TSRA Content:
Author: Rebekah Boyd, MD
This is a revision and update from the previous edition of the TSRA Primer in Cardiothoracic Surgery written by Mara Antonoff, MD and David Odell, MD
Hemodynamics are the hallmark of cardiothoracic surgery and can largely be divided into noninvasive (obtained by blood pressure (BP) cuff) and invasive measurements (obtained by pulmonary artery catheter or right or left heart catheterization). Noninvasive hemodynamic measurement includes systolic (SBP) and diastolic blood pressures (DBP) as measured by a blood pressure cuff (either manual or automatic) and the mean arterial blood pressure (MAP) which can be derived from the formula (2(DBP) + SBP)/3 or DBP + 1/3(pulse pressure or SBP-DBP). Many of the original studies investigating vasopressor use utilized noninvasive blood pressure management strategies to study the dose-effect relationship between vasopressors and MAP. Thus, if an invasive hemodynamic measurement is not available, this does not preclude the ability to appropriately titrate vasoactive medications. When relying on noninvasive hemodynamic measurements, it is critical to ensure that the proper size BP cuff is selected. The cuff width should be ~ 40% of the circumference of the arm and the bladder cuff (inflatable portion of the cuff) size should be ~ 80% of the circumference of the patient’s arm. If the cuff is too small, the blood pressure readings will be artificially elevated. If the cuff is too large, the readings will be artificially low. The discrepancies in readings can be as high as 40 mmHg, so size of the cuff should be assessed when responding to concerns for hypo- or hypertension if relying on noninvasive hemodynamic measurement.
Invasive hemodynamic measurements that can be obtained via pulmonary artery catheter include right atrial (or true central venous) pressure, right ventricular pressure, pulmonary artery systolic/diastolic/mean pressures, pulmonary capillary wedge pressure, cardiac output and index, and stroke volume variation. Pulmonary artery (PA) catheters are placed through introducer sheaths (commonly referred to as "Cordis" sheaths) which have been placed in either the internal jugular or subclavian veins. If an appropriate sheath is not already in place, this may require placement of a new central venous catheter or rewiring a previously placed triple-lumen catheter to a larger PA introducer sheath. After the sheath has been secured, the sterile field is created/maintained, and the PA catheter is calibrated ("zeroed") at the level of the patient's 4th intercostal space at the mid-axillary line. The balloon is tested and discarded if any abnormality/eccentric shape is found. Abnormalities of the balloon shape increase the risk of PA perforation. Prior to placing the PA catheter into the sheath, it is passed through a clear plastic "accordion-type" sterile covering. This covering is placed onto the sheath to maintain the sterility of the PA catheter during positioning. The catheter is passed through the sheath to a length of 20 cm (the tick marks on the catheter identify distances; 1 cm intervals are marked with single ticks, while a double tick indicates 20 cm, triple indicates 30 cm, etc.).
Once in the central venous system, the balloon is inflated. A PA CATHETER SHOULD NEVER BE ADVANCED WITHOUT THE BALLOON INFLATED. The catheter tip has the potential to perforate the myocardium and/ or the PA if advanced with a deflated balloon. LIKEWISE, A PA CATHETER SHOULD NEVER BE WITHDRAWN UNLESS THE BALLOON IS DOWN. The telemetry monitor must be kept in view while advancing (floating) the catheter. As the catheter is advanced, the clinician can follow the progress from the right heart into the PA via changes in the pressure waveform on telemetry. Distinct pattern changes for right atrium (RA), right ventricle (RV), PA, and pulmonary capillary wedge pressure (PCWP) are recognizable as each of these chambers are passed. Once wedged in the pulmonary artery, the balloon is deflated, and the PA waveform can be appreciated. If a wedge tracing is still seen, with the balloon deflated, the catheter has advanced too far and should be withdrawn 1-2 cm (or until a PA tracing is obtained). Once the catheter is correctly positioned, the locking mechanism is secured to keep the PA catheter at a set distance within the sheath. Placement can be confirmed via observation of an appropriate PA waveform and chest x-ray. One way to estimate if the PA catheter is positioned correctly on chest x-ray is to make sure that the tip does not go below the middle third of the lung field. The most proximal port of the PA catheter can be transduced to measure the right atrial or central venous pressure. The most distal port can be used to draw a mixed venous oxyhemoglobin saturation (SvO2) allowing for a true central assessment of tissue extraction of oxygen after mixing. There is an additional port that can be used to administer vasoactive medications as through a central line.
