Cardiovascular Medicine

Cardiovascular Medicine • • • • • • • • • • • • • • • • • • • • • • Cardiac anatomy Cardiac excitation Cardiac cycle Cardiac function Haemodynamics Control of blood vessels Blood pressure Hypertension ECG o Heart block o Arrhythmias o SVTs AMI Non Q Wave infarct / Unstable Angina Angina Oedema Cardiac failure Acute pulmonary oedema Congestive cardiac failure Intracardiac defects Haemorrhage Cardiac surgery Heart valve disease Endocarditis Venous thromboembolic disease CVS 1 2 4 5 6 9 10 12 14 18 25 28 29 31 32 34 36 38 38 40 41 42 45 Cardiac anatomy • Draw a simple diagram of the circulatory system in man • Name the chambers and valves of the heart together with the major arteries and veins. IVC & SVC RA Tricuspid (AV) valve RV Pulmonary Valve Pulmonary Artery Head, neck, upper limbs Right Lung Left Lung Pulmonary Veins LA Bicuspid / mitral / AV valve LV Aortic Valve Aorta LA RV LV Coronary Liver GI Tract Volume output LHS = RHS 70ml/beat = 5l/min@rest Renal Pressure Skeletal Muscle LHS = 4X RHS 120mmHg LHS, 30mmHh RHS • RA Skin List the major components of blood. 55% Plasma (90% water, 8% Proteins, 2% acids & salts) 45% Cells (99% erythrocytes, 0.6-1% thrombocytes, 0.2% leukocytes) • List the classification of blood vessel types. Large Arteries – elastic conducting vessels (e.g. aorta, common carotid) Medium Artieries – muscular distributing vessels (e.g. brachial) Small Arterioles – resistance vessels (unnamed) Capillaries / sinusoids Small Venule – merging of capillaries Medium Vein – capacitance / reservoir vessels Large Vein – inc sinuses (thin walled with larger lumen) Tunica Intima • cuboidal/squamous epithelium with BM, connective tissue and… • internal elastic lamina – only in medium sized arteries, assists in maintaining blood pressure Tunica Media • mixture of elastic and concentrically arranged smooth muscle. Well developed in medium arteries, used for redistributing blood • external elastic lamina – discreet layer only in muscular arteries Tunica Adventitia • loose connective tissue with vasa vasorum, nerve (nervi vasorum) and smooth muscle cells CVS 2 Coronary arteries and veins 1. Right coronary artery 2. Small cardiac vein 3. Circumflex branch of left coronary artery 4. Coronary sinus 5. Middle cardiac vein 6. Posterior descending branch of left coronary 7. Left anterior descending artery (off LCA) 8. great cardiac vein 9. circumflex branch of LCA 10. Left coronary artery CVS 3 Cardiac excitation 99% cardiac are contractile 1% are “autorhythmic” (capable of spontaneously firing) = pacemaker cells. Pacemaker cells are found at 3 locations • Sino-Atrial Node (70-80 AP/min) • Atrio-Ventricular Node (40-60 AP/min) • Bundle of His, branches and Purkinje fibres (20-40 AP/min) The fastest cells set the rate so SA Node is natural pacemaker The excitation spreads in a co-ordinated manner • SA node (pacemaker) • Rapid spread through atria (approx 1m/s) • AV Node (slow conducting (0.05m/s = delay)) • Rapid spread through bundle of His, bundle branches and Purkinje fibres (1-4m/s) • Spread through the ventricular muscle cells Spread is facilitated by intercalated discs (gap junctions/nexus) where cardiac muscle fibres meet. These are low resistance connections à muscle functions as a syncitium. Excitation is followed by contraction of entire muscle (all-or-nothing). Coordination ensures that atria contract before ventricles to enable efficient emptying of blood and that the ventricles contract from the base upwards to expel blood efficiently. Ventricular excitation occurs from endo à epicardium and from apex to base. Action potential of contractile cell • is triggered by an influx of Ca2+, which triggers further release of Ca2+ from sarcoplasmic reticulum. The free Ca2+ activates contraction of the myocardial fibres (SYSTOLE). The amount of calcium determines the force of the contraction • The uptake of Ca2+ by the sarcoplasmic reticulum and expulsion of Ca2+ by Na+/Ca2+ exchange and outward Ca2+ pump à lower free Ca2+ à relaxation (DIASTOLE) • The long plateau phase provides a long refractory period so protects from tetany – contractions (unlike skeletal muscle) cannot summate Ca2+ Influx • • • • • • • • K+ Efflux Na+ Influx Na+ channels open (fast) Na+ influx Na+ channels inactivated Ca2+ channels open (slow) Ca2+ from outside & SR K+ channels open (slow) Ca2+ channels shut Repolarisation Action potential of a pacemaker cell K+ efflux Ca2+ influx Threshold potential Na+ influx (via if channel) Resting membrane potential (-60mV) Pacemaker potential Activates “if” channel CVS 4 • The spontaneous firing of the pacemaker cells can be influenced by neurotransmitters, ions and drugs o o o Neurotransmitters § Sympathetic - NA acts on B receptors à increases rate by increasing slope of pacemaker potential (increases “if” & “iCa2+” channels) § Parasympathetic – ACh acts on muscarinic receptor à decrease rare by increasing K+ permeability so makes RMP more negative (hyperpolarizes), also