Ala Z. Jamal, Amir A. Sarkeshik, and Bob Kiaii
Background
Optimal cardiac function is vital to ensure adequate tissue perfusion and oxygenation. Cardiac dysfunction, even for a short period of time, can result in organ function impairment, leading to potential life-threatening complications. In this text, basic principles of cardiac hemodynamics will be reviewed, along with cardiac parameters important for cardiac function monitoring. Disease-specific pathophysiological changes (e.g. valvular dysfunction, pericardial disease, and cardiomyopathies) will be discussed in the corresponding chapters.
Basic principles
Cardiac parameters
Cardiac output (CO) is the volume of blood being ejected from the heart per minute time, which is determined by the stroke volume (SV) and the heart rate (HR); (CO = SV X HR). Stroke volume is equal to the difference between left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV), it can also be calculated using the CO equation as seen in Table 47-1. SV is highly influenced by preload, contractility, and afterload.
- Preload refers to ventricular end-diastolic fiber-length which reflects the ventricular volume at end-diastole (i.e. venous return). Preload can be measured by echocardiogram; however pulmonary artery (PA) catheter (i.e., Swan-Ganz) provides more accurate assessment. Swan-Ganz catheter also provides measures for PA pressure, PA wedge pressure, CO, systemic vascular resistance (SVR), and mixed venous oxygen saturation (SvO2).
Central venous pressure (CVP) parameter extracted by Swan-Ganz is the measured pressure in the caval venous system which is equal to right atrial pressure normally; CVP represent right ventricular (RV) preload. Pulmonary capillary wedge pressure (PCWP) which is an indirect measure of left atrial pressure is a measure of left ventricular (LV) preload. In normal heart with normal compliance, filling volume correlates with filling pressure. In hypertrophic ventricles (e.g. systemic hypertension, aortic valve stenosis), ventricles are less compliant with diastolic dysfunction requiring higher filling volume to achieve adequate filling pressure (e.g. PCWP 18-20). The opposite is true in dilated ventricles (e.g. Aortic valve regurgitation, dilated cardiomyopathy).
Compliance can be temporarily affected post cardiopulmonary bypass due to myocardial edema and/or myocardial inflammation, which makes interpreting PCWP less accurate in the immediate postop period.
Rt atrial pressure waveform (CVP waveform)
- V-wave, refers to atrial pressure due to passive venous filling
- A-wave, refers to pressure change due to atrial contraction
- C-wave, refers to pressure change due to closure and protrusion of tricuspid valve leaflets
- X-descent refers to pressure change due to Rt atrium relaxation and pulling tricuspid leaflets downward during ventricular contraction.
- Y-descent, refers to pressure change due to tricuspid valve opening and Rt atrium emptying into RV
Common abnormal waveforms:
- Increased A-wave, seen in tricuspid stenosis, pulmonary stenosis, RV failure, and pulmonary hypertension
- Canon A-wave, seen in ventricular tachycardia, complete heart block (Rt atrium contracts against closed tricuspid valve)
- Absent A-wave, seen in Atrial fibrillation
- Elevated V-wave, seen in tricuspid regurgitation
- Prominent Y-descent, seen in tricuspid regurgitation
- Slow Y-descent, seen in tamponade and tricuspid stenosis
- Contractility refers to the intrinsic strength of myocardial contraction at fixed preload and afterload. However, it is highly driven by preload, HR, inotropic stimulation, and afterload; increased contractility is noted with increased preload, HR, and decreased afterload. Ejection fraction (EF) reflects contractility, which is indirectly related to CO (e.g., CO can be low in cases with high EF due to sever bradycardia).
- Afterload refers to LV systolic wall tension which reflects the vascular resistance that ventricles must override to pump blood against.
Table 47-1. Hemodynamic parameters used in monitoring and diagnosing cardiac dysfunction. Note that all parameters can be measured by the Swan-Ganz catheter, except MAP which is measured through an arterial pressure catheter.
Myocardial O2 demand (MvO2) is increased with increased preload, contractility, or HR, and with decreased afterload. Myocardial O2 supply is determined by coronary blood flow which in turn is specific to length of diastole, coronary perfusion pressure, Hb and SaO2. The following measures aid in increasing myocardial O2 supply postoperatively:
- HR of 80-90 bpm to ensure adequate diastole time
- MAP >70 to provide adequate coronary perfusion pressure
- Avoid excessive preload and afterload to minimize ventricular wall distension and stress
- Maintain adequate hematocrit
Intra-cardiac pressures and oxygen saturation
| Table 47-2: Intracardiac blood pressures and oxygen saturation | ||
| Intra-chamber pressure in mm Hg | Oxygen saturation | |
| SVC & IVC | 2-6 (CVP) | 70% |
| Rt Atrium | 2-6 | 72% |
| Rt ventricle | 25/3 | 70% |
| PA | 25/10 | 70% |
| Lt Atrium | 6-12 | 100% |
| Lt ventricle | 120/5 | 100% |
| Aorta | 120/80 | 100% |
Understanding the physiology of intracardiac pressures help troubleshooting Swan-Ganz catheter placement. (e.g. only diastolic recorded wave form changes when advancing catheter from RV to PA and systolic pressure stays the same)
Tissue oxygenation
Mixed venous oxygen saturation (SvO2). is a measure of oxygen (O2)saturation in the pulmonary artery. Venous return from coronary sinus (maximal O2 extraction) is mixed with the caval venous return; hence the word “mixed.” SvO2 measurement can be obtained from the Swan-Ganz catheter as mentioned (normal range: 60-80%).
