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Cardiovascular system

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Human cardiovascular system
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Cardiovascular system

  1. 1. CARDIOVASCULAR SYSTEM Dr Jahanzaib Sheikh
  2. 2. Heart: Structure • It is divided into 4 chambers: (Two upper & Two lower) • The two upper chambers are called – Atria (Right & Left) • The two lower chambers are called – Ventricles (Right & Left) • The two atria are separated by the – Inter-Atrial Septum • The two ventricles are separated by the – Inter-Ventricular Septum • The atrium and ventricle communicate with each other via Atrioventricular orifice
  3. 3. Heart Acts as a pump and has 4 chambers. Upper two smaller chambers – Atrium Lower two larger chambers – Ventricles Volume of each chamber is the same Ventricles are larger due to thicker walls. Largest Chamber is the Left Ventricle which pumps blood all over the body. Thick wall between the Right and Left sides of heart – Septum. Blood -- Rt. Atrium -- Rt. Ventricle – Lungs -- Left Atrium -- Left Ventricle
  4. 4. Heart Interior Rt Atrium Rt Ventricle Lt Ventricle Lt Atrium Septum Heart is divided into 4 chambers where a muscular wall or Septum divides them
  5. 5. Circulatory System • Heart – Pumps blood • Arteries and arterioles – Carry blood away from heart • Capillaries – Exchange nutrients with tissues • Veins and venules – Carry blood toward heart
  6. 6. Heart Valves • Heart valves act as gates between the heart chambers • This orifice between atria and the ventricles is guarded by – A-V valve or the AtrioVentricular Valve • They allow blood to pass between – Heart chambers – From heart chambers to their blood vessels • They include the: – Tricuspid – Pulmonary – Bicuspid (or mitral) – Aortic valves
  7. 7. Aortic Valve Bicuspid Valve Pulmonary Valve Tricuspid Valve Heart Valves
  8. 8. Cardiac Cycle Sup Vena Cava brings deoxygenated blood from upper body to the heart Inf Vena Cava brings deoxygenated blood from lower body to the heart Pulmonary Artery takes deoxygenated blood to the lungs Pulmonary Veins brings oxygenated blood from lungs back to the Lt Atrium of the heart Aorta takes blood to body Blood from both veins is received by Rt Atrium and is pushed into the R Ventricle RA LA RV LV SVC IVC Aorta Pul A Blood enters L Ventricle from L Atrium and is then pumped into the Aorta
  9. 9. Cardiac Output - Q • Q = HR x SV or Q = (FH) (Vs) • Where: • Q = volume of blood pumped by left ventricle each minute (L.min) • FH = heart rate (b/min) • Vs = stroke volume (average volume of blood pumped per each contraction (L/b)
  10. 10. Cardiac Output • Range of normal at rest is 4 – 6 L.min • During aerobic activity the increase in cardiac output is roughly proportional to intensity. • Max. Q is in range of 20 – 40 L.min, depending on size, heredity, and conditioning.
  11. 11. Heart Rate • Range of normal at rest is 50 – 100 bpm • Increases in proportion to exercise intensity • Max. HR is 220 – age • Medications or upper body exercise may change normal response
  12. 12. Stroke Volume • Range of normal at rest is 60 – 100 ml/b • During exercise, SV increases quickly, reaching max. around 40% of VO2 max. • Max. SV is 120 – 200 ml/b, depending on size, heredity, and conditioning. • Increased SV during rhythmic aerobic exercise is due to complete filling of ventricles during diastole and/or complete emptying of ventricles during systole.
