We are now in a place to manage heart failure from a physiological level. By understanding the physiology, good choices can be made when the patient does not fit the guidelines. I am hoping that as we work through the management of LV dysfunction people will feel more comfortable treating this patient population.
This post will focus on LV systolic dysfunction as the cause of decompensated heart failure. Heart failure secondary to valvular disease and outflow obstruction will be discussed next. I will discuss diastolic heart failure at some point in more depth in the future as well.
Managing LV Dysfunction
Types of heart failure:
Differentiating the types of heart failure is important to understand who needs what type of treatment.
Heart failure can be differentiated using volume status and perfusion status.
Figure 1: Heart Failure Subtypes
Table 1: Heart failure subtypes and mortality
The focus will be on patients who come in congested. Patients presenting Cold & Dry are significantly less common.
Differentiating the congested patient:
1. Congestive Heart Failure
2. Decompensated Heart Failure
3. Cardiogenic Shock
Correctly identifying these patients will ensure that sick patients are identified. All of them with have congestion, but decompensated heart failure and cardiogenic shock patients will have decreased perfusion as well.
Clinical Presentation:
Table 2: Clinical presentation of decompensated heart failure/cardiogenic shock
Hemodynamic Presentation:
Figure 2: Breaking Down Cardiac Output
Is there congestion?
Congestion, or volume overload, is seen hemodynamically with increased filling pressures or increased preload (CVP, PAOP).
Is there low cardiac output?
Low cardiac output leads to low oxygen delivery, and therefore a low mixed venous oxygenation and organ dysfunction. Low cardiac output activates RAAS and causes vasoconstriction and an increase in afterload (SVR).
Is there shock?
Shock is when there is organ ischemia and lactate production.
Table 3: Hemodynamic Abnormalities of the Heart Failure Spectrum
Physiological Presentation:
Figure 3: Starling Curve
Figure 4: Pressure-Volume Loop
Medical Management of Decompensated Heart Failure:
Problem List
1. Increased Preload
2. Decreased Contractility
3. Increased Afterload
Step 1: Decreasing afterload
Decreasing afterload is the most essential first step, as discussed in part 3. This can be done with PO or IV medications. If the patient is able to tolerate PO meds, ACE inhibitors (ACEI) should be the first-line medication, unless contraindicated. ACEIs can reduce afterload and block RAAS, this helps stop the feedback loop more directly. Other options include ARBs and hydralazine. Frequently, the patient has an acute kidney injury and ACEIs and ARBs are not able to be given. So, hydralazine is given as an alternative. If the patient has a borderline blood pressure or is in the ICU, captopril is often the ACEI prescribed since it is every 8 hours and able to be titrated more quickly or discontinued more easily if not tolerated. The captopril can be changed to a longer-acting ACEI when they are closer to discharge, or frequently is changed to an ARB to bridge to Entresto (sacubitril/valsartan). Hydralazine is also every 8 hours and a reasonable alternative but remains every 8 hours for discharge, which makes it a high risk for non-compliance. If PO cannot be tolerated, these medications can be given as IV pushes.
If the patient would benefit more from an IV infusion formulation, nitroprusside is the best medication to use. It is a potent vasodilator and works well in heart failure patients. It has a short half-life, but since it is potent it is given at low doses and titrated carefully. It is usually only given when there is an arterial line in place.
PO/IV Push Afterload Reducers:
1. ACE inhibitors
2. ARBs
3. Hydralazine
IV Infusion Afterload Reducers:
1. Nitroprusside
Step 2: Decreasing preload
Decreasing preload can be done in two different ways. In this situation, it is due to too much volume in the ventricle. Treatment can involve removing the volume with diuretics or dilating the venous system which allows more blood to stay in the venous system and reduces the blood volume in the ventricle.
PO/IV diuretics:
1. Loop: Furosemide/torsemide/bumetinide
2. Thiazide: Chlorothiazide/metolazone
3. CAI: Acetazolamide
PO/IV venodilators
1. Nitroglycerin
Step 3: Increasing contractility
Medications that increase contractility are split into two categories. There are beta-1 agonists (B1 agonists) and phosphodiesterase-3 (PDE-3) inhibitors, both of which are IV. B1 agonists include dobutamine and epinephrine, and the only PDE-3 is milrinone. I will place digoxin on the list, since it has some inotropic properties, but it is not really used for this purpose. This means that there are no great PO inotrope options, another reason why it is important to focus on afterload. If the patient can be compensated on just vasodilator medications, then IV can be transitioned to PO, whereas, if the patient can only become compensated on an inotrope, the patient must be able to qualify for home IV therapy.
IV Inotropes:
B1 agonist:
1. Dobutamine
2. Epinephrine
PDE-3 inhibitors:
1. Milrinone
Digoxin
Choosing the right inotrope:
Dobutamine and milrinone both have vasodilator properties and will lower SVR. This can cause hypotension. They are often referred to as inodilators. Epinephrine has vasopressor properties and increases SVR and is referred to as an inopressor. Another factor is that epinephrine and dobutamine are both fast-acting, and milrinone takes 3-4 hours to reach a steady state. These factors may change the provider’s choice of inotrope.
The SOAP II trial showed worse outcomes using dopamine in a subset analysis of cardiogenic shock compared to norepinephrine, due to its positive bathmotropic properties and increased dysrhythmias.
