CVS Revision PDF

WEEK WEEK 2 – ISCHAEMIC HEART DISEASE LO1 Explain the basic embryology of the heart and X. Septation of atria, ventricles 5. Ductus venosus becomes the the fetal circulation. and vessels ligamentum venosum...

WEEK WEEK 2 – ISCHAEMIC HEART DISEASE LO1 Explain the basic embryology of the heart and X. Septation of atria, ventricles 5. Ductus venosus becomes the the fetal circulation. and vessels ligamentum venosum 6. Ductus arteriosus becomes the Basic embryology : STAGE 5 : Development of Heart ligamentum arteriosum STAGE 1 : Formation of the heart Valves XI. AV valves – form from LO 2 Describe the macroscopical structure fields ( day 18) and characteristics of the heart, conduction I. Heart starts to form mesoderm endocardial cushions system (middle layer of the embryo) XII. Semilunar valves – swellings in II. Mesoderm then forms both the truncus arteriosus that RA : primary and secondary heart reshape into thin, cusp-like 1. SINUS VENOSUS field. structures Smooth wall, embryological III. Primary heart field = atria (left remnant and right) and left ventricles Fetal circulation : 2. CHRISTA TERMINALIS IV. Secondary heart field = right Junction between pectinate muscle Before birth.. ventricle, PA and aorta and smooth wall 3. SAN 1. Blood leaves placenta via the STAGE 2 : Formation of the heart Located near the SVC umbilical vein (80% of this is tube (day 21) Junction of christa terminalis saturated with o2) V. Primary and secondary heart 4. AVN 2. Half to fetal liver fields fold and fuse in the Triangle of Koch 3. Other half is diverted into the IVC midline to form a single heart 5. EUSTACHIAN VALVE via the ductus venosus (plus poorly tube Directs the oxygenated blood in the 02 saturated blood) VI. Specific sections from top to foetus into FO 4. Resulting in 67% O2 saturated bottom: mixture a. TRUCTUS ARTERIOSUS (aorta 5. Blood empties into the RA and PA) MUSCLES OF THE HEART 6. RA – LA (Foramen ovale) b. BULBUS CORDIS (RV) 7. LV Ventricles.. c. PRIMITIVE VENTRICLE (LV) 8. LV – Systemic circulation 1. CHORDAE TENDINAE d. PRIMITIVE ATRIUM (parts of 9. Another portion of blood : PA (via a. Attach to the valves and both atrias) the ductus arteriosus) papillary muscle e. SINUS VENOSUS (RA and 10. PA – Aorta 2. PAPILLARY MUSCLE Coronary sinus) 11. Descending Aorta – common and a. RIGHT – 3x Papillary muscle , internal iliac arteries – 2x umbilical prevents blood flow from STAGE 3: Looping of the heart arteries RV to RA tube (day 23-28) 12. Goes back to fetus b. LEFT – 2x papillary muscle, VII. Straight heart tube begins to prevents blood flow from fold and loop After birth.. LV to LA VIII. Essential for the heart to 1. Pulmonary vascular pressure 3. TRABECULAR TENDINAE takes its final shape falls below systemic pressure a. Internal wall surfaces of IX. Tube loops in a rightward 2. Pulmonary vasodilation both ventricles of the fashion 3. RA pressure drops! heart 4. Foramen ovale becomes fossa b. More abundant in LV STAGE 4 : SEPTATION : Formation ovalis of chambers  Atriums.. 2. LCA originates from left aortic 1. PECTINATE MUSCLE sinus - Exterior surface of the atrium - LAD – Anterior part of the IV Septum - Stretch and increase SA and thus (2/3), anterior wall of LV, Apex of atrial volume the heart 2. CHORDAE TENDINAE - LCX – wraps around the LA to supply - ONLY IN RA!!! the lateral and posterior wall of - Runs perpendicular to the pectinate the LV muscle o Left marg – LV LAD – Most common occluded artery CORONARY VEINS : 1. Great – LAD 2. Middle – PDA 3. Small – RCA CONDUCTION SYSTEM OF THE HEART 1. SA node (primary pace maker, -each phase represents how volume of blood in regulated by vagus nerve) the LV changes relative to the pressure within depolarises the ventricle (week 1 for more detail) 2. Travels to the AV node (located at the triangle of Koch, secondary 1. ISOVOLUMETRIC CONTRACTION pacemaker, causes 2. EJECTION atrioventricular delay) 3. ISOVOLUMETRIC RELAXATION 4. FILLING 3. Bundle of His (distal to AV node just next to Tricuspid valve) Preload – amount of blood in the ventricle 4. Purkinje fibres (runs through the LO 4 Describe the normal cardiac cycle including Increased preload, increased EDV, Increased SV heart endocardium of the entire pressure-volume loops. (because increased contractility and CO), No ventricle, tertiary pacemaker) LO 3 Describe the coronary arterial and venous anatomy and the usual pattern of regional coronary supply to the myocardium. 