For everyone to be on the same page with hemodynamics, I think it is important we all speak the same language. Many intensivists only discuss hemodynamics when deciding what type of shock a patient has and otherwise do not seem invested.
Every patient should have their hemodynamics evaluated and discussed daily on rounds, not just patients in a CCU or CVICU. Critically ill patients usually have some degree of organ dysfunction. By evaluating and optimizing hemodynamics, it optimizes cardiac output and blood pressure, which will increase oxygen delivery and organ perfusion. Reversing organ dysfunction is much of what intensivists do daily and so being good at optimizing hemodynamics is an invaluable skill.
In this discussion of hemodynamics, I am going to talk about the five –tropies. These are considered the fundamentals of heart function. By knowing these, it will increase understanding of how the heart works at a physiological level. It will also help with prescribing medications that alter hemodynamics.
The first four –tropies were described in 1897 by TW Engelmann. TW Engelmann was a physicist, botanist, and microbiologist. He taught physiology in Germany in the late 1800s and early 1900s. These first four –tropies were inotropy, chronotropy, dromotropy, and bathmotropy.
Figure 1:
1. Inotropy: Cardiac contractility.
Origin: From the Greek root “in“ meaning sinew (fiber)
The end result of the different pathways is an increase in intracellular calcium. The increase in intracellular calcium strengthens the actin/myosin bridge and improves cardiac muscle contraction (Figure 2) (1).
Figure 2:
https://www.anaesthesiajournal.co.uk/article/S1472-0299(15)00167-8/abstract
When treating a decompensated heart failure patient reducing ventricular filling (preload) can move them to a better location on the Frank-Starling curve and optimize stroke volume. By improving inotropy, they move to a whole new curve with improved stroke volume at the same preload (Figure 3).
Figure 3:
Inotropy increases stroke volume and therefore increases the width and area of the pressure-volume loop meaning a lower LV volume and pressure at end-diastole (Figure 4).
Figure 4:
Positive inotropic medications: milrinone, dobutamine, epinephrine, digoxin, calcium
Negative inotropic medications: beta-blockers, calcium channel blockers.
2. Chronotropy: Rate through the SA node (time)
Origin: From the Greek root “chron“ meaning time
When things affect chronotropy they affect the emission frequency or timing of the SA node. With positive chronotropy there is an increase in the intrinsic rate and with negative chronotropy a decrease in the rate (Figure 5).
Figure 5:
Medications that alter chronotropy act on the sympathetic or parasympathetic system
Positive chronotropes: dopamine, dobutamine, epinephrine, atropine
Negative chronotropes: amiodarone, beta blockers, non-dihydropyridine calcium channel blockers, digoxin
3. Dromotropy: Conduction through the AV node
Origin: From the Greek root “dromos“ meaning running
When things affect dromotropy they affect the action potential conduction speed of the AV node. This means that positive dromotropes will increase the speed and shift the action potential to the left. Negative dromotropes shift the action potential to the right by slowing conduction (Figure 6).
Negative dromotropes are commonly used for atrial fibrillation or atrial flutter with rapid ventricular rates. Negative dromotropes will slow the conduction through the AV node and slow down the ventricular rate.
Negative dromotrope medications (ABCD): Amiodarone, Beta-blocker, Calcium channel blockers and Digoxin. Adenosine will stop conduction through the AV node with very short half-life but is a negative dromotrope
Positive dromotrope medications: isoproterenol
Figure 6:
4. Bathmotropy: Excitability of the heart
Origin: From the Greek root “bathmos“ meaning degree
When things affect bathmotropy they affect the amount of response to stimulus the heart will have. Positive bathmotropes increase the degree of excitability of the heart and increase excitation.
An easy way to think about it is irritability. Positive bathmotropes will increase ectopy and dysrhythmias by making it easier for the action potentials to fire.
Positive bathmotropic medications: norepinephrine, epinephrine, digoxin, dopamine, dobutamine
Negative bathmotropic medications: beta-blockers, amiodarone
1982:
It was not until 1982 that the 5th –tropy was described. This was due to a misunderstanding of the cardiac cycle. Cardiac relaxation was discovered to be an active process and therefore a fifth term, lusitropy, was introduced.
