Cardiodynamics

Case Studies

Cardio Shock Septic Shock Hypovolemic Shock Mixed Shock

Background Information

The development of diagnostic human cardiac catheterization for evaluation of patients with ischemia or infarction dates back to the early 1900s, though it required rigid catheters and fluoroscopic guidance which posed significant limitations due to the need to transport critically ill patients to the catheterization lab, the increased risk of inducing cardiac arrhythmias, and the requirement of remarkable catheter manipulation due to varying anatomy. Recognizing these difficulties and limitations as well as the need for an improved way to evaluate these seriously ill patients, in 1970, Swan et al. set out to find a more acceptable way of catheter placement. To meet their standard, there were 3 major criteria required: placement without induction of ventricular arrhythmias, quick and easy passage to the pulmonary artery, and placement without the need for fluoroscopy.

Similar to catheters used in dogs by Lategola and Rahn at the time, Swan et al. constructed a flexible flow-guided balloon catheter and tested 100 total catheter passages in humans, 60 without fluoroscopic guidance and 40 with fluoroscopic guidance. 92% of these 100 insertions passed into the pulmonary artery, no severe arrhythmias occurred, and the average passage time was 36 seconds which was much faster than with conventional catheters. Additionally, the insertion of these new catheters was able to be successfully completed by inexperienced staff, whereas conventional catheters required experienced personnel. Without fluoroscopic guidance, the average passage time was 49 seconds and 95% of passages enter the pulmonary artery which showed promise in the use of these catheters in severely ill patients who were unable to be transferred to the catheterization lab or in which fluoroscopy was not readily available.

The use of these catheters became widespread after this study, and the following new information changed the future by providing a more robust understanding of abnormal hemodynamics of acute cardiac conditions such as myocardial infarction, altering management of these patients, giving prognostic insight, and allowing for the monitoring of therapies that affect hemodynamics.

(Resources: Swan et al, Lategola & Rahn, and Mitchell’s Invasive Hemodynamic Monitoring)

Preload

Cardiac preload is defined as the ventricular wall stress at the end of diastole via stretching of the cardiac myocytes, and, clinically, preload for the left ventricle is measured as the left ventricular end-diastolic volume.
Increases in preload can be caused by increased ventricular compliance, increased atrial contraction, reduced heart rate providing more filling time, atrioventricular valve regurgitation, and increased central venous pressure via increased blood volume, increased skeletal pump activities, decreased venous compliance from sympathetic activation, and respiratory augmentation.
Decreases in preload can be caused by impaired atrial contraction in the case of atrial arrhythmias, increased heart rate reducing filling time, atrioventricular valve stenosis, and decreased central venous pressure via decreased blood volume such as from dehydration or blood loss.

Afterload

Afterload is the resistance the heart must overcome following systole, and, clinically is affected by aortic pressure and systemic vascular resistance.
Changes in afterload are affected by the blood viscosity, the autonomic nervous system, and vasoactive hormones such as norepinephrine, epinephrine, angiotensin II, and vasopressin to name a few.

Contractility

Contractility is the ability of the ventricle to contract at a certain preload and afterload. Unlike skeletal muscle that can change contractile force through changes in motor nerve activity and motor unit recruitment, cardiac muscle contraction involves activation of all muscle fibers. For this reason, contractile force can only be changed by varying the fiber length, which is dependent on preload, and changes in inotropy, which is the strength of contraction.

(Resources: hemodynamic adaptive mechanisms in heart failure)

The first step in inserting a Swan-Ganz catheter involves placing an introducer sheath into the right internal jugular vein, subclavian vein, or less commonly, the antecubital or femoral veins. After placement of the introducer sheath, the Swan-Ganz catheter is passed through and advanced into the central vein where the balloon is inflated with 1.5cc of air. The catheter is advanced slowly, with the balloon flowing through the right atrium, right ventricle, and pulmonary artery until there is a wedge position achieved in the distal branch of the pulmonary artery.

Physiologic Measurements and Interpretation

Preload/pulmonary artery wedge pressure

Pulmonary artery wedge pressure is used to approximate left ventricular preload. Because proximal blood flow is occluded when the catheter is in the wedge position due to the inflated balloon, the distal catheter tip of the catheter is able to measure pressures distally in the pulmonary arterioles which closely approximates left atrial pressure. Subsequently, when the mitral valve is open at the end of diastole, this pressure approximates left ventricular end-diastolic pressure which is equal to the preload.

CO/Cardiac index

Thermodilution method

This method uses a thermistor or thermocouple to continuously measure the temperature of blood in the heart. Typically, cold saline is injected into the right atrium which causes a drop in temperature of the blood. This produces a thermodilution curve, and the area under the curve is automatically calculated which is inversely related to CO.

