110 likes | 117 Views
This text provides an in-depth overview of short-term and long-term control mechanisms regulating cardiac cycle through autonomic nerve impulses. It covers factors affecting heart rate, including chemical regulation, hormones, and various stimuli. It also discusses the impact of autonomic regulation on heart rate and contractility, as well as the role of vasopressin in blood pressure control. The content includes information sourced from "Introduction to Cardiovascular Physiology" by J.R. Levick.
E N D
Regulation of Cardiac Cycle Autonomic nerve impulses alter the activities of the S-A and A-V nodes
Overview of short-term control mechanisms From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
Heart rate Autonomic regulation (medullary CV center): Receives input from higher brain centers and variety of sensory receptors • Proprioceptors • Chemoreceptors • Baroreceptors • Sympathetic output ↑HR and contractility • Parasympathetic impulses ↓ HR • Little effect on contractility (does not innervate ventricular myocardium)
Heart rate • Several factorscontribute to regulation of heart rate: • Chemical regulation • Cardiac activity depressed by • Hypoxia • Acidosis • Alkalosis • Hormones • Catecholamines and thyroid hormones increase HR and contractility • Cations • Alterations in balance of K+, Na+ and Ca2+ alter HR and contractility
Heart rate • Several other factorscontribute to regulation of heart rate: • Age • Gender • Female HR higher • Physical fitness • Resting bradycardia • Body temperature • Increase causes SA node to discharge more rapidly
PNS • Vagus nerve (via ACh) ↓ HR by ↓ slow inflow of Na+ and Ca++ and by ↑ the subsequent outflow of potassium (K+). • Acts at SA and AV nodes. • May treat SNS-driven heart attack by gagging or massage of carotid arteries activate vagal reflexes PNS counteracts SNS.
The Cardiovascular Stress Response • Get the heart to beat faster: ↑ SNS tone, ↓ PNS tone • Norepinephrine (NE) and epinephrine (Epi) ↑ slow inflow of Na+ and Ca++ increase rate of re-excitation in SA node. • This ↑ Ca++ also increases contractility. • SNS terminals also excite AV node and whole myocardium: enhances contractility everywhere.
Summary of long term BP control • Cardiac output and BP depend on renal control of extra-cellular fluid volume via: • Pressure natriuresis, (increased renal filtration) • Changes in: • Vasopressin • Aldosterone • Atrial natiuretic peptide All under the control of altered cardiovascular receptor signaling
Vasopressin • Enhances water retention • Causes vasoconstriction • Secretion increased by aortic baroreceptors and atrial sensors http://www.cvphysiology.com/Blood%20Pressure/BP016.htm
Aortic arch Carotid sinus Nucleus tractus solitarius Cardiac inhibition Vasoconstriction Cardiac stimulation Constriction of veins & arterioles Increased heart rate Increased stroke volume Increased peripheral resistance Increased cardiac output Baroreceptor reflex Blood pressure falls Sensors Neural integration Effectors Increased blood pressure