acts on slope of pacemaker potential by “if” and “iCa2+” Ions § K+ increase or decrease extracellular à RMP less negative (depolarise) § Ca2+ increase extracellular à raises threshold potential à stabilises membrane = less excitable. Decrease à lowers TP à destabilises Drugs § Local Anaesthetic (e.g. lignocaine) blocks fast Na+ channels § Beta Blockers (e.g. propranolol) blocks the action of NA at B receptors à slows the heart § Ca2+ channel blockers (e.g. verapamil) block iCa2+ à slow and stabilise § Cardiac glycosides (e.g. digitalis) block Na+/K+ ATPase & enhance parasympathetic effects CVS 5 Cardiac cycle • Given a diagram which shows the pressure profiles in the left atrium, left ventricle and the aorta for a single cardiac cycle in a healthy adult, perform the following tasks: a. Label the pressure axes b. Label the time-base (assuming heart rate = 60b.min-1) c. Indicate the points at which the cardiac valves open and close d. Draw the profile of the volume changes in the left ventricle, labelling the axis e. Indicate the positions of the 1st and 2nd heart sounds f. Draw the profile of pressure changes in the external jugular vein, labelling the three component waves g. Draw a "classical" ECG waveform on the same time-base. Aortic Pressure (120/80 mmHg) if PAo > PLV valve is closed LV Pressure (120/10 mmHg) if PLV > PLA valve is closed LA Pressure (10/0 mmHg) = pressure wave of JVP LV Volume (50-120ml) Phase 1 - Atrial Contraction Phase 2 - Isovolumetric Contraction Phase 3 - Rapid Ejection Phase 4 - Reduced Ejection Phase 5 - Isovolumetric Relaxation Phase 6 - Rapid Filling Phase 7 - Reduced Filling • Explain the origin of the 1st and 2nd heart sounds. HS I – Left AV Valve closing HS II – Aortic Valve closing HS III – Pulmonary Valve closing HS IV – Right AV Valve closing CVS 6 Cardiac function • Define the terms cardiac output, heart rate and stroke volume and give approximate (± 10%) values for these in a healthy adult at rest. Explain the relationship between them Cardiac Output = volume of blood passing through the heart (5 litres/min @ rest) Stroke Volume = volume of blood expelled from heart in one beat (70 ml/beat @ rest) Heart Rate = (70 beats/min @ rest) Cardiac Output = Stroke Volume X Heart Rate Factors affecting Rate Intrinsic factors – pacemaker (SA node) and conduction speed (AV node) Influenced by: • Autonomic NS o Sympathetic NS – NA on B adrenoceptors à increased rate o Parasympathetic NS – ACh on muscarinic receptors à decreased rate • Hormones o Adrenalin acts on B adrenoceptors à increased rate o Thyroid hormones enhance contractility and rate • Extra & Intracellular ions o Increased serum K+ (blocks APs) or Na+(blocks Ca2+ inflow) à decrease rate & contractility o Increased Ca2+ à increased rate & contractility • Temperature o Hyperthermia à SA node discharges more frequently à increased rate o Hypothermia à decreases rate & contractility Factors affecting stroke volume • Length – tension relationship – increasing starting length (preload = end diastolic volume) à increased force (until overstretched then elasticity is lost) • Force – velocity relationship – increasing load à decreasing velocity as insufficient force (f=ma). Afterload = force to be overcome before contraction can start causing movement = diastolic BP • Contractility (innate strength) – increasing contractility à increased force (for any given pre/afterload) • Define the terms preload, afterload and contractility and describe how a change in each of these will affect cardiac performance. Preload – degree of stretch on the heart before it contracts Greater the stretch on the fibres à greater contractility Preload = end diastolic volume 2 factors affect this Duration of diastole – affected by heart rate (increased rate above 160 à reduced filling time) Venous return – to right side of heart. Increased venous return à increased preload . Depends on venomotor tone, venous valve competence, skeletal muscle pump & respiration. Contractility – the forcefulness of contractions of the muscle Substances which increase contractility are positive ionotropes (promote Ca2+ inflow à strengthens next contraction Positive ionotropes - epinephrine, norepinephrine, digitalis CVS 7 Negative ionotropes – anoxia, acidosis, some anaesthetics (e.g. halothane), high K+, calcium channel blockers Afterload – the pressure that must be exceeded before ejection of blood from the ventricles can occur A higher systemic (or pulmonary) pressure à less pressure difference à reduces stroke volume. e.g. hypertension, atherosclerosis • Define Starling’s Law of the heart (the Frank-Starling relationship) & describe the influences of noradrenaline and adrenaline, myocardial ischaemia, myocardial failure (heart failure) and digitalis in the failing heart. Force of contraction is proportional to initial fibre length Or stroke vol is proportional to end diastolic volume Pressure mmHg C 120 B 80 D 70ml A 140ml Volume ml A Aà B B BàC B–C C CàD D DàA starting