MEDICATIONS

1. Analgesics / Antipyretics / Sedation

Non-opioid Analgesic / Antipyretic

  • Tylenol (Acetaminophen)

    • MoA:

      • inhibits COX enzymes centrally (brain) leading to prostaglandin synthesis inhibition—> decreased body temp, decreased pain

    • SIDE EFFECTS:

      • LIVER DAMAGE:

        • liver failure from overdose (>4g/day)

        • monitor:

          • AST, ALT, bilirubin, INR

NSAIDS

  • MoA:

    • inhibit COX enzymes which inhibits prostaglandins, thrombaxanes, and prostacyclins which are created from arachidonic acid

      • leads to:

        • decreased inflammation, pain, and fever (desired)

        • decreased GI protection→ ulcer risk

        • decreased renal blood flow→ AKI risk

        • decreased platelet aggregation→ bleeding risk

  • Ibuprofen/Advil/Motrin

    • COX selectivity: non-selective

    • Use: mild-moderate pain, fever, inflammation

    • Duration: short-intermediate (q6-8hr)

    • OTC or Rx: both

    • Key points:

      • common first line NSAID

      • moderate GI risk

      • reversible platelet inhibition

  • Naproxen/Aleve

    • COX selectivity: non-selective

    • Use: arthritis, musculoskeletal pain, menstrual cramps

    • Duration: longer acting (q12)

    • OTC or Rx: both

    • Key points:

      • longer half-life than ibuprofen

      • often preferred for chronic inflammatory conditions

      • possibly lower CV risk compared to some NSAIDs

  • Aspirin

    • MoA: inhibits COX enzymes→ decreased prostaglandin synthesis (Reduces pain, fever, and inflammation) and inhibits thromboxane A2 production in platelets→ reduced platelet aggregation

    • COX selectivity: non-selective

    • Use:

      • low dose→ antiplatelet (MI, stroke prevention) (cardioprotection)

      • higher dose→ pain, fever, inflammation

    • Duration:

      • pain/fever dosing: q4-6

      • antiplatelet effect: lasts 7-10 days (life of platelet due to irreversible inhibition

    • OTC or Rx: both

    • Key points:

      • high ulcer and bleeding risk

      • salicylate toxicity:

        • salicylates directly stimulate the medullary respiratory center→ hyperventilation→ blow off CO2→ respiratory alkalosis

        • salicylates uncouple oxidative phosphorylation in mitochondria→ decreased ATP production→ cells switch to anaerobic metabolism→ increased lactic acid, increased ketones→ metabolic acidosis→ tinnitus & mixed acid-based disorder

      • reye syndrome risk:

        • occurs when aspirin is given during viral infections (influenza or varicella))

        • viral infection already stresses mitochondria + aspirin causes mitochondrial dysfunction in hepatocytes→ decreased ATP production, impaired fatty acid oxidation→ fat accumulates in liver cells→ microvesicular fatty liver→ ammonia rises (liver cant detoxify)→ ammonia crosses BBB→ cerebral edema + acute liver failure

      • aspirin-induced asthma:

        • bronchospasm triggered by aspirin or NSAIDs in susceptible patients

        • when COX is blocked, arachidonic acid gets shunted to→ lipoxygenase pathway → increased leukotrienes→ bronchoconstriction, mucus production, airway inflammation

  • Celecoxib/Celebrex

    • COX selectivity: selective

    • Use: arthritis, chronic inflammatory pain    

    • OTC or Rx: rx only

    • Key points: less GI ulcer risk, no platelet inhibition, higher cardiovascular risk compared to nonselective NSAIDs

  • Indomethacin

    • COX selectivity: non-selective

    • Use: acute gout, inflammatory conditions

    • Duration: closes PDA in neonates

  • Ketorolac/Toradol

    • COX selectivity: non-selective     

    • Use: short-term management of moderate-severe acute pain (post-op)

    • Key points:

      • very potent analgesic (near opioid-level pain relief)

      • strong platelet inhibition

      • high GI and renal risk

Opioid Analgesics

  • Morphine sulfate

    • MoA:

      • full opioid receptor agonist→ decreased cAMP, decreased Ca+ influx, increased K+ efflux→ neurons become hyperpolarized→ decreased neurotransmitter release→

        • increased release of substance P and glutamate (pain neurotransmitter→ blocks ascending pain signals, alters perception of pain in brain→ decreased pain transmission AND decreased emotional response to pain

        • suppresses responsiveness to CO2 + decreased firing of respiratory neurons→ slower respiratory rate, decreased tidal volume, increased CO2 retention

        • decreased excitatory neurotransmission + reduces cortical arousal→ less neuronal firing→ sedation, drowsiness, possible decreased LOC

        • decreased acetylcholine release in GI tract→ reduced peristalsis→ slower stool movement, harder stool, constipation, ILEUS RISK

        • stimulates mast cell→ histamine release→ vasodilation, increased capillary permeability, pruritus→ HYPOTENSION!