1. RCA originates from right aortic sinus - Right Marginal Artery – RV - PDA –Posterior IV septum (1/3) and part of RV (2/3) - SA Node (60% of people) change to ESV, Increased afterload. - AV Node (80% of people)  LO 6 Discuss the pharmacology of anti-platelet LO 7 Discuss the pathology of coronary agents, nitro-vasodilators, heparin, low atherosclerosis, coronary thrombosis and acute Afterload – pressure against which the heart is molecular weight heparin and thrombolytics. coronary syndromes (unstable angina, non-ST pumping (resistance) elevation myocardial infarction, ST elevation Increased afterload, increase pressure in ANTICOAG’S myocardial infarction). 1. HEPARIN - Acts on antithrombin 3 to increase its Atherosclerosis – narrowing and hardening of binding affinity to factors 2a and 10a to arterial vessels due to accumulation of plaque inhibit their actions 2. FACTOR 10A INHIBITORS (DOACs) 1. Chronic stress of endothelium (e.g. HTN) - Inhibit factor 10a and activation of 2a 2. Endothelial dysfunction - Cannot be reversed 3. Invasion of inflammatory cells 3. DIRECT THROMBIN INHIBITORS (macrophages and lymphocytes) through - Inhibit 2a formation the disrupted endothelial barrier - Dabigatran can be reversed 4. Adhesion of platelets to the damaged 4. WARFARIN vessel wall 5. Platelet derived growth factor and ventricle needed to overcome resistance, ejection - Inhibit Vit-k reductase cytokines are released. occurs at a higher pressure, aortic valve closes - No reduced vit-k 6. PDGF stimulates migration and earlier. No change to EDV, reduced SV, Increased - No activation of factors 2,7,9,10 proliferation of Smooth muscle cell in ESV tunica media and mediate differentiation ANTIPLATELET of fibroblasts – MYOFIBROBLAST LO 5 Describe the causes of angina, cardiac pain 1. ASPIRIN 7. Inflammation of the Bessel wall pathways, pain pattern of referred cardiac pain - Irreversible inhibition of COX-1 pathway 8. Macrophages and smooth muscle cells and the treatment for relief of angina pain. - Stops production of thromboxane A2 ingest cholesterol from oxidized LDL - TXA2 stimulates platelet aggregation 9. Transformed it into foam cells ANGINA 2. P2Y12 INHIBITORS 10. Foam cells accumulate - Chest pain due to reduced blood flow to - P2Y12 allows platelet aggregation to 11. Form fatty streaks the heart (MI) occur 12. ECM produced called atheroma (by SMCs - Caused by an imbalance between 3. GP 2b/3a Antagonists and lipid laden macrophages) coronary blood supply and oxygen - GP 2b/3a is a GP that sits on the platelet 13. Inflammatory cells in the atheroma demand surface which eventually allows secret matrix metalloproteinases - Symptoms : platelet aggregation 14. Causes weaking of the fibrous cap due to o Chest pain that may radiate to - The antagonists binds to the breakdown of the ECM – any minor stress left arm, jaw, neck, back, glycoprotein to stop platelet can rupture the fibrous cap epigastrium aggregation 15. Calcification of the intiama 16. ACUTE – plaque ruptures and exposes STABLE ANGINA UNSTABLE ANGINA THROMBOLYTICS thrombogenic material Occurs after 70% of Unexpected chest pain - Carries a very high risk of bleeding and major coronary BV occurs after a plaque has been occluded rupture generally reserved for lysis of clots in ACUTE CORONARY SYNDROMES Better with rest Even occurs during acute MI or stroke when surgical 20mins ECG – possible ST NITRATES depression/ T wave - GTN, dinitrate Primary cause: inversion ATHEROSCHLEROSIS - Metabolised to release NO - Activates Primary cause: protein kinase – Smooth muscle ATHEROSCHLEROSIS relaxation – vasodilation - Dilate veins – decrease preload - Dilate arteries – decrease afterload  identify changes 3. U WAVES STABLE ANGINA - Represent repolarisation of the purkinje - Stable atherosclerotic plaque 1. P WAVE fibres - Angina resolves at rest - Atrial contraction – atrial 4. ST SEGMENT depolarisation - Intervals between ventricular 2. Q WAVE UNSTABLE ANGINA - Normal left-to-right depolarisation of - Existing plaque ruptures the IV septurm - Thrombus forms around the rupture 3. R WAVE - Causing a partial occlusion - First upward deflection - Angina occurs at rest - Represents early ventricular - ST depression depolarisaiton 4. QRS WAVE - Ventricular contraction (depolarisation) N-STEMI - Ventricles contracting shortly after - Plaque ruptures the peak of R wave - Partial occlusion severe enough to 5. T WAVE cause infarction to the sub-endocarium - Ventricular repolarisation - Subendocaridal infarc - ST depression depolarization and repolarization STEMI - Plaque ruptures 1. Leads 2,3, avF – Inferior wall of the heart - Complete occlusion (right coronary artery) - Severe enough to cause a transmural 2. Leads V1- V2 – Septal view, views the IV infarction septum (LAD) 3. Leads V3 – V4 – Anterior view, views the - ST ELEVATION!!! anterior wall of the LV (LAD) 4. Leads 1, avL, V5, V6 – Lateral wall of the heart (left circumflex artery) LO 8 Discuss the differential diagnoses of patients presenting with acute dyspnea or chest pain. LO 10 Outline the epidemiology of coronary artery LO9 Describe the normal electrocardiogram and disease and myocardial infarct in relation to risk factors. LO 11 Calculate drug dosages for application.  1g – 1000mg  1mg – 1000micrograms (mcg or ug) 1. PR INTERVAL  1 microgram – 10000nanogram - Reflects conduction through the AV node LO 12 Define the pathology of myocardial infarct. 2. QT INTERVAL - Time required for the ventricles to 1. PARTIAL CORONARY ARTERY OCCLUSION undergo a single cycle of depolarisation - Decreased myocardial blood flow and repolarisation - Supply-demand mismatch - Myocardial ischaemia - Usually affects the inner layer of the myocardium (subendocardial infarction) - Unstable Angina, NSTEMI 2. COMPLETE CORONARY ARTERY OCCLUSION - Impaired myocardial blood flow - Sudden death of myocardial cells - Transmural infarction - STEMI 3. ST ELEVATION = IRREVERISBLE INFARCTION - Benefits of PCI decreases with each hour patient is out of the hospital WEEK 3 – HYPERTENSION AND VASCULAR oedema 1. Increased sympathetic constriction 2. Increased rate and depth of SYSTEM breathing LO 3 Explain factors that determine blood flow and blood pressure including the range of RAAS LO 1 Describe the anatomical and histological 'normal' blood pressure values. structure of blood vessels. - BP = CO X TPR INNERMOST TO OUTERMOST : - CO = HR X SV - BP = HR X SV X TPR 1. TUNICA INTIMA - Thin inner layer. LO 4 Explain the physiological control of normal - Endothelial cell monolater supported BP; acute and long term. by connective tissue - Endothelial cells lining the vascular lumen are sealed by tight junctions. CVS is externally regulated by autonomic - Endothelial cells have a crucial role in reflexes. These works closely with the RAAS and controlling vascular permeability, ADH systems. ANP/BNP vasoconstriction, homeostasis and - Vasodilation, Decreased renin angiogenesis - Thicker in larger arteries CVS refluxes involve… 2. INTERNAL ELASTIC LAMINA 1. Afferent nerves sense a change and - ELASTIN communicate this to the brain 3. TUNICA MEDIA 2. Processes the information - Middle layer 3. Implements appropriate response - Smooth muscle cells are embedded in the 4. Altering the activity of efferent ECM composed mainly of collagen. nerves 4. EXTERNAL ELASTIC LAMINA 5. TUNICA EXTERNA/ ADVENTITIA - Collagenous tissue supporting the BARORECEPTOR (mechanoreceptor) REFLEX – fibroblast and nerves short term 1. Found in the carotid sinus and the aortic arch LO 2 Discuss the changes in the heart and changes 2. They sense a stretch in the wall in the limbs that cause oedema in limbs and 3. Low BP, shortness of breath. 4. Increased afferent signals to the CNS 5. Efferent activity from CNS HYDROSTATIC PRESSURE – 6. Increased vagal drive pressure that drives water out of the capillaries 7. Decreased sympathetic drive - Decrease BP 8. Increased heart rate and contractility COLLOID OSMOTIC PRESSURE – pressure that draws water into the capillaries 2 types of baroreceptor : 1. A fibres – larger, myelinated axons and are activated over lower 1. Discuss the pharmacology of major OEDEMA – levels of pressure classes of anti-hypertensive drugs, High capillary hydrostatic pressure leading to 2. C fibres – small, unmyelinated axons including: β-adrenergic receptor fluid build-up in tissue regions and are activated over higher antagonists; ACE inhibitors; Angiotensin levels of pressure receptor antagonists; Thiazide diuretics; Calcium channel blockers; and α- LEFT HEART FAILURE RIGHT HEART FAILURE CHEMORECEPTORS REFLEX – short term adrenergic receptor antagonists. Blood not ejected Decreased function of