Blood Pressure Definition: Measurement of the force of the blood pushing against the aortic wall. Described as a fraction = Systolic = Force the blood exerts on the arteries when ejected from the left ventricles (systole) working phase Diastolic = Force in the arteries in the ventricles are relaxed during diastole CO = SV x HR BP = CO x PVR (this expresses the interaction of the 2 variables) BP = SV x HR x PVR Pulse Pressure = The difference between systolic and diastolic pressure Ex: 120/80 = Pulse Pressure = 40 Stroke Volume = the amount of blood from the heart with each heartbeat or contraction Determinants of BP: 1) Cardiac output (L/min) : Normal CO = 4-8 (L/min) - If CO inc. then BP inc. - Amount of the blood the heart (specifically the left ventricles pumping chamber), pumps in 1 minute - Is important because it predicts the oxygen delivering to cells 9 2) Peripheral vascular resistance: increases as the diameter of blood vessel By ↑ - If PVR inc. then BP inc. - Is the force that is opposing the blood flow, especially the arterial vessels - PVR inc. the pressure needed to push the blood - PVR inc. as the diameter of the vessel inc. 3) Volume of circulating blood - When volume inc. pressure is exerted 4) Viscosity : thickness of the blood - The thicker the blood, the higher the pressure 5) Elasticity of arterial walls * - Also known as the flexibility of the blood vessels - When the elasticity inc, the BP dec. - The more elastic the blood vessels the lower the blood pressure → pressure ⑧ T 6) Afterload: the pressure that the LV must exert to get the blood out of the heart during systole (↑PVR ≈↑ T t SV) T BP, ↓ afterload → ↑ - Systemic Vascular Resistance = the amount of the heart must overcome to open the aortic valve and push blood volume into the systemic circulation. - The PVR affects the afterload p volume 9 preload → 9 7) Preload: the volume of blood in the ventricles at the end of diastole (↑ ? SV, 9 ? BP) - When preload inc. the stoke volume dec. - End diastolic pressure : the amount of ventricular stretch at the end of diastole. The more volume in the ventricles, the more comes out. - When the pressure inc, the stroke volume inc. - When there is low cardiac output, this means that the body does not receive enough oxygen to the tissues - If more blood is pumped, the volume increases - Arteriole Sclerosis = thickening + hardening of the artery, the elasticity is decreased so the BP inc. BP Regulators (long term) - Receptors in the kidneys monitor disruption in homeostasis (mainly regulate blood volume) - Release in the response to the low fluid vol. + high serum osmolarity - Antidiuretic hormone (ADH): (also known as vasopressin) made in the hypothalamus, stored in the posterior pituitary gland 9 blood volume, ↑ 9 BP - Increases water absorption: ↑ 9 PVR, ↑ BP - Secondary function: Vasoconstriction → ↑ 99 - Renin-angiotensin-aldosterone (RAA) system : secreted from the kidney - Angiotensin II ( also a vasoconstrictor)= the active form, this stimulates the adrenal gland cortex to release aldosterone - Aldosterone: reabsorbs Na in the kidneys, water follows, excretes K → ↑ BP - ADH + RAA = activate when there is a decrease in blood volume - Low blood volume = low BP - In response to low blood volume that reaches the kidney, the glomerulus releases renin - Renin converts angiotensin 1, angiotensin concerting enzyme comes in and converts to Angiotensin II. - Short Term : receptors in the brain, heart , and blood vessels regulate short term BP & maintain homeostasis Lymphatic System : part of circulatory + immune system, due to their function. Organs such as Spleen and Tonsils, they have lymphocytes residing there. Spleen acts as a filter for blood. • Includes lymphatic vessels, lymph, lymph nodes, organs • Important part of the immune system • Lymph nodes = (stations that filter out bacteria + fight out bacteria/infection) , organs - Lymph,is extra fluid that was not pushed to the Venus end, flow of lymph is really slow - Push pressure - arterial end , osmotic pressure = Venus end • Lymphatic vessels transport lymph only in one direction (same as in veins) = they need valves, they prevent back flow • Lymph: clear fluid collected from fluid pushed out of the blood capillaries (~ 10%) → lymph vessels and lymph nodes → left and right lymphatic duct → Subclavian veins, back to venous system • Production/entering = removal (if not equal, it can lead to edema) • I removal → Edema 9 production and/or ↓ ↑ - Hydrostatic pressure ( water pushing pressure), is higher when it just came out of the heart. Pushing pressure is higher than osmotic pressure. Alterations In the Cardio Vascular System ( dec. cardiac output ) 1) Pericardial Effusion - Pericardial Sac = too much fluid in there so causes effusion - Pericardium = outer layer, this reduces friction which allows the membrane to glide with each heart beat - Fluid shift occurs b/c of the inflammatory process, so vasodilation occurs - Inc vascular permeability = causes fluid to flow more into the pericardial cavity • Accumulation of fluid in the pericardial sac, which contains (nl: ~ 50 ml) of fluid by the serious membrane • Cause: pericarditis, autoimmune disorders ( can both cause inflammation ) 9 pressure within the pericardial sac → heart compression •↑ • Effects as pericardial fluid increases: L cardiac output (CO) • ↑ 