      • triggers release of histamine→ vasodilation

  • Fentanyl/Sublimaze

    • MoA:

      • Full MOR agonist, highly lipophilic (rapid CNS penetration)→ decreased cAMP, decreased Ca+ influx, increased K+ efflux→ neuron hyperpolarization + decreased neurotransmitter released

        • decreased substance P and decreased glutamate (pain neurotransmitter)→ potent pain suppression (100x more morphine)

        • minimal histamine release→ more hemodynamically stable

        • increased muscle→ chest wall rigidity + impaired ventilation

        • vagus nerve stimulation (vagal stimulation)→ released acetylcholine→ bradycardia

  • Methadone

    • MoA:

      • Full MOR agonist, NMDA receptor agonist (reduces CENTRAL sensitization (chronic pain)), inhibits serotonin + norepinephrine uptake

        • NMDA blockade→ better for reduction of neuropathic pain

        • blocks cardiac potassium channels→ delays ventricular repolarization, prolongs QT interval→ increased risk torsades de pointes

  • Oxycodone

    • same as other opioids

    • increased risk for abuse, moderate sedation, mild hypotension

Benzodiazepines

  • bind to GABA-A receptor→ increased frequency of Cl- channel opening→ increased GABA inhibitory effect → decreased neuronal excitability→ CNS Depression: decreased anxiety, anticonvulsant, respiratory depression (especially paired with opioid), decreased HR & BP

    • risk for paradoxical agitation: enhance GABA-A inhibition (GABA inhibits excitatory neurons)→ some inhibitory interneurons suppress OTHER inhibitory neurons→ possible inhibition of inhibitory neurons→ disinhibition→ increased dopamine activity, increased behavioral activation→ restlessness, crying combativeness, hyperactivity, inconsolability

  • FLUMAZENIL- REVERSAL AGENT

    • Competitive antagonist at the benzodiazepine binding site on GABA-A receptor → displaces benzos, doe NOT activate the receptor→ reversed sedation

  • Lorazepam/Ativan

    • onset: moderate

    • duration: interpediate

    • key point: seizure managment

  • Midazolam/Versed

    • onset: rapid

    • duration: short (unless infusion)

    • key point: intubation + procedural

  • Diazepam/Valium

    • onset: rapid

    • duration: long (Active metabolites)

    • key point: muscle spasm + seizures

Sedatives

  • selective alpha 2 adrenergic receptor agonist + acts primarily on brainste

  • alpha 2 receptors are G-protein coupled receptors linked to the Gi subunit→ inhibition of enzyme adenylyl cyclase→ reduced intracellular cAMP→ decreased norepinephrine→ decreased sympathetic outflow

  • Dexmedetomidine/Precedex

    • MoA:

      • decreased norepi→ decreased sympathetic tone→ calm, arousable sedation

      • decreased pain signal transmission

      • minimal respiratory depression becasued it does not suppress medullary CO2 responsiveness

      • decreased nroepi→ decreased SA node stimulation→ decreased SVR, hypotension, decreased HR→ decreased cardiac output

      • uses:

        • sedation for extubated patients, sedation during weaning from ventilatory

        • junctional ectopic tachycardia management (decreased sympathetic tone)

        • post-op congenital heart surgery

  • Propofol/Diprivan

    • MoA:

      • potentiates GABA-A receptor→ increased Cl- channel opening duration→ direct CNS depression

        • increased Cl- influx→ hyperpolarization→ profound CNS suppression→ deep sedation, hypnosis, anesthesia

        • cortical suppression→ memory impairment

        • direct depression of medullary respiratory centers→ decreased CO2 responsiveness, decreased tidal volume, apnea

        • enhanced GABA-A activity in central sympathetic pathways→ decreased norepinephrine release, decreased alpha-1 receptor stimulation, relaxation of arterial smooth muscle→ systemic vasodilation, decreased SVR, myocardial depression→ decreased contractility, decreased stroke volume, decreased cardia output

Dissociative Anesthetic

  • Ketamine

Reversal Agent/Withdrawal Adjunct

  • Narcan (Naloxone) – opioid antagonist

  • Flumazenil/Romazicon

  • Methadone

  • Clonidine/Catapres

Oral Sucrose (Analgesic for neonates)

  • Sweet Ease

Cardiovascular Medications

Vasopressors

  • Epinephrine

    • MoA:

      • mixed alpha 1, alpha 2, beta 1, and beta 2 adrenergic agonist

        • (β₁): ↑ HR (β₁) → ↑ cardiac output + tachyarrythmias (VT, SVT)

