Applied cardiovascular physiology

With moving from supine to standing -

Initially,

RV preload falls due to gravity (70% of venous blood is redistributed to lower limbs, decreasing stress volume and MSFP)

Cerebral perfusion pressure falls

Then,

Decreased pressure at the aortic arch + carotid sinus (due to lower CO and also being located above the hydrostatic indifference point)

Sensed by baroreceptors \(\to\) vagus and glossopharyngeal \(\to\) vasomotor + cardiac centers of rostral medulla \(\to\) increased heart rate and vasoconstriction

Cerebral blood vessels vasodilate

Ultimately,

Cerebral blood flow is stable

Heart rate is higher, blood pressure is higher

Cardiac output is slightly lower

Immediately:

\(\uparrow\) Blood volume \(\to \ \uparrow\)MSFP \(\to \ \uparrow\)Preload \(\ \xrightarrow{\text{Frank-Starling}} \ \uparrow\)Cardiac output \(\to \uparrow\)MAP

Over seconds to minutes:

\(\uparrow\)Atrial stretch \(\xrightarrow{\text{Bainbridge reflex}} \ \uparrow\) heart rate (transiently)

\(\uparrow\)MAP \(\xrightarrow{\text{Baroreceptor reflex}} \ \uparrow \text{Vagal tone} \ \downarrow \text{SNS} \ \to \downarrow{HR} \downarrow{\text{contractility}} \downarrow{TPR}\)

Due to this BP remains stable

Over minutes to hours:

\(\uparrow\)Capillary hydrostatic pressure \(\to \) net movement of solute out of vascular space until ~\(\frac{3}{4}\) infused volume is interstitial

\(\uparrow\)Atrial stretch \(\to \ \downarrow\)ANP \(\to \ \uparrow Na+H_2O\) renal excretion

\(\uparrow\)Renal perfusion \(\to \ \downarrow\) Renin \(\to \ \downarrow\) ATII / Aldosterone \(\to \ \downarrow Na+H_2O\) renal excretion

Prior to exercise,

CNS anticipates effort

Vagus nerve \(\to\) increased HR

SNS \(\to\) adrenaline release \(to\) increased splanchnic and skin resistance (\(\alpha_1\)), decreased SkM resistance (\(\beta_2\)), increased contractility

During exercise,

Working muscles release CO2, lactate, and potassium

Endothelium releases NO, prostacyclin

Results in regional vasodilation

TPR falls \(\to\) MAP falls \(\to\) baroreceptor reflex \(\to\) tachycardia and vasoconstriction

Ultimately,

CO increases massively (~30L/min) due to decreased afterload + increased contractility + tachycardia

MAP, CVP, and PCWP all rise

Pulse pressure increases, diastolic BP falls

TPR decreases

Myocardium

• Concentric hypertrophy; LVOT narrowing
• Valvular sclerosis
• Increased systolic function
• Decreased diastolic function due to increased afterload
• Decreased cardiac output
• Increased reliance on atrial kick
• Atrial dilation and increased propensity for AF; increased ANP

Vasculature

• Decreased vascular compliance \(\to\) increased afterload, widened pulse pressure, hypertension
• Dilation of aorta and large arteries
• Endothelial dysfunction \(\to\) impaired autoregulation, procoagulant state

Autonomic nervous system

• Blunting of baroreceptor response
• Decreased sympathetic innervation of myocardium

Conduction system

• Decreased maximum heart rate
• SA node atrophy
• Loss of conductive tissue

Total body oxygen demand increased due to increased lean body mass (adipose itself low O2 requirement)

Leptin synthesized by adipose \(\to\) RAAS activation \(\to\) fluid retention

\(\uparrow\) Blood volume \(\to \ \uparrow\) MSFP \(\to \ \uparrow\)Cardiac output, atrial pressures

Increased parrellel capillaries usually decrease TPR, but leptin-induced RAAS causes vasospasm, increases TPR, and OSA causes chronic \(\uparrow\)SNS, increases TPR \(\to\) LV afterload typically increased

PVR increased (LV diastolic failure and OSA\(\to\) chronic hypoxic pulmonary vascoconstriction)

Ultimately increased preload and afterload for both ventricles leads to remodelling

• Concentric hypertrophy
• Chamber dilation
• Diastolic dysfunction