Increased Contractility and Stroke Volume (SV) Occur With:
✅ Catecholamine Stimulation via β1 Receptors – Activates protein kinase A (PKA), enhancing calcium dynamics.
✅ PKA Activation Leads to:
- Phosphorylation of phospholamban, which boosts Ca²⁺ ATPase activity, increasing Ca²⁺ storage in the sarcoplasmic reticulum (SR).
- Phosphorylation of calcium channels, enhancing Ca²⁺ entry into myocytes and promoting Ca²⁺-induced Ca²⁺ release from the SR.
✅ Higher Intracellular Ca²⁺ Levels – Strengthens myocardial contraction.
✅ Reduced Extracellular Na⁺ – Decreases Na⁺/Ca²⁺ exchanger activity, leading to increased intracellular Ca²⁺.
✅ Digoxin (Na⁺/K⁺ Pump Inhibitor): - Inhibits the Na⁺/K⁺ ATPase, raising intracellular Na⁺.
- Decreases Na⁺/Ca²⁺ exchanger activity, allowing Ca²⁺ to accumulate inside the cell, enhancing contractility.
Decreased Contractility and Stroke Volume (SV) Occur With:
❌ β1-Blockers – Lower cAMP levels, reducing PKA activation and calcium influx.
❌ Systolic Dysfunction in Heart Failure (HFrEF) – Weakens myocardial contraction.
❌ Acidosis – Reduces calcium binding to troponin C, impairing contraction.
❌ Hypoxia/Hypercapnia – Low oxygen (↓ PaO₂) and high carbon dioxide (↑ PaCO₂) compromise cellular energy production.
❌ Nondihydropyridine Calcium Channel Blockers (e.g., Verapamil, Diltiazem) – Reduce calcium entry, decreasing contractility.
Optimizing heart contractility is crucial for managing conditions like heart failure, cardiogenic shock, and arrhythmias. Understanding these physiological mechanisms helps in effective treatment planning and pharmacological interventions.