        • (β₁): ↑ contractility → ↑ stroke volume

        • (α₁ at higher doses): ↑ SVR → ↑ BP + peripheral ischemia

        • (β₂): Bronchodilation → useful in asthma/anaphylaxis

        • (β₂): ↑ glycogenolysis→ hyperglycemia + lactic acidosis

      • dose-dependent effects:

Dose

Dominant Effect

Low

β₁ → ↑ HR, ↑ contractility

Moderate

β₁ + β₂ → HR ↑, some vasodilation, bronchodilation

High

α₁ → vasoconstriction dominates

  • Norepinephrine

    • MoA:

      • predominantly alpha 1 agonist, some beta 1 activity

      • minimal beta 2 activity

        • (α₁): ↑ SVR → ↑ BP→ ischemia of extremities/organs

          • reflex bradycardia may occur due to ↑ BP

        • (β₁): mild ↑ contractility → ↑ stroke volume

    • indications:

      • post-op hypotension/low SVR

      • septic shock with low BP

      • often first-line for pediatric vasodilatory shock

  • Dopamine

    • low dose: “renal dose” (D1 receptors)

      • location: renal, mesenteric, coronary, cerebral arterioles

      • MoA:

        • dopamine binds D1 Gs-coupled receptors→ increased adenylyl cyclase→ increased cAMP in smooth muscle→ activation of PKA→ decreased intracellular Ca2+→ smooth muscle relaxation→ vasodilation→ increased renal blood flow→ increased GFR, increased urine output

          • mild decreased SVR

          • minima effect on HR or contractility

    • moderate dose: “inotropic dose” (beta 1 receptors)

      • location: SA node, AV node, atrial & ventricular myocardium

      • MoA:

        • dopamine binds beta 1 Gs-coupled receptors→ increased adenylyl cyclase→ increased cAMP→ increased PKA→ PKA phosphorylates L-type Ca+ channels→ increased Ca2+ influx during systole→ increased actin-myosin cross-bridge cycling→ increased contractility (inotropy) and increased HR (chronotropy)→ increased SV & CO

      • uses:

        • post-op congenital heart disease with low CO but normal BP

        • avoid in patients prone to tachyarrythmias

    • high dose: “vasopressor dose” (alpha 1 receptors)

      • location: vascular smooth muscle (arterioles)

      • MoA:

        • dopamine binds alpha Gq-coupled receptors→ activates phospholipase C→ increased IP3 (triphosphate)→ increased Ca2+ in smooth muscle→ Ca2+ binds to calmodulin→ myosin light chain kinase→ contraction

        • alpha 2 receptors→ increased SVR→ increased BP→ increased afterload→ increased coronary perfusion pressure

    • dose-dependent receptor activity:

Dose

Receptor

Signaling

Key Physiologic Effect

Clinical Use

1–5 µg/kg/min

D1

Gs → ↑ cAMP → ↓ Ca²⁺ in smooth muscle

Renal & mesenteric vasodilation → ↑ urine output

Renal perfusion / mild low CO

5–10 µg/kg/min

β1

Gs → ↑ cAMP → ↑ Ca²⁺ influx

↑ HR, ↑ contractility → ↑ CO

Post-op low cardiac output

>10 µg/kg/min

α1

Gq → ↑ IP₃ → ↑ Ca²⁺ in smooth muscle

Vasoconstriction → ↑ SVR & BP

Hypotensive shock

  • Vasopressin/ADH: peptide hormone

    • MoA:

      • V1 receptors- vascular smooth muscle→ vasoconstriction

        • vasopressin binds V1 Gq- coupled receptors→ activates phospholipase C→ IP3→ increased intracellular Ca2+→ Ca2+ binds calmodulin→ activates myosin light chain kinase→ smooth muscle contracts→ arterial vasoconstriction→ increased SVR→ increased BP→ ischemia of gut, extremities, and coronary d/t intense vasoconstriction & reflex bradycardia

          • uses: useful in catecholamine-resistant vasodilatory shock

          • works independently of adrenergic receptors, so it’s effective even if patients are tachyphylactic to norepinephrine or epinephrine

      • V2 receptors- renal collecting ducts→ water reabsorption

        • vasopressin binds V2 Gs-coupled receptors→ increased adenylyl cyclase→ increased cAMP→ PKA activation→ phosphorylates aquaporin-2 channels→ aquaporin-2 translocates to the apical membrane→ water is reabsorbed from the urine back into the circulation→ increased free water retention→ increased blood volume→ increased BP→ hypernatremia from water retention

          • uses: can help maintain BP in hypovolemic states, but not the primary ICU effect

