Cardiac Muscle & Circulatory Physiology Review
Circulatory Overview
- Primary role of the heart: generate pressure to move blood ➔ maintains two distinct but linked circuits.
- Systemic circulation = oxygen-rich blood delivery to entire body.
- Pulmonary circulation = oxygen-poor blood to lungs for gas exchange.
- Sequence (starting in systemic side for orientation):
- Left ventricle (LV) contracts ➔ ejects blood into aorta.
- Aorta repeatedly bifurcates → arteries → arterioles → capillary beds serving all tissues ("big toe, brain, GI tract, pancreas, skeletal muscle, kidneys," and even the myocardium itself via coronary arteries).
- After oxygen drop-off & waste pick-up, de-oxygenated blood returns via superior + inferior vena cavae to right atrium (RA) ➔ right ventricle (RV).
- RV pumps through pulmonary arteries → lungs (located lateral to heart in thoracic cavity/mediastinum) ➔ CO₂ unloaded, O₂ loaded.
- Oxygen-rich blood moves through pulmonary veins → left atrium (LA) ➔ LV and the cycle repeats.
- Side distinction shorthand:
- Right side = "oxygen-poor".
- Left side = "oxygen-rich".
Heart Anatomy & Spatial Orientation
- Human-anatomy convention: described from specimen’s point of view (patient facing you). Your left hand = specimen’s right side, etc.
- Chambers
- 2 atria (RA, LA)
- 2 ventricles (RV, LV)
- Atria—especially LA—are more posterior; anterior heart views mainly show both ventricles + RA auricle.
- Heart sits in mediastinum between right & left lungs inside thoracic cavity.
- Drawings sometimes place aorta exit anteriorly for clarity; reality: aorta ascends from LV’s superior border and arches posteriorly.
Systemic vs Pulmonary Circuit Pressures
- Blood flows down pressure gradients (higher ➔ lower); absolute value less important than relative difference.
- Typical systemic arterial blood pressure: 120\,\text{mmHg}/80\,\text{mmHg}
- 120 = LV systolic (contracted)
- 80 = LV diastolic (relaxed)
- Returning venous pressure to RA is single-digit mmHg.
- RV/pulmonary circuit operates at much lower peak pressures than LV/systemic circuit.
Physics of Pressure–Volume Relationships
- Two distinct “volumes” to track:
- Volume of the container (chamber or vessel diameter changes).
- Volume of the fluid (amount of blood present).
- Container rule (inverse relationship):
- ↑ Chamber volume ➔ ↓ Pressure.
- ↓ Chamber volume (e.g.
ventricular systole) ➔ ↑ Pressure.
- Fluid rule (direct relationship):
- ↑ Blood volume ➔ ↑ Pressure (balloon filling analogy).
- ↓ Blood volume ➔ ↓ Pressure (hemorrhage → hypovolemia → hypotension).
- Water-balloon metaphors illustrate both:
- Adding water (fluid increase) raises pressure until balloon bursts.
- Squeezing fixed-volume balloon (container decrease) likewise raises internal pressure until rupture.
Phases of the Left Ventricular Cycle
- End-Systolic Volume (ESV)
- Blood remaining in LV immediately after contraction.
- Passive Ventricular Filling (early diastole)
- Blood flows LA → LV mainly via gravity + pressure gradient while LV pressure is lower than LA pressure.
- Atrial Systole (late diastole)
- LA contracts to push final blood into LV once LV pressure nears LA pressure.
- End-Diastolic Volume (EDV)
- Max blood in LV just before it contracts.
- Aortic pressure still > LV pressure, so aortic valve closed.
- Ventricular Systole / Ejection
- LV muscle contracts (container shrinks) + has full EDV (fluid increase) ➔ rapid pressure rise.
- When P{LV} > P{aorta}, aortic valve opens; blood ejected into systemic circulation.
- Dual mechanisms raising LV pressure before ejection:
- Increased fluid volume (EDV).
- Decreased chamber size (muscle contraction).
Cardiac Output (CO) Calculations
- Definition: Volume of blood pumped by LV per unit time (≈ L · min⁻¹).