vol (EDV) = 140mls isometric contraction PV > PAo = 80mmHg à Valve opens blood ejected = Stroke Volume PAo > PV = 120mmHg à Valve closes isometric relaxation AV valve opens filling phase Increase EDV à increase stroke volume (e.g. venous tone, blood vol, posture, pericardial & thoracic pressure) Increase Afterload (Aortic pressure = diastolic BP) à decrease stroke volume (e.g. aortic stiffness, peripheral resistance, blood vol) Pressure mmHg Increase contractility à increase stroke volume (e.g. increased by sympathetic NS, NA/A, Ca2+, +ve ionotrophic drugs, decreased by hypoxia, acidosis, hypercapnia, infarction) D 70ml Volume ml CVS 8 Haemodynamics • State how flow through a blood vessel is influenced NB: Blood is not a simple Newtonian fluid (due to cells etc suspended in it) & Blood vessels are not uniform straight tubes Poiseuille’s Law (Flow) Q = pPi-Po R4 / 8 l h Q Pi r l h • = flow (ml/min) = inflow pressure, = Radius of tube = length of tube = viscosity of fluid Po = outflow pressure à pressure gradient Given values for the perfusion pressure and for the resultant flow through a vascular bed, calculate a numerical value of the resistance to flow and state its units. Darcy’s Law (Resistance) Resistance = Pressure Difference / Flow = 8 l h / p r4 As length and viscosity are fixed (for the most part) in medicine resistance is mostly influenced by radius As vessel diameter changes the pressure also changes – highest in the aorta, diastolic drops to approx 15mmHg by arterioles and flow is steady rather than pulsatile Total resistance = arterial (100) – venous pressure (0) / CO (5l/min) = 0.02units Renal resistance = arterial (100) – venous (0) pressure / renal flow (600ml) = 0.17units NB: Pressure difference for any vascular bed is constant • Define the term total peripheral resistance in relation to mean systemic arterial pressure and cardiac output. The sum of all the vascular resistances throughout the body Mainly regulated by arterioles (by changing diameter) BP = CO x TPR Resistance depends on Length of vessels Vessel radius Viscosity of blood • State the meaning of the term compliance as applied to arteries and state what structures in the arterial wall confer elasticity. State simply what structural pathology of arteries reduces compliance. Compliance = change in volume for a given change in pressure Determined by the extent of elasticity Less compliant means less distensible e.g. atheroscelosis Arterial compliance is for smoothing flow Venous compliance provides capacity for storage CVS 9 Control of blood vessels • Describe, in simple mechanistic terms, how the calibre of an arteriole may be altered. Vessel Radius depends on… Active tension exerted by smooth muscle Passive elastic properties of wall Blood pressure inside vessel Tissue pressure outside vessel LaPlace’s Law Distending pressure (intra – extra vascular pressure) = wall tension / radius Wall tension = Pressure X radius As vessel radius decreases, the pressure required to keep the vessel open increases If the distending pressure is too high the vessel will rupture NB: an increase in radius increases tension (e.g. an aneurysm) • Factors affecting contraction of vascular smooth muscle Sympathetic – Predominantly NA à alpha 1 adrenoceptors à constriction In some places NA à Beta 2 adrenoceptors à dilatation Hormones – Angiotensin & Vasopressin à vasoconstriction Histamine & Bradykinin à vasodilataion Intrinsic – Nitric oxide à dilatation Endothelin à constriction Increased O2, decreased CO2 à constriction (Except the lungs) Increased lactate, H+, K+, CO2, decreased O2 à dilatation (except the lungs) • Define the term blood flow autoregulation. Autoregulation – the maintainence of a constant rate of blood flow throughout a range of blood pressures by alteration of the resistance of vascular beds. Best seen in the brain • Cerebral circulation 50ml/100g/min 14% CO High metabolic requirement – autoregulation between 60-160mmHg Flow is dependent on CO2 – increased à increased flow Hyperventilation à blow off CO2 à decreased flow à decreased O2 à dizzy High CSF pressure à decreased blood flow due to limited space in skull Cushing Response = high intracranial pressure à decreased blood flow à increased BP à increased cerebral flow • Coronary circulation 70ml/100g/min 4% CO O2 extraction is near maximum at rest, so increased demand requires increased flow Sympathetic innervation à increases HR à increase Stroke vol à increased CO à increased metabolic demand à increased coronary blood flow CVS 10 Peak flow to cardiac muscle is in early diastole Flow is backward in systole Sys • Skin circulation Dia 1-200ml/100g/min Sys 4% CO Skin is used for thermoregulation so blood flow can vary greatly Contains low resistance AV shunts though which the capillary beds can be bypassed Pseudomotor nerves à sweat glands (sympathetic cholinergic) à bradykinin à vasodilatation Reactive hyperaemia – post occulusion à over perfusion • Skeletal muscle circulation