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PY5.1-16 | Cardiovascular Physiology — Part 4

Microcirculation and Regional Circulations (PY5.12, PY5.13)

Before understanding what goes wrong in shock and heart failure, we need to understand where the actual exchange of nutrients and waste occurs — the microcirculation.

Figure: Microcirculation and Regional Circulations (PY5.12, PY5.13)

The capillary: the functional unit of the circulation. Total length of all capillaries: ~96,000 km. Wall is a single layer of endothelial cells — thin enough for diffusion.

Starling forces govern capillary exchange:

Fluid movement depends on the balance of 4 pressures:
• Capillary hydrostatic pressure (Pc) — pushes fluid OUT (arteriolar end ~35 mmHg, venular end ~15 mmHg)
• Interstitial hydrostatic pressure (Pi) — pushes fluid IN (slightly negative, ~-3 mmHg)
• Plasma oncotic pressure (pi-p) — pulls fluid IN (~25 mmHg, due to albumin)
• Interstitial oncotic pressure (pi-i) — pulls fluid OUT (~8 mmHg)

At the arteriolar end: net filtration pressure = (35 + 3 + 8) - 25 = +21 mmHg -> fluid moves OUT.
At the venular end: net absorption pressure = (15 + 3 + 8) - 25 = +1 mmHg -> slightly OUT, but mostly balanced. Excess interstitial fluid is drained by lymphatics.

Oedema occurs when fluid accumulates in the interstitium: increased Pc (heart failure, venous obstruction), decreased pi-p (nephrotic syndrome, liver cirrhosis — low albumin), increased capillary permeability (inflammation, burns), lymphatic obstruction (filariasis, post-surgical).

Regional circulations (PY5.13):
• Coronary circulation — 250 mL/min at rest (5% of CO). Flow occurs mainly during DIASTOLE (systolic compression occludes intramural vessels). Metabolic autoregulation is dominant — adenosine is the key vasodilator.
• Cerebral circulation — 750 mL/min (15% of CO). Autoregulation maintains constant flow between MAP 60-150 mmHg. CO2 is the most potent cerebral vasodilator.
• Splanchnic circulation — 1400 mL/min (25% of CO). Acts as a blood reservoir; sympathetic stimulation redistributes blood away from the gut during exercise or shock.

Cardiovascular Responses to Exercise and Posture (PY5.14)

Exercise — the ultimate cardiovascular stress test:

Figure: Cardiovascular Responses to Exercise and Posture (PY5.14)

During maximal exercise, the cardiovascular system must increase oxygen delivery from ~250 mL/min (rest) to ~3,000 mL/min (maximal exercise) — a 12-fold increase.

How does the body achieve this?

1. Cardiac output increases — from ~5 L/min to ~25 L/min (5-fold). Both HR (up to ~190 bpm in a young adult) and stroke volume (from ~70 mL to ~120 mL via Frank-Starling mechanism + increased contractility) increase.

1. Blood flow is redistributed — skeletal muscle blood flow increases from ~1 L/min to ~20 L/min (20-fold!). Coronary and cerebral flow also increase. Blood flow to the gut, kidneys, and skin DECREASES (sympathetic vasoconstriction redirects blood to working muscles).

1. Peripheral resistance decreases — local vasodilation in working muscles (metabolites: K+, adenosine, CO2, lactic acid) overwhelms the sympathetic vasoconstriction elsewhere. Net result: TPR falls, which allows the increased CO to flow through without excessive BP rise.

1. Blood pressure changes — SBP increases significantly (to ~200 mmHg during heavy exercise), but DBP stays the same or slightly decreases (because TPR falls). Pulse pressure widens.

Postural changes:

On standing, ~500 mL of blood shifts to the lower limbs due to gravity -> venous return decreases -> CO drops transiently -> baroreceptor reflex compensates within seconds (increased HR, vasoconstriction). Orthostatic (postural) hypotension = a fall of >20 mmHg systolic or >10 mmHg diastolic within 3 minutes of standing. Causes: dehydration, autonomic neuropathy (diabetic patients), drugs (antihypertensives, diuretics), elderly.

