The heart and circulatory system

Blood group systems

• 43 total blood group systems

• Most important: ABO and Rhesus (Rh +/-)

ABO blood types

• 4 types: A, B, AB, O

• Determined by antigens on red blood cells (RBCs) and antibodies in plasma

• A and B antigens are sugars

• Discovered by Karl Landsteiner (1901)

Type A

A antigen, anti-B antibody

Type B

B antigen, anti-A antibody

Type AB

A & B antigens, no antibodies (universal recipient)

Type O

No antigens, anti-A & anti-B antibodies (universal donor)

Transfusion reactions

• Wrong type: antibodies bind foreign RBCs → agglutination → clumping → thrombosis

• Agglutination used in blood typing

Blood type inheritance

• 3 alleles: IA (A), IB (B), i (O)

• A and B are codominant, O is recessive

Haemolytic Disease of the Newborn

• Maternal antibodies attack fetal RBCs

• Common when mother is O and fetus is A/B

• Results in jaundice, anaemia, ↑ bilirubin

• Severe cases: phototherapy or exchange transfusion

Location

• Mediastinum, level of 2nd rib

• Angled L to R (anatomically)

Apex

Points left

Base

Towards right

Pericardium function

Encloses heart; provides lubrication and protection

3 layers of pericardium

• Fibrous pericardium

• Serous pericardium (parietal + visceral layers with cavity)

• Epicardium

Acute Pericarditis

inflammation, chest pain, friction rub, resolves with NSAIDs

Chronic effusive pericarditis

fluid build-up

Chronic constrictive pericarditis

fibrotic thickening

Heart wall layers

• Epicardium

• Myocardium (muscle)

• Endocardium (inner lining)

Atrioventricular valves

• Tricuspid (RA → RV)

• Mitral/Bicuspid (LA → LV)

• Prevent backflow into atria

Semilunar valves

• Pulmonary (RV → Pulmonary artery)

• Aortic (LV → Aorta)

• Prevent backflow from arteries

Valve disorders

• Incompetent: doesn't fully close (leaky)

• Stenosis: narrowed opening (less flow)

• May have both

Chordae Tendinae

Prevent AV valves from swinging back

Pulmonary Circulation (RHS)

Vena cavae → RA → RV → Pulmonary artery → Lungs

Systemic Circulation (LHS)

Pulmonary veins → LA → LV → Aorta → Body

Coronary Circulation

• L/R coronary arteries from aorta

• Supply myocardium during diastole

• Reperfusion injury can occur after blockage

Blood vessel structure (All vessels have 3 layers)

• Tunica intima

• Tunica media – smooth muscle (resistance control)

• Tunica externa (adventitia) – structural support

Tunica intima

endothelial (smooth inner)

Tunica media

smooth muscle (resistance control)

Tunica externa (adventitia)

Structural support

Vasoconstriction/Vasodilation

Alters lumen size → affects blood flow and pressure

Blood flow resistance

Inversely proportional to 1 / radius^4

Large arteries

elastic, withstand high pressure, not resistance vessels

Small arteries/arterioles

resistance and regulation, innervated, hormone-sensitive

Capillaries

exchange vessels, slow velocity for diffusion

Types of Capillaries

• Continuous

• Fenestrated

• Sinusoid

Continuous capillaries

tight junctions (CNS, muscle)

Fenestrated capillaries

pores (kidney, endocrine)

Sinusoid capillaries

large gaps (bone marrow, liver)

Venous system

• Low pressure

• Thin walls, less muscle

• Valves in large veins

• Venules

Venules

Porous, allow exchange

Blood Volume Distribution (Upright)

• Veins: 65%

• Arteries: 13%

• Arterioles: 2%

• Capillaries: 5%

• Central: 15%

Blood volume distribution (supine)

Veins: 54%, Central: 30% (↑ in heart & lungs)

Cardiac cycle

One full heartbeat (0.8s at 75bpm)

Systole

Contraction (mainly ventricular)

Diastole

Relaxation and filling

Phases of cardiac cycle

1. Atrial systole

2. Isovolumetric contraction

3. Ventricular ejection

4. Isovolumetric relaxation

5. Ventricular filling

Atrial systole

0.1s) – Atria contract → push blood into ventricles

• AV valves open; semilunar valves closed

• ~10% extra blood added (End Diastolic Volume ~130 ml)

Isovolumetric contraction

Ventricles start to contract

• All valves closed

• Pressure increases → AV valves shut → First heart sound (LUBB)

• No volume change yet

Ventricular ejection

(0.3s total for systole)

• When ventricular pressure > aortic/pulmonary pressure

• Semilunar valves open → blood ejected

• No heart sounds in healthy people

• L side: Pressure up to 120 mmHg

• R side: Pressure up to 25–30 mmHg

Isovolumetric relaxation

• Ventricles relax; all valves shut

• Pressure falls → semilunar valves close → Second heart sound (DUPP)

• Volume = End Systolic Volume (~60 ml)

ventricular filling

(0.4s total diastole)

• AV valves open; semilunar valves closed

• Blood flows in passively → Rapid then reduced filling

• Third heart sound may occur (usually inaudible)

1st heart sound (LUBB)

AV valves close (start of systole)

2nd heart sound (DUPP)

