Cardiovascular Physiology

Hypovolaemic

Cardiogenic

Distributive

Obstructive

Cytotoxic

• Mitchondrial toxicity e.g. sepsis, cyanide

SNS activated by peripheral nerves

Increase pituitary hormones - ADH

Increase ACTH and cortisol

Cytokine release IL6, IL1 TNF alpha

• Autonomic effects

  • Arterial hypotension causes baroreflex activation.

  • Decreased cardiac output causes chemoreceptor activation.

  • Both reflexes result in autonomic phenomena:

    • Decreased vagal stimulus; thus increased heart rate

    • Sympathetic activation, which has multiple effects:

      • Increased peripheral vascular resistance

      • Redistribution of blood flow away from the cutaneous and splanchnic circulation

      • Stimulation of systemic catecholamine release from adrenal glands, which produces an increased systemic effect in addition to the peripheral sympathetic nervous system effects

      • Stimulation of vasopressin release via the projections from the nucleus of the solitary tract to the hypothalamus

      • Stimulation of renin release by sympathetic stimulation of the juxtaglomerular cells, and due to lower renal perfusion

• Neurohormonal effects

  • Renin secretion causes:

    • Vasoconstriction (by angiotensin)

    • Increased sodium retention (by aldosterone)

  • Vasopressin release causes:

    • Vasoconstriction (by V1 receptors)

    • Increased water retention (by V2 receptors)

  • Venous hypotension decreases atrial natriuretic peptide secretion, which causes:

    • Decreased renal blood flow

    • Decreased urinary water and sodium excretion

  • The net effect is decreased urine output and increased retention of sodium and water

Fick’s

Indicator dilution

Pulse contour analysis

Doppler Velocity Measurement

Flow rotometer

CO = VO2/Ca-Cv

The total uptake of oxygen is equal to the product of the cardiac output and the arterial-venous oxygen content difference.

Direct measurements of these things can be difficult.

Indirect measurements introduce inaccuracies

e.g.:

• VO2 estimate from nomograms

• Use CVC O2 or venous estimates

• Estimate Ca from SpO2

VO2 measurement takes time - CO may change during this

Can substitute CO2 for this too!

• Estimation of CaCO2 on the basis of end-tidal CO2

• Estimation of CvCO2 on the basis of EtCO2 during rebreathing 

Inject indicator or change property of blood and measure its concentration distally (or the effect of change of property)

CO = indicator dose/area under [ ] time curve

Prone to error!

• delivery technique (flow, volume, temp, timing with resp) changes results

• sampling rate must be high

• corrections needed for thermodilution

Limitations

• Indicator limits repeat observations (recycling)

• Relies on uniform mixing and unidirectional flow

Arterial waveform converted into volume measurement using a calibration factor based either on

• estimate from nomogram

• derived from indicator measurement

These are a signifcant source of error. Calibration is dependent on properties of the vascular system.

If this changes recalibration is needed e.g. vasoconstriction

CO = HR x CSA aorta x VTI (velocity time integral)

Measure velocity over time in 5 chamber view and integrate. Need serial measurements to account for resp cycle variation. Further serial measurments for AF.

Beam angle needs to be right.

Gives a fair estimate in experienced hands.

PP = SBP - DBP, usually 40mmHg

PP = SV / Compliance

Systolic

• Arterial compliance ***

• Stroke volume

• Peripheral resistance

Diastolic

• Peripheral resistance (increases DBP) ***

• Arterial compliance

• Time constant of vessels (and therefore HR)

Note that increased resistance generally reduces compliance as constricted vessels don’t expand as well.

• Respiratory pulse pressure variation:

  • As intrathoracic pressure changes, so do preload and afterload, and this gives rise to a variation in stroke volume, which is in turn a major determinant of systolic pressure. 

• Pulse pressure variation in shock:

  • In hypovolemia the pressure gradient for venous return becomes more sensitive to changes in intrathoracic pressure.

  • In cardiac tamponade, changes in preload exaggerate the normal inspiratory drop in blood pressure through interventricular interdependence.

• Pulse pressure variation with stress and exercise:

  • Increased sympathetic activity increases the stroke volume and therrefore the systolic blood pressure 

• Pulse pressure variation due to arterial compliance:

  • As arterial compliance decreases, systolic pressure increases  and diastolic pressure drops because of the steeper pressure-volume curve

• Pulse pressure variation due to heart rate

  • With a slower heart rate, the diastolic pressure decline occurs over a longer time period, and is therefore deeper, and the diastolic filling is longer, resulting in a higher stroke volume and higher systolic pressure

• Pulse pressure difference according to the site of measurement:

  • Distal pulse pressure amplification due to constructive interference of reflected waves increases the systolic and decreases the diastolic pressure in distal arteries

• Pulse pressure variation with pathological states:

NARROW PP

Shock - more susceptible to standard changes in preload associated with respiration

Tamponade - intrathoracic pressure changes lead to interventricular dependence

Any decrease in SV

• Aortic stenosis

• Heart failure

• High afterload

Increased compliance - AV fistula

WIDE PP

Increase in stroke volume

• hyperdynamic, early sepsis

• thyrotoxicosis

• anaphylaxis

Decreased compliance

• age

• atherosclerosis

• aortic aneurysm (no Windkessel)

Structural

• Aortic regurg