  13. 13. Coronary Circulation • Exclusive arterial blood supply to heart muscle and electrical conduction system originates from the aorta Aorta Lt Coronary A Lt Anterior Descending Br Rt Coronary A
  14. 14. Cardiac Cycle & Circulation L Atrium Aorta L Ventricle SVC 3. Capillary Bed 3. Arteriole4. Venule Pul V R Ventricle R Atrium IVC Pul A 2. Artery5. Vein Oxygenation Of blood in the lungs
  15. 15. Blood Vessels • Arteries • Arterioles • Veins • Venules • Capillaries
  16. 16. Major Arteries and Veins • Aorta • Pulmonary • Carotid • Femoral • Brachial • Radial • Superior vena cava • Inferior vena cava • Pulmonary • Jugular
  17. 17. Arterial Structure Outer most layer: Adventitia Made up of Collagen & Elastic fibres Middle layer: Media Made up of Smooth Muscle Cells Innermost layer: Intima Made up of Endothelial Cells Lumen: Hollow Blood: Cells & plasma etc Longitudnal section Cross Section *Higher the Arterial resistance Higher will be the Afterload
  18. 18. Arteries: Physiological Effect NORMAL STATE: (Results in) • Smooth blood flow • No risk of injury to artery VASOCONSTRICTION: (Results in) • Turbulent / fast blood flow • High internal pressure • High risk of injury to artery VASODILATATION: (Results in) • Slow blood flow • Low internal pressure • High risk for blood to escape circulation Artery Normal Lumen Dilated Lumen Narrow Lumen
  19. 19. Capillaries • Extremely narrow— 8-10 micrometer wide. • One-cell thick walls composed mostly of epithelium with a basement membrane • Total surface area in humans is 6,000 m2 • Capillary beds present throughout body • Oxygen and nutrients diffuse out of capillary into tissue fluid that surrounds cells • Wastes (CO2)diffuse into capillary • Heart and vessels of CV system can be thought of as means by which blood is conducted to and from capillaries • Each capillary bed has arteriovenous shunt
  20. 20. Veins • They arise from the organs • They carry deoxygenated blood – Exception: Pulmonary Vein which carries oxygenated blood • They return blood from the tissues back to the heart • They are thin walled vessels • They do not have muscular or elastic walls • They do not have the ability to: • Contract: Vasoconstriction • Dilate: Vasodilatation • They are helped by valves and skeletal muscles in returning blood back to the heart
  21. 21. Venous Structure Thin Venous Wall Valve prevent backflow of blood Valve allows blood to move forward
  22. 22. Veins: Venous Return B Contracting Skeletal muscle Applies pressure on vein and squeazes it to push blood up against gravity A Relaxed muscles allow Valves to close up and prevent the back flow of blood under the influence of gravity Gravity Gravity Gravity Higher the Venous Return Higher will be the Preload
  23. 23. Pulmonary and Systemic Circulations • Essentially two separate pumps: – Right Side • moves deoxygenated blood to the lungs for oxygenation – Left Side • moves oxygenated blood to the body • Which leads to two distinct circulatory systems: – Pulmonary • vessels to and from the lungs – Systemic • vessels to and from the rest of the body • Vessels that move blood away from the heart are called arteries and vessels that return blood to the heart are called veins.
  24. 24. Systemic Circulation • Each time the heart beats, a bolus (~ 80 mL) of blood is ejected from the left ventricle into the aorta (the largest artery). • Blood flows into the medium-sized arteries and arterioles (small muscular arteries) which branch off the aorta. • These vessels further subdivide into the capillaries (smallest blood vessels that carry oxygenated blood).
  25. 25. • SA Node is called the pacemaker • Keeps heartbeat regular • If SA node fails to work properly, heart still beat due to impulses generated by the AV node • However, beat is slower • To correct this situation, it is possible to implant an artificial pacemaker • Automatically gives an electrical stimulus to heart every 0.85 seconds Heart Conducting system
  26. 26. • SA node initiates heartbeat and automatically sends out an excitation impulse every 0.85 second • Causes atria to contract • When impulses reach AV node, there is a slight delay that allows atria to finish their contraction before ventricles begin their contraction Heart Conducting system
  27. 27. • Signal for ventricles to contract travels from AV node through two branches of AV bundle before reaching numerous and smaller Purkinje fibers. • The AV bundle, its branches, Purkinje fibers consist of specialized muscle fibers that efficiently cause ventricles to contract Heart Conducting system
  28. 28. Electrocardiogram (ECG) • The entire electrical event can be measured by the electrocardiogram (ECG).
  29. 29. Lipids- Dyslipidaemias
  30. 30. 32
  31. 31. 33
  32. 32. The story of lipids • Chylomicrons transport fats from the intestinal mucosa to the liver • In the liver, the chylomicrons release triglycerides and some cholesterol and become low-density lipoproteins (LDL). • LDL then carries fat and cholesterol to the body’s cells. • High-density lipoproteins (HDL) carry fat and cholesterol back to the liver for excretion.
