QUIZ/TEST REVIEW NOTES SECTION 2 CARDIAC OUTPUT [CARDIOLOGY]

Transcription

1 QUIZ/TEST REVIEW NOTES SECTION 2 CARDIAC OUTPUT [CARDIOLOGY] Learning Objectives: Construct and interpret graphs of ventricular pressure, ventricular volume, heart sounds, and ECG during a cardiac cycle Identify how EDV and ESV change during exercise I. CARDIAC CYCLE AND VOLVUMES a. Location systole and diastole on an ECG 1. Atrial Systole - P QRS complex 2. Atrial Diastole - QRS complex P 3. Ventricular Systole - QRS complex T 4. Ventricular Diastole - T QRS complex b. Ventricular Volumes 1. End-Diastolic Volume (EDV) - The maximum filling that occurs at the end of ventricle diastole (relaxation) - Ejection Fraction: Percentage of EDV ejected with one contraction (stoke volume/edv) - Normal EDV for 70kg man = 135ml - During exercise EDV<135 because ventricles do not completely fill 2. End-Systolic Volume (ESV) - The amount of blood left in the ventricle at the end of ventricular systole (contraction) - The minimum amount of blood the ventricle will contain during one cycle - Normal ESV for 70kg man = 65 ml [Meaning that nearly half of the 135mL that was in the ventricle at the start of the contraction is still there at the end of contraction] - Functions as reserve during exercise or times of high bodily exertion 3. Stroke Volume (SV) a. Defined: - The amount of blood pumped by one ventricle during a contraction - EDV-ESV=Stroke Volume 1

2 [Volume of blood before contraction Volume of blood after contraction = Stroke Volume] - Normal SV for a 70kg man is 135mL-65mL=70mL - Is homeostatically regulated - Is directly related to the force generated by cardiac muscle during a contraction b. SV Resting: 135mL-65mL=70mL (Normal EDV and ESV) c. SV Exercising: 135mL-35mL=100mL (Normal EDV but ESV Increases) c. Ascultation (heart sounds) 1. Sounds caused by - ASCULTATIONS; Heart sound correspond to closing of valves and turbulence of blood flow 2. S1 - Vibrations created by atrioventricular valves closing and semilunar valves opening - Occurs during QRS wave at beginning of ventricular systole - LUB 3. S2 4. S3 5. S4 - Vibrations created by semilunar valves closing and atrioventricular valves opening - Occurs after T wave in the end of ventricular systole (beginning of diastole) - DUB - Turbulence during ventricular diastole (filling of blood) - Occurs after S2 - Turbulence during atrial systole (blood pushing down into ventricles) - After P wave 2

3 HR x SV = CO HR = Parasympathetic Control SV = Sympathetic Control II. CARDIAC OUTPUT (CO) a. Defined - The volume of blood pumped by one ventricle in a given period of time - Cardiac Output (CO) is an indicator of total blood flow through the body b. Calculations - Can be calculated by multiplying heart rate (beats per minute) by stroke volume (ml per beat or per contraction) - Average total blood volume is about (Male: 5 liters/female: 4.2 liters) meaning that at rest one side of the heart pumps all the blood in the body through it in only minute - Normally cardiac output is same for both ventricles [If one side of heart begins to fail the CO become mismatched causing the blood to pool in the circulation behind the weaker side of the heart] - During exercise CO can increase from 5 liters a minute (at rest) to 35 liters a minute (meaning that one side of the heart pumps all the blood in the body 7 times in one minute; opposed to 1 time at 5 liters) c. Regulation of Stroke Volume - SV is directly related to force generated by cardiac muscle during a contraction - A large contraction force will generate a large SV - Ventricular contraction is affected by two parameters (a) Length of muscle fibers at the beginning on contraction (b) Contractility of the heart 1. Preload a. Definition - Degree of myocardial stretch before contraction begins - Stretch represents the load placed on cardiac muscle before they contract (EDV and Venous Return) 1. Length-Tension - The force generated by a myocardial muscle fiber is directly related to the length of the sarcomeres > By the increase length, contraction force increases Preload Main Points: - Directly proportion to SV - EDV/Venous Return - Stretching of walls 3 2. Duration of diastole - The volume of blood in the ventricle at the beginning of contraction ( EDV) determines the length of the muscle - As EDV increases the SV increases 3. Venous Return - Determines EDV; the amount of blood that enters the heart from the venous circulation - Effecting factors of Venous Return

4 (1) Skeletal muscle pump [Skeletal muscle contractions that squeeze veins; helps return blood to heart; when sitting or standing motional the pump does not assist venous return] (2) Respiratory muscle pump [Created by movement of thorax during inspiration; increased pressure in abdominal veins and decreased pressure in thoracic veins; breathing deeply helps] (3) Sympathetic Innervations of Veins [When veins constrict their volume decreases and squeeze more blood out of them and into the heart] (4) Exercise [Exercising and body movement increases use of respiratory muscle pump, skeletal pump, and sympathetic innervations] Contractility Main Points: - Directly proportion to SV - Contractile force 2. Contractility a. Strength of contraction at any preload - The intrinsic ability of a cardiac muscle fiber to contract at any given fiber length - Is a function of Ca2+ interaction with the contractile filaments - Contractility is dissimilar from length-tension relationship [Muscle can remain one length but show increased contractility] - Contractility increases as the amount of calcium available for contraction increases b. Calcium levels - Volume of blood in the ventricle at beginning of contraction (EDV) determines the length of the muscle - Increasing the sarcomeres length also makes cardiac muscle more sensitive to Ca2, thus linking contractility to muscle length - Catecholamine(s) > Ca2+ increase by > Molecules bind to and activate Beta 1-Adrenergic Receptors > Increase cardiac contraction force > Decrease Duration of contraction b. Chemicals - Any chemical that affects contractility is called an inotropic agent, and its influence is called an inotropic effect (1) Positive inotropic agents > Increases the force of contraction > Beta 1 Agonists > Hypercalcomia > Digoxin (cardiac glycosides) (2) Negative inotropic agents > Decreases the force of contraction > Anoxia > Acidosis > Anesthetics (halothane) > Hyperkalemia > Beta 1 Blockers/Ca-Channel Blockers 4