SvO2,physiologically, represents the difference betweenO2 delivery to tissue and O2 consumption by that tissue; “O2 delivery” per se is determined by the CO and the “O2-carrying-capacity, which in turn, depends mainly on arterial O2 saturation (SaO2) and partially on the pressure of the dissolved arterial O2 (PaO2).This explains why a drop in hematocrit causes a significant drop in O2 delivery compared to drop in PaO2.
Medical literature has suggested that absolute SvO2 values are unreliable when it comes to CO assessment; however, trending SvO2 along with other parameters can offer insight for cardiac performance and tissue perfusion.
Factors increasing O2 extraction/consumption, on the other hand, are shivering, pain, hyperthermia, and agitation. Hypothermia and systemic shunting are associated with decreased O2 extraction/consumption.
In summary, a decrease in SvO2 can be due to a decrease in CO, PaO2, SaO2, Hb, or due to increase in O2 extraction/consumption. Increase in SvO2 can be seen in decreased O2 extraction/consumption (hypothermia, shunting), increased O2 delivery (high FiO2), or a wedged pulmonary artery catheter.
Management of low cardiac output postoperatively
The following are the major principles in addressing a low cardiac output condition and the resulting low tissue perfusion and oxygenation (e.g., elevated lactate, low urine output). Table 47-3 describes major hemodynamic medications and their effect on hemodynamic parameters.
- Rule out non cardiac causes (respiratory, acid-base, electrolytes)
- Correct ischemia or coronary spasm (Nitroglycerin, Diltiazem)
- Optimize preload (CVP and/or PCWP 18-20) with intravenous fluid infusion
- Optimize HR at 90-100 with pacing
- Control arrhythmia
- Inotropic support if CI <2.0 L/min/m2
- Epinephrine
- Dopamine (if low SVR)
- Dobutamine (if high SVR)
- Milrinone (if high SVR/pulmonary pressure or in RV failure)
- Vasodilator to lower afterload if SVR >1500 & high MAP
- Nitroprusside (if high SVR, MAP and normal kidney function)
- Nicardipine (if high SVR, MAP and abnormal kidney function), but be aware of pulmonary shunting and drop in O2 saturation
- Nitroglycerin (if evidence of coronary ischemia or spasm)
- Vasoconstrictor if SVR <800
- Norepinephrine if marginal CO
- Vasopressin/Phenylephrine if satisfactory CO
- Blood transfusion if Hct 26%
- Intra-aortic balloon pump (IABP) if refractory to above measures
- Ventricular assist device (VAD) if refractory to above measures [both IABP and VAD will be discussed in detail in the corresponding chapters]
| Table 47-3: Medications and impact on hemodynamic parameters | ||||||
| Medication & receptors | PCW | HR | CI | SVR | MAP | MvO2 |
| Dopamine (α1,β1,β2, DA1) | variable | +++ | + | variable | variable | + |
| Dobutamine (β1,β2) | – | +++ | + | – | variable | variable |
| Isoproterenol (β1,β2) | – | ++++ | + | — | variable | ++ |
| Epinephrine (α1,β1,β2) | variable | ++ | + | variable | + | = |
| Milrinone (PDEI) | – | + | + | — | – | variable |
| Calcium chloride | + | variable | + | + | ++ | + |
| Norepinephrine (α1,β1) | ++ | ++ | + | ++ | +++ | + |
| Phenylephrine (α) | + | variable | variable | ++ | ++ | variable |
| Vasopressin (V) | + | variable | variable | ++ | +++ | variable |
| Nesiritide (BNP analogue) | — | variable | + | – | – | — |
| MvO2 = Myocardial O2 demand; PDEI = Phosphodiesterase Inhibitor Note that effect may vary with dosage level (Dopamine & Epinephrine). Also, for some medications, increase in MAP might be due to inotropic effect despite reduction in SVR. |
Suggested Readings
- Yuh, D. D. (2014). Johns Hopkins manual of cardiothoracic surgery. New York: McGraw-Hill Companies.
- Bojar, R. M. Manual of perioperative care in adult cardiac surgery. Chichester, UK: Wiley Blackwell.