mass) 3-60ml/100g/min 15%CO (40% of body As skeletal muscle is 40% of body mass v/c has a large effect on TPR Resting = alpha mediated contstriction B2 adrenoceptors à vasodilatation enabling increased activity (active hyperaemia) • Splanchnic circulation SMA = 10% CO, Hepatic = 25% CO Liver can store upto 15% of blood volume Venoconstriction allows regulation ¾ of inflow to liver is hepatic portal vein (low O2) ¼ on inflow is via hepatic artery (high O2) Gut peptides (cholecystokinin = CCK) are generated by breakdown of food à increased gut flow = functional hyperaemia • Renal circulation 25% CO Renin à angiotensin à vasoconstriction Good autoregulation ability • Pulmonary 100% CO Hypoxic vasoconstriction (only place in the body) – endothelin involved NO inhaled can cause vasodilatation Pulmonary arterial pressure = 25mmHg CVS 11 Blood pressure • Define the terms systemic arterial pressure, systolic pressure, diastolic pressure, pulse pressure and mean arterial pressure. Systolic BP Is influenced by: Stroke volume – increase Stroke vol à increased SBP Aortic elasticity – decrease elasticity (in elderly) à systolic HT (increased SBP) Diastolic BP is influenced by: Peripheral resistance – increased TPR à increased DBP Aortic elasticity – decrease elasticity à decreased DBP (no spring back) Heart rate – decrease HR à decreased DBP (more time for blood to distribute between pulse) Mean Arterial Pressure MAP e.g. SYSTEMIC e.g. PULMONARY = DBP + 1/3 PP = CO x TPR MAP = 100mmHg, CO = 5l/min, TPR = 20 units MAP = 10mmHg, CO = 5l/min, Pulmonary R = 2 units Systolic BP (120mmHg) Pulse Pressure Mean BP (DBP + 1/3 PP) Diastolic BP (70mmHg) • State the controlling factors of arterial blood pressure Pressure sensors in circulation = afferent input Arterial baroreceptors (high pressure) – in carotid sinus & aortic arch. Increase in transmural pressure à increased afferent nerve discharge (carotid sinus/aortic nerves, IX & X) Cardiopulmonary baroreceptors (low pressure) – in pulmonary vessels, atrial-vena cava junction and ventricular walls. Aka “volume receptors”. Increase in transmural pressure à afferent nerve discharge (vagus) à integration centre in medulla = efferent output Afferent input à Nucleus of tractus solitarus à Cardiac vagal nuclei (nucleus ambiguous) à parasympathetic cardiac vagal efferent activity à Caudal ventrolateral medulla “depressor” à decreases sympathetic efferent activity à decreases BP NB: depressor is NOT tonically active & activated by baroreceptor à Rostral ventrolateral medulla “pressor” à increases sympathetic efferent activity à increases BP. NB: pressor is tonically active & inhibited by baroreceptor à effector mechanisms (via autonomic NS) Parasympathetic (Ach, muscarinic receptors à decrease HR) Sympathetic (NA, B1 adrenoceptors à increase HR & St Vol) CVS 12 • Use your diagram of the baroreflex to describe the changes in efferent discharge from the medullary cardiovascular centres which would be expected to follow (a) a rise and (b) a fall in mean systemic arterial pressure. Decreased arterial BP Unloads arterial baroreceptors Decreases afferent nerve discharge Decreases tonic inhibition at pressor area Increases sympathetic nerve activity Increases HR, Str Vol à increased CO (via B1 adrenoceptors) Increases peripheral resistance (A1 adrenoceptors) by v/c Increases BP back to normal Increased arterial BP Increases afferent nerve discharge Activates depressor & inhibits pressor Decreases sympathetic nerve activity Decreases HR, Str Vok à decreased CO (via B1 adrenoceptors) Decreases peripheral resistance (A1 adrenoceptors) by v/d Decreases BP back to normal Postural Reflexes Supine à standing causes blood to pool in legs & abdomen à decreases venous return à decreases BP à decreases afferent discharge (decreases vagal, increases sympathetic) à increases HR, Str Vol, vasocontriction (increases TPR) à restore BP to normal CVS 13 Hypertension • Outline the difficulties of defining whether blood pressure is raised in view of its normal distribution and the graded risk associated with increasing pressure. Blood pressure varies based on • Age (increases with increasing age) • Gender • Individual (based on health Etc) • Stress (increases BP) • Ethnic Background (increased in black Africans) High blood pressure is associated with increased morbidity & mortality Isolated systolic hypertension --> 2-3 x Increase in cardiac mortality • Outline the levels of blood pressure currently defined as normal, borderline or raised Optimal 120/80 Normal 120/85 High Normal 130-139/85-89 Hypertension Grade 1 (mild) 140-149/90-99 Grade 2 (mod) 160-179/100-109 Grade 3 (severe) > 180/110 Isolated systolic hypertension Grade 1 140-149/90 Grade 2 > 160/90 NB: due to multiple factors affecting BP – 3 separate readings, on 3 occasions are required to make a diagnosis • Define the terms primary (essential) and secondary hypertension. Essential HT – 90% of all cases - no known cause, possible connection with