      • V3 receptors- pituitary→ ACTH release

        • vasopressin binds→ ACTH release→ increased cortisol

Receptor

Mechanism

Effect

V₁

Gq → ↑ IP₃ → ↑ Ca²⁺ → smooth muscle contraction

↑ SVR, ↑ BP

V₂

Gs → ↑ cAMP → PKA → aquaporin-2 insertion

↑ water reabsorption → ↑ blood volume

V₃

Pituitary

↑ ACTH → ↑ cortisol (minor)

Inotropes

  • Dobutamine: synthetic catecholamine

    • MoA:

      • predominantly beta 1 adrenergic agonist→ increased contractility

        • increased HR→ may slightly increase CO

      • mild beta 2 agonist→ vasodilation→ decrease afterload

      • weak alpha 1 agonist→ minimal vasoconstriction

    • uses:

      • post-op low CO with normal or low BP

      • short-term inotropic support

      • often used when SVR is not extremely high

    • good if BP is adequate; risk of tachycardia

  • Milrinone: phosphodiesterase-3 (PDE3) inhibitor

    • MoA:

      • increases cAMP in cardiac myocytes→ increased intracellular Ca2+→ increased contractility + vasodilation (decreased SVR, decreased PVR)→ decreased afterload

    • uses:

      • decreased PVR helps in post-op single ventricle (glenn or fontan) or pulmonary hypertension (with low CO)

      • usually HR unchanged or slightly increased

    • ideal when afterload reduction and pulmonary vasodilation are needed; hypotension possible

  • Digoxin: cardiac glycoside

    • MoA:

      • inhibits Na+/K+ ATPase on cardiac myocytes

      • increased intracellular Na+→ reduces Na+/Ca2+ exchanger activity→ increased intracellular Ca2+→ increased contractility→ increased SV

      • vagal stimulation→ decreased SA node firing→ decreased HR→ increased diastolic filling time→ increased coronary perfusion

      • slows AV conduction→ prolong PR interval- useful for rate control in atrial arrythmias

    • uses:

      • heart failure with low CO

      • ventricular dysfunction post-op

      • SVT/atrial tachyarrythmias (slows AV conduction)

      • useful for HR control + inotropy; narrow therapeutic window

Antiarrhythmics

CLASS I antiarrythmics

  • targets: phase 0 of ventricular cells

    • block fast Na+ channels (Na+ stays OUT)→ slowing conduction velocity

  • CLASS 1A:

    • examples:

      • procainamide

      • quinidine

    • MoA:

      • moderate Na+ block→ slows phase 0

      • also blocks K+→ prolongs phase 3

        • increased action potential duration

        • increased QT interval

    • use:

      • atrial and ventricular arrythmias

  • CLASS 1B:

    • examples:

      • lidocaine

    • MoA:

      • weak Na+ block

      • shortens action potential duration

      • acts mainly on ischemic tissue

    • use:

      • ventricular arrythmias

      • post MI VT

  • CLASS 1C:

    • examples:

      • flecainide

    • MoA:

      • strong Na+ block

      • markedly slows conduction

      • minimal effect on QT

    • use:

      • SVT, atrial fib

      • avoid in structural heart disease

CLASS II antiarrythmics/Beta blockers

  • targets: phase 4 of nodal cells

  • examples:

    • metoprolol

    • propanolol

    • esmolol

    • atenolol

  • MoA:

    • block beta 1 receptors→ decreased cAMP→ decreased Ca2+ influx

      • decreased slope of phase 4

      • decreased AV node conduction→ decreased HR, decreased myocardial oxygen demand, rate control for AF

      • increased PR interval→ prevents SVT

CLASS III antiarrythmics/Potassium channel blockers

  • targets: phase 3 of ventricular cells

    • block K+ channels (K+ stays in)→ prolonging repolarization

      • increase action potential duration

      • increase QT interval

      • increase refractory period

  • Amiodarone

    • class III antiarrythmic, potassium channel blocker

    • MoA:

      • blocks delayed rectifier K+ channels→ decreased potassium efflux during phase 3 of cardiac action potential→ prolonged repolarization→ prolonged action potential duration→ prolonged QT interval→ increased refractory period

CLASS IV antiarrythmics/ Ca+ channel blockers

  • targets: phase 0 in nodal cells

  • examples:

    • verapamil

    • diltiazem

  • MoA:

    • block L-type Ca2+ channels→

      • slow phase 0 depolarization in AV node→ rate control in AF, decrease HR

      • decreased conduction velocity

      • increased PR interval → SVT termination

  • Adenosine

    • enedogenous nucleoside; AV nodal blocking agent

    • MoA:

      • acts on A1 adenosine receptors (Gi coupled) in the AV node:

        • decreases cAMP

        • increased K+ efflux

        • hyperpolarizes AV nodal cells

        • decreases Ca2+ influx

          • profound slowing of AV node conduction

          • temporary AV block

            • makes the cell EXTREMELY negatively polarized→ flatline (asystole)

    • uses:

      • first line for SVT

      • diagnostic tool (reveals atrial flutter)

      • rapid termination of AVNRT (atrioventricular nodal reentrant tachycardia/paroxsysmal SVT)

ACE Inhibitors

  • Captopril

  • Enalapril

    • MoA:

      • inhibits angiotensin-converting enzyme→

        • decreased angioteNSIn II

          • decreases vasoconstriction→ decreased SVR→ decreased afterload + decreased BP

          • hypotension

        • decreased aldosterone

          • decreased Na+ reabsorption→ decreased water retention→ decreased preload

          • hyperkalemia

        • increased bradykinin

          • ACE normally breaks down bradykinin

          • blocking ACE→ bradykinin accumulation→

            • vasodilation

            • cough

            • angioedema- life-threatening

    • uses:

      • chronic heart failure

        • reduces wall stress, reduces remodeling, improves survival, improves ejection fraction overtime

Vasodilators

  • Hydralazine

    • direct arterial vasodilator

    • MoA:

      • acts directly on arteriolar smooth muscle

        • increases nitric oxide signaling, decreases intracellular Ca+→ smooth muscle relaxation→ decreased SVR→ decreases afterload

          • reflex increased HR (baroreceptor response)

  • Nipride (Nitroprusside)

    • potent arterial & venous vasodilator

    • MoA:

      • nitroprusside releases NO

        • NO→ activates guanylate cyclase→

          • cGMP, decreases Ca2+→ smooth muscle relaxation → arterial vasodilation (Decreases afterload) + venous vasodilation (decreases preload)

        • decreases BP→ increased SV (if HF present)

  • Sildenafil

    • PDE-5 inhibitor

    • MoA:

      • blocks phosphodiesterase-5 in pulmonary vasculature

      • normally:

        • NO→ increased cGMP→ vasodilation

        • PDE-5 breaks down cGMP

      • sildenafil blocks PDE-5:

        • sustains cGMP

        • pulmonary vasodilation → decreased pulmonary vascular resistance

          • decreased RV afterload→ decreased RV wall stress, increased RV stroke volume

  • Alprostadil/Prostaglandin E1

    • prostaglandin analog

    • MoA:

      • binds prostaglandin receptors→ increased cAMP→ increased smooth muscle relaxation

        • vasodilation

        • keeps ductus arteriosus open→ allows mixing of blood

    • side effects:

      • APNEA

      • hypotension

      • fever

      • flushing

  • Remodulin (Treprostinil)

    • prostacyclin analog

    • MoA:

      • binds prostacyclin receptors→

        • increased cAMP

        • smooth muscle relaxation→ mild systemic vasodilation

        • pulmonary vasodilation→ decreased PVR→ decreases RV afterload→ decreased RV wall stress→ improves RV stroke volume

        • inhibits platelet aggregation

    • side effects:

      • hypotension

      • flushing

      • jaw pain

      • infusion site pain

      • bleeding risk

Diuretics

Loop Diuretics

  • Diuril (Chlorothiazide)

  • MoA:

    • massive Na+ loss→ water follows→ decreased ability to concentrate urine

  • elyte:

    • decreased Na+, K+, Mg2+, Ca2+

      • can lead to metabolic alkalosis

  • hemodynamic effects:

    • decreased blood volume→ decreased EDV

    • decrease preload→ decreased LV wall stretch

    • decreased pulmonary congestion→ decreased pulmonary edema

    • mild decreased BP

  • side effects:

    • hypokalemia→ arrythmias

    • ototoxicity

    • dehydration

    • AKI

    • metabolic alkalosis

  • Furosemide/lasix

    Bumetanide/bumex

Thiazides

  • MoA:

    • less potent than loop diuretic

    • water loss→ decreased preload

  • electrolytes:

    • decreased Na+, K+

    • Ca2+ retention

  • Spironolactone

    • aldosterone agonist (potassium-sparing)

    • MoA:

      • blocks aldosterone receptor→mild diuresis + K+ retention

        • subtle preload reduction

      • normally aldosterone:

        • increased Na+ reabsorption

        • increase K+ excretion

        • increases water retention

    • electrolytes:

      • increases K+

      • decreases Na+

        • mild acidosis possible

  • Diamox (Acetazolamide)

    • carbonic anhydrase inhibitor

    • MoA:

      • blocks carbonic anhydrase (allows bicarbonate reabsorption)→ increased bicarbonate excretion, mild diuresis, metabolic acidosis

      • weak diuretic effect

      • MAIN USE→CORRECTING METABOLIC ALKALOSIS

    • electrolytes:

      • decreases HCO3-

      • metabolic acidosis

      • mild hypokalemia

Anticoagulants / Antiplatelets / Thrombolytics

  • Aspirin – antiplatelet

    • COX inhibitor

    • MoA:

      • aspirin irreversibly inhibits COX-1 in platelets

        • normally:

          • arachidonic acid→ COX-1→ thromboxane A2 (TXA2)

          • TXA2 causes:

            • platelet activation

            • platelet aggregation

            • vasoconstriction

        • aspirin block COX-1→

          • decreased TXA2→ decreased platelet activation and platelet aggregation

      • **platelets cannot make new COX enzyme- effect lasts for the life of the platelet (~7-10 days)

    • uses:

      • arterial clot prevention

  • Enoxaparin – LMWH

    • MoA:

      • enhances antithrombin III activity

        • AT3 normally inhibits:

          • factor Xa

          • Thrombin (factor IIa)

        • LMQH mainly enhances factor Xa inhibition

          • blocks prothrombin→ thrombin→ fibrin→decreased clot propagation

    • monitor: anti-Xa levels

    • Side effects:

      • bleeding

      • HIT

      • injection site hematoma

  • AT3 (Antithrombin III)

    • natural anticoagulant protein

    • MoA:

      • AT3 inactivates by binding to these factors and neutralizing them: heparin works by accelerating AT3 activity

        • thrombin (Factor 2a)

        • factor Xa

        • factor IXa

        • factor XIa

  • Alteplase (tPA) – thrombolytic

    • fibrinolytic

    • MoA:

      • activates plasminogen→ plasmin (breaks down fibrin mesh in clots)

        • dissolves EXISTING clots

  • Aminocaproic acid – antifibrinolytic (clot stabilizer)

    • MoA:

      • competitively inhibits plasminogen activation→ blocks plasmin formation→ prevents fibrin breakdown

        • opposite of tPA

        • stabilizes existing clot

  • Heparin:

    • sulfated polysaccharide

    • MoA:

      • heparin binds to AT3→ conformational change→ increase AT3 activity by 1,000 fold→ AT3 rapidly inactivates:

        • thrombin

        • factor Xa→ no thrombin→ no fibrin→ unstable clot→ no clot formation

    • *if AT3 levels are low→ heparin doesnt work

    • monitor:

      • unfractionated heparin:

        • PTT

        • anti-Xa

        • ACT (in ECMO)

      • LMWH: anti-Xa only

    • **does not break down existing clots (tPA)

    • side effects:

      • bleeding

      • HIT

      • osteoporosis

Respiratory Medications

Bronchodilators (Beta Agonists)

  • Albuterol

    • short acting beta 2 agonist

    • MoA:

      • beta 2 receptor stimulation→ increased cAMP→ bronchial smooth msucle relaxation→ bronchodilation

    • Uses:

      • asthma exacerbation

      • bronchospasm

      • hyperkalemia

    • side effects:

      • tachycardia

      • tremor

      • hypokalemia

      • anxiety

  • Xopenex (Levalbuterol)

    • selective S-enantiomer beta 2 agonist

    • MoA:

      • same as albuterol but more beta 2 selective→ theoretically less tachycardia

    • uses:

      • asthma

      • patients sensitive to albuterol-induced tachycardia

    • side effects:

      • tachycardia

      • tremor

      • hypokalemia

  • Racemic Epinephrine

    • non-selective alpha and beta agonist

    • MoA:

      • beta 2→ bronchodilation

      • alpha 1→ mucosal vasoconstriction→ decreased airway edema

    • uses:

      • croup

      • post-extubation stridor

    • side effects:

      • tachycardia

  • Theophylline

    • Methylxanthine bronchodilator

    • MoA:

      • phosphodiesterase inhibition→ increased cAMP

      • adenosine receptor blockade→ bronchodilation + mild respiratory stimulation

    • uses:

      • refractory asthma

      • neonatal apnea

    • side effects:

      • narrow therapeutic index

      • arrythmias

      • sezures

      • n/v

Mucolytic

  • Mucomyst (Acetylcysteine)

    • mucolytic; antidote for acetaminophen toxicity

    • MoA:

      • breaks disulfide bonds in mucus→ decreases viscosity, replenishes glutathione

    • Uses:

      • thick secretions (CF, intubated patients)

      • acetaminophen overdose

Pulmonary Hypertension

  • Sildenafil

    • PDE-5 inhibitor

    • MoA:

      • blocks PDE-5→ increased cGMP→ pulmonary vasodilation

    • uses:

      • pulmonary hypertension

      • congenital heart disease with increased PVR

    • side effects:

      • hypotension

      • headache

      • flushing

  • Remodulin

    • prostacyclin analog

    • MoA:

      • activates prostacyclin receptors

        • increases cAMP→ pulmonary vasodilation

        • inhibits platelet aggregation

    • uses:

      • severe pulmonary arterial hypertension

    • side effects:

      • hypotension

      • jaw pain

      • bleeding risk

RSV Prevention

  • Palivizumab

    • monoclonal antibody (RSV F protein inhibitor)