  33. 33. The story of lipids (cont.) • When oxidized LDL cholesterol gets high, atheroma formation in the walls of arteries occurs, which causes atherosclerosis. • HDL cholesterol is able to go and remove cholesterol from the atheroma. • Atherogenic cholesterol → LDL, VLDL, IDL
  34. 34. Normal Arterial Wall Tunica adventitia Tunica media Tunica intima Endothelium Subendothelial connective tissue Internal elastic membrane Smooth muscle cells Elastic/collagen fibers External elastic membrane
  35. 35. Development of Atherosclerotic Plaques Normal Fatty streak Foam cells Lipid-rich plaque Lipid core Fibrous cap Thrombus
  36. 36. Atherosclerosis Timeline Stary et al. Circulation. 1995;92:1355-1374. Foam Cells Fatty Streak Intermediate Lesion Atheroma Fibrous Plaque Complicated Lesion/Rupture Endothelial Dysfunction From first decade From third decade From fourth decade Growth mainly by lipid accumulation Smooth muscle and collagen Thrombosis, hematoma
  37. 37. Atherosclerosis
  38. 38. Lumen Fibrous Cap Lipid Core Lipid Core Fibrous Cap Lumen Vulnerable Plaque Stable Plaque • Thick fibrous cap • Smooth muscle cells: more extracellular matrix • Lipid-poor plaque • Thin fibrous cap • Inflammatory cell infiltrates: proteolytic activity • Lipid-rich plaque Libby P. Circulation. 1995;91:2844-2850. Vulnerable vs Stable Atherosclerotic Plaques
  39. 39. Thrombosis Influences the Severity of a Cardiovascular Event Nonocclusive thrombus Occlusive thrombus • Unstable angina • Non—Q-wave MI • Q-wave MI • Sudden death • Minor plaque disruption • High flow • Low thrombotic tendency • Major plaque disruption • Low flow or vasospasm • Thrombotic tendency Kullo IJ, et al. Ann Intern Med. 1998;129:1050-1060. Factors favoring thrombosis:Factors limiting thrombosis:
  40. 40. Causes of Hyperlipidemia • Diet • Hypothyroidism • Nephrotic syndrome • Anorexia nervosa • Obstructive liver disease • Obesity • Diabetes mellitus • Pregnancy • Obstructive liver disease • Acute heaptitis • Systemic lupus erythematousus • AIDS (protease inhibitors)
  41. 41. Dietary sources of Cholesterol Type of Fat Main Source Effect on Cholesterol levels Monounsaturated Olives, olive oil, canola oil, peanut oil, cashews, almonds, peanuts and most other nuts; avocados Lowers LDL, Raises HDL Polyunsaturated Corn, soybean, safflower and cottonseed oil; fish Lowers LDL, Raises HDL Saturated Whole milk, butter, cheese, and ice cream; red meat; chocolate; coconuts, coconut milk, coconut oil , egg yolks, chicken skin Raises both LDL and HDL Trans Most margarines; vegetable shortening; partially hydrogenated vegetable oil; deep-fried chips; many fast foods; most commercial baked goods Raises LDL
  42. 42. Hereditary Causes of Hyperlipidemia • Familial Hypercholesterolemia • Codominant genetic disorder, coccurs in heterozygous form • Occurs in 1 in 500 individuals • Mutation in LDL receptor, resulting in elevated levels of LDL at birth and throughout life • High risk for atherosclerosis, tendon xanthomas (75% of patients), tuberous xanthomas and xanthelasmas of eyes. • Familial Combined Hyperlipidemia • Autosomal dominant • Increased secretions of VLDLs • Dysbetalipoproteinemia • Affects 1 in 10,000 • Results in apo E2, a binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL) • Increased risk for atherosclerosis, peripheral vascular disease • Tuberous xanthomas, striae palmaris
  43. 43. Hyperlipidaemias There are 6 types of hyperlipidemia which are differentiated by the type(s) of lipids that are elevated in the blood. Some of the types may be due to a primary disorder such as a familial hyperlipidemia, and some are due to secondary causes. Secondary causes of hyperlipidemia are related to diseases associated with hyperlipidemia, dietary risk factors, and drugs associated with hyperlipidemia.
