Physiology
Ohm’s Law: I(Flow)=V(Pressure)/R(Resistance)
Hydraulic analogy
Echocardiography
Flow*time = Volume, but cardiac flow is not steady so the VTI compensates for that. The doppler line is placed on a valve, and the stroke volume is calculated from the integral of the doppler velocity and the diameter (eg LVOT)
Vascular resistance
Peripheral vascular resistance is mediated locally by metabolites, and over a distance on a neuro-hormonal level
The central dictation of peripheral vascular resistance occurs at the level of the arterioles. The arterioles dilate and constrict in response to different neuronal and hormonal signals.
In the human body there is very little change in blood pressure as it travels in the aorta and large arteries, but when the flow reaches the arterioles, there is a large drop in pressure, and the arterioles are the main regulators of SVR.
R is the resistance of blood flow [change in pressure between the starting point and end point]
There are several mechanisms by which systemic vascular resistance may be altered
Renin-Angiotensin system - Vasoconstriction
The autonomic nervous system - Alpha-1 receptors for vasoconstriction, Beta-2 receptors for vasodilation
At the endothelial level, nitrous oxide is released for vasoconstriction and endothelin for vasoconstriction
Several other molecules have uncertain effects (ANP, thromboxane, bradykinin)
Flow resistance in the pulmonary circulation is only about 10% of the total peripheral resistance in the systemic circulation
Typical pulmonary vascular resistance is 1,8 Wood units and a typical pressure drop of 10 mmHg
Low PVR maximizes the distribution of blood to the peripheral alveoli and ultimately allows for proper gas exchange
During increased CO the PVR decreases to allow increased flow, primarily by capillary recruitment (mostly from the apical zone where cap pressures are lowest) and capillary distension (the ovular vessels become more circular)
Lung collapse increases resistance in associated vessels (by increasing pressure from parenchyma)
Additionally, low resistance allows for the pulmonary system to pump the entire cardiac output at low pressures
Disease processes that cause chronic hypoxia will increase pulmonary vascular resistance through hypoxic pulmonary vasoconstriction
Typical systemic vascular resistance is 18 Wood units and a typical pressure drop of 100 mmHg
Ohm’s Law: ΔP (Pressure difference, mmHg) = Q(flow, L/min)R (resistance, mmHg*min/L (Wood Units))
The blood pressure in the pulmonary artery is much lower than the aortic pressure. The pulmonary vessels have relatively thin walls and their environment (air- filled lung tissue) is highly compliant. Increased cardiac output from the right ventricle therefore leads to expansion and thus to decreased resistance of the pulmonary vessels. This prevents excessive rises in pulmonary artery pressure during physical exertion when cardiac output rises.
On coronary blood flow control:
Adaptation of the myocardial O2 supply according to need is therefore primarily achieved by adjusting vascular resistance. The (distal) coronary vessel resistance can nor- mally be reduced to about 1/4 the resting value (coronary reserve). The coronary blood flow Q. cor (approx. 250 mL/min at rest) can therefore be increased as much as 4–5 fold. In other words, approx. 4 to 5 times more O2 can be supplied during maximum physical exertion.
Compliance
C=ΔV/ΔP (volume change/pressure change)
Veins have 30x the compliance of arteries
Afterload
When the aortic pressure load (afterload) increases, the aortic valve will not open until the pressure in the left ventricle has risen accordingly. Thus, the stroke volume (SV) in the short transitional phase (SVt) will decrease, and End Systolic Volume will rise (ESVt). Consequently, the start of the isovolumic contraction shifts to the right along the passive Pressure–Volume curve. SV will then normalize despite the increased aortic pressure (D2), resulting in a relatively large increase in ESV (ESV2).