diet, sodium, environment, stress, genes Secondary HT – 10% of cases – cause known. E.g. renal artery disease / stenosis à poor renal perfusion à high renin à RAA system à Na & H2O retention E.g. adrenal tumour – cortex = high steroids, medulla = high catecholamines Hypertension is a risk factor for other mortality (heart failure, IHD, CVA, Renal disease) Isolated systolic hypertension has 2-3 x risk of cardiac mortality • Discuss the possible causes of secondary hypertension Renal Disease = 80% of 2o HT • Diabetic nephropathy • Chronic glomerulonephritis • Adult polycystic disease • Chronic tubulointerstitial nephritis • Renovascular disease Endocrine Disease • Conn’s syndrome • Adrenal hyperplasia • Phaeochromocytoma • Cushings syndrome • Acromegaly Congenital Cardivascular • Co-arctation of the aorta Drugs • NSAIDs – esp if pre-existing renal disease CVS 14 • Oral contraceptives • Steroids, Carbenoxolone, Liquorice, Sympathomimetics, Vasopressin • MAO inhibitors + tyramine --> malignant HT Pregnancy • Pregnancy induced HT – 8-10% of women, Pre-eclampsia • Describe the clinical and pathological features of 'accelerated phase' or 'malignant' hypertension. Rapid rise in BP to a diastolic > 120mmHg à fibrinoid necrosis of the vessel walls Untreated à renal / heart failure / aortic dissection / stroke Signs Increased BP Proteinuria / Haematuria Cotton wool spots / Flame haemorrhages Papilloedema 1 yr survival < 20% untreated • Describe the pathological consequences of hypertension as they affect the cardiovascular, cerebrovascular and renal systems • • • • • • Artery wall thickening & hyaline arteriolosclerosis --> decreased lumen, tissue ischaemia & increased fragility of cerebral vessels --> predispose to haemorrhage Increased pressure --> left ventricular myocardial hypertrophy --> insufficient coronary blood flow --> IHD --> Left ventricular failure Microinfarctins in brain --> Hypertensive lacunae Progressive ischaemia of nephrons --> chronic renal failure --> benign Hypertensive nephrosclerosis Predisposition to severe atheroma, AAA & aortic dissection Outline possible physical signs in the examination of a patient with hypertension including left ventricular hypertrophy, radio-femoral delay, renal artery bruits, enlarged kidneys and hypertensive retinopathy. Mild = Asymptomatic à • Headaches • Epistaxis • Nocturia • Breathless (LVF) • Angina • Renal Artery Bruits – renovascular hypertension • Radio-femoral delay – co-arctation of aorta • Hypertensive retinopathy - Increased retinal vessels, Flame haemorrhages, Cotton wool exudates, papilloedema • Discuss common investigations to exclude a secondary cause of hypertension • • • • • ECG Urine Stix – for protein & blood Fasting blood – for total lipids, HDL & glucose Serum U+E & Creatinine (for renal disease or Conn syndrome) Urinary catecholamines – 24hour urine collection (phaemochromocytoma) CVS 15 • Discuss the treatment of hypertension Goals • Systolic < 140 • Diastolic < 85 (80 if DM) Young (<55), non black, high renin Old (>55), black, low renin ACEi / B Blocker Ca2+ antag / diuretic Conservative management • Decrease alcohol, weight, salt & fat intake • Increase exercise, fruit & oily fish • Stop smoking • Reduce stress if possible ACEi / B Blocker + Ca2+ antag / diuretic MAP = CO x TPR ACEi / B Blocker + Ca2+ antag + diuretic Can target resistance, Str Vol, HR, venous return or contractility + A-Blocker OR + Spironolactone OR + other diuretic B-blocker NA à B1 àé HR & force CNS NA à A à v/c 2+ Ca blocker A-blocker Vessels Angiotensin II à v/c Peripheral resistance Baroreceptors feedback to CNS B-blocker NA à B àé Renin Kidney Heart Diuretic ACEi RAA system à Na+ & H2O retention Cardiac Output Arterial BP ACE Inhibitors e.g. Captopril, enalapril, rampril Mechanism of action ACE converts Angiotensin I (inactive) to Angiotensin II (active v/c) AND bradykinin (active v/d) to bradykinin 1-7 (inactive) Therefore - Lower angiotensin II à reduce v/c à reduce aldosterone à reduce Na & H2O retention à potentiates bradykinin à v/d Side Effects Cough – bradykinin increases airway sensitivity & à inflammation 1st dose hypotension – give first dose at night Can increase K+ & cause renal damage. ALWAYS monitor creatinine before starting and after 1 week to check renal function Other uses Heart Failure, left ventricular hypertrophy, DM protein nephropathy CVS 16 B – adrenoceptor anatagonists (B-blockers) e.g. propranolol – non selective (B1 & B2) for angina & HT e.g. atenolol / metoprolol – B1 selective (for action on heart) Mechanism of Action Block receptors in SA node and ventricular muscle à decrease HR & force à reduce O2 demand – used in angina Decrease renin secretion (& therefore angiotensin II & aldosterone) Decrease sympathetic activity (some cross BBB) Decrease NA release (blocks presynaptic B receptors which increase NA release) Side Effects Bronchoconstriction – block B2 mediated bronchodilatation (less with B1 selective). AVOID in asthma / COPD Can reduce