressures beyond the ideal ventricular size and dilatation with overstretching ensues. As progressive increases in fluid retention occur, the mean systemic filling pressures are translated to the heart, which then leads to the gradual rise and fall of cardiac output.

If the cardiac output never reaches a point of providing sufficient perfusion, specifically to the kidney, then cardiac failure is imminent, leading to systemic edema and pulmonary edema, hypoxia, pump failure and eventually death.

The Frank-Starling mechanism or Starling’s Law of the heart dictates that with increasing volume in the heart there is an increase in myocardial performance that includes an increased stroke volume (Fig. 2.4) [9]. This is a manifestation of the sarcomere length-tension relationship. As the ventricle fills with blood there is distention of cardiac myocytes and less sarcomere overlap. As the myocytes are “stretched”, the heart is able to increase the volume of blood it ejects. After the optimal point of overlap, the ventricle can be overstretched leading to a decrease in the amount of volume ejected from the heart. The ascending portion of the Starling curve illustrates how the increase in preload leads to the increase in cardiac output. Ventricular over filling can be detrimental. End diastolic pressures rise, and the overly “stretched” myocardium transitions to the descending portion of the Starling curve and a decrease in stroke volume and systolic pressure.

Normal valvular function provides a mechanism for unidirectional flow without resistance. The limitation of blood flow during diastole or systole is cause by a stenosis in the atrio-ventricular or ventricular-arterial valves respectively.

Aortic stenosis and pulmonic stenosis result in a decrease in cardiac output due to increased resistance to emptying of the ventricle. This increase in resistance to cardiac output results in a measurable pressure gradient across the valve which can be measured via a dual lumen pigtail catheter, separate aortic root and left ventricular catheters, or arterial sheath and left ventricular catheter. In aortic stenosis with preserved left ventricular function, as the severity in aortic valvular stenosis increases, there is an increase in the LV chamber pressure generation. Aortic and left ventricular pressure tracings are used to measure peak to peak, maximum, and mean pressure gradients (Fig. 2.5) [10]. With the advent of increased diagnostic accuracy of echocardiography, the utilization of direct hemodynamic measurement is most strongly indicated when there is a discrepancy between clinical and echocardiographic findings.

After analysis of hemodynamic tracings, the Gorlin formula is utilized in the calculation of aortic valve area. Special circumstances with decreased systolic function, “low-output, low gradient aortic stenosis”, are a subset of patients that pose diagnostic dilemmas.

Illustrated in Fig. 2.6 is the potential findings during dobutamine challenge in patients with “low-output, low gradient” aortic stenosis [10, 11].

The far left clinical scenario both cardiac output and aortic valve mean gradient increase as a result of dobutamine infusion, thus true aortic stenosis. The middle scenario finds an increase in cardiac output with no dramatic increase in aortic valve pressure gradient, a finding of mild aortic stenosis. In the right most clinical scenario, there was no change in the aortic valve pressure gradient as a result of dobutamine infusion, truly severe aortic stenosis.

In addition to valvular stenosis that limits cardiac output, is valvular stenosis that limits cardiac filling. Mitral and tricuspid valvular stenosis affects the ability to provide adequate chamber preload. Hemodynamic findings result in an elevation in PCWP but inaccurately reflect LVEDP. PCWP in mitral stenosis is reflection of left atrial pressure but not left ventricular end diastolic pressure. Mitral stenosis results in a pressure gradient between the left atrium and the left ventricle. The classic finding on hemodynamic tracings is the elevation of pulmonary pressures, prominent “a” and “v” waves on PCWP (Figs. 2.7a, b) [12]. Simultaneous tracings within the left ventricle reveal an evident pressure gradient between PCWP and LVEDP.