Ancillary Therapies in STEMI

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Indication:
- Relief of chest pain and discomfort
Mechanism:
- Activation of μ-opioid receptor, reducing perception of pain
Dose:
- 0.1 to 0.2 mg/kg IV every 5 minutes, max dose 10 mg
Pharmacokinetics:
- IV Onset: 1-5 min; Duration: 2-4 hr; Metabolism: Liver
Adverse Effects:
- Respiratory depression, hypotension, nausea, vomiting
Clinical Pearls & Practical Considerations:
- There is limited evidence to support the routine use of morphine in ACS, and its use should be reserved for patients with severe pain and not as a first-line therapy..
- Morphine should be used with caution in patients receiving P2Y12 inhibitors, as it can increase the risk of bleeding and delay the onset of action of these drugs.
- Multiple studies linking its use with increased mortality

Oxygen

Indication:
- Oxygen therapy (O2) is indicated for the treatment of hypoxemia in patients with acute coronary syndromes, specifically those with ST-segment elevation myocardial infarction, to improve patient outcomes.
Mechanism:
- O2 therapy increases oxygen concentrations in the arterial blood and thus, the oxygen delivered to the myocardium.
- Clinical Pearls & Practical Considerations:
- The AHA and ESC recommend using oxygen therapy in patients with acute coronary syndromes who are hypoxic.

Indication:
- Used to treat angina, acute coronary syndrome (including MI), and hypertension
Mechanism:
- Relaxes vascular smooth muscle and reduces venous return to the heart, decreasing preload and myocardial oxygen demand
Dose:
- 0.4mg SL every 5 minutes up to 3 doses; 5–20mcg/min IV infusion
Pharmacokinetics:
- Rapidly absorbed after oral, SL and IV administration; metabolized in the liver
Adverse Effects:
- Headache, hypotension, reflex tachycardia, nausea, vomiting
- Clinical Pearls & Practical Considerations:
- Nitroglycerin should not be given to patients with hypotension, right ventricular infarction, or suspected obstructive hypertrophic cardiomyopathy.

Mechanism:
- Block beta-adrenoceptors, decreasing cardiac output and peripheral vascular resistance
Pharmacokinetics:
- Metabolized in the liver, half-life of 6-12 hours
Adverse Effects:
- Bradycardia, hypotension, fatigue, insomnia, depression
Clinical Pearls & Practical Considerations:
- Beta Blockers reduce myocardial oxygen demand and decrease the risk of recurrent myocardial infarction and ventricular arrhythmias.
- Caution in those with Asthma, COPD, or bradycardia
- Should be started within 24 hours of ACS unless: There are signs of HF, Active evidence of other shock states, If at increased risk of cardiogenic shock (SBP < 120 mm Hg, HR > 110 beats/min or < 60 beats/min, age > 70, and increased time since onset of symptoms)

Mechanism:
- Block ACE enzyme, reduce aldosterone and bradykinin, vasodilation
Pharmacokinetics:
- Oral, rapid absorption, high bioavailability, excreted in urine
Adverse Effects:
- Cough, hypotension, hyperkalemia, renal impairment
Clinical Pearls & Practical Considerations:
- Contraindications: Hypersensitivity, renal impairment, hyperkalemia

Mechanism:
- Statins are lipid-lowering medications that inhibit the enzyme HMG-CoA reductase, which is involved in cholesterol synthesis. By reducing cholesterol levels in the body, statins can help prevent the buildup of plaque in the coronary arteries and reduce the risk of cardiovascular events.
Pharmacokinetics:
- Statins are absorbed in the small intestine and undergo extensive first-pass metabolism in the liver.
- They are metabolized by the liver and excreted in the feces.
Adverse Effects:
- muscle pain, liver enzyme abnormalities, and gastrointestinal symptoms.
Clinical Pearls & Practical Considerations:
- Statins are an essential component of the treatment of ACS and are recommended for all patients unless contraindicated.
- Patients should be monitored for muscle pain and liver enzyme abnormalities while taking statins
- It is also important to check for potential drug interactions when prescribing statin