Inferior wall infarct in lvp lv volume eg aortic

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Unformatted text preview: and the strength of contraction decreases when the parasympathetics are blocked Interaction of ANS •  From the previous results it can be concluded that under resting conditions: –  Parasympathetic NS exerts a dominate inhibitory influence on heart rate –  Sympathetic NS exerts a dominate stimulatory influence on strength of contraction Remove both symp. and para. The heart rate increases but the strength of contraction decreases Interaction of the SNS & PSNS •  SNS Cardiac cell β - NE β ACh Gs Gi ⇑ cAMP Ad. Cycl. NPY NE ACh M ⇓ •  PARA Atropine is a mechanoblocker Propranolol is a beta blocker The release of NE by symoathetics can effect the release of ACh by parasympathetics and visa versa Direct vs. Indirect SNS influence •  Direct innervation of Cardiac cells accounts for most of the SNS effect. –  Norepinephrine acting on β-1 receptors. (85%) Cardioacclerator reflex •  Stretch on right atrial wall + stretch receptors which in turn send signals to medulla oblongata + SNS outflow to heart –  AKA Bainbridge reflex –  Helps prevents damning of blood in the heart & central veins –  •  Indirect effects would be due to circulating catacholamines (epinephrine & norepinephrine) released primarily from the adrenal medulla (blood borne) which would find their way to the cardiac β-1 receptors. (15%) Indirect effects are due to circulating blood Direct accounts of the most effect because it gets there faster and by the time the indirect effects reach the point the receptors are already full 12 Neurocardiogenic syncope •  Benzold-Jarisch reflex (Baroreceptors in ventricles) –  Stimulation of sensory endings mainly in the ventricles (some in the atria) that reflex via the X CN to the CNS •  Inferoposterior wall of LV which is supplied by the circumflex artery is site of majority of receptors •  Reflex effects results in hypotension & bradycardia Major Hormonal Influences •  Thyroid hormones –  + inotropic Increases strength of contraction –  + chronotropic Increases heart rate –  also causes an increase in CO by ⇑ BMR –  Reflex stimulated by •  Occlusion of circumflex artery (inferior wall infarct) •   in LVP & LV volume (eg. Aortic stenosis) Calcium: - causes spastic contraction - Ca ions initiate the cardiac contractile process - deficiency causes flaccidity 112 Ionic influences •  Effect of elevated [K+]ECF –  dilation and flaccidity of cardiac muscle at concentrations 2-3 X normal (8-12 meq/l) –  decreases resting membrane potential Effect of body temperature •  Elevated body temperature –  HR increases about 10 beats for every degree F elevation in body temperature –  Contractile strength will increase temporarily but prolonged fever can decrease contractile strength due to exhaustion of metabolic systems •  Effect of elevated [Ca++] ECF –  spastic contraction •  Decreased body temperature –  decreased HR and strength Potassium: -Large quantities can block impulses from going through the AV bundle -Elevation of 2-3x can cause death -decreases resting membrane potential in cardiac fibers -makes the contractionof the heart weaker Energy substrate for cardiac cells •  Heart is versatile & can use many different energy substrates •  Fatty acids-70% preferred •  Glucose •  Glycerol •  Lactate •  Pyruvate •  Amino acids Relationship of energy to work •  75% of energy the heart utilizes is converted to heat •  The remainin...
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