How can stroke volume and heart contractility be increased in patients?

Increasing Stroke Volume and Heart Contractility

Stroke volume and heart contractility can be increased through inotropic agents (dobutamine, phosphodiesterase inhibitors), fluid optimization using goal-directed therapy in hypovolemic patients, and vasopressors when hypotension persists despite adequate preload. 1, 2

Pharmacologic Approaches to Increase Contractility

Inotropic Agents

Dobutamine is the primary inotropic agent for increasing contractility and stroke volume, working through β-receptor stimulation to enhance myocardial contractility while producing mild chronotropic effects. 2 The drug increases cardiac output primarily through:

• Enhanced left ventricular contractility leading to increased stroke volume at low plasma concentrations (2.5 μg/kg/min), with onset of action within 1-2 minutes 2, 3
• Decreased systemic vascular resistance facilitating ventricular emptying 2, 4
• At higher doses, heart rate becomes the dominant mechanism for cardiac output augmentation rather than stroke volume 3

Phosphodiesterase III inhibitors (milrinone) increase contractility through a different mechanism by inhibiting cyclic AMP breakdown, resulting in increased myocardial contractility and peripheral vasodilation. 5 Key advantages include:

• Effectiveness during concomitant beta-blocker therapy since they work distal to beta-adrenergic receptors 5
• Less tachycardia and fewer arrhythmias compared to dobutamine 5
• Significant increases in cardiac output and stroke volume with decreased pulmonary wedge pressure 5

Critical limitation: PDE inhibitors should only be used short-term in hospitalized patients as long-term oral therapy increases mortality in heart failure patients. 5

When to Use Inotropes

Inotropes should be considered when cardiac index is <2.5 L/min indicating reduced contractility, particularly after fluid optimization has failed to improve stroke volume. 1 The European Heart Journal recommends inotropes for patients with peripheral hypoperfusion refractory to diuretics and vasodilators at optimal doses. 5

Fluid Optimization to Increase Stroke Volume

Goal-Directed Fluid Therapy (GDFT)

Fluid boluses can increase stroke volume only when two conditions are met: (1) fluid infusion significantly increases cardiac preload, and (2) the heart is operating on the steep portion of the Frank-Starling curve. 6

GDFT uses minimally invasive cardiac output monitoring to optimize patients on their individual Frank-Starling curve by administering colloid boluses when stroke volume increases >10% with fluid challenge. 1 This approach is:

• Strongly recommended for high-risk patients and those undergoing surgery with large intravascular fluid loss 1
• Weakly recommended for low-risk patients as recent studies within enhanced recovery programs showed minimal benefit 1

Fluid Selection and Volume Status

Isotonic crystalloids (0.9% saline) at 1-4 ml/kg/h maintain homeostasis while avoiding the cerebral edema risk associated with hypotonic solutions. 1

Large volume saline infusion (when appropriate) increases stroke volume through both preload-dependent and preload-independent mechanisms, including decreased end-systolic volumes and increased contractility indices. 7 However, approximately 50% of fluid boluses fail to improve cardiac output as intended, and excess fluid worsens outcomes. 8

Arterial pulse pressure variation predicts fluid responsiveness by determining whether stroke volume will increase when preload increases. 6 If pulse pressure variation is low, only inotropic drugs can improve cardiac output. 6

Vasopressor Support

When fluid boluses fail to increase stroke volume significantly (≤10% increase), vasopressors should be used to treat arterial hypotension. 1 Norepinephrine is the primary agent, increasing mean arterial pressure through:

• Increased systemic vascular resistance without significant pulmonary vasoconstriction 1
• Decreased preload dependency by shifting unstressed to stressed venous volume 1
• Transient increase in cardiac output through increased venous return 1

Clinical Algorithm

1. Assess volume status and fluid responsiveness using pulse pressure variation and volumetric preload markers 6
2. If hypovolemic with positive fluid responsiveness: Administer isotonic crystalloid boluses targeting stroke volume increase >10% 1, 6
3. If euvolemic or fluid non-responsive with cardiac index <2.5 L/min: Initiate dobutamine starting at 2.5 μg/kg/min, titrating to effect 1, 2
4. If hypotensive despite adequate preload: Add vasopressor (norepinephrine) 1
5. If on beta-blockers: Consider PDE inhibitor instead of dobutamine for short-term use only 5

Critical Pitfalls

Avoid fluid overload as perioperative weight gain >2.5 kg worsens outcomes; maintain near-zero fluid balance. 1 Never use intra-aortic balloon counterpulsation in acute aortic regurgitation despite the need for inotropic support. 1 Do not rely on clinical examination or vital signs alone to predict fluid responsiveness as they are unreliable. 8