hypoglycaemic awareness so avoid in DM Poor execise tolerance, muscle cramps, cold extremities – blocked B2 mediated vasodilatation (skeletal muscle) à unopposed A-mediated v/c. Should be less with B1 selective Other uses of B-blockers IHD Arrhythmias Glaucoma (raised intraoccular pressure) Ca2+ channel blockers e.g. Verapamill, amilodipine, felodipine, nifedipine Mechanism Act on heart & smooth muscle à reduce contractility and propagation of action potentials à v/d & lower BP Side effects Peripheral oedema, postural hypotension, constipation Good for afro-caribeans, isolated systolic hypertension Diuretics (see renal notes) e.g. thiazide first line - bendroflumethiazide 2.5mg Method of Action Reduce sodium reabsorption in kidney à reduce circulating volume, some also vasodilate Side effects Volume depletion, hypokalaemia, increases urination, impairs glucose control, may cause impotence. Avoid in gout A-Adrenoceptor Antagonists (A-blockers) e.g. doxazosin, prazosin – A1 selective Mechanism of action Reduce A-mediated vasoconstriction Side Effects Postural Hypotension – loss of A-mediated v/c with baro reflex Angina, Arrhythmias, Tachycardia – reduced A2 mediated presynaptic inhibition of NA release à more NA available to act on cardiac Breceptors Other Uses Pheochromocytoma (catecholamine secreting tumour of adrenal medulla) – used with B-blocker pre & post op Peripheral vascular disease – raynauds Hypertensive emergencies – cheese reaction Sx relief from prostatic hypertrophy CVS 17 ECG DEPOLARISATION – towards a positive electrode gives and upward deflection AMPLITUDE – is maximal when the positive electrode is on the vector • Given electrocardiograms label the components of the waveform (P, Q, R, R’, S, T where present) and relate each to its generative cardiac vector. P (P) = atrial depolarisation Q (R) = septal depolarisation L à R R (S) = depolarisation of ventricular base (endo to epicardium) S (R’) = depolarisation of base of R ventricle (endo to epi) T (T) = ventricular repolarisation R R P R ’ T Q P T S P = 0.08s PR interval = 0.2s QRS duration = 0.1s S • Draw diagrams indicating the ‘viewing’ positions achieved with the 6 standard limb lead recordings (I, II, III, aVr, aVL, aVF) and the 6 standard chest leads (V1 V6). VI V II V III V IV VV V VI 4th IC space, R sternal edge 4th IC space, L sternal edge between II & IV 5th IC space, mid clav line / APEX between IV & VI Mid axillary line, same level as IV Paper speed 1 large square = 0.02 sec HR = 300 / R-R interval • aVR aVL -30o I Normal Axis II III aVF 90o Axis deviation • Find the iso-electric lead (where Q=R=S). The axis is 90o clockwise from that lead o > 90o = Right Axis deviation o < -30o = Left axis deviation • OR Look at leads I & III – if the QRS complexes are o Reaching toward each other = Right axis deviation § R.Ventricular Hypertrophy § PE § WPW syndrome § Anterolateral MI o Leaving each other = Left axis deviation § Inferior MI § LBBB § VT • Classify heart block and identify the ECG features of each type of heart block 1st Degree heart block • Prolonged PR interval (<0.2s) • Sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturnbance CVS 18 2nd Degree heart block • Mobitz type II o Most P waves are followed by QRS, occasionally QRS missing o Can à 3rd degree block • Wenckebach o Progressive lengthening of the PR interval, then failure of a QRS à resets system o Usually benign • Alternate 2:1 / 3:1 o Regular pattern of QRS’s conducted or not conducted o NB: spare P wave may only show as a distorted T wave is summation occurs 3rd Degree (complete block) • Atrial contraction is normal, no conduction t o ventricles • P waves regular at 90/min • QRS complexes regular at 36/min • NO LINK between timing of P and QRS • QRS abnormal shape due to unco-ordinated spread through the ventricles • Can be acute (e.g. MI) or chronic (e.g. fibrosis in bundle or L+RBBB) • May need pacing • Describe the ECG features of atrial arrhythmias (including atrial fibrillation, atrial flutter and re-entrant tachycardia) & ventricular arrhythmias (including ventricular tachycardia and fibrillation) NB: most arrhythmias are named after their origin Sinus rhythms o Sinus Arrhythmia – change in HR assoc with respiration o Sinus Bradycardia (HR <60) – normal in athletes, fainting attacks (sick sinus syndrome), hypothermia, myxoedema, post MI, B-blockers, digoxin, diltiazem, verapamil o Sinus Tachycardia – during exercise, fear, pain, haemorrhage, thyrotoxicosis Terms o o Supraventricular – have normal QRS (but abnormal if also BBB) Ventricular – have wide abnormal QRS & abnormal T (repolarisation affected) Bradycardia escape rhythms – are a fail safe for conduction pathways. Commonly seen post MI & should not be interrupted o SA node = 70bpm o Atrial / Junctional = 50 bpm o Ventricular = 30 bpm o Atrial escape – if SA node slows / stops the atrium takes over. A single abnormal P CVS 19 o o wave followed by a normal QRS is seen hopefully f.b. return to normal