MRCS

Inotropes and Vasopressors

Definition Recap:

MAP = mean arterial pressure

CO = cardiac output
HR = heart rate
SV = stroke volume
SVR = systemic vascular resistance
EDV = end-diastolic volume

CO = HR x SV

Stroke volume = end-diastolic volume - end-systolic volume (80ml)

Ejection fraction = SV/ EDV (0.67)

Arterial pressure = CO x SVR

MAP estimation = diastolic pressure + 1/3(systolic pressure - diastolic pressure)

Pulse pressure = systolic pressure - diastolic pressure

Frank-Starling law - the stroke volume of the heart increases in response to the volume of blood
entering the heart (end diastolic volume). Note: An increase in myocardial contractility causes an
increase to the stroke volume.

Inotropic: Effects myocardial contractility i.e. +ve inotrope increases force of contraction - causes
an upward and left shift in the Starling curve.

Chronotropic: Effects heart rate i.e. +ve chronotrope increases rate

Dromotropic: Effects conduction speed and therefore rate of electrical impulses

Core receptors:

• Alpha adrenergic receptors -

• Increase systemic vascular resistance.
• Vasoconstriction of coronary arteries, venous constriction, reduced gut motility.
• A1 - smooth muscle contraction.
• A2 - negative feedback inhibits insulin release, NA release.
• Beta adrenergic receptors -
• B1 - Chronotropic/Dromotropic/Inotropic = increased CO, increases renin
secretion, increases ghrelin.
• B2 - Smooth muscle relaxation - bronchi/gi tract. Lipolysis, Anabolism, Insulin
secretion. Skeletal artery dilatation.
• Non-CNS Dopamine receptors -
• Various subtypes
• Vasodilatory, Inotropic
• Vasopressin receptors -
• V1 mediates constriction of vascular smooth muscle.
• V2 water reabsorption by enhancing renal collecting duct permeability.
 MRCS Inotropes and Vasopressors

Common Vaso-active Drugs:

Drug Receptor Effect Application Side Effects

Dopamine DA+++ +ve Inotrope. Often 1st Choice Hypotension,

β1++++ Low dose: splanchnic Shock - ventricular
α1+++ vasodilatation, increased Cardiogenic, arrhythmias,
β2++ renal and hepatic flow. Vasodilatory, cardiac/tissue
High dose: symptomatic ischaemia in high
vasoconstriction, bradycardia. doses.
increased SVR

Dobutamine β1+++ +ve Inotrope, weaker Low CO - Tachycardia

β2 ++ chronotrope. Decompensated Increased
α1+ Mild vasodilatation HF, Cardiogenic ventricular
shock. response rate in
patients with
Sepsis-induced atrial fibrillation
myocardial Ventricular
dysfunction, arrhythmias
Symptomatic Cardiac ischemia
bradycardia. Hypertension

Noradrenaline α1++++ Arteriolar Septic shock with Arrhythmias

β1++ vasoconstriction - low SVR Bradycardia
β2+ Increased systemic Peripheral
vascular resistance (digital) ischemia
Hypertension

Adrenaline α1++++ +ve Inotrope and Shock: Ventricular

β1++++ chronotrope Cardiogenic, arrhythmias
β2+++ High doses - septic. Severe
vasoconstriction Cardiac arrest hypertension risk
Bronchospasm/ of cerebral
anaphylaxis hemorrhage
Symptomatic Cardiac ischemia
bradycardia Sudden cardiac
death

Vasopressin V1, V2 Vasoconstriction, less Shock: Arrhythmias

(antidiuretic direct coronary/cerebral Vasodilatory, Hypertension
hormone) vasoconstriction. Cardiogenic. Decreased CO
Increased systemic Cardiac arrest Cardiac ischemia
vascular resistance. Peripheral
ischemia
Splanchnic
vasoconstriction
Reference:
Christopher B. Overgaard, Vladimír Džavík, Contemporary Reviews in Cardiovascular Medicine. Inotropes and
Vasopressors. Review of Physiology and Clinical Use in Cardiovascular Disease Circulation. 2008; 118: 1047-1056