Pharmacology Flashcards
4 sites of drug metabolism
Lungs
Liver
Kidneys
Cells
4 sites of drug excretion
Kidneys
Lungs
Bowels
Skin
Contraindications for Succinylcholine
- Hyperkalemia
- Rhabdomyolysis (burns/crush > 72hrs) due to up regulation of ACh receptors
- History of malignant hyperthermia
- Neuromuscular disease (safe in mysthenia gravis)
- Spinal cord injury
- Stroke, over 72 hours old
- Unable to BVM
- Pseudoactylcholinestrase deficiency
Succinylcholine administration cautions
- Can affect muscarinic receptors in myocardium and cause bradycardia (or the hyperkalemia can).
- Can increase ICP so avoid in TBI/CVA patients.
- Masseter spasm (*rarely associated with malignant hyperthermia)
- Will temporarily increase serum potassium levels by 0.5-1.0 mmol.
Rocuronium administration cautions
- Difficult BVM
- Anaphylaxis (can occur hours after administration)
MOI of most Pressors/Inotropes
- Modifies intracellular cyclic adenosine monophosphate (cAMP) levels
- Increases release of Ca++ from sarcoplasmic reticulum
- Increases sensitivity of troponin to Ca++
Effects of pH on SNS receptors
Mutates alpha and beta receptor sites and inhibits their binding with catecholamines. This often occurs with pH < 7.12. Consider NaHCO3 if vasopressors are ineffective.
Succinylcholine induction dose:
- 5mg/kg (actual body weight)
* Larger doses can potentially spill over and cause muscarinic activation –> bradycardia
Rocuronium induction dose:
0.6 to 1.2mg/kg (ideal body weight)
Rocuronium pharmacokinetics
Onset: 60-90 seconds
Duration: 30-45 minutes
Succinylcholine pharmacokinetics
Onset: <60 seconds (look for fasiculations)
Duration: 4-10 minutes
Ketamine doses
Induction: 0.5-4mg/kg
Maintenance: 0.5-4mg/kg/hr
IVP: 0.01 to 0.03mg/kg or just 5-20mg
*Going over won’t ‘dissociate’ the patient deeper, it will just prolong the effect of dissociation. It may, however, cause respiratory arrest!
Ketamine pharmacodynamics
- Antagonizes NMDA receptors and reduces catecholamine reuptake.
- Interrupts pathways between limbic system (emotions/memories) and the cortex (higher functions, wakefulness, perception) causing dissociation.
- Increases HR, BP and cardiac output.
- Can cause bronchodilation.
- Is associated with significant oropharyngeal secretions (can be dried with 0.2mg atropine).
Propofol doses
Induction: 2 to 4mg/kg (Will cause hypotension!!)
Maintenance: 5-100mcg/kg/min
IVP: 10-30mg
Propofol infusion syndrome can occur at doses of 80mcg/kg/min over 24 hours. Severe, refractory bradycardia leading to asystole. Crank up the milliamps and pace!
Propofol pharmacodynamics
- Works on GABA and NMDA receptors and modulates hypothalamic sleep pathways. Also, upregulates Mu receptors to make opioids more responsive.
- Amnesic, anxiolytic, anti-convulsant, anti-emetic, bronchodilatory effects, and muscle relaxing effects. No analgesia!
- Will sequester itself into adipose tissue to delay clearance. Elimination is not affected by renal/liver dysfunction.
Fentanyl doses
Induction: 50-100mcg (less for patients > 65)
Maintenance: 1-3mcg/kg/hr (50-200mcg/hr)
IVP: 20-50mcg
*Large doses of opioids for induction can cause “frozen chest wall.” The only treatment is paralytics or naloxone.
Ketamine pharmacokinetics
Onset: 1 minute
Duration: 15-20 minutes
Fentanyl pharmacokinetics
Onset: Immediate
Duration: 30-60 minutes
Is midazolam safe for pregnant patients?
No. All benzodiazepines are recognized as class D. Evidence shows strong risk to the fetus.
Choose another agent to treat eclampsia (MgSO4, phenytoin etc.)
Midazolam pharmacokinetics
Onset: 2-5 minutes
Duration: <2 hours
*Benzodiazepines can alter higher cognitive function in older adults for up to 6 months after administration!
Midazolam doses
Induction: 5-10mg
Maintenance: 5-10mg/hr
- Cut in half for anybody >65.
- Will have significant duration for anybody with renal/hepatic dysfunction since both drug and metabolite are active!
Low dose epinephrine receptor activation
Alpha: +
Beta 1: +++
Beta 2: ++
*Increases CO, decreases SVR
High dose epinephrine receptor activation
Alpha 1: +++
Beta 1: +++
Beta 2: +
Increases CO and increases SVR
Low dose (1-2mcg/kg) dopamine receptor activation
Alpha: -
Beta 1: +
Beta 2: -
Dopaminergic: ++ (causes selective vasodilation of renal, coronary, mesenteric and cerebral vessels)
Medium dose (5-10mcg/kg) dopamine receptor activation
Alpha: +
Beta 1: ++
Beta 2: -
Dopaminergic: ++
High dose (10-20mcg/kg) dopamine receptor activation
Alpha 1: ++ Beta 1: ++ Beta 2: - Dopaminergic: ++ *Be wary of dysrhythmias!
Dobutamine receptor activation
Alpha 1: - Beta 1: +++ Beta 2: ++ Dopaminergic: - *lower doses cause more inotropy while higher doses cause more vasodilation!
Vasopressin properties
- Works like anti-diuretic hormone (ADH) and exclusively works on V1 receptors.
- Increases water reabsorption in the kidney’s collecting ducts. Pulls more water than sodium so can cause relative hyponatremia. This is good for diabetes insipidus but bad for cerebral edema.
- Causes vasoconstriction, particularly in the splanchnic vessels so can be useful for esophageal varices.
- Unlike levophed, will constrict efferent renal arterioles, thus increasing glomerular flow.
- Considered second line agent for sepsis refractory to levophed or anaphylaxis refractory to sepsis
- Dose: 0.01 to 0.04 units/min. Doses higher than 0.03u/min are associated with mesenteric and coronary ischemia and increased pulmonary artery pressures.
- Particulalry useful in septic shock since there is possible reduced endogenous ADH in this shock state.