9 pressure in all cardiac chambers → ↓ L venous return due to atrial compression • ↓ • Large or uncontrolled pericardial effusion may progress to cardiac tamponade 2) Cardiac Tamponade - blockage • Clinical syndrome resulting from compression of the heart, b/c now too much fluid • Ventricles are unable to distend and fill → ↓ L CO • Clinical manifestation: •↓ 9 HR (tachycardia), distant heart sounds, chest pain L BP, ↑ • ↓arterial pressure: may be life-threatening → HF ( heart failure, b/c not pump enough blood) cardiogenic shock, death : • ↑ venous pressure = edema occur or jugular vein dissension - pressure in veins, blood accumulates in the veins • Management: • Treat the underlying cause (e.g., antibiotics) • Analgesics, O2 therapy, bed rest • Pericardiocentesis = puncture the sac + drain fluid 3) Valvular Disorders • Causes disruption of normal blood flow through the heart • Causes: congenital defects, endocarditis (inflammation of the endocardium), rheumatic fever (untreated staph infection), HTN, age-related • Stenosis: narrowing of the heart valves - Valves prevent back flow 9 • Blood moving through the valve ↓→ →9 ↑ chamber pressure, ↑ d backs up to the chamber just before the valve & ↓CO d workload, ↑ 9 O2 demand → hypertrophy, dilation → failure L CO, ↑ T after load, LV hypertrophy, pulmonary edema, b/c of lack of backup • Aortic valve stenosis: ↓ • Regurgitation: occurs when the valves do not completely close r O2 demand → hypertrophy, dilation → failure • Blood flows in both directions → ↓ r workload, ↑ t CO, ↑ • Management: valve repair, prosthetic replacement, which comes from a pig 4) Cardiomyopathy * • Heart muscle disease (usually occurs in the ventricles) → difficult to pump blood • Classification: dilated ( the most common ), hypertrophic, restrictive 1) Dilated: occurs when the ventricles become enlarged and weakened • Most common type • Inherited, CAD (coronary artery disease), MI (myocardial infarction = artery that supplied blood to heart, narrowing occurs here, which affects the systolic muscles), chronic HTN t myocardial contractility → ↓ 9 pulmonary pressure • Affects systolic function: ↓ d CO, ↑ I BP, ↑ • S/sx: fatigue, dyspnea, dizziness, activity intolerance, angina, weak pulse, cool/pale extremities, ↓ 9 HR, thrombi ( stagnation is occurring) , JVD, edema • Management: mainly supportive - symptom management , medication needed to dec. the work load + dec. fluid + inc. contractility - or transplant needed 2) Hypertrophic: abnormal thickening of the heart muscle • Causes: inherited, chronic HTN ( more work load the heart has to do ), valvular disorders, HF • Affects both systolic and diastolic function • Hypertrophied ventricle walls become stiff (so they do not contract or relax)→ unable to relax during diastole and contract L during systole → ↓CO, ↑ 9 pulmonary pressure • S/sx: similar to dilated cardiomyopathy • Management: mainly supportive 5) Heart Failure • - The ventricles are less efficient Causes: congenital heart defects, valvular disorders, MI (myocardial cells die + muscles get weaker which leads to heart failure) , HTN, cardiomyopathy • Usually considered a secondary disease , this means that it is caused by a pre existing heart disease. - Normal EF = 55-70% - < - 40% = Systolic HF t GFR -T ↑ BUN/Cr , ↓ • Classification: by cardiac phase (systolic HF = contraction (work phase), Diastolic = due to weakened cardiomyocytes , anatomically • Systolic HF: problems with contraction d pumping ability (= ejection fraction) t force of contraction & CO, ↓ • ↓ • Causes: CAD (coronary artery disease , MI, ? cardiomyopathy (dilated) • Diastolic HF: problem with diastolic = filling + resting phase • Not filling with enough blood → ↓ t CO & blood ejection (reserved EF) - less filling = less coming out (ejection) t compliance): HTN, AVS (active valve stenosis), hypertrophy (problem with filling), cardiomyopathy • Hypertrophy, stiffness (↓ • Mixed: systolic + diastolic HF HF : Compensation & Decompensation • t CO & BP ↓ Loss of cardiomyocyte function (cause) → ↓ d - cause of heart failure is MI in left ventricle • Compensation I. 9 contractility/SV, vasoconstriction = this lead to inc. CO + BP 9 HR, ↑ Activate SNS (sympathetic nervous system)(: ↑ 9 SV, Na ↑K↓ 9 t II. RAA activation (Renin) - sweat glands get activated (↑ 9 preload): ↑ - renin inc, in attempt to inc. fluid volume T contractility III. Ventricle hypertrophy: ↑ - inc. muscled mass to inc contractility T workload & O2 demand T CO temporarily → ↑ →↑ • T ↓ L contractility → blood backs up to pulmonary d CO (eGFR ↓ L , BUN/Cr ↑), Decompensation: heart weakens → left-sided HF, ↓ circulation → ↑ resistance in right ventricle → right-sided HF (total) : Anatomical Classification • Left-sided HF: decreased CO and Pulmonary congestion • Forward effects: fatigue, weakness, ↓urine output • Backup effects: Pulmonary congestion/edema •Right-sided HF: decreased CO and systemic congestion N - right side has to pump harder , pump directly to lungs - COPD = pulmonary + vascular changes occur lung - pumping back into system, the fluid in lower extremity is going back , urine output • Forward effects: fatigue, weakness, ↓ • Backup effects: systemic congestion (JVD, LE edema, wt gain, nocturia) • Cor pulmonale = “pulmonary heart disease” ( most common HF) prob w stlysfmimcanifistatdmfeah foot swelling
