The Dossier

Stroke Volume can vary from 5-40L/min.

Increased tension produced from a fixed preload is called positive contractility or positive inotropy. (NE)

Ventricles are not well innervated with parasympathetics, so the PNS is more important for HR.

For same internal pressure a larger sphere has greater wall stress. During isovolumetric phase, wall tension increases 25X. Increases to 50x during systole.

Treppe or Staircase phenomenon describes rate induced regulation. Increase HR and you increase force due to cytoplasmic Ca.

Bainbridge Reflex and atrial receptors, stretch induced, ensure inflow and outflow are equal. Increase in venous return will accelerate HR.

Thyroid Hormone increases HR and cardiac output. Also influences myosin ATPase in cardiac cells.

Hypoxia – modest reduction – causes increase in HR and contractility.

Marked reduction causes depressed function

Alkalosis – mild decrease in Co2 – augments cardiac function via effects on myocardium

Acidosis – mild increase in Co2 – depresses heart function

Adrenergic fibers from lower cervical and upper thoracic ganglia. Right nerves work on SA node to increase HR. Left nerve increases contractility via ventricles.

Activation of cAMP dependent kinases phosphorylate Ca channels and phospholamban.

Cannot regulate heart on beat to beat basis, slow fx

B-blocker propanolol

Phosphodiesterase inhibitors slow down removal of Ca, but increase myocardial oxygen need.

Parasympathetics. Right works on SA node to slow HR. Left slows the AV node. Acts on muscarinic receptor, opens K channels, slows phase 4 depolarization.

Blocked by atropine

Fast effects. Keeps HR down at 70 when at rest. Exercise increases vagal tone and decreases HR. This can also happen with increased intracranial pressure.

Thalamic and medullary centers are critical in the control of vasculature

Frontal lobes and orbital cortex have input

Baroreceptor reflex: High BP causes vagal firing and inhibits sympathetics. Receptors in aortic arch and carotid sinus. Acute hypertension may cause bradycardia.

Sinus arrhythmia: HR varies with breathing, increases with inspiration. Due to increased sympathetic firing  due to parallels to phrenic nerve>vasomotor center and increases venous return/Bainbridge reflex. HR decreases during expiration due to increased parasympathetics, decreased venous return.

Chemoreceptor reflex – low o2 or high co2 have small effects on lungs and heart, but bigger effects on vaculature.

Ventricular Receptor Reflex – sensory receptor in wall of ventricle may slow the HR and lower peripheral vascular resistance when stimulated. Mechanical or chemical.