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PY5.1-16 | Cardiovascular Physiology — Part 2

SELF-CHECK

During isovolumetric ventricular contraction, which valves are open and which are closed?

A. AV valves open, semilunar valves closed

B. All four valves closed

C. AV valves closed, semilunar valves open

D. All four valves open

Reveal Answer

Answer: B. All four valves closed

During isovolumetric contraction, ALL FOUR valves are closed. The AV valves have just closed (causing S1), and the semilunar valves haven't opened yet (ventricular pressure hasn't exceeded aortic/pulmonary pressure). Similarly, during isovolumetric relaxation, all four valves are closed — semilunar valves have just closed (causing S2), and AV valves haven't opened yet.

Arterial Blood Pressure (PY5.9, PY5.10)

Arterial Blood Pressure — Key Values and Formulas

Parameter Normal Value Formula Clinical Significance
Systolic BP (SBP) 120 mmHg Peak pressure during ejection Reflects stroke volume and aortic compliance
Diastolic BP (DBP) 80 mmHg Lowest pressure during diastole Reflects total peripheral resistance
Pulse Pressure 40 mmHg SBP - DBP Wide in aortic regurgitation; narrow in heart failure
Mean Arterial Pressure (MAP) 93 mmHg DBP + 1/3(PP) Perfusion pressure for organs; must be >60 mmHg
Blood Pressure 120/80 mmHg CO x TPR Determined by cardiac output and vascular resistance

Arterial blood pressure is the lateral force exerted by blood on the walls of the arteries. It has two components:

Arterial Blood Pressure (PY5.9, PY5.10)

Figure: Arterial Blood Pressure (PY5.9, PY5.10)

Arterial pressure waveform diagram showing systolic peak (120 mmHg), diastolic trough (80 mmHg), pulse pressure (40 mmHg), and mean arterial pressure (93 mmHg). Includes the formula MAP = DBP + 1/3(Pulse Pressure). A second panel shows the factors affecting arterial blood pressure: cardiac output (HR x SV) and total peripheral resistance, with sub-factors branching out.
  • Systolic blood pressure (SBP) — the peak pressure during ventricular ejection. Normal: ~120 mmHg.
  • Diastolic blood pressure (DBP) — the lowest pressure during ventricular diastole. Normal: ~80 mmHg.
  • Pulse pressure = SBP - DBP = ~40 mmHg. It reflects stroke volume and arterial compliance.
  • Mean arterial pressure (MAP) = DBP + 1/3(Pulse pressure) = 80 + 1/3(40) = ~93 mmHg. MAP is the average pressure driving blood through the systemic circulation. MAP below 60 mmHg = inadequate organ perfusion.

Factors affecting arterial BP:
1. Cardiac output (CO) — BP = CO x Total Peripheral Resistance (TPR)
2. Peripheral resistance — mainly determined by arteriolar smooth muscle tone
3. Blood volume — more volume = more pressure (think: overfilled balloon)
4. Elasticity of arterial walls — loss of elasticity (arteriosclerosis) increases systolic BP and pulse pressure
5. Viscosity of blood — increased viscosity (polycythaemia) increases resistance

The arterial pulse (PY5.10) — the pressure wave that travels along the arterial wall with each heartbeat. It travels much faster (4-12 m/s) than the blood itself (~0.5 m/s). The radial pulse at the wrist is where you routinely feel it.

Characteristics to assess: Rate, Rhythm, Volume (amplitude), Character (contour), Condition of the arterial wall, Symmetry (compare both sides).

Abnormal pulses: Pulsus paradoxus (exaggerated fall in BP during inspiration — cardiac tamponade), water-hammer pulse (wide pulse pressure — aortic regurgitation), pulsus alternans (alternating strong and weak beats — left ventricular failure).

Venous Pressure and JVP (PY5.11)

Venous blood pressure is much lower than arterial — about 10-15 mmHg in peripheral veins, falling to nearly 0 mmHg in the right atrium (central venous pressure, CVP). The veins are a capacitance system — they hold ~60-70% of total blood volume.

Venous Pressure and JVP (PY5.11)

Figure: Venous Pressure and JVP (PY5.11)

Two-panel figure. Panel A: JVP waveform showing a, c, v waves and x, y descents with their causes labelled. Panel B: Diagram of factors aiding venous return — skeletal muscle pump, respiratory pump, venous valves, and sympathetic venoconstriction.