Fick

This method is based on the principle that oxygen delivery/consumption to the organs is the product of blood flow (or cardiac output) to the organs and the arteriovenous concentration difference of oxygen.
- O2 consumption (mL/min) = CO (L/min) x (A-V) concentration difference (mL/L)
Therefore, if we solve for cardiac output, the Fick equation is
- CO (L/min) = O2 consumption (mL/min) / (A-V) concentration difference (mL/L)
Things to know
- Arteriovenous difference:
  - To find the A-V concentration difference, the A-V saturation difference must be multiplied by the theoretical O2-carrying capacity
    - Theoretical O2-carrying capacity occurs when Hgb is 100% saturated
    - Theoretical O2-carrying capacity = Hgb (g/dL) x 1.36 (mL/O2/g Hgb) x 10 dL/L
  - Blood is drawn from the tip of the Swan-Ganz catheter to assess PA O2 saturation
  - Ao O2 sat can be assessed with an oximeter or with arterial blood
- At rest, O2 consumption can be assumed to be 125 mL/m²

SVR

Computed value using measurements from the PA catheter and blood pressure measurements
SVR = (mean arterial pressure – right atrial pressure) / CO
Mean arterial pressure = (1/3 x [systolic pressure – diastolic pressure]) + diastolic pressure

PVR

Computed value using measurements from the PA catheter
PVR = (mean pulmonary artery pressure – pulmonary capillary wedge pressure) / CO

Indications and Considerations

(Resources: bedside hemodynamic monitoring)

Indications

Shock

Management of cardiogenic shock, especially in the setting of end-organ compromise
Differentiate causes of shock and guide management after failing a trial of intravascular volume expansion
Determine the presence of pericardial tamponade when clinical assessment is inconclusive and echocardiography is unavailable

Heart failure

Differentiation of cardiogenic and noncardiogenic pulmonary edema after failing a trial of diuretic and/or vasodilator therapy
Management of congestive heart failure refractory to standard medical therapy

Acute MI

Diagnosis of mechanical complications of MI if echocardiogram has not been performed
Progressive hypotension unresponsive to fluids post-MI
Short-term guidance of management of acute mitral regurgitation before surgical correction
Diagnosis of intracardiac shunts and severity of these shunts prior to surgical correction

Pulmonary hypertension

Diagnosis and severity of pulmonary hypertension

Contra-indications

Absolute

Right-sided endocarditis
Mechanical tricuspid or pulmonic valves
Presence of thrombus or tumor in the right side of the heart

Relative

Coagulopathy
Recent permanent pacemaker or defibrillator placement
Left bundle branch block
Bioprosthetic tricuspid or pulmonic valves

Common Interventions in Shock

(Resources: Inotropes and vasopressors, amboss)

Sympathomimetic drugs

Receptors

Alpha-1: increases vascular smooth muscle contraction
Beta-1: increases heart rate (chronotropy) and cardiac contractility (inotropy)
Beta-2: increases vasodilation
Dopamine-1: induces vasodilation in renal vasculature

Dobutamine

Beta-1 > beta-2 >> alpha-1
Inotropic effects > chronotropic effects
No change or decrease in blood pressure, raises heart rate, increases cardiac output

Norepinephrine

Alpha-1 > beta-1
Increase in blood pressure (secondary to vasoconstriction) with possible reflex bradycardia

Epinephrine

Alpha-1 > beta-1 (at high doses)
Increases blood pressure, heart rate, and cardiac output

Dopamine

D > beta-1 > alpha-1
Low dose: greater beta-1 → increases heart rate and cardiac output
High dose: greater alpha-1 → increases blood pressure

Phenylephrine

Alpha-1 only
Increased vasoconstriction → increased blood pressure with possible reflex bradycardia

Milrinone

PDE3 inhibitor (beta-1/beta-2 like effect)
In myocardium: phosphodiesterase type 3 inhibitor → increased cAMP → activation of calcium channels → cardiostimulatory effects → increased heart rate and inotropy
In peripheral vasculature: phosphodiesterase type 3 inhibitor → increased cAMP → inhibition of myosin light chain kinase → smooth muscle relaxation → vasodilation
Increased cardiac output and heart rate, unchanged or decreased blood pressure (decreased systemic vascular resistance)

Vasopressin

Vasopressin-1 (alpha-1 like effect) → increased vasoconstriction → increase in blood pressure

Nitrates

Nitroprusside

Nitric oxide → activation of guanylyl cyclase → increase cGMP → activation of protein kinase G
Peripheral vasodilation → decreased preload and afterload
Coronary dilation → improved myocardial perfusion

Nitroglycerin

Nitric oxide → activation of guanylyl cyclase → increase cGMP → activation of protein kinase G
Peripheral vasodilation (vein > arteries) → decreased preload and afterload
Coronary dilation → improved myocardial perfusion

Fluids

Giving fluids increases central venous pressure via increased blood volume, which then causes an increase in preload and subsequently, contractility

Lasix

Giving Lasix decreases central venous pressure via decreased blood volume, which then causes a decrease in preload and subsequently, contractility

Beta blockers

Inhibit beta-1 → decrease heart rate and cardiac contractility → decrease blood pressure

Table Summary

Alpha-1: increases vascular smooth muscle contraction
Beta-1: increases heart rate (chronotropy) and cardiac contractility (inotropy)
Beta-2: increases vasodilation
Dopamine-1: induces vasodilation in renal vasculature

Resources for Further Education

Swan et al
Bedside hemodynamic monitoring
Invasive hemodynamic monitoring
Lategola M, Rahn H: A self-guiding catheter for cardiac and pulmonary arterial catheterization and occlusion. Proc Soc Exp Biol Med 84:667-668, 1953
Hemodynamic adaptive mechanisms in heart failure
Inotropes and vasopressors

Surveys