  44. 44. Type I IIa IIb III IV V Lipids Cholesterol N, > >> >> N, >> N, > N, >> Triglycerides >> N >> N, >> >> >> Lipoproteins Chylomicrons >> N N N N >> VLDL N, > N, << << N, > >> >> ILDL >> LDL << >> >> >> N, < << HDL << N N N N, < << Treatment Diet Diet, Statins, Bile Acid Sequestrants, Nicoti nic Acid Diet, Statins, Bile Acid Sequestrants, Fibrates, Nicotinic Acid Diet, Fibrates, Nicotinic Acid Diet, Fibrates, Nicotinic Acid Diet, Fibrates, Nicotinic Acid
  45. 45. Lipid Parameter Function: Latest Commentary  VLDL Carries triglycerides to peripheral cells High levels may be associated with increased CHD risk2  LDL Carries cholesterol to cells High levels linked to increased CHD risk Primary target of cholesterol-reducing therapy3  HDL Removes cholesterol from cells High HDL considered protective against CHD HDL >60 mg/dL decreases CHD risk1  Lipoprotein(a) A complex of LDL and apolipoprotein(a) Prevents LDL from being taken up by the Liver Elevated Lp(a) is an independent risk factor for premature CHD4  Triglycerides A neutral fat stored in adipose cells Positively correlated with risk for CHD1
  46. 46. Clinical Manifestations of Atherosclerosis • Coronary heart disease – Stable angina, acute myocardial infarction, sudden death, unstable angina • Cerebrovascular disease – Stroke, TIAs • Peripheral arterial disease – Intermittent claudication, increased risk of death from heart attack and stroke American Heart Association, 2000.
  47. 47. Risk Factors for CHD • Modifiable – Dyslipidemia Raised LDL Low HDL Raised TGs – Smoking – Hypertension – Diabetes mellitus – Obesity – Dietary factors – Thrombogenic factors – Sedentary lifestyle Wood D, et al. Atherosclerosis. 1998;140:199-270. • Nonmodifiable – Age – Sex – Family history of premature CHD
  48. 48. DYSLIPIDEMIA (A consequence of abnormal lipoprotein metabolism) • Elevated Total Cholesterol (TC) • Elevated Low-density lipoproteins (LDL) • Elevated triglycerides (TG) • Decreased High-density lipoproteins (HDL)
  49. 49. PRIMARY DYSLIPIDEMIA ETIOLOGY • SINGLE OR MULTIPLE GENE MUTATION – RESULTING IN DISTURBANCE OF LDL, HDL AND TRIGYLCERIDE, PRODUCTION OR CLEARANCE. • Should be suspected in patients with – premature heart disease – family hx of atherosclerotic dx. – Or serum cholesterol level >240mg/dl. – Physical signs of hyperlipidemia.
  50. 50. SECONDARY DYSLIPIDEMIA (Most adult cases of dyslipidemia are secondary in nature in western civilizations) • Sedentary lifestyle • Excessive consumption of cholesterol – saturated fats and trans-fatty acids.
  51. 51. Secondary Dyslipidemia (Medical Conditions Associated with dyslipidemia) • Diabetes • Hypothyroidism • Cholestatic liver disease. • Nephrotic syndrome • cigarette smoking
  52. 52. SECONDARY DYSLIPIDEMIA (Drugs causing mild to moderate degrees of dyslipidemia) • Beta-blockers • Thiazide diuretics • Antiretroviral drugs • Hormonal agents
  53. 53. Why Do We Care? According to the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Cholesterol in Adults (NCEP ATP-III): High LDL levels are a leading cause of coronary heart disease (CHD) and should be the main target of any cholesterol lowering regimen
  54. 54. Checking lipids • Nonfasting lipid panel • measures HDL and total cholesterol • Fasting lipid panel • Measures HDL, total cholesterol and triglycerides • LDL cholesterol is calculated: – LDL cholesterol = total cholesterol – (HDL + triglycerides/5)
  55. 55. LDL Cholesterol • Remains the cornerstone of dyslipidemia therapy1 • Strongly associated with atherosclerosis and CHD events1 • 10% increase results in a 20% increase in CHD risk1 • Most patients with elevated LDL untreated – Only 4.5 million out of 28.4 million treated2,3 1. Wood D et al. Atherosclerosis. 1998;140:199-270. 2. National Centre for Health Statistics. National Health and Nutrition Examination Survey (III), 1994. 3. Jacobson TA, et al. Arch Intern Med. 2000;160:1361-1369.
  56. 56. HDL Cholesterol • Low HDL cholesterol is a strong independent predictor of CHD1 • The lower the HDL cholesterol level the higher the risk for atherosclerosis and CHD2 • Low HDL is defined categorically as a level < 40 mg/dL (a change from < 35 mg/dL in ATP II)1 • HDL cholesterol tends to be low when triglycerides are high2 1. NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497. 2. Wood D, et al. Atherosclerosis. 1998;140:199-270.
