Terminology for Cardiac Drugs
Inotropes = Contractility
Vasopressors = SVR
Chronotropes = HR
These can be positive or negative too. For example, beta-blockers are negative chronotropes.
Deal with contractility.
Deal with SVR
Deal with HR
Receptors of the Nervous System
Muscarinic (ACh) in the Parasympathetic
Adrenergic (a & B) in the Sympathetic
Role of Parasympathetic
"Rest and Digest"
Decreases HR and SVR
Role of Sympathetic
"Fight or Flight"
Increase HR, SVR, and bronchiolar dilation
Located on vascular smooth muscle and a little bit in the heart.
Activation leads to increased contractility of the heart, increased HR, and greatly increased SVR.
Located selectively where vasodilation may be beneficial during shock, such as the brain.
Activation leads to selective decrease in SVR.
Located in the heart.
Leads to greatly increased contractility and greatly increased HR.
Located in smooth muscle of vessels and bronchi.
Activation leads to decreased SVR and bronchial dilation.
Endogenous release from the adrenal medulla.
Activates a-1, a-2, B-1, B-2 receptors.
Results in increased cardiac output, and greatly increased SVR.
For cardiac arrest, the IV bolus is 1 mg of 1:10,000
For anaphylaxis, the IM dose is 0.3 mg of 1:1000
Natural catecholamine which is a precursor to norepinephrine.
Increases both CO and SVR.
Effects are dose-related. At lower doses it is more of a beta-effect, and at higher doses it exhibits more of an alpha effect.
Used only as a bridge to buy time to get to the cath lab. Increasing SVR is not good in the long-term for MI. Very easy to give. Will actually make an MI worse, but will keep the patient from dying.
An anticholinergic agent. It is a competitive inhibitor of muscarinic receptors.
Blocks the parasympathetic system to increase HR without increasing SVR or CO.
An alpha-1 receptor agonist with minimal beta-1 activity.
Greatly increases SVR and keeps CO relatively neutral.
Can be used for uncontrolled bleeding.
Beta-1 receptor agonist with minimal beta-2 or alpha activity.
Greatly increases CO with a slight decrease in SVR.
Be careful. In heart failure, the cardiac output may increase but it may not increase above the point where the SVR drops, and the problem may be made worse. This can be supplemented with norepinephrine which will keep CO the same, but will greatly increase SVR.