    • MoA:

      • binds RSV fusion protein → preventing viral entry into respiratory cells

    • uses:

      • high-risk infants (prematurity, CHD, BPD)

      • RSV season prophylaxis

Respiratory Stimulant (Neonatal apnea)

  • Caffeine citrate

    • methylxanthine CNS stimulant

    • MoA:

      • adenosine receptor antagonist→ stimulates medullary respiratory center→ increases diaphragmatic contractility

    • uses:

      • apnea of prematurity

Neurologic Medications

Antiepileptics

  • Levetiracetam/Keppra

    • antiepileptic (SV2A modulator)

    • MoA:

      • binds to synaptic vesicle protein SV2A→ modulates neurotransmitter release→ decreases excessive neuronal firing→ seizure stabilization

      • unlike benzos or phenobarbital, it does NOT directly enhance GABA

    • Uses:

      • first-line for focal and generalized seizures

      • status epilepticus

  • Phenobarbital

    • barbiturate; long-acting anticonvulsant

    • MoA:

      • enhances GABA-A receptor activity→ prolongs chloride channel opening→ neuronal hyperpolarization→ CNS depression

      • at high doses: can directly open GABA channels (strong CNS depression)

    • Uses:

      • first-line for neonatal seizures

      • refractory status epilepticus

      • sedation in some ICU settings

Benzodiazepines

  • MoA:

    • enhances GABA-A receptor activity→ increased freqeuncy of Cl- channel opening→ rapid neuronal inhibition

    • stops seizures activity quickly

  • uses:

    • first-line for status epilepticus

    • acute seizure control

  • side effects:

    • respiratory depression

    • hypotension

    • oversedation

    • paradoxical agitation (Rare)

Antibiotics / Antimicrobials

Penicillins

  • Amoxicillin

  • Ampicillin

  • Nafcillin

  • Piperacillin-Tazobactam

Cephalosporins

  • Cefazolin

  • Cefotaxime

  • Ceftazidime

Aminoglycosides

  • Gentamicin

  • Tobramycin

Glycopeptide

  • Vancomycin

Sulfonamide

  • Sulfamethoxazole/Trimethoprim

Rifamycin

  • Rifampin

Antiviral

  • Oseltamivir

    • uses:

      • influenza A & B treatment

      • high-risk pt (peds, cardiac disease, immunocompromised)

      • post-exposure prophylaxis

Antifungal

  • Nystatin

    • uses:

      • oral thrust (candida)

      • diaper rash (candida)

Endocrine / Metabolic

Insulin

  • Rapid-Acting Insulin

    • onset: ~15 min

    • peak: ~1 hr

    • duration: ~2-4 hrs

    • types:

      • glulisine (apidra)

      • lispro (humalog)

      • aspart (novolog)

    • uses:

      • post-op hyperglycemia correction

      • insulin drop transition

  • Short-acting (regular insulin)

    • onset: ~30 min

    • peak: 2-3 hr

    • duration: 3-6 hrs

    • types:

      • humulin R

      • novolin R

    • uses:

      • hyperkalemia tx (IVP with dextrose)

      • DKA (only insulin approved for IV)

  • intermediate-acting (NPH)

    • onset: 2-4 hrs

    • peak: 4-12 hrs

    • duration: 12-18 hrs

    • types:

      • insulin NPH

    • uses:

      • outpatient glycemic control hypoglycemic risk

  • Long-acting insulin

    • onset: hours

    • peak: minimal/no peak

    • duration: ~24 hours

    • types:

      • determir

      • glargine

    • uses:

      • basal insulin in chronic diabetes

      • transition off insulin drop

  • Calcitriol

    • active form of vitamin D

    • active vitamin D analog

    • uses: 

      • hypocalcemia

      • hypoparathyroidism

      • renal dysfunction with low Ca2+

  • D-Vi-Sol (Vitamin D)

    • vitamin D supplement

    • uses:

      • vitamin D deficiency

      • bone health in premature infants

      • long-term supplementation

  • Phytonadione (Vitamin K)

    • fat-soluble vitamin

    • uses:

      • elevated INR

      • vitamin K deficiency

      • reversal of warfarin

      • newborn prophylaxis

  • Rasburicase

    • uric acid oxidase enzyme

    • uses:

      • tumor lysis syndrome

      • severe hyperuricemia

        • d/t severe renal injury with uric acid elevation

  • Carnitine/levocarnitine

    • metabolic supplement

    • uses:

      • carnitine deficiency

      • certain metabolic disorders

      • valproic acid toxicity

  • Filgrastim (Filgastrin) – colony-stimulating factor

    • uses:

      • neutropenia

      • bone barrow suppression

      • severe infection with low ANC

      • Post-op immunosuppressed

      • oncology + cardiac patient

      • ECMO patients with infection risk

Electrolytes / Acid-Base / Supplements

Electrolytes

  • Potassium chloride

    • uses:

      • hypokalemia

        • low K+→ delayed repolarization

      • post-bypass

        • diuretics

        • insulin therapy

        • alkalosis

  • Magnesium sulfate

    • torsades de pointes

    • post-op arrythmia prevention

    • low Mg→ refractory hypokalemia

      • Mg2+ stabilizes myocardial membrane

      • regulates Ca2+ influx

    • risks:

      • hypotension

      • respiratory depression

      • loss of reflexes

  • Calcium gluconate 10%

    • uses:

      • hypocalcemia

      • hyperkalemia (membrane stabilization)

        • calcium does NOT lower K+→ stabilizes cardiac memebrane

      • low BP with poor contractility

        • calcium = phase 2 plateau→ myocardial contraction strength

  • Calcium chloride 10%

    • same as calcium gluconate BUT more potent

  • Calcium glubionate

    • chronic hypocalcemia

    • oral supplementation

  • Sodium chloride

    • uses

      • volume resuscitation

      • hyponatremia correction

  • Sodium bicarbonate / Na Bicarbonate     

    • uses:

      • severe metabolic acidosis

      • cardiac arrest

      • hyperkalemia

        • alkalosis shifts K+ intracellularly

  • THAM tromethamine

    • uses:

      • laternative buffer for metabolic acidosis

        • binds H+ directly

        • does NOT generate CO2

          • good for ventilated patients who cannot blow off CO2

          • severe respiratory compromise

Iron / Vitamins / Supplements

  • Ferrous sulfate

    • iron supplement

    • uses:

      • iron deficiency anemia

      • chronic cyanotic heart disease

      • post-op blood less

  • Vitamin C

    • water-soluble vitamin

    • iron absorption

    • wound healing

    • antioxidant

  • Zinc

    • trace element

    • uses:

      • poor wound healing

      • growth delay

      • chronic illness malnutrition

      • immune support

  • Poly-Vi-Sol

    • multivitamin supplement

    • uses:

      • failure to thrive

      • poor enteral intake

  • D-Vi-Sol

    • vitamin d supplement

    • uses:

      • vitamin d deficiency

GI Medications

Acid Suppression

  • Famotidine

    • h2 receptor antagonist

    • uses:

      • stress ulcer prophylaxis

      • GERD

      • ventilated patients

  • Lansoprazole

    • proton pump inhibitor

    • uses:

      • GERD

      • esophagitis

      • GI bleed prevention

Antiemetic / Prokinetic

  • Metoclopramide/reglan

    • dopamin antagonist; prokinetic

    • uses:

      • delayed gastric emptying

      • feeding intolerance

      • GERD

    • risks:

      • extrapyramidal symptoms

      • dystonia

      • QT prolongation

Antiflatulent

  • Mylicon (Simethicone)

    • anti-foaming agent

    • uses:

      • gas discomfort

      • abdominal distention

        • less abdominal distention→ less diaphragmatic compromise

Hepatobiliary

  • Ursodiol

    • bile acid

    • uses:

      • cholestasis

      • TPN-associated liver dysfunction

        • long-term TPN in complex CHD

Potassium Removal

  • Kayexalate

    • postassium-binding resin

    • uses:

      • hyperkalemia

        • exchanges Na+ for K+ in colon→ removes K+ in stool

Octreotide (Somatostatin analog)

  • Used for GI bleeds, varices, etc.

    • hormone analog

    • uses:

      • GI bleeding

        • decreases GI hormones secretion

      • portal hypertension

        • decreases splanchnic blood flow

      • chylothorax

        • common post cardiac surgery

        • decreases lymphatic flow + reduces lymph production

Steroids / Anti-inflammatory

  • Decadron (Dexamethasone)

    • corticosteroid

    • uses:

      • airway edema (post-extubation)

      • inflammation

      • shock adjunct

      • brain edema

    • side effects:

      • hyperglycemia

      • hypertension

      • infection risk

      • GI bleeding

      • immunosuppression

  • Hydrocortisone

    • corticosteroid

    • uses:

      • adrenal insufficiency

      • refractory shock

      • vasopressor-resistant hypotension

🦴 10. Allergy / Immune

  • Benadryl (Diphenhydramine)

    • H1 antihistamine

    • uses:

      • allergic reaction

      • transfusion reaction prophylaxis

  • IVIG – immunoglobulin therapy

    • immunomodulator

    • uses:

      • kawasaki disease

        • reduces coronary artery aneurysm risk

      • immune deficiency

      • myocarditis

      • severe infection

Neuromuscular Blocker

  • Vecuronium

    • uses:

      • intubation

      • ventilator synchrony

      • prevent shivering post-op