Cardiac Output, Blood Flow, and Blood Pressure PDF

# Chapter 14: Cardiac Output, Blood Flow, and Blood Pressure ## Cardiac Output (CO) - Is volume of blood pumped/min by each ventricle - Stroke volume (SV) = blood pumped/beat by each ventricle - CO = SV x HR - Total blood volume is about 5.5L ## Regulation of Cardiac Rate - Without neuronal infl...

# Chapter 14: Cardiac Output, Blood Flow, and Blood Pressure ## Cardiac Output (CO) - Is volume of blood pumped/min by each ventricle - Stroke volume (SV) = blood pumped/beat by each ventricle - CO = SV x HR - Total blood volume is about 5.5L ## Regulation of Cardiac Rate - Without neuronal influences, SA node will drive heart at rate of its spontaneous activity - Normally Symp & Parasymp activity influence HR (chronotropic effect) - Autonomic innervation of SA node is main controller of HR - Symp & Parasymp nerve fibers modify rate of spontaneous depolarization ## Regulation of Cardiac Rate (Continued) - NE & Epi stimulate opening of pacemaker HCN channels - This depolarizes SA faster, increasing HR - ACH promotes opening of K+ channels - The resultant K+ outflow counters Na+ influx, slowing depolarization & decreasing HR - _Figure 14.1: Diagram of pacemaker potential showing how sympathetic and parasympathetic nerve fibers interact with the SA node_. ## Regulation of Cardiac Rate (Continued) - Cardiac control center of medulla coordinates activity of autonomic innervation - Sympathetic endings in atria & ventricles can stimulate increased strength of contraction ## Effects of Autonomic Nerve Activity on the Heart | Region Affected | Sympathetic Nerve Effects | Parasympathetic Nerve Effects | | ---------------- | ------------------------------------------------------------------------------------------------------------------- | -------------------------------------------------------------------------------------------------------- | | SA node | Increased rate of diastolic depolarization; increased cardiac rate | Decreased rate of diastolic depolarization; decreased cardiac rate | | AV node | Increased conduction rate | Decreased conduction rate | | Atrial muscle | Increased strength of contraction | No significant effect | | Ventricular muscle | Increased strength of contraction | No significant effect | ## Stroke Volume Is determined by 3 variables: - End diastolic volume (EDV) = volume of blood in ventricles at end of diastole - Total peripheral resistance (TPR) = impedance to blood flow in arteries - Contractility = strength of ventricular contraction ## Regulation of Stroke Volume - EDV is workload (preload) on heart prior to contraction - SV is directly proportional to preload & contractility - Strength of contraction varies directly with EDV - Total peripheral resistance = afterload which impedes ejection from ventricle - Ejection fraction is SV/EDV - Normally is 60%; useful clinical diagnostic tool ## Frank-Starling Law of the Heart - States that strength of ventricular contraction varies directly with EDV - Is an intrinsic property of myocardium - As EDV increases, myocardium is stretched more, causing greater contractions & SV - _Figure 14.2: Diagram showing the relationship between stroke volume and ventricular end-diastolic volume (EDV) with and without sympathetic stimulation_ ## Frank-Starling Law of the Heart (Continued) - (a) is state of myocardial sarcomeres just before filling - Actins overlap, actin-myosin interactions are reduced & contraction would be weak - In (b, c & d) there is increasing interaction of actin & myosin allowing more force to be developed - _Figure 14.3: Diagram showing the relationship between sarcomere length and tension._ ## Extrinsic Control of Contractility - At any given EDV, contraction depends upon level of sympathoadrenal activity - NE & Epi produce an increase in HR & contraction (positive inotropic effect) - Due to increased Ca2+ in sarcomeres - _Figure 14.4: Diagram showing the relationship between muscle length and relative tension in skeletal muscle, cardiac muscle with epinephrine, and cardiac muscle without epinephrine. ## _Figure 14.5: Diagram showing the relationship between cardiac output, cardiac rate, stroke volume, contraction strength, end-diastolic volume, and mean arterial pressure._ ## Venous Return - Is return of blood to heart via veins - Controls EDV & thus SV & CO - Dependent on: - Blood volume & venous pressure - Vasoconstriction caused by Symp - Skeletal muscle pumps - Pressure drop during inhalation - _Figure 14.7: Diagram showing the relationship between venous return, end-diastolic volume, negative intrathoracic pressure, blood volume, venous pressure, breathing, urine volume, tissue-fluid volume, venoconstriction, skeletal muscle pump, and sympathetic nerve stimulation._ ## Venous Return (Continued) - Veins hold most of blood in body (70%) & are thus called capacitance vessels - Have thin walls & stretch easily to accommodate more blood without increased pressure (=higher compliance ) - Have only 0-10 mm Hg pressure - _Figure 14.6: Diagram showing the distribution of blood in different parts of the body._