The Cardiovascular System PDF

The Cardiovascular System Organization of Neural System CNS: brain & spinal cord PNS: everything Afferent: ascending to CNS...

The Cardiovascular System Organization of Neural System CNS: brain & spinal cord PNS: everything Afferent: ascending to CNS Efferent: exiting the brain Autonomic: involuntary Sympathetic (fight or flight) Parasympathetic (rest & digest) Somatic: voluntary The Cardiovascular System: The heart Impetus for blood flow 2/3 lies on left side of chest cavity 4 chambers: R & L atria, R & L ventricles Right and left side separated by intraventricular septum Output: ~6000L/day Myocardium: cardiac muscle Intercalated disks: complex junctions connecting Striated striations of cardiac muscle Involuntary Allows electrical activity to travel between cardiac Intercalated disks muscle cells Cardiac vs Skeletal Similarities: Differences: Striated Intercalated disks Response to stretch/tension Involuntary control 1 or 2 centrally located nuclei Ventricular Diastole: ventricles relax & fill with blood Ventricular Systole: ventricles contracts, push blood through Systemic Circulation Capillaries Arterial System Venules Aorta, arteries, arterioles Veins Carry blood away from the heart Sup/Inf Vena Cava Most carries oxygenated blood except pulmonary artery Right Atrium Tricuspid valve Capillaries: carry both oxygenated nd deoxygenated blood Right ventricle Pulmonary semilunar valve Venous System Lungs Venules, Veins, and Inferior and Superior Vena Cava Left atrium Most carries deoxygenated blood except pulmonary vein Bicuspid/mitral valve Return blood to the heart Left ventricle Aortic semilunar valve Pulmonary Artery: only arteries to carry deoxygenated blood Aorta Arterials Pulmonary Veins: only veins to carry oxygenated blood Arteries Systole: phase of ventricular contraction Diastole: phase of ventricular relaxation End-Systolic Volume (ESV): blood volume remaining in ventricles after contraction. End-Diastolic Volume (EDV): blood volume in ventricles just prior to contraction Increasing EDV results in: Stretching of the myocardium ↑ ESU 4 contractility greater force , = Increases in the strength of the contraction Increased volume of blood ejected during systole  blood ejected ~ Stroke Volume (SV): volume of blood ejected from the left ventricle with heart contraction SV = EDV-ESU max blood in ventricles - blood left over Ejection fraction: ratio of SV to EDV T = SV EDU Preload: end-diastolic pressure ,extent which the heart chambers stretch when they fill with blood during diastole. stretch ventricle walls on e Afterload: resistance to the heart pumping blood into circulation (ventricular emptying) which increases workload for the heart. Ex, jelly donut. If artery is blocked (plague), less blood will be ejected as it would be hard for the blood to leave. Arteries: carry oxygenated blood away from the heart Thick-walled, elastic - blood flow is pulsatile Arterioles Smaller than arteries Major source of resistance Surrounded by smooth muscle Smooth muscles (precapillary sphincter) can change shape of vessel by vasodilation/ vasoconstriction Capillaries 7-10 micrometers (RBC pass one at a time) Site of gas exchange and nutrient exchange Greatest cross sectional area in vascular system (collective) Increased vasculature results in slower blood flow Slower blood flow passing muscle ensures good nutrient and gas exchange Venules Empty into veins Similar in size to arterioles Microcirculation = Venules + capillaries Veins: carry deoxygenated blood back to the heart Low resistance vessels Contain smooth muscle Distensible- can pool large volumes of blood One way valves prevent backward flow Venous Return: smaller veins empty into the sup/inf vena cava before returning to the heart Low blood pressure makes venous return difficult. One-way valves Muscle pump aids in venous return (needs movement) Vasoconstriction Why do people faint if they stand for a prolonged period of time? Muscle pump is taken away so blood pools therefore no blood is returns to the heart and brain. You lose consciousness as a protective function. compression socks on an airplane why people wear ~ Varicose Veins: blood pools in the vein, compression helps construct veins to prevent pooling. Blood Pressure: force exerted on blood vessel walls by blood Hypertensive: too high (diet, exercise, weight, age, ethnicity) 14098 Normotensive: normal 110 130 systolic to diastolic want to be 6 to 85 -> on lower end Hypotensive: too low -90/60 BP has no preliminary symptoms. Hypertension is often called the “silent killer” and is the leading cause of premature death in the world. More than 50 % with high will develop hypertension years normal BP lifestyle changes , not made within 4 if are. Untreated high blood pressure can also lead to: Heart attack Memory loss