Vasopressors Lecture Notes

Introduction

• Importance of vasopressors in clinical settings.
• Follow along with comprehensive notes and illustrations available on the website.
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Categories of Vasopressors

1. Inodilators
2. Inopressors
3. Pure Vasopressors
4. Methylene Blue

Inodilators

Definition

• Inodilators increase heart contractility (inotropic) and cause vasodilation.
• Indications: Cardiogenic shock, low cardiac output.

Major Drugs

1. Dobutamine
   • Receptors: Primarily beta agonist (beta-1, beta-2), minimal alpha-1.
   • Mechanism: Increases contractility and heart rate by acting on beta receptors in nodal and myocardial cells.
   • Effects: Increases cardiac output and stroke volume, slight vasodilation due to minimal alpha activity.
2. Milrinone
   • Receptors: PDE-3 inhibitor, not acting on adrenergic receptors.
   • Mechanism: Increases cAMP leading to increased contractility in the heart and vasodilation in vessels.
   • Effects: Increases cardiac output, decreases afterload and blood pressure.
3. Isoproterenol
   • Receptors: Strong beta agonist (beta-1 and beta-2).
   • Mechanism: Strongly increases heart rate, contractility, and causes mild vasodilation.

Clinical Uses

• Cardiogenic Shock: Dobutamine and milrinone are preferred.
• Septic Shock: Used in combination therapy for patients with low ejection fraction or cardiac output.
• Bradycardia: Isoproterenol is a strong choice for patients on the verge of cardiac arrest.

Titration

• Goal: Titrate to cardiac output, not blood pressure.
• Methods: Echocardiogram, urine output, central venous pressure, SVO2, lactate levels.

Pros and Cons

1. Dobutamine
   • Pros: Short half-life, easily titratable.
   • Cons: Beta receptor desensitization, not ideal for Afib with RVR.
2. Milrinone
   • Pros: More effective vasodilation.
   • Cons: Renal elimination, risk of accumulation in renal dysfunction.
3. Isoproterenol
   • Cons: Expensive, available in limited hospitals.

Inopressors

Definition

• Increase cardiac contractility and peripheral vasoconstriction.
• Indications: Septic shock, cardiogenic shock.

Major Drugs

1. Norepinephrine
   • Receptors: Alpha-1, Beta-1 agonist.
   • Effects: Increases contractility, heart rate, systemic vascular resistance.
2. Epinephrine
   • Receptors: Dose-dependent; low doses (beta-1, beta-2), high doses (alpha-1).
   • Effects: Increases heart rate, contractility, systemic vascular resistance, lactate production.
3. Dopamine
   • Receptors: Dose-dependent; low doses (dopamine receptors), moderate doses (beta-1), high doses (alpha-1).
   • Effects: Variable; difficult to titrate, associated with higher mortality in shock states.

Clinical Uses

• Septic Shock: Norepinephrine (first-line), epinephrine (second-line).
• Cardiogenic Shock: Epinephrine more effective, sometimes combined with inodilators.
• Bradycardic Periarrest: Epinephrine drip can stabilize heart rate temporarily.

Titration

• Goal: Mean arterial pressure (MAP) >= 65 mmHg.
• Methods: Monitor MAP, sometimes heart rate in bradycardic conditions.

Pros and Cons

1. Norepinephrine
   • Pros: Effective in septic and cardiogenic shock, reliable increase in BP.
   • Cons: Increased heart rate could be problematic in Afib with RVR.
2. Epinephrine
   • Pros: Effective in multiple shock states, added bronchial dilation, histamine inhibition.
   • Cons: Increases lactate, care needed in Afib.
3. Dopamine
   • Cons: Difficult to titrate, associated with higher mortality, risk of tissue necrosis if extravasated.

Pure Vasopressors

Definition

• Primary function: Vasoconstriction, little effect on heart rate.
• Indications: Vasodilatory shock, especially septic shock.

Major Drugs

1. Phenylephrine (Neo)
   • Receptors: Alpha-1 agonist.
   • Effects: Increases preload, systemic vascular resistance, BP.
2. Vasopressin
   • Receptors: V1 (arterioles), V2 (kidneys).
   • Effects: Increases systemic vascular resistance, water reabsorption, lowers pulmonary arterial pressure.
3. Angiotensin II (Giapreza)
   • Receptors: Acts on angiotensin II receptors.
   • Effects: Causes vasoconstriction, increases aldosterone and ADH.

Clinical Uses

• Septic Shock: Phenylephrine, vasopressin, and angiotensin II.
• Vasopressin: Central diabetes insipidus, hepatorenal syndrome.

Titration

• Goal: MAP >= 65 mmHg.
• Methods: Monitor heart, urine output, clinical status.

Pros and Cons

1. Phenylephrine
   • Pros: Useful in Afib with RVR, aortic stenosis; reflex bradycardia.
   • Cons: May be less effective in low ejection fraction unless volume responsive.
2. Vasopressin
   • Pros: Can help with urine output, pulmonary vasodilation.
   • Cons: Risk of tissue necrosis if extravasated.
3. Angiotensin II
   • Cons: Potential for thrombosis, pro-inflammatory effects.

Methylene Blue

Definition

• Used for refractory vasoplegic shock of any etiology.
• Indications: Severe cases where traditional vasopressors are ineffective.

Mechanism

• Inhibits nitric oxide synthase, lowers cyclic GMP, increases calcium in cytoplasm, vasoconstriction.

Titration

• Procedure: Initial dose (2 mg/kg), followed by infusion.
• Goal: Titrate to MAP >= 65 mmHg.

Pros and Cons

• Pros: Effective in life-threatening vasoplegic shock.
• Cons: Pulmonary vasoconstriction, serotonin syndrome, false low oxygen readings, hemolytic anemia in G6PD deficiency, P450 inhibition.

Peripheral vs Central Lines

• Peripheral IV acceptable briefly in emergent situations.
• Central lines preferable for higher doses or prolonged use.
• Arterial lines provide accurate MAP readings, useful in complex cases.

Oral Vasopressors

1. Midodrine
   • Mechanism: Oral alpha-1 receptor agonist.
   • Indications: Weaning off IV vasopressors, hepatorenal syndrome.
   • Cons: Renally excreted, can cause reflex bradycardia.