Nodal Cells Action Potential Myocardial Action Potential

The reasons there is concentric left ventricular hypertrophy in

response to systemic hypertension is that increased wall
thickness decreases wall stress by offsetting increased wall
tension

via law of Laplace, Ws = P*r / 2T, Wall tension = P*r); increased

wall thickness also allows increased pressure generation, which
is necessary to overcome the increased aortic pressure
Heart Sounds

Key Points about Cardiac cycle

 During isovolumetric relaxation, there is a v wave on the jugular venous pressure curve
as there is atrial filling against a closed tricuspid valve. As there is rapid ventricular
filling, the presure goes down and becomes a x wave.
Jugular Venous Pulse ( a = atrial contraction marks the end of ventricular filling, c= ventricular
ejection bulging on tricuspid valve, x= end of ventricular ejection, v=isovolumetric relaxation
or atrial filling, y=rapid ventricular filling)
PAVA - conduction velocity Purkinje fastest

Increased hydrostatic capillary pressure --> edema caused by (constriction of venules, dilation
of arteries, inc. venous return)
Greater the pulse pressure, greater the stroke volume
Increased compliance, decreased pulse pressure
Renal artery --> segmental --> lobar --> acruate --> interlobular --> afferent arterioles -->
efferent arterioles --> peritubular capillaries --> renal venule --> renal vein

 
Regulation of Na Balance

Sympathetic Activity --> contraction of afferent arteriole and increase sodium uptake at the PCT
in response to AT2 which upregulates the Na/H+ pump there (contraction alkalosis here) as the
H+ is converted to bicarbonate and brought into the cell and blood in addition to water

ANP is secreted in response to high ECF volume and functions as a diuretic to excrete excess
pee --> mechanistically this works by dilation of afferent and constriction of efferent and
increased GFR to pee out more

Starling force mechanism --> decrease in ECF leads --> higher oncotic pressure in the
peritubular capillaries so more Na plus reabsorption at the PCT
also higher ECF volume --> leads to decreased oncotic pressure --> less Na plus reabsorption

RAAS ---> activated in response to decrease blood volume, decreased arterial pressure and
decreased renal perfusion pressure so know the AT2 mechanism (PCT Na/H reabsorption),
aldosterone at the late distal and collecting duct (proteins to increase Na plus reabsorption)

High Na intake --> higher ECF volume

Low Na intake --> lower ECF volume