Junctional escape – no P waves (absent / lost in QRS) but normal QRS seen Ventricular escape – most commonly seen in complete heart block. (Regular P waves, wide regular QRS with no relationship between ). Can occur without heart block (atrial failure) and can occur singly o Accelerated idoventricular rhythm – assoc with acute MI. Appears similar to VT but is faster than a normal ventricular rhythm, is benign & doesn’t require treatment. Extrasystoles – are extra beats which occur earlier than they should, usually from an abnormal location o Atrial extrasystole – abnormal P wave o Junctional extrasystole – no P wave o Ventricular extrasystole – abnormal wise QRS, common & of little importance. Can have inverted T wave. NB: If QRS occurs over the T wave of preceding beat can à VF Supra Ventricular Tachycardias Sinus tachycardia – originates in the SA node. E.g. sick sinus syndrome Atrial tachycardia Regular > 150bpm. Set focus within the atria causing impulses P wave superimposed on QRS but QRS is normal. AV node has maximum conduction of 200/min which if faster can à AV block. Rx: adenosine Atrial fibrillation Causes: poor flow to muscle à dilation of heart à impaired conduction pathway. E.g. post MI, IHD, mitral stenosis / regurg, hypertension, hyperthyroidism, binge drinking Pattern: Originates aroud the L atrium (usually around the origin of the pulmonary veins) ECG findings: No P waves, irregular baseline, normal QRS shape. (Top – lead II, Below - V1). NB: will decrease cardiac output by approx 20% so vital to restore early if valve disease Rx: ABC and fluid challenge to try improve BP (slow bec heart pathology) ECG to confirm rhythm Slow rate – B-blocker (-ve chronotrope) or Ca2+ blocker (verapamil / diltiazem – NB: only if normal LVF as also –ve ionotrope) Digoxin Cardioversion – Electrical - preferred if low BP / not responded to chemical conversion. Requires an anesthetist and NBM for 4 hrs. CVS 20 Chemical Amiodarone = class 3 anti-arrhythmic, K+ blocker. Give as IV loading dose f.b. maintainence. Irritant so give centrally or with large flush Fleconide = class 1C anti-arrhythmic. Almost 100% success in conversion (within 10 mins) & can be given peripherally BUT assoc with increased mortality in IHD so only give in no MI / Angina Ablation: is possible to prevent the abnormal conduction initiation. Relatively new so only available at regional centres NB: only cardiovert if known onset within the last 48 hrs due to risk of embolism beyond that time. Otherwise anticoagulate with LMWH at treatment dose à warfarin > 3 weeks and confirm no clot (echo) before converting. Keep on warfarin for 3-4 months post Atrial flutter Causes: assoc with structural problems (HT, valve disease) Pattern: Abnormality originates around the tricuspid valve origin ECG: Sawtooth appearance rate 250350/min. Ventricular rate is normally 150 (2:1) or 100 (3:1) Rx: treat by the same protocol as AF as risks are similar. Ablation is possible to block the pathway NB: Carotid sinus pressure – activates a reflex à vagal stimulation on AV & SA node à lowers rate. Has no effect on ventricular tachycardia AV node re-entry tachycardia Usually occur in young women à palpatations Pattern: Micro-reentry tachy as the circuit is only within the node ECG: small regular complex tachycardia with no P’s but QRS are regular Rx: benign and no stroke risk. Not assoc with serious pathology or outcome. Adenosine can be used as AVN blocker (lasts 7-10 sec) to reset the node B-blocker to slow the AVN can help Ablation is possible but dangerous as if too much is burnt à heart block! AV re-entry tachycardia = Wolff-Parkinson-white syndrome Pattern: Extra connecting bundle usually on LHS of heart ECG: Short PR interval, Slurred upstroke (delta wave) on QRS, End of QRS is normal Rx: block the AVN to reset the cycle (e.g sinus massage / vaso-vagal / head in cold water. Can ablate pathay NB: avoid digoxin / Ca2+ antag as will slow AVN making the accessory pathway dominant à increased ventricular rate (= dangerous) Anti-arrhythmic drugs Class I antiarrhythmics Class II antiarrhythmics Class III antiarrhythmics Class IV antiarrhythmics Lidocaine Inhibition of Na-channels. VT B-blockers (including sotalol) Amiodarone, sotalol Verapamil Antagonism of B-adrenoceptors. Paroxysmal AF. Blockade of K-channels leading to action potential prolongation. Blockade of Ca-channels. AF. CVS 21 SVT • • Ventricular fibrillation – totally disorganised, usually assoc with loss of consiousness = CARDIAC ARREST • Ventricular tachycardia – wide abnormal QRS in all leads. o CHECK PULSE – if pulseless = cardiac arrest o Rx lignocaine , if acute à shock (if conscious then contact anaesthetist Left & Right Atrial Hypertrophy • Right Atrial Hypertrophy (p-pulmonale) o Due to tricuspid stenosis / pulmonary hypertension o Peaked P waves on ECG • Left Atrial Hypertrophy o Due to mitral stenosis o Broad and Bifid P wave • Describe the ECG features of AMI and how they change with time Q Waves