Factors aiding venous return:
1. Skeletal muscle pump — contraction of leg muscles squeezes blood upward through one-way venous valves ('peripheral heart')
2. Respiratory pump — inspiration decreases intrathoracic pressure, creating a suction effect on the great veins
3. Venous valves — prevent backflow (especially important in the lower limbs)
4. Sympathetic venoconstriction — reduces venous capacitance, pushing blood toward the heart
5. Cardiac suction — ventricular relaxation creates a suction effect
6. Vis a tergo — the 'push from behind' — the residual pressure from arterial blood flowing through capillaries into veins

Jugular Venous Pressure (JVP) — examined in the internal jugular vein, it reflects right atrial pressure. The JVP waveform has 3 positive waves (a, c, v) and 2 descents (x, y):

  • a wave — atrial contraction (right atrial systole)
  • c wave — bulging of the tricuspid valve into the right atrium at the start of ventricular systole
  • x descent — atrial relaxation + descent of the AV ring during ventricular systole
  • v wave — passive filling of the right atrium while the tricuspid valve is closed
  • y descent — opening of the tricuspid valve, blood flowing from atrium into ventricle

Clinical significance: Raised JVP = right heart failure, fluid overload, cardiac tamponade. Giant 'a' waves = tricuspid stenosis, pulmonary hypertension. Cannon 'a' waves = complete heart block (atrium contracts against a closed tricuspid valve). Absent 'a' waves = atrial fibrillation.

Blood Pressure Regulation — Baroreceptors and Beyond (PY5.8)

Blood Pressure Regulation Mechanisms

Mechanism Time Scale Sensors/Organs Effectors Response to Low BP
Baroreceptor reflex Seconds Carotid sinus (CN IX), Aortic arch (CN X) Heart, blood vessels (ANS) Increased HR, vasoconstriction
Chemoreceptor reflex Seconds-minutes Carotid body, Aortic body Cardiovascular centre Vasoconstriction, increased ventilation
CNS ischaemic response Seconds (emergency) Medullary neurons Massive sympathetic discharge Extreme vasoconstriction (Cushing reflex)
RAAS Hours-days Juxtaglomerular cells (kidney) Angiotensin II, Aldosterone Vasoconstriction + Na/water retention
ADH (Vasopressin) Hours Hypothalamic osmoreceptors Collecting ducts (kidney) Water retention, vasoconstriction
ANP Hours Atrial cardiomyocytes Kidney, vessels Natriuresis, vasodilation (counter-regulatory)

Blood pressure must be maintained within a narrow range — too low and organs don't get blood; too high and vessels are damaged. The body has short-term and long-term mechanisms.

Blood Pressure Regulation — Baroreceptors and Beyond (PY5.8)

Figure: Blood Pressure Regulation — Baroreceptors and Beyond (PY5.8)

Flow diagram of blood pressure regulation showing short-term (baroreceptor reflex arc with carotid sinus, aortic arch, NTS, vagal/sympathetic outputs) and long-term (RAAS pathway and renal fluid-volume mechanism) in two linked panels.

SHORT-TERM REGULATION (seconds to minutes) — Neural:

  1. Baroreceptor reflex — THE most important short-term mechanism. Baroreceptors are stretch receptors in the carotid sinus (CN IX — glossopharyngeal nerve) and aortic arch (CN X — vagus nerve). When BP rises: baroreceptors fire more -> nucleus tractus solitarius (NTS) in medulla -> increased parasympathetic output (vagus) + decreased sympathetic output -> decreased HR, decreased contractility, vasodilation -> BP falls. When BP falls: the opposite occurs.

The baroreceptor reflex operates continuously — it is the reason your BP doesn't crash every time you stand up.

  1. Chemoreceptor reflex — peripheral chemoreceptors in the carotid body and aortic body respond to hypoxia, hypercapnia, and acidosis. They primarily regulate respiration but also cause vasoconstriction (increasing BP) when stimulated.
  1. CNS ischaemic response (Cushing response) — when cerebral blood flow is severely reduced, the vasomotor centre fires massively, causing intense vasoconstriction and hypertension. This is a last-resort mechanism — it operates only at MAP < 60 mmHg. The Cushing triad (hypertension + bradycardia + irregular respiration) is a sign of raised intracranial pressure.

LONG-TERM REGULATION (hours to days) — Renal and Hormonal:

  1. Renin-Angiotensin-Aldosterone System (RAAS) — when renal perfusion falls, the kidneys secrete renin -> angiotensinogen is converted to angiotensin I -> ACE (in lung capillaries) converts it to angiotensin II -> vasoconstriction + aldosterone release (Na+ and water retention) -> increased blood volume and BP.
  1. ADH (vasopressin) — released from the posterior pituitary when osmolarity rises or blood volume falls. Causes water retention and vasoconstriction.
  1. ANP (atrial natriuretic peptide) — released from atrial myocytes when the atria are stretched (volume overload). Causes Na+ and water excretion, vasodilation -> reduces BP. It opposes RAAS.
  1. Pressure natriuresis — the ultimate long-term mechanism. When BP rises, the kidneys excrete more Na+ and water, reducing blood volume until BP returns to normal. Guyton called this the 'infinite gain' mechanism — given enough time, it can return BP to its set point regardless of what other mechanisms do.