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The Five -tropies of the Heart

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 increases the actin/myosin connection and improves the cardiac muscle contraction (Figure 2) (1).

Figure 2:
Figure 2.png

https://www.anaesthesiajournal.co.uk/article/S1472-0299(15)00167-8/abstract

When decompensated heart failure patients reduce ventricular filling they can move to a better part of the Frank-Starling curve to optimize stroke volume. But, by improving inotropy they move to a whole new curve (Figure 3).

Figure 3:

Figure 3.png

Inotropy increases stroke volume and therefore increases the width and area of the pressure-volume loop with a lower LV volume and pressure at end-diastole (Figure 4).

Figure 4:

Figure 4.png

https://www.cvphysiology.com/Cardiac%20Function/CF025

Positive inotropic medications: milrinone, dobutamine, epinephrine, digoxin, calcium

Negative inotropic medications: beta-blockers, calcium channel blockers.

 

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).

 

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

Figure 5:

Figure 5.png

https://memorang.com/flashcards/84624/111+-+Electrical+Properties+of+Heart

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 afib or aflutter 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:

Figure 6.png

https://www.cvphysiology.com/Arrhythmias/

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

 

 

Lusitropy: Cardiac relaxation.

Origin: From the Greek root “lusis” meaning a loosening

 

Cardiac relaxation was discovered to be an active process and therefore a fifth term was introduced.

 

Cardiac relaxation occurs at the start of diastole and officially begins when the actin-myosin bridge dissociates. Calcium levels in the cytosol are lowered 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.

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Figure 7:

Figure 7.png

https://www.discoverymedicine.com/Mihai-Gheorghiade/2011/08/23/combining-serca2a-activation-and-na-k-atpase-inhibition-a-promising-new-approach-to-managing-acute-heart-failure-syndromes-with-low-cardiac-output/

Positive lusitropic agents with lead to relaxation of the left ventricle and allow more venous return (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:

Figure 8.png

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

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Clinical Practice:

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.

Figure 11.png

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 can increase in dysrhythmias, but that is more accurately an increase in bathmotropy. One huge benefit of milrinone that is often overlooked is its positive lusitropy. It is great at relaxing the left ventricle and lowering filling pressures and will help with diastolic dysfunction.

 

It is estimated 30-50% of extubation failures are related to diastolic dysfunction (2,3).

Figure 9: (2)

Figure 9.png

Many times, BP 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 great choices in this situation if blood pressure is adequate. Milrinone should definitely be considered as well if the patient continues to have flash pulmonary edema/decompensated diastolic dysfunction.

Figure 10: Hemodynamics 24 hours after milrinone administration (4)

Figure 10.png

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.

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Resources:

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