Activated by hypoxia, hypocapnia and properly, right heart leads to acidosis leading to a backup of backup of blood in the Located in the aortic and carotid bodies LO 6 Compare and contrast essential and blood in pulmonary systemic circulation secondary hypertension and the mechanisms circulation, Leads to.. underlying their current therapy. causes pulmonary  HYPERTENSION = Persistent BP more than or SECONDARY HTN satans) Decrease preload and after load equal 140mm Hg CALCIUM First line. - Primary HTN = HTN with no identifiable CHANNEL Binds to and block calcium cause 1. Cushings syndrome – rare endocrine BLOCKERS channels on vascular smooth - Secondary HTN = HTN caused by underlying disorder that the body is exposed to (-dipine) muscle cell condition great amounts of cortisol for a long Causes vasodilation and time decreases BP Dihydropyridines have been shown to be especially effective in the elderly and are safe in the pregnancy THIAZIDE First line DIURETICS Inhibition of Na/Cl cotransporter Decrease Na/Cl reabsorption Decrease water reabsorption Decreases BP Vasodilation properties when given in low doses No for pts with gout BETA Second line BLOCKERS Blocks b1 and b2 receptors in the 2. Hyperaldosteronism – LOTS OF (-olol) heart peripheral vasculature ALDOSTERONE (bronchi, pancreas, uterus, brain 3. Aortic Coarctation – narrowing of aorta, etc) Decrease cardiac HTN SUBTYPES : harder for blood to get pumped out contractility 4. Pheochromocytoma – rare tumour Decrease HR, CO growing on top of the adrenal gland BB also binds to beat receptors in WHITE COAT HTN MASKED HTN the JG complex= decrease renin, Elevated bp readings Normal bp readings in decrease RAAS in a clinical setting a clinical setting but Effects of HTN but normal readings consistently elevate when measured d reading when No for pts with beta blockers elsewhere measure elsewhere 1. CEREBROVASCULAR DISEASE ALPHA Second line. a. Stroke BLOCKERS Causes vasodilation by inhibiting 2. VASCULAR DISEASE constriction of arteries by NA In-office – a. Coronary artery disease 140/90 and up – 160/100 3. LEFT VENTRICULAR HYPERTROPHY STEPPED TREATMENT (if no use, go to next step Out of office – 130/80 1. ACE I or ARB (white, >> the acute SYMPTOMS Angina asymptomatic for systemic venous congestion increase in (exertional) years volume and LV LA pressure Dyspnoea EDP rises rises rapidly (exertional) - Dyspnoea - Fatigue LV EDP causes PV pressure - Palpiatio the early increases ns closure of - RHF REGURGITATION – the mitral valve Pulmoary - PND oedema - Orthopno ea  Valve does not close properly so most of the blood moves back Resulting in - Haemopty CHRONIC :-  ‘Forward failure’ – less blood flow into inadequate LV sis the net chamber filling, CVS  ‘Backward failure’ – too much blood collapse! Dilation and AUSCULTATION Crescendo- Decrescendo pooling behind causing an increased in hypertrophy of FINDINGS * decrescend pressure, stretch and congestion the LV CHRONIC :- o AORTIC MITRAL LV Increased S4 REGURGITATION REGURGITATION hypertrophy volume capacity Aetiology ACUTE PRIMARY of the LV (infective (caused by the Begins with endocarditis, direct Aortic valve ejection aortic involvement of never Increased EDV click dissection, the valve completely chest trauma, leaflets or closes, no LV following av chordae isovolumetric Slow rising  relaxation 6. MITRAL VALVE PROLAPSE phase - Most common cause of mitral valve regurgitation in developed countries 1. VENTRICULAR SEPTAL DEFECT (L-R SHUNT) 7. TETRALOGY OF FALLOT - Defects in ventricular septum - Pulmonary stenosis AUSCULTAT ACUTE Holosystolic - Pathophysiology : - RV hypertrophy ION o RV volume increase - Overriding aorta FINDINGS o RV hypertrophy - VSD Sudden, Decreased S1 o Excessive pulmonary blood flow severe, Soft o Increased PA pressure S1, Short LO 6 Discuss the aetiology and complications of early S3 2. ATRIAL SEPTAL DEFECT infective and non-infective endocarditis. diastolic - Defect in atrial septum murmur - Initially asymptomatic and if small may close spontaneously NON-INFECTIVE ENDOCARDITIS - Larger shunts may lead to pulmonary HTN - Often occurs in hypercoagulable states CHRONIC - Pathophysiology: - Histology: o Allow oxygenated blood to o Deposition of small sterile Asymptomatic, flow from the higher-pressure vegetables of fibrin S3, High- LA to lower pressure RA o NO polymorphonuclear pitched o Increases