Shock — When Blood Pressure Fails (PY5.15)

Shock is a state of inadequate tissue perfusion — cells don't get enough oxygen and nutrients. It is NOT simply 'low blood pressure' — BP may be initially normal due to compensatory mechanisms.

Figure: Shock — When Blood Pressure Fails (PY5.15)

Types of shock (classified by cause):

1. Hypovolaemic shock — reduced blood volume. Causes: haemorrhage (most common in India — road accidents, obstetric haemorrhage), dehydration (cholera, severe gastroenteritis), burns (plasma loss). This is the most common type in India.

1. Cardiogenic shock — the heart fails as a pump. Causes: massive MI (loss of >40% of myocardium), severe arrhythmias, acute valvular regurgitation. Mortality: 70-80%.

1. Distributive shock — widespread vasodilation reduces effective circulating volume. Subtypes: septic shock (most common in ICU), anaphylactic shock (acute allergic reaction), neurogenic shock (spinal cord injury causing loss of sympathetic tone).

1. Obstructive shock — physical obstruction to blood flow. Causes: cardiac tamponade, tension pneumothorax, massive pulmonary embolism.

Compensatory mechanisms (why BP may be initially normal):
1. Baroreceptor reflex -> tachycardia, vasoconstriction
2. Sympathetic discharge -> catecholamines -> increased HR, contractility, vasoconstriction
3. RAAS activation -> angiotensin II (vasoconstriction) + aldosterone (Na+/water retention)
4. ADH release -> water retention + vasoconstriction
5. Capillary fluid shift -> reduced Pc draws interstitial fluid into capillaries ('autotransfusion')

Stages of shock:
• Compensated — BP maintained by above mechanisms. Patient is tachycardic, cool, clammy (peripheral vasoconstriction), anxious. Urine output decreasing.
• Decompensated (progressive) — mechanisms overwhelmed. BP drops. Tachycardia worsens. Lactic acidosis (anaerobic metabolism). Oliguria.
• Irreversible — cellular death. Multi-organ failure. No response to treatment. Fatal.

Heart Failure — When the Pump Weakens (PY5.16)

Heart failure (HF) is a clinical syndrome where the heart cannot pump enough blood to meet the body's metabolic demands, OR can only do so at elevated filling pressures.

Causes:
• Systolic failure (reduced ejection fraction, HFrEF) — weakened contraction. Causes: ischaemic heart disease (most common in India), dilated cardiomyopathy, myocarditis, chronic alcoholism.
• Diastolic failure (preserved ejection fraction, HFpEF) — impaired filling. Causes: hypertensive heart disease (LVH), hypertrophic cardiomyopathy, constrictive pericarditis.

Pathophysiology — the vicious cycle:

1. Decreased cardiac output -> inadequate tissue perfusion
2. Compensatory mechanisms activate (initially helpful, ultimately harmful):
- Frank-Starling mechanism: increased preload -> increased stretch -> more forceful contraction. But excessive stretch leads to ventricular dilation and worsening function.
- Sympathetic activation: increased HR and contractility. But chronically increased catecholamines are toxic to cardiac myocytes.
- RAAS activation: Na+ and water retention -> increased blood volume -> increased preload. But fluid overload causes pulmonary oedema (left heart failure) and peripheral oedema (right heart failure).
- Ventricular remodelling: the heart dilates and hypertrophies. But a dilated heart is less efficient (Laplace's law: wall stress = pressure x radius / 2 x wall thickness).

1. The compensatory mechanisms themselves worsen the disease -> vicious cycle -> progressive deterioration.

Clinical features:
• Left heart failure -> pulmonary congestion: dyspnoea (breathlessness), orthopnoea (breathlessness lying flat), paroxysmal nocturnal dyspnoea (PND), pulmonary crackles, S3 gallop.
• Right heart failure -> systemic congestion: raised JVP, hepatomegaly, peripheral oedema (ankle swelling), ascites.
• Biventricular failure -> features of both. This is the most common presentation because left heart failure eventually causes pulmonary hypertension -> right heart failure.

Key concept: Treatment of heart failure targets the harmful compensatory mechanisms — ACE inhibitors (block RAAS), beta-blockers (block sympathetic overdrive), diuretics (reduce fluid overload). This is why understanding the pathophysiology matters for treatment.