  57. 57. Triglycerides • Recent data suggest that elevated triglycerides are an independent risk factor for CHD • Normal triglyceride levels: < 150 mg/dL • Borderline-high triglycerides: 150 to 199 mg/dL • High triglycerides: 200 to 499 mg/dL • Very high triglycerides: ( 500 mg/dL) increase pancreatitis risk – Initial aim of therapy is prevention of acute pancreatitis NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.
  58. 58. Non-HDL Cholesterol • Non-HDL Cholesterol = TC – HDL Cholesterol1 • Secondary target of therapy when serum TG 200 mg/dL1 • New non-HDL-C goal for patients with elevated TG is LDL-C goal + 30 mg/dL1 • Non-HDL-C includes all atherogenic lipoprotein particles including LDL-C, Lp(a), IDL-C, and VLDL-C2 1. NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497. 2. Cui Y, et al. Arch Intern Med. 2001;161:1413-1419.
  59. 59. National Cholesterol Education Program, Adult Treatment Panel III (NCEP ATP III) • The National Cholesterol Education Program’s updated clinical guidelines for cholesterol testing and management announced in May 2001 • Establishes goals for patients with varying levels of risk • ATP III builds on previous ATP reports and expands the indications for intensive cholesterol- lowering therapy NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.
  60. 60. New Concepts for ATP III Modified Risk Factor Assessment • Inclusion of more patients in the high-risk category (greater focus on diabetes, noncoronary atherosclerosis, multiple risk factors) • Incorporation of global risk assessment in the guidelines • Complete fasting lipoprotein profile recommended • Definition of low HDL-C is now < 40 mg/dL for males and females • Triglyceride cut points lowered from 200 mg/dL to 150 mg/dL NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.
  61. 61. New Concepts for ATP III (cont) Modified Treatment Guidelines • LDL-C < 100 mg/dL identified as optimal • LDL-C goal of < 100 mg/dL expanded to include CHD patients and those with CHD risk equivalent NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.
  62. 62. New Concepts for ATP III (cont) More Intensive Lifestyle Intervention: Therapeutic Lifestyle Changes (TLC) • Therapeutic diet lowers saturated fat (< 7% of total calories) and cholesterol (< 200 mg/d) intakes to levels of previous Step II diet • Adds dietary options to enhance LDL-C lowering – Plant stanols/sterols (2 g/d) – Viscous (soluble) fiber (10-25 g/d) • Increased emphasis on weight management and physical activity NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.
  63. 63. LDL Cholesterol Goals for Therapeutic Lifestyle Changes (TLC) and Drug Therapy According to NCEP ATP III Risk Category LDL-C Goal (mg/dL) LDL-C Level for Initiation of TLC (mg/dL) LDL-C Level for Consideration of Drug Therapy (mg/dL) CHD or CHD Risk Equivalents (10-y risk > 20%) 2 + Risk Factors (10-y risk 20%) 0-1 Risk Factor < 100 < 130 < 160 100 130 160 130 (100-129: drug optional) 10-y risk 10%-20%: 130 10-y risk < 10%: 160 190 (160-189: LDL-C-lowering drug optional) NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.
  64. 64. Advanced Lipid Analysis: Size Does Matter
  65. 65. LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Different Risk Categories Risk Category LDL Goal (mg/dL) LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) (mg/dL) LDL Level at Which to Consider Drug Therapy (mg/dL) CHD or CHD Risk Equivalents (10-year risk >20%) <100 100 130 (100–129: drug optional) 2+ Risk Factors (10-year risk 20%) <130 130 10-year risk 10– 20%: 130 10-year risk <10%: 160 0–1 Risk Factor <160 160 190 (160–189: LDL- lowering drug optional)
  66. 66. LDL Cholesterol Goal and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Patients with CHD and CHD Risk Equivalents (10-Year Risk >20%) 130 mg/dL (100–129 mg/dL: drug optional) 100 mg/dL<100 mg/dL LDL Level at Which to Consider Drug Therapy LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) LDL Goal
  67. 67. LDL Cholesterol Goal and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Patients with Multiple Risk Factors (10-Year Risk 20%) LDL Goal LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) LDL Level at Which to Consider Drug Therapy <130 mg/dL 130 mg/dL 10-year risk 10– 20%: 130 mg/dL 10-year risk <10%: 160 mg/dL
  68. 68. LDL Cholesterol Goal and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Patients with 0–1 Risk Factor 190 mg/dL (160–189 mg/dL: LDL-lowering drug optional) 160 mg/dL<160 mg/dL LDL Level at Which to Consider Drug Therapy LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC)LDL Goal
  69. 69. THANK YOU