volume of blood leukocyte blowing entering RA and RV - Complication Decrescendo o Causing Right side heart volume o May produce emboli – stroke TREATMENT Vasodilators ACE-I and BB overload - Treatment (mild) o Anticoagulation 3. PATENT DUCTUS ARTERIOSUS AV - Arises when the ductus does not close INFECTIVE ENDOCARDITIS replacement Surgical mitral properly - Infectious inflammation of the valve repair - More common in females endocardium that typically affects one (moderate to - Pathophysiology : or more heart valves severe) o Allows persistent - Infectious pathogens : S. aureus communication between aorta - Pathogenesis and PA o Infectious agent enters TRICUSPID REGURGITATION o Volume overload in pulmonary bloodstream vessels o Leading to bacteraemia o Continuous RV (and/or LV) strain o Bacterial colonisation - Uncommonly primary valve disease o Heart failure o Mitral valve is most frequently - Backflow of blood into RA during involved systole 4. EISENMENGER’S SYNDROME - Clinical consequences - Reaction when patient with initially o Fever noncyanotic heart defects that leads to o Roth’s spots LO 5 Discuss Congenital Heart Disease (atrial and the reversal of the left-to-right shunt o Osler nodes ventricular septal defects, mitral valve and the development of a cyanotic heart o Murmur prolapse, bicuspid aortic valve). disease o Janeway lesion - Pathophysiology : o Anaemia o Irreversible pulmonary HTN due o Nail bed haemorrhage L-R SHUNT R-L SHUNT to permanent remodelling of o Emboli Ventricular septal Tetralogy of fallot pulmonary vessels defect, o RVH to compensate for patent ductus pulmonary HTN arteriosus, atrial septal defect 5. BICUSPID AORTIC VALVE Cyanosis - Very common (1% of population) (no cyanosis) - Results from 2 of the cusps fusing L-R : LateR cyanosis R-L : eaRLy cyanosis together during development LO 1 Explain the macroscopical structure and  As the heart fills up with more blood microscopical characteristics of the heart during diastole, it contracts harder and including chambers, valves. pumps out more blood during systole  Cardiac contractility is directly related Explain the LaPlace relationship between  Sarcomeres are the smallest muscle of to the wall tension of the myocardium pressure and cardiac wall tension. the heart that is capable of contracting  Stroke volume increases an EDV Discuss the hormones affecting the vascular increases system: the renin-angiotensin system, vasopressin,  Increased EDV causes increased stretch bradykinin. of cardiac myocytes Describe the conduction system of the heart.  Increased CO, Increased SV Discuss the pharmacology of digoxin, loop diuretics, ACE inhibitors, aldosterone-receptor antagonists, and β-blockers. Discuss the pharmacology of inotropic agents. Discuss the major complications of myocardial infarction for cardiac function. Discuss the pathophysiology and management of acute cardiogenic pulmonary oedema. Discuss the pathophysiology and management of chronic heart failure. Describe mechanisms and management (drugs) of  M line – myosin filaments ventricular tachyarrhythmia.  Z line – Actin Discuss the epidemiology of heart failure.  During contraction, myosin heads grab Define and understand the basic types of onto the actin filaments and pull them cardiomyopathy and myocarditis. towards the M-line which brings both Z line together and closer to M line  The force of muscle contraction depends on the number of myosin heads that binds to actin  Which directly depends of the length of the overlapping section between actin and myosin filament  Overlapping section between actin and myosin directly depends on the overall length of the sarcomere  Which depends on how much blood fill the ventricles LO 2 Describe Starling’s law of the heart. LO 7 Describe the physiological basis and significance of added heart sounds. LO 8 Explain the etiology and management of rheumatic fever. Rheumatic fever = acute symptoms associated with post-strep inflammation event RHD = chronic condition occurring because of the initial insult. - 75% mitral valve - 25% aortiv valve Aetiology of Rheumatic Fever : 1. Acute infection with Strep pyogenes 2. Cross reactivity of antibodies and T cells with heart valves 3. Causes valvular changes and nodules within the heart LO 9 Discuss the epidemiology and demography of cardiovascular diseases, especially rheumatic heart disease.