EXPH 386 Leary Notes 7-8 PDF

○ 0.06 seconds time till ventricles contract upon stimulation Electrocardiogram (ECG/EKG) ○ Records the electrical activity of the heart ○ P wave Atrial depolarization ○ QRS complex Ventricular depolarization and atrial repolarization simultane...

○ 0.06 seconds time till ventricles contract upon stimulation Electrocardiogram (ECG/EKG) ○ Records the electrical activity of the heart ○ P wave Atrial depolarization ○ QRS complex Ventricular depolarization and atrial repolarization simultaneously ○ T wave Ventricular repolarization ○ ECG abnormalities may indicate coronary heart disease ST segment depression can indicate MI Relationship between Pressure Changes and ECG ○ We have atrial depolarization which signals atrial contraction which has a small increase in blood volume which acts on the ventricular walls increasing pressure ever so slightly ○ Polarization passes AV node and into ventricles which causes contraction and generates maximal pressure which signals ventricular repolarization Areas of the Heart That Can Initiate a Rhythm and Intrinsic Rate ○ The slower the lower ○ Sinus node: 60-100 BPM ○ Atrial Tissue: 60-100 BPM ○ AV node: 40-60 BPM ○ Ventricular Tissue: 20-40 BPM Extrinsic Heart Rate Regulation ○ Neural influences superimpose on the inherent rhythm of the myocardium To accelerate HR in anticipation of exercise and adjust HR as exercise intensity increases or decreases ○ Range 20-200 BPM (dependent upon physical fitness) Sympathetic and Parasympathetic Control ○ Sympathetic stimulation Catecholamine (NE/Epinephrine) Results in tachycardia Increases SA node depolarization, increases HR Increases contractility ○ Parasympathetic influence Acetylcholine- vagal influence Results in bradycardia Slow SA node depolarization, slows HR Exercise and Blood Flow  Parasympathetic Neural Control ○ Periphery Excitation of iris, gallbladder, coronary arteries Inhibits gut sphincters, intestines, and skin vasculature During the onset of exercise, HR increases by inhibition of PNS Sympathetic Control on Blood Flow ○ Mechanism is NE via adrenergic fibers that lie within smooth muscle of small arteries, arterioles, and precapillary sphincters ○ Inactive Tissue (vasoconstriction) Renal, splanchnic, and inactive skeletal muscle Produces systemic vasoconstriction of inactive muscle ○ Active Tissue (vasodilation) Active muscle Decreases SNS activity Neural Response During Exercise ○ Anticipatory response Decrease parasympathetic Increase sympathetic ○ Exercise Parasympathetic inhibition (early) Sympathetic stimulation (more intense) ○ What happens? Increased HR and contractility Increase in arterial blood pressure Vasodilation of active skeletal muscles Vasoconstriction of skin gut spleen etc. Vasoconstriction increases venous return Functional Sympatholysis ○ Sympathetic neural activity on blood vessels = vasoconstriction ○ So how do we get increased blood flow to active tissues? Local changes in muscle metabolites and other substances reduce vascular responsiveness to alpha adrenergic receptor activation Peripheral Input Control of CV response ○ Initial signal to “drive” cardiovascular system comes from higher brain centers ○ Fine-tuned by feedback from Chemoreceptor Sensitive to blood, O2, CO2, and pH levels Baroreceptors Sensitive to changes in arterial blood pressure Muscle mechanoreceptors (heart, skin, joints)