Right atrial (or true central venous) pressure is often used as a surrogate for overall intravascular volume status, however, caution with interpretation should be utilized in patients with right heart dysfunction or failure or in disease processes such as cardiac tamponade or other obstructive phenomena as this number may be falsely elevated leading to an inaccurate assessment of volume status. In general, a normal right atrial pressure is ~ 2-6 mmHg. In the immediate post-operative setting following cardiac surgery, a higher filling pressure of ~8-10 mmHg may be desirable and can be achieved with judicious use of fluid administration and vasoactive agents to maintain vascular tone if profound vasoplegia is present.
Right ventricular systolic pressure is typically ~ 20-30 mmHg with a diastolic pressure of 3-7 mmHg. Measurement of right ventricular pressures can be useful when there is concern for right-sided heart failure, pulmonary valve stenosis, or pulmonary valve regurgitation. Notably, pulmonary artery catheters are also able to estimate right ventricular ejection fraction and right ventricular end diastolic volume (see TSRA primer right ventricular failure)
Pulmonary artery systolic pressure ranges from ~ 18-25 mmHg with a mean pressure of 12-16 mmHg. Traditionally, a mean PA pressure of > 25 mmHg is indicative of pulmonary hypertension. Pulmonary capillary wedge pressure (PCWP) is normally between 4-12 and can be viewed as a surrogate of left atrial pressure and left ventricle end diastolic pressure; thus, an elevated PCWP is concerning for left heart failure or mitral stenosis. In patients with a pulmonary artery catheter, the balloon can be inflated while the catheter is in the pulmonary artery to obtain a PCWP measurement.
Cardiac output (CO) is equal to heart rate x stroke volume (HR x SV); a normal cardiac output is between 4-8 L/min. Cardiac index refers to the cardiac output per body surface area (CO/BSA), and is typically between 2.5-4 L/min/m2. Cardiac output and index can be measured continuously with a continuous cardiac output pulmonary catheter that utilizes thermal energy and thermodilution principles. In a post-operative patient, attention should be given to both the overall volume status of the patient (i.e., is the stroke volume low) and heart rate to optimize CO. Stroke volume variation (SVV) can also be obtained via the pulmonary artery catheter in intubated patients to assess fluid-responsiveness. This measurement assesses the differences in stroke volume ejected with each systole and should be less than 10-13% in an euvolemic patient. Higher ranges of SVV indicate that the patient is fluid responsive; it is important to note that SVV should only be relied on as a volume indicator in a mechanically intubated patient as the variation in volume is directly related to the use of negative pressure ventilation.
When titrating vasoactive medications or administering fluid boluses, the general guiding principle is to aim for a MAP of 60-65 as the MAP is most indicative of end-organ tissue perfusion. It is important to assess the overall volume status of the patient as hypotension may be driven by factors other than hypovolemia or hemorrhage (see TSRA primer hypotension).
Vasoactive medications can be loosely grouped into those acting on vascular tone and cardiac inotropy/chronotropy. Many vasoactive medications act on multiple domains. The following is a short list of medications that are commonly used in the cardiac population in the post-operative setting for hemodynamic management:
Norepinephrine – has inotropic properties (beta-1) but primarily used as vasopressor due to strong vasoconstrictive effect (alpha-1). This is the initial vasopressor used in a variety of pathologies including cardiogenic shock. Initial dose 0.05 mcg/kg/minute – can titrate up to 3.3 mcg/kg/minute.
Epinephrine – acts equally on alpha-1 and beta-1 and 2 receptors. Displays inotropy, chronotropy and vasoconstrictive activity. Initial dose 0.01-0.2 mcg/kg/minute – can titrate up to 2 mcg/kg/minute)
Phenylephrine – pure alpha-1 agonist primarily used for arterial vasoconstriction. May cause a reflex bradycardia due to its selective nature. Initial dose 40-160 mcg/minute – can titrate up to 730 mcg/minute.
Vasopressin – synthetic ADH monolog, acts on V1 receptors, pure vasoconstrictor. Usually used as an adjunct to norepinephrine, not first line monotherapy. Initial dose 0.03 units/minute – run at 0.01-0.04 units/minute
Dopamine – dose-dependent effects, at doses between 5-15 mcg/kg/min, acts on both alpha and beta receptors. At doses greater than 15 mcg/kg/min primarily acts as vasopressor at alpha receptors. Initial dose 2-5 mcg/kg/minute – can titrate up to 20 mcg/kg/minute
Milrinone – phosphodiesterase inhibitor used as inotrope in heart failure, particularly right-sided heart failure and cardiogenic shock. Initial dose 0.125-0.25 mcg/kg/minute – can titrate up to max 0.75 mcg/kg/minute.
Dobutamine – inotrope, beta-1 effects outweigh beta-2 and alpha. Can be used to increase CO with minimal effects on blood pressure (may have vasodilatory effect so should be avoided in patients with refractory hypotension). Initial dose 2-5 mcg/kg/minute – can titrate up to 20 mcg/kg/minute