- Formula: CO = HR \times SV
- HR = heart rate (beats · min⁻¹)
- SV = stroke volume (mL · beat⁻¹)
- SV = EDV - ESV
- Numerical example from transcript:
- Given EDV = 100\,\text{mL}
- ESV = 20\,\text{mL}
- SV = 100 - 20 = 80\,\text{mL}
- Assume HR = 70\,\text{beats·min}^{-1}
- CO = 70\,\text{beats·min}^{-1} \times 80\,\text{mL·beat}^{-1} = 5600\,\text{mL·min}^{-1}
- Convert: 5600\,\text{mL} = 5.6\,\text{L} ➔ CO \approx 5.6\,\text{L·min}^{-1}
- Matches total blood volume (≈5-6 L) ➔ entire blood volume circulates once per minute.
Cardiac Muscle Cell Types
- Myocardium ("myo" = muscle, "cardium" = heart) contains two cell classes:
- Myocardial Contractile Cells (MCCs)
- Perform force generation & ejection, analogous to skeletal muscle fibers.
- Myocardial Autorhythmic Cells (MACs)
- Generate & propagate electrical impulses that dictate timing/rate; covered in later lecture.
Excitation–Contraction Coupling in MCCs
- Structural parallels to skeletal muscle
- Sarcoplasmic reticulum (SR)
- T-tubules
- Troponin/tropomyosin regulated thin filaments
- Key molecular players (with cardiac twists):
- Voltage-gated Calcium Channel (VGCC) in T-tubule membrane (analogue of DHP receptor).
- Voltage-sensitive but permits actual Ca²⁺ influx (unlike skeletal DHP which is voltage sensor only).
- Ryanodine Receptor (RyR) on SR membrane is ligand-gated (not mechanically gated).
- Ligand = Ca²⁺ (coming from VGCC ingress).
- Process (Calcium-Induced Calcium Release, CICR):
- MAC depolarization reaches MCC ➔ action potential travels along sarcolemma/T-tubule.
- VGCC opens ➔ extracellular Ca²⁺ enters cell.
- Ca²⁺ binds RyR ➔ SR releases large Ca²⁺ pool into cytosol.
- Cytosolic Ca²⁺ binds troponin ➔ tropomyosin moves ➔ cross-bridge cycling & contraction (sliding-filament theory same as skeletal muscle from here).
Ion Removal & Homeostasis Post-Contraction
- SR Ca²⁺-ATPase (SERCA) pumps Ca²⁺ back into SR (primary active transport).
- Na⁺/K⁺-ATPase restores Na⁺ & K⁺ gradients (3 Na⁺ out / 2 K⁺ in per ATP).
- NCX (Na⁺/Ca²⁺ Exchanger)
- Secondary active antiporter: 3 Na⁺ in (down gradient) drive 1 Ca²⁺ out (against gradient).
- Prevents cytosolic Ca²⁺ overload & permits relaxation.
- Potential depolarizing Na⁺ influx instantly countered by Na⁺/K⁺-ATPase to avoid unintended action potentials; ensures MCCs fire only when orchestrated by MACs.
Skeletal vs Cardiac Muscle – Key Differences Highlighted
- Skeletal: Mechanical coupling between DHP & RyR; no need for external Ca²⁺ entry.
- Cardiac: CICR—requires initial extracellular Ca²⁺ influx; RyR is Ca²⁺-gated.
- Functional consequence: Cardiac muscle cannot enter tetanus because refractory period matches contraction length (topic foreshadowed for future lecture).
Examples, Analogies, & Real-World Relevance
- Water-balloon analogy used twice: illustrates both fluid-volume–pressure (fluid addition) and container-volume–pressure (squeezing) principles.
- Hypovolemia (severe bleed) ➔ ↓ plasma volume ➔ ↓ pressure gradients ➔ impaired tissue perfusion.
- Coronary arteries = systemic branches specifically serving myocardium (heart "feeds itself").
- Understanding LV pressure/volume important for diagnosing heart failure, calculating ejection fraction, and managing blood pressure therapeutically (e.g., antihypertensives target systemic pressure).
- Normal CO ≈ 5 – 6 L·min⁻¹ reaffirms why alterations in HR or SV (exercise, disease) have systemic implications.
Ethical & Clinical Considerations (Implicit)
- Maintaining adequate perfusion critical for organ health; rapid recognition/management of hypovolemia can be lifesaving.
- Pharmacologic manipulation of Ca²⁺ channels or NCX affects contractility—therapeutic potential (e.g., calcium channel blockers) but requires caution to avoid compromising CO.