Decompensated heart failure go-to medications:
Afterload reduction: Captopril
Preload reduction: Furosemide
Contractility agent: Milrinone
Medical Management of Cardiogenic Shock:
Problem List:
1. Hypotension
2. Increased Preload
3. Decreased Contractility
4. Increased Afterload
Hypotension:
To be able to reverse the shock, the patient must be able to perfuse their organs. Organ perfusion is usually MAP – CVP, with a goal MAP ≥ 65mmHg. Sometimes adding an inotrope can increase the blood pressure without adding vasopressors. However, often, vasopressors have to be added to ensure an appropriate MAP. Norepinephrine is the vasopressor of choice. Phenylephrine and dopamine should not be used as vasopressors in cardiogenic shock patients. Vasopressin is also not used unless added to norepinephrine to decrease its requirements.
Vasoplegic cardiogenic shock
As mentioned in part 3, patients can present in vasoplegic cardiogenic shock and will have a low SVR and need vasopressors, and should be able to wean off as the vasoplegia improves.
Non-vasoplegic cardiogenic shock
If vasopressors are used in non-vasoplegic cardiogenic shock they are counterproductive as they increase SVR in patients that already have a significantly elevated SVR. In these situations, if the vasopressor requirement cannot be removed, they would need mechanical support which is for another blog.
Otherwise, the afterload, preload, and contractility meds are the same as decompensated heart failure.
Clinical Examples:
All of these patients are presumed to be a Cold & Wet profile and fit the cardiogenic shock hemodynamics and none of these patients have cardiogenic shock secondary to a primary valvular abnormality.
1. 60 yo M with BP 106/71 (83), HR 92, Lactate 3, EF 21%
This patient shows signs of poor perfusion with a mildly elevated lactic acid, but their blood pressure is normal. This means that there is room to start afterload reduction. I would start PO captopril at a low dose, IV furosemide for diuresis. I would consider adding nitroglyercin IV or PO if the patient was dyspneic and needed immediate relief.
Captopril
Furosemide
+/- Nitroglycerine
Good Tip: If the patient's diastolic blood pressure is higher than your MAP goal they can tolerate more afterload reduction.
2. 42 yo M with BP 98/84 (89), HR 112, Lactate 7, EF 21%
This patient shows worse perfusion compared to patient 1, additionally, their pulse pressure is considerably more narrowed and diastolic BP much higher. This patient has a very low stroke volume and is very clamped down (high afterload). For this patient, I would start IV nitroprusside and continue to up titrate until the MAP is 65-70 mmHg. I would also add IV furosemide.
Nitroprusside
Furosemide
3. 62 yo M with BP 64/49 (53), HR 120, Lactate 10, EF 21%
This patient is hypotensive in shock with a MAP below 65 mmHg. This means that there are perfusion issues due to low flow and low MAP. I would try this patient on dobutamine since it is short-acting. If this does not improve the MAP then add norepinephrine. If the vasopressor requirement is high, I would change dobutamine to epinephrine. I would also start IV furosemide.
Dobutamine +/- Norepinephrine
Furosemide
4. 45 yo W with BP 72/52 (59), HR 30, Lactate 5, EF 35%
This patient is hypotensive and has a low EF, but is probably in cardiogenic shock due to bradycardia. This patient would probably benefit more from a transvenous pacer if the rate is not able to be increased with dopamine or epinephrine. Dopamine is an option since the source of the shock is heart rate related as opposed to stroke volume related. I would also start IV furosemide.
Dopamine
Furosemide
5. 61 yo W with BP 91/32 (52), HR 112, Lactate 9, EF 21%
This patient probably has vasoplegic cardiogenic shock. They have a low EF and elevated lactate, but their diastolic blood pressure is also extremely low. They likely are a mixed cardiogenic and distributive picture. I would either start immediately with epinephrine or try dobutamine with norepinephrine. The dose of norepinephrine would be less worrisome since these patients will usually improve their vasoplegia over time and wean off of vasopressors. Since the patient is vasoplegic, I would not be as aggressive with diuresis and either hold diuresis or give a lower dose compared to the patients above.
Dobutamine
Norepinephrine
Summary:
Understanding the hemodynamics of left ventricular systolic dysfunction and being able to recognize decompensated heart failure and cardiogenic shock is important. Not every patient fits the guidelines, and it is important to know why medications are given and how to use them effectively.
Left Ventricular Heart Failure Series:
Part 1a: Introducing Preload
Part 1b: Measuring Preload
Part 2a: Physiological Contractility
Part 2b: Clinical Contractility
Part 3a: Simplifying Afterload
Part 3b: The Physiology of Afterload
Part 4: Managing LV dysfunction
Other Left-Sided Heart Failure:
Part 1: Valvular disease
Part 2: LVOT obstruction/SAM
Cardiogenic Shock:
Part 1: Why a Protocol is Needed
Part 2: Cardiogenic Shock Protocols
References:
1. Crystal GJ, Assaad SI, Heerdt PM. 24 - Cardiovascular Physiology: Integrative Function. In: Hemmings HC, Egan TD, eds. Pharmacology and Physiology for Anesthesia (Second Edition). Philadelphia: Elsevier; 2019:473-519.
2. Klabunde, R., 2017. CV Physiology | Cardiac Afterload. [online] Cvphysiology.com. Available at: <https://cvphysiology.com/Cardiac%20Function/CF008> [Accessed 16 January 2022].
3. Yartsef A. Determinants of afterload | Deranged Physiology. Derangedphysiology.com. https://derangedphysiology.com/cicm-primary-exam/required-reading/cardiovascular-system/Chapter%20025/determinants-afterload. Accessed January 16, 2022.
4. Greim C, Roewer N, Meissner C, Bause H, Schulte am Esch J. Abschätzung akuter linksventrikulärer Nachlaständerungen. Untersuchung mit der transösophagealen Echokardiographie bei beatmeten Patienten [Estimation of acute left ventricular afterload alterations. Transesophageal echocardiography in artificially respirated patients]. Anaesthesist. 1995;44(2):108-115. doi:10.1007/s001010050137