5 Afterload Main Points: - Indirectly proportion to SV - Peripheral resistance 3. Afterload a. Ventricular pressure needed to overcome peripheral resistance - Combined load of EDV and arterial resistance during ventricular contraction - To maintain constant SV when afteload increases the ventricle must increase its force of contraction [increasing need for O2 and ATP synthesis] - Peripheral Resistance > Resistance of blood leaving > Increase Peripheral Resistance. Decrease S.V. [Blood has to work harder against an outside force to reach the heart, so less blood will fill the heart; decreasing EDV S.V.] > Myocardial Hypertrophy - Increased thickness of ventricular walls because of chronic high afteload; 5

6 d. Regulation of Heart Rate [Neural Innervations] 1. Autonomic Division - Divided into Sympathetic and Parasympathetic branches - Sympathetic branch dominates flight or fight situations - Parasympathetic branch dominates during rest and digest functions 2. Antagonistic Control is Hallmark of Autonomic Division - Autonomic division is primary under Antagonistic control - Sympathetic innervations increases heart rate while parasympathetic stimulation decreases it - Exceptions to this are sweat glands, smooth muscle control in most blood vessels (tonically controlled by sympathetic branch) 3. Pathways - Preganglionic Neuron > Originates in the CNS - Autonomic Ganglion > Ganglion: Is a cluster of nerve cell bodies that lie outside the CNS (equivalent in the CNS is a nucleus) - Postganglionic Neuron > Divergence: Each postganglionic neuron may innervate a different target, meaning that a single signal from the CNS can affect a large number of target cells simultaneously 6

7 - Autonomic Neurotransmitter Modulation (1) Both sympathetic and parasympathetic preganglionic neurons release acetylcholine (ACh) onto nicotinic cholinergic receptors on postganglionic cells (2) Most postganglionic sympathetic neurons secrete norepinephrine onto adrenergic receptors (3) Most postganglionic parasympathetic neurons secrete acetylcholine onto muscarinic cholinergic receptors ACh (parasympathetic) NE, E (sympathetic) Cholinergic Adrenergic Nicotinic Alpha 1, 2 Muscarinic Beta 1, 2 Postganglionic Autonomic Neurotransmitters Parasympathetic Division Sympathetic Division Neurotransmitter Acetylcholine (ACh) Norepinephrine Receptor Types Nicotinic and Muscarinic (Cholinergic) α and β (Adrenergic) Varicosity membrane transports Norepinephrine Choline PARASYMPATHETIC BRANCH [Rest and Digest] - Secrete ACh at their targets - Muscarinic cholinergic receptors are found at the neuroeffector junctions of the parasympathetic branch - Muscarinic receptors are all G protein-coupled receptors - Pathways laves the CNS at the brain stem (Vagus Cranial Nerve) and in the sacral region of the spinal cord/ganglia are located close to or in the target tissue SYMPATHETIC BRANCH [Flight or Fight] - Secrete catecholamine s that bind to adrenergic receptors on their target cells - Adrenergic receptors come has α (alpha) or β (beta) β 1 = Respond equally strongly to Norepinephrine and epinephrine Found on contractile cells of the heart β 2 = More sensitive to epinephrine than to Norepinephrine (are not innervated; no sympathetic neurons terminate near them which limits their exposure to the neurotransmitter Norepinephrine Coronary Arteries Arteries of liver and skeletal muscle Bronchioles β 3 = Found primary on adipose tissue, are innervated and more sensitive to Norepinephrine than to epinephrine - All Adrenergic receptors are G protein-coupled receptors and not ion channels [Target cell response is slower to start and usually last longer] - Pathways originate in the thoracic and lumbar regions of the spinal cord/ganglia are located close to the spinal cord (are paravertebral) Adrenal Medulla Secretes Catecholamine s o Adrenal medulla is specialized neuroendocrine tissue associated with sympathetic nervous system o Sympathetic branch of nervous system secrets Norepinephrine and the adrenal medulla secretes epinephrine primarily 7

8 o o Adrenal Cortex (outer region) is true endocrine gland of epidermal origin that secretes steroid hormones Adrenal Medulla forms the small core of the gland, develops from the same embryonic tissue as sympathetic neurons and is a neurosecretory structure Adrenal Medulla: Modified sympathetic ganglion; preganglionic sympathetic neurons project from spinal cord to adrenal medulla to synapse; the postganglionic neurons lack axons that would project to target cells, so these axonless cell bodies are called chromaffin cells the secrete neurohormone epinephrine directly into the blood 8

9 SYMPATHETIC Stimulation Location Receptor Effect SA + AV Nodes β1 Increase rate of conduction (Cardiac Output) Contractile Cells β2 Increase force (Cardiac Output) Coronary Arteries β2 Vasodilatation (Afterload) Systemic Arteries (Afterload) Α Vasoconstriction SYMPATHETIC Stimulation Location Receptor Effect SA + AV nodes m-ach-r Slows rate of conduction Contractile Cells None No Effect 9

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