Semilunar valves close (start of diastole)

3rd heart sound

Rapid ventricular filling (abnormal if audible in adults)

4th heart sound

Atrial contraction (often audible in stiff ventricles)

Cardiac output

CO = HR × SV

Stroke volume

SV = EDV − ESV

• EDV ~130 ml (max fill)

• ESV ~60 ml (after contraction)

Regulation of heart function via neural control

• Sympathetic (SNS): ↑ HR & contractility (via SA node)

• Parasympathetic (PNS): ↓ HR

Regulation of heart function via ions

• Ca²⁺: ↑ = stronger, longer contractions

• K⁺: Imbalance disrupts rhythm/conduction

Frank-Stirling Law

“The heart pumps out what it receives)

• ↑ Preload (EDV) → ↑ stretch → ↑ contraction → ↑ SV

• More venous return → More ejection

• Exercise = ↑ venous return via skeletal muscle pump + breathing

Blood pressure

Cardiac Output × Total Peripheral Resistance (TPR)
Normal: 120/80 mmHg

Pulse pressure

PP = SBP – DBP

Mean arterial pressure

MAP = DBP + (PP/3)

BP regulation via homeostasis

Stimulus: ↑ BP / ↑ CO₂ / ↓ O₂
Sensors:

• Baroreceptors: Aortic arch + carotid sinus (pressure)

• Chemoreceptors: Carotid & aortic bodies (O₂, CO₂, pH)

Response:
→ CNS control (medulla)
→ ↓ SNS / ↑ PNS
→ ↓ HR, ↓ contractility
→ ↓ CO → BP returns to normal

Total peripheral resistance

It refers to the resistance to blood flow offered by all of the systemic (non-pulmonary) blood vessels, especially the small arteries and arterioles.

Increased by

• Vasoconstriction (SNS, cold, atherosclerosis)

• ↑ Blood viscosity (e.g., high RBC count)

• ↑ Blood volume (salt retention)

Ways to decrease bp

• Low salt diet

• ACE inhibitors (block vasoconstriction)

• Stress reduction (↓ SNS activity)

Skeletal muscle pump

• Surrounding muscle contractions squeeze veins

• One-way valves prevent backflow

• ↑ Venous return during exercise

Cardiac muscle cellular characteristics

• Myogenic

• Mononucleated

• Branched

• Striated

Myogenic

contracts spontaneously without neural input

Branched

To increase connectivity

Striated

Z-bands visible like in skeletal muscle ~100µm long

Intercalated Discs

• Connect cardiomyocytes.

• Contain:

  • Desmosomes

  • Gap junctions

• Enable functional syncytium: heart contracts as one coordinated unit

Desomosomes

Mechanical strength

Gap junctions

allow ion flow → rapid action potential (AP) transmission

Non-Pacemaker (Ventricular) Cardiomyocytes

• Resting potential: ~-90 mV

• Duration: 200–400 ms (vs 1–5 ms in neurons/skeletal muscle)

• Prevents tetany via long refractory period

Phases of non-Pacemaker (Ventricular) Cardiomyocytes

• Rapid Na⁺ influx (depolarisation)

• Ca²⁺ influx via slow L-type channels (plateau)

• K⁺ efflux (repolarisation)

• Return to RMP

Effect of hypoxia

Reduces RMP → Na⁺ channels inactivated → can lead to arrhythmia

Pacemaker Cells (SAN & AVN)

• Spontaneous depolarisation due to:

  • Funny current (If): Na⁺ influx

  • T-type Ca²⁺ channels

• Once threshold reached → L-type Ca²⁺ channels open → AP

• Phase 4: pacemaker potential

• SAN: ~100 bpm intrinsic rate

• AVN: slower (40–60 bpm); usually driven by SAN

Conduction system pathway

• SA Node (right atrium): primary pacemaker

• Signal spreads across atria → atrial contraction (P wave)

• AV Node: delay allows complete atrial emptying

• Bundle of His → left/right bundle branches

• Purkinje Fibres → ventricular contraction (QRS complex)

Regulation by the Autonomic Nervous System: Sympathetic pathway

To increase HR:

• Via β1 receptors: ↑ rate, ↑ force

• Stimulated by stress, adrenaline, catecholamines

Regulation by the Autonomic Nervous System: Parasympathetic pathway

To decrease HR:

• Via Vagus nerve (ACh on muscarinic receptors)

• Decreases SAN activity

Other influences that increase HR

• β-agonists, catecholamines

• Hyperthyroidism, hyperthermia

• Hyperkalaemia

• Stress, caffeine, nicotine

Other influences that decrease HR

• β-blockers

• Hypothyroidism, hypothermia

• Hypokalaemia

• Ischaemia, Na⁺/Ca²⁺ channel blockers

Abnormal heart rate conditions

• Tachycardia - fast

• Bradycardia - slow

• Fibrillation - Uncoordinated, rapid contractions

ECG

• Measures electrical activity, not contraction.

• Leads on chest detect signal.

Waves in an ECG

• P wave

• QRS complex

• T wave

P wave

Atrial depolarisation

QRS complex

Ventricular depolarisation

T wave

Ventricular repolarisation

ECG uses

• Time HR

• Diagnose arrhythmias

• Correlate with cardiac cycle phases