Pharmacology Flashcards
Catecholamines
Augment arterial BP, contractility and cardiac output
They will not work without cortisol so may require glucocorticoid given simultaneously in the critically ill
Increase the metabolic O2 demand
Addressing hypotension
- Anticholinergic or reversal is a2
- Fluid bolus if Hypovolaemia
- Start dopamine CRI at pressor rates (lower rates will vasodilate)
- Give antiarrhthmics
- If no response to dopamine consider norepinephrine
- No response to catecholamines consider vasopressin and/or hydrocortisone
Dopamine
Precursor to epinephrine
B and A properties depending on dose (b at lower and a at higher)
Modest vasoconstriction and increase in BP
Dobutmaine
Synthetic analog to dopamine with primary b1 agonism
Moderately vasodilate and increases forward blood flow in the face of normal BP (increasing CO)
Ephedrine
Increases norepinephrine release from the SNS and is a bronchodilator
Modest decrease in HR whilst increasing CO, SVR and arterial BP
Can deplete norepinephrine stores
Norepinephrine
Primarily a agonism
Potent vasoconstriction to increase arterial BP
Will have varying affect on HR and CO depending on volume status
Used when ineffective to dopamine
Phenylephrine
A agonism only
Raises the BP after dopamine ruled ineffective
Vasopressin
Not technically a catecholamine but is a pure vasoconstrictor that may be useful if no response to catecholamines
Will increase SVR due to baroreceptor reflex in response to a decrease in HR/Vol
Epinephrine
Works on all receptors
Not usually a first choice unless CPR
Increases HR, SVR and CO
Increases arterial BP and pacemaker activity
Cardiovascular support drug choice
- Dopamine and/or dobutamine as increases heart rate and contractility and potentially CO. Modestly increases vasomotor tone; dopamine “pressure” and dobutamine “output”.
- Norepinephrine
Combining catecholamines does what?
Midway effects of both drugs I.e. increases in heart rate and BP without arrhythmia (norepinephrine and dopamine)
Which of vascular resistance and cardiac output is more powerful in determining arterial BP
Vascular resistance
Arterial vasomotor tone
Primary determinant of visceral and tissue perfusion
Vasoconstriction
Good thing unless affecting perfusion in which case dobutamine may be used to modestly vasodilate without affecting BP but improving the forward flow
Cortisol and catecholamines
The cardiovascular system doesn’t operate well without cortisol; low cortisol causes vasoparesis and impaired response to catecholamines (CIRCI/RAI) and so low dose hydrocortisone in the critically ill that aren’t responding to catecholamines will likely help improve catecholamine activity
What are some affects other than cardiovascular catecholamines can have
Increased glucose and lactate
Increased K uptake so Hypokalaemia
Increasing metabolic O2 demand
Impaired PLT
Vasopressin
Or known as ADH or AVP
Normally released in response to an increase in osmolality, decreased blood volume or decreased BP
G-coupled receptors that primarily induce vasoconstriction
Inhibited by glucocorticoids, opiates, natriuretic factors and GABA
V1 receptors
Smooth muscles
Vasoconstriction (vasodilation at cerebral, renal, pulmonary and mesenteric vessels)
V2 receptors
Renal collecting ducts, endothelial cells, platelets and vascular endothelium
Increased water permeability
Increased vWF release
Stimulation of aggregation
Vasodilation
V3 receptors
Posterior pituitary
ACTH release
Oxytocin (vasopressin receptor)
Mammary gland, uterus, GIT and endothelium
Contraction
Vasodilation
In vitro vasopressin
More potent vasoconstrictor compared to norepinephrine, angiotensin II, phenylephrine
Apart from vaso effects what is AVP involved in
Sleep
Memory
Temperature regulation
ACTH release
Uses of vasopressin
CPR
Vasodilatory shock
Central diabetes insipidus (desmopressin) - increased ADH action
vWD (desmopressin)
GI disease
Haemorrhagic shock