Introduction to the Cardiovascular System PDF

Summary

This document provides an introduction to the cardiovascular system. It covers vascular aspects, circulation, function of blood, relevant biological topics, and related concepts. The document is intended for educational purposes, possibly for an undergraduate level class.

Full Transcript

Introduction to the cardiovascular system Vascular aspects Circulation refers to movement in a circle, circular motion or course, movement around or about, orderly movement in a circuit Function of blood and circulation:...

Introduction to the cardiovascular system Vascular aspects Circulation refers to movement in a circle, circular motion or course, movement around or about, orderly movement in a circuit Function of blood and circulation: Circulates oxygen and removes carbon dioxide Provides cells with nutrients Removes the waste products of metabolism to the excretory organs for disposal Protects the body against disease and infection Clotting stops bleeding after injury Transports hormones to target cells and organs Helps regulate body temperature Introduction to the cardiovascular system 1 Introduction to the cardiovascular system 2 Introduction to the cardiovascular system 3 In laminar flow, the fluid travels in parallel layers, with no disruption between the layers The fluid in the centre of the tube moves fastest, while the fluid near the edges moves slower due to friction Flow rate is proportional to the fourth power of the radius This means that even small changes in radius of the tube can have a large effect on flow. Larger radius = significantly more flow Flow rate is inversely proportional to viscosity Higher viscosity (thicker fluid) will reduce flow, but the effect is smaller compared to changes in radius While Poiseuille’s law is useful for understanding fluid flow in tubes, it is not perfect for predicting blood flow in the body because blood vessels are not rigid, and blood is not a simple fluid (it contains cells, and the vessel walls can expand and contract). Introduction to the cardiovascular system 4 Introduction to the cardiovascular system 5 Introduction to the cardiovascular system 6 Elastic tissues within the elastic arteries allow continuous flow & prevent damage They are the most abundant tissue in elastic arteries Muscular Tone playing roles in regulating the circulation & regional flow Walls of the smaller arteries, arterioles - more muscular (less elastin) than aorta Introduction to the cardiovascular system 7 Vascular smooth muscle - always has basal vascular tone at systemic level - altering blood pressure - ‘resistance vessels’ at local level - modulate local blood flow (arterioles, pre-capillary sphincter) Systemic and local regulators respond to Vasoconstriction ← 1-adrenergic (AR), AngII, Endothelin and other circulating mediators Vasodilation ← B2-AR and parasympathetic nerves and Histamine, NO and prostglandins PGE2 and prostacyclin Local paracrine effects Stretch itself - myogenic response local chemicals especially -interstitial pO2 ⬇, pCO2 ⬆, pH ⬇ → vasodilate (opposite to pulmonary) but also [K+], lactate, ATP/ADP/adenosine (including via P2YR, A2R) Veins can collapse while arteries remain spring open. The valves in the veins support against gravity Their ability to collapse and expand allows the venous system to accommodate varying blood volumes without causing significant changes in blood pressure. When there is a need to redistribute blood, veins can constrict or expand accordingly Introduction to the cardiovascular system 8 Arteries and veins respond very differently to changing volume Introduction to the cardiovascular system 9 Introduction to the cardiovascular system 10 Continuous Capillaries: Tight junctions, low permeability, found in most tissues. Fenestrated Capillaries: Pores for increased permeability, found in kidneys and intestines. Allow for a larger volume Sinusoidal Capillaries: Large openings, very permeable, found in the liver and spleen. Oxygen & Nutrient delivery The lymphatic system is a low pressure system with valves Introduction to the cardiovascular system 11 Oedema Caused by a higher hydrostatic pressure and a lower oncotic pressure. Higher hydrostatic pressure → to interstitium Caused by heart failure venous obstruction incompetence in valves in veins Lower oncotic pressure - returning to circulation Caused by Protein tlosing (nephrotic, protein losing enteropathy) protein synthesis less - hepatic disease / failure malnutrition, acute illness Increased capillary permeability Lymphatic dysfunction The interstitial fluid moves with gravity Introduction to the cardiovascular system 12 Swelling of ankles, standing, increasingly when standing / sitting sacral oedema - when in bed, overnight - easier to miss pulmonary oedema in pulmonary circulation worse lying flat - orthopnoea, paroxysmal nocturnal dyspnoea (PND) Specialised parts of the circulation Kidney → excretion, autoregulation Gut → liver (2 blood supplies) CNS → autoregulation, blood brain barrier → CSF Fetal circulation + Change at birth Introduction to the cardiovascular system 13 Introduction to the cardiovascular system 14 Cardiac cycle 1. Atrial filling rapid ventricular filling 2. Further slower passive. Ventricular filling (diastasis) 3. Atrial systole 4. Ventricular systole: Flow → Arteries Introduction to the cardiovascular system 15 Cardiac cycle 4 phases: 1-3 diastol, 4 = ventricular systolic A-D points of opening/shutting of A-V, semilunar valves. A-B = inflow→ ventricular filling, B-C = isovolumetric contraction, C-D = outflow→ ventricular ejection, D-A isovolumetric relaxation Introduction to the cardiovascular system 16 CO = SV x HR CO will match venous return (in = out) VR = preload to the cardiac pump Preload = LVEDP Left Ventricle Pre-contraction load Venous return Amount of blood entering ventricle in diastole determines the LV filling → preload (and CO) Preload affected by venous capacitance (sympathetic NS effects) venous filling (plasma volume and ECF regulation) Heart failure results in: venous return less efficiently cleared preload may rise and usually boost CO if there is a limited cardiac function reserve to respond, venous backpressure may lead to oedema Introduction to the cardiovascular system 17 Frank-Starling Mechanism Frank-starling mechanism is important in: ensuring the heart can deal with wide variations in venous return balancing the outputs of the two sides of the heart Also a separate intrinsic rate-induced regulation - allows increased cardiac forces to develop at higher heart rate largely via changes muscle Ca2+ dynamics + sensitivity Extrinsic influences on the heart Autonomic Nervous System Both PNS (vagus) and SNS - at rest PNS tone seems greater complete block of both HR → 100 Both can affect heart rate and contractility (PNS slows, SNS speeds) Introduction to the cardiovascular system 18 Reflexes Baroreceptors Others - Chemoreceptor, Brainbridge (Volume load), respiration effects Circulating factors Adrenal Medulla Atrial Natriuretic Peptide Other hormones Co-ordinated responses To exercise, serious changes in haemodynamics (eg haemorrhage) CO = ABP/TPR CO, cardiac output ABP: arterial blood pressure TPR: Total Peripheral Resistance TPR Largely due to vascular tone / damage in resistance arterioles Key determinant of afterload (and so affects ABP + CO) Increased TPR → Increased Afterload → Increased ABP for same CO Afterload is the LV myocardial wall load (wall stress/pressure) during systolic ejection of stroke volume Afterload is affected by Factors affecting resistance vessel tone autonomic control, circulating hormones Local factors including vascular damage or hindrance to LV outflow eg aortic valve opening restricted (aortic stenosis) Introduction to the cardiovascular system 19 In heart failure - maladaption Reducing cardiac function → homeostatic mechanism to restore CO + ABP may lead to neuroendocrine activation - can exacerbate heart failure Renin-AngII prevents the blood pressure from becoming too low It does this through boosting Na and water retention, as well as vasoconstriction A preload and afterload that increases too much may lead to heart failure Beta blockers help to slow the heart rate down Introduction to the cardiovascular system 20 Vicious cycle of Heart Failure Introduction to the cardiovascular system 21 Uptake of oxygen in Lungs - pulmonary arterioles / small arteries dilate with increased pO2 (decreased pH and increased CO2) Delivery of oxygen to tissues - systemic arterioles / small arteries dilate with decreased pO2, decreased pH and increased CO2 In the longer term, new vessels form in response to same stimuli to meet demand. Systemic mechanisms respond to optimise oxygen delivery / CO2 clearance The baroreceptor reflex is required to maintain a good cardiac output / blood pressure Risk factors for Atherosclerosis and coronary heart disease: Hypertension Hyperglycaemia Lifestyle risk factors (smoking, poor diet, poor sleep) Genetics (eg family history of cardiovascular disease) Introduction to the cardiovascular system 22 Poor fitness Obesity Insulin resistance Kidney disease Dyslipidaemia Types of heart disease Coronary artery disease Aneurysm Valve disease Cardiac arrhythmia Heart failure Cardiomyopathy Perciarditis Introduction to the cardiovascular system 23 Introduction to the cardiovascular system 24 Introduction to the cardiovascular system 25

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