Lusitropy: Cardiac relaxation.
Origin: From the Greek root “lusis” meaning a loosening
Cardiac relaxation occurs at the start of diastole and officially begins when the actin-myosin bridge dissociates. The result of lusitropy is a decrease in calcium levels in the cytosol by transferring the calcium into the sarcoplasmic reticulum.
ATP activates the calcium channel on the sarcoplasmic reticulum and lowers calcium levels in the cytosol
The decreased levels cause the release of calcium from troponin C and detachment of the actin-myosin cross-bridges.
The detachment returns the sarcomere to its resting length
ATP starts this process meaning energy is required for cardiac relaxation.
Figure 7:
Positive lusitropic agents with lead to relaxation of the left ventricle and allow more venous return and ventricular filling (preload). Positive lusitropes will drop the end-diastolic line on the pressure-volume loop, meaning that for the same amount of volume the ventricle will have less pressure (Figure 8).
Figure 8:
https://www.researchgate.net/figure/The-effects-of-adrenergic-stimulation-on-the-pressure-volume-relationship-The-slope-of_fig3_8244616
Positive lusitropic medications: milrinone, dobutamine, nitroglycerine, nitroprusside
Negative lusitropic medications: beta-blockers
Putting it all together clinically:
When prescribing medications that act on the heart it is important to understand what your goals are so that you can make the best possible decision for the patient.
The best example I have is milrinone. It has multiple effects on the heart. It is mainly known as an inotropic agent and is given to patients with reduced LV or RV function. It is also well-known as a systemic and pulmonary vasodilator and can be beneficial in pulmonary hypertension with RV failure. A side effect is an increase in dysrhythmias, but that is more accurately an increase in bathmotropy. One huge benefit of milrinone that is often overlooked is its positive lusitropic properties. It is great at relaxing the left ventricle and lowering filling pressures and helping with diastolic dysfunction.
It is estimated 30-50% of extubation failures are related to diastolic dysfunction(2,3).
Figure 9 (2):
Many times blood pressure control alone will prevent an increase in diastolic dysfunction causing increased filling pressures and worsening pulmonary edema. But, occasionally it is not enough and other measures are needed. Nitroglycerin and nitroprusside are lusitropic and great choices in this situation if blood pressure is adequate. However, milrinone should definitely be considered if the patient continues to have flash pulmonary edema/decompensated diastolic dysfunction. Adding milrinone will allow more ventricular filling/cardiac relaxation and significantly decrease the central venous pressure (CVP) and pulmonary artery occlusion pressure (PCWP) as shown below (Figure 10). PCWP <18mmHg will decrease the risk of pulmonary edema and improve extubation success rates.
Figure 10: Hemodynamics 24 hours after milrinone administration(4)
Below is a list of commonly used medications to alter hemodynamics and their expected change on these factor.
Understanding the fundamentals of hemodynamics can really help with the understanding of the patient and the understanding of how medications can help.
Here is how I think about cardiac output and where I can intervene to help the patient.
Remember the five -tropies of the heart.
References:
1. Klabunde. R. Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops. CV Physiology. 2017. Accessed 3/15/2021. https://www.cvphysiology.com/Cardiac%20Function/CF025
2. Papanikolaou, J., Makris, D., Saranteas, T., Karakitsos, D., Zintzaras, E., Karabinis, A., Kostopanagiotou, G., Zakynthinos, E. New insights into weaning from mechanical ventilation: left ventricular diastolic dysfunction is a key player. Intensive Care Medicine. 2011;37:1976-1985. doi:10.1007/s00134-011-2368-0
3. Roche-Campo, F., Bedet, A., Vivier, E., Brochard, L., Mekontso Dessap, A. Cardiac function during weaning failure: the role of diastolic dysfunction. Annals of Intensive Care. 2018;8. doi:10.1186/s13613-017-0348-4
4. Albrecht CA, Giesler GM, Kar B, Hariharan R, Delgado RM 3rd. Intravenous milrinone infusion improves congestive heart failure caused by diastolic dysfunction: a brief case series. Tex Heart Inst J. 2005;32(2):220-223.