and dementia Stroke Arteriosclerosis Bison problems Heart disease Sexual dysfunction Kidney failure Uncontrollable risk factors: age, sex (males are higher at risk, family history Controllable risk factors: poor diet, lack of exercise, prolonged stress Even small reductions in BP can significantly I risks Hypertensive Treatment Options Lose excess weight For every 20lbs reduced Follow a DASH diet Lower diet vegetables fat rich in , Fruit and low-fat dairy Foods Daily physical activity 30 mins/day aerobic activity of Limit sodium No than 2400mg more Limit alcohol No than drinks (male) and more 2 drink (female) daily One BP = Cardic Output x Total Peripheral Resistance = SVXHR Systolic Blood Pressure (SBP): force that blood exerts on the arterial walls during ventricular systole (ventricular contraction) Estimates work of the heart Diastolic Blood Pressure (DBP): pressure exerted on the walls of the arteries during ventricular diastole (relaxation phase of the cardiac cycle) Estimates peripheral resistance - ease of blood flow from arterioles into capillaries Mean Arterial Pressure (MAP): the average force exerted by blood on arterial walls during an entire cardiac cycle. Spend more time in diastole MAP = DBP + 0. 33 SBP-DBP Blood Pressure is affected by: BP QX TPR = Peripheral resistance - Decreased heart rate Increased blood pressure Vessel elasticity Decreased cardiac output Increased cardiac output Blood volume Decreased blood pressure Increased heart rate Cardiac output (Q) resistance ↑ BP in peripheral = 3 Sources of Peripheral Resistance: 4th topower * Vessel diameter - ↑ resistance to Flow Narrow-more diameter = friction = ↑ resistance to Flow ; plague , vasoconstriction Blood viscosity ↑ viscosity ↑ ↑ thickness = resistance = ↑ resistance Blood , changes viscosity sweating ; Blood vessel length ↑ length ↑ = resistance Poiseuille’s Law: expresses relationship among pressure differential, resistance and flow. Pressure difference = high to low Length and viscosity remains somewhat constant, radius affects blood flow the most. Atherosclerosis: narrowing of the arteries Decreased diameter due to build up of plaque Both result in increased blood pressure Arteriosclerosis: hardening of the arteries Less elasticity to absorb the force of pulsitile flow If hardened cannot distend to absorb force so force bounces off Blood flows because of a pressure gradient (pressure differential). BP is highest in the aorta and arteries and lowest in the veins and right atrium of the heart. High to low Coronary Circulation: the heart itself needs its own blood supply coronary arteries branch off the aorta, just past the aortic valves 2 coronary arteries (R & L) - each branch into 2 more Coronary blood flow occurs mostly during diastole (relaxation) Blood returns to the right atrium via the coronary veins (coronary sinus (LV) & anterior cardiac vein (RV) Myocardial blood flow = 250ml/min (5% of Q) Coronary heart blockage: myocardial infarction aka heart attack is caused by thrombus (blood clot) Coronary O2 Consumption Muscle oxygen utilization a-vO2 difference: arterial-venous oxygen difference IsmO(() Comloron/ombo a Sm) Q: cardiac output ① 20-15 = 5m/ Muscle O2 utilization Resting 2 Consumption = a -vOz diff X Q 20-5 = 15 m/ muscle Myocardium will consume 70-80% of the O2 from the circulated blood. During exercise, coronary blood flow increases due to an increase in HR, increase in force of contraction and vasodilation. Myocardial oxygen consumption (work) can be calculated as Rate Pressure Product: j RPP = HRX SBP RPP correlates highly with myocardial O2 consumption. Rate pressure Heart rate x systolic blood pressure product CARDIOVASCULAR REGULATION & INTEGRATION Regulation of Heart Rate: heart maintains its own rhythm (autorhythmic) SA node: stimulus for heart action (“pacemaker”) Intrinsic rhythm high = 100 to allow blood from atria into 0 10 sec delay to pass SA node signal sent to both atria and AV node. Low HR down=low intrinsic rate. ventricles below AV node gives rise to the AV bundle (Bundle of His) AV node transmits signals via purkinje fibres to ventricle for contraction time ↑ NEDV ↑stretch ↑ contraction ↑ SV distribute blood filling = more ore , , , , , Slow down ↑ = in ventricular filling SA node → Atria → AV node → AV bundle (Bundle of His) → Left and Right Bundle Branches → Perkinje fibres (of the ventricles) Cardiovascular Control Centre: located in the medulla in the brain stem. Regulates: Heart’s outputs (SA and AV Node input) Flow via vasoconstriction vasodilation = Flow via Distribution of blood on the body (viscera, muscle, etc.) Vasomotor tone in active muscle (vasoconstriction, vasodilation) Autonomic Nervous System S Sympathetic Parasympathetic Catecholamine release Acetylcholine release (epinephrine & Leads to bradycardia norepinephrine) (HR