Heart – pump (≈300–350 g; consumes ≈10 % of resting O₂)
Vasculature – arteries, arterioles, capillaries, venules, veins
Blood – formed elements (≈40 %) + plasma (≈60 %)
Transport – O₂, CO₂, nutrients, wastes, hormones
Homeostatic regulation – fluid balance, BP, pH, thermoregulation (heat transfer via blood)
Protection – hemostasis (clotting), immune defense, blood-flow prioritization during loss
Right heart (pulmonary): pumps de-oxygenated blood → lungs → picks up O₂
Left heart (systemic): pumps oxygenated blood → entire body
SVC / IVC → Right Atrium (RA)
Tricuspid Valve (Right AV) – prevents RA⇆RV backflow
Right Ventricle (RV)
Pulmonary Semilunar Valve → Pulmonary Artery → Lungs
Pulmonary Veins → Left Atrium (LA)
Bicuspid / Mitral Valve (Left AV)
Left Ventricle (LV) – thickest wall (~3× RV); systemic pump
Aortic Semilunar Valve → Aorta → Arterial tree → Capillaries → Veins → (step 1)
Valves = one-way; disease/leakage alters preload/afterload
Coronary arteries/veins nourish myocardium (critical in MI)
Definition: volume ejected per minute
Formula: Q = HR \times SV
Typical resting values:
HR_{rest}\approx 60–80\;\text{b·min}^{-1}
SV_{rest}\approx 60–80\;\text{mL·beat}^{-1}
Q_{rest}\approx 5\;\text{L·min}^{-1} (♀ slightly lower, ♂ higher)
Exercise increase: Q_{max}\approx 20–25\;\text{L·min}^{-1} (untrained) → 40+\;\text{L·min}^{-1} (elite endurance)
Age sets max HR; training mainly augments SV
Endothelium (tunica intima)
Smooth muscle (tunica media) – thicker in arteries ⇒ vaso-control
Fibrous/elastic connective (tunica adventitia)
Elastic (central) arteries – Aorta, iliacs; Windkessel effect dampens pulsatility
Muscular arteries – named regionals (ulnar, femoral); rich smooth muscle; main site of exercise redistribution
Arterioles – resistance vessels; greatest pressure drop; SNS & local metabolites dictate dilation/constriction
Capillaries – single-cell wall; huge cross-sectional area; slow flow for gas exchange; vulnerable to HTN damage
Venules / Veins – capacitance vessels (≈60 % blood volume at rest); thin wall, valves, low pressure (≈10–30 mmHg); venous return aided by:
Skeletal muscle pump
Respiratory pump
Sympathetic venoconstriction
Flow follows ΔP / Resistance (Ohm’s law for fluids)
Blood flows high → low pressure; valve timing hinges on this fact
Windkessel effect: aortic elasticity stores energy during systole, sustains flow in diastole (prevents zero-flow periods)
Central (aortic) BP < peripheral (brachial) BP
Formed elements (≈40 %)
Erythrocytes – carry O₂ via hemoglobin
Leukocytes – immune defense
Thrombocytes (platelets) – clotting; contribute to athero-plaque
Plasma (≈60 %) – ≈90 % water + proteins, nutrients, hormones
Dehydration → ↓plasma → ↑hematocrit → ↑viscosity → ↑resistance → ↑BP & clot risk
Duration at HR 75 b·min⁻¹ ≈ 0.8 s (HR 60 → 1 s)
Isovolumetric Contraction (IVC) (all valves closed)
LV pressure ↑ steeply (≈5 → 80 mmHg)
Volume constant (EDV)
Ventricular Ejection
Aortic valve opens when P{LV}>P{aorta}
Rapid then reduced ejection; volume ↓ to ESV
Isovolumetric Relaxation (IVR)
Aortic valve closes when P{aorta}>P{LV} (dicrotic notch)
All valves closed; LV pressure ↓ rapidly, volume constant (ESV)
Ventricular Filling
Rapid inflow: Mitral valve opens when P{LA}>P{LV}
Diastasis: slower passive filling
Atrial systole (A-wave; P-wave on ECG): last ~10 % of filling
Valves operate on pressure gradients (no neural trigger)
Heart sounds: S₁ = AV valve closure (start systole), S₂ = semilunar closure (start diastole)
Stroke Volume: SV = EDV - ESV
Ejection Fraction: EF = \dfrac{SV}{EDV}\times100\% (clinical pump metric)
EDV\approx 120\;\text{mL}
ESV\approx 50\;\text{mL}
SV\approx 70\;\text{mL}
P{systolic}\approx 120\;\text{mmHg} ; P{diastolic}\approx 80\;\text{mmHg} (aortic)
Left Ventricular Hypertrophy (LVH)
Physiologic (endurance training) vs pathologic (HTN, valve disease)
Blood Pressure refers exclusively to arterial pressure
High BP end-organ risk: brain (stroke), heart (MI), kidneys (nephropathy), micro-capillary damage
Hydration status directly modifies plasma volume → influences SV and BP
Venous return & preload enhanced by active muscle – rationale for cool-down walking
Post-prandial exercise: splanchnic vasodilation competes with muscle blood flow → GI discomfort/“swim rule”
Master heart diagram; trace flow w/o notes
Practice Wiggers diagram interpretation (pressure, volume, ECG, sounds)
Use Huff “ECG Workout” rhythm strips for self-quizzing (exam source)
Expect lab practical: setup 12-lead ECG and strip interpretation
Canvas assignments auto-repeat until 100 %; completion boosts grade
Review material nightly—fast-paced term!