indicate MI if > 2mm deep • The location of the Q waves indicate the area with damage • Gives no indication of time since MI I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 INF = Right coronary artery ANT = Left anterior descending artery LAT = Circumflex NB: posterior MI will show prominent R wave in V1 and ST depression in the chest leads (turn the ECG upside down or ask for V7-12 leads. True posterior MI is an indication for thrombolysis T wave Inversion • T wave inversion is normal in aVR, V1 and V2 • Shows ischaemia post MI ST segment should be isoelectric • Elevation shows acute MI or pericarditis • Depression shows ischaemia • Downsloping shows digoxin overdose (with T wave inversion) • Depression in Chest leads with clear clinical features of evolving MI may indicate a posterior MI Changes over time • ST Elevation takes hours • Over days the elevation lessens and there is a sign of underlying T-wave inversion and deeper Q waves, the R wave is decreased • Over weeks the R&Q wave changes stay similar to days but there is pronounced T wave inversion. CVS 22 • • Describe the typical ST segment/T wave changes of angina. • • • • After months, there is a larger Q, and smaller R ST depression showing ischaemia Transient ST depression, T wave inversion and ventricular arrhythmia may be seen as a result of ischaemia. If Prinzmetals can get ST depression, but is still angina Describe the ECG features of left and right ventricular hypertrophy. Hypertrophy à increased muscle mass à Increased height of QRS complexes • • • • Right Ventricular hypertrophy o Best seen in V1 (R higher than S) and o Deep S wave in V6 o Usually accompanied by R axis deviation, peaked P waves (& in extremes inverted T in V1 & V2 Left Ventricular hypertrophy o Peaked tall R waves (> 25mm) in V 5/6 o Deep S in V 1/2 o Can get inverted T in I, aVL, V5/6 Pulmonary Embolus o May just show sinus tachycardia o But can show as R.Vent hypertrophy o Peaked P wave o R axis deviation o Tall R in V1 o RBBB o Inverted T in V1(2&3) o Q wave in III (like inferior infarct) Describe the ECG appearances of left and right bundle branch block. • • P wave & PR interval normal Abnormal conduction à delay in depolarisation à Widening of QRS complex (>120ms) Prominent R wave only Right Bundle Branch Block (RBBB) = MARROW • Can be due to atrial septal defect • Septum depolarises R-->L as normal • Left Ventricular depolarisation normal • Right ventricle depolarisation is delayed NB: Prominent R wave in V1 with left axis deviation = left anterior hemiblock (bifascicular block) has 2 causes RBBB or posterior MI V1 V1 V6 V6 Left Bundle Branch Block = WILLIAM • Can be due to aortic stenosis / ischaemia • Septum depolarises R --> L (inverse of normal) • Right ventricular depolarisation (small wave) • Ventricular depolarisation (large wave) • Can also show as T wave inversion in I, V2, V5 & V6 (lateral leads) • List the symptoms that a patient with paroxysmal arrhythmia most commonly complains about and outline the reasons for those symptoms CVS 23 Syncope, dizziness, palpitations and sudden death All except for palpitations are from the decreased filling time and reduced oxygen flow to brain and heart muscle. • Explain the rationale for the use of cardiac glycosides (eg digoxin) in the treatment of certain types of arryhthmia. If arrhythmia is Atrial then blocking conduction through AV node will stop Ventricular manifestation. Digoxin etc poisons AV node and reduces Ventricular rate. • Describe briefly the likely mode of action of â-adrenoceptor antagonists (eg atenolol), Ca2+ antagonists (eg verapamil) and local anaesthetic drugs (eg lignocaine), in the treatment of arrhythmias. Explain the use of anticoagulants (eg warfarin) in this condition • • • • • Atenolol reduces the rate of discharge of the SA node and reduces the AV node conduction speed. It also give a prolonged period of atrial refraction. Verapamil acts on Calcium channels. There is a greater density of these in the SA and AV nodes and it therefore can be used to slow heart rate from atrial tachycardia. Lidocaine blocks sodium channels, can stop action potentials, very dangerous if heart block or bradycardia but useful in tachyarrhythmias, can even slow VT/VF. If patient has prolonged arrhythmia then the muscle is uncoordinated and turbulent flow & incomplete ejection occurs, these increase risk clotting within the heart (specifically the atria). Treat with warfarin to reduce risks of later MI / Stroke, aim for INR 2-3. State the principal sites of action of the phenylalkylamine Ca2+ channel antagonists (eg verapamil) and the dihydropyridines (eg nifedipine) Verapamil SA / VT node and vessels. Therefore rate limiting Nifedipine acts on cardiac muscle and vascular smooth muscle • Discuss the types of pacemaker A pacemaker will only help if there is already electrical activity in the heart (e.g. if no atrial activity then don’t pace the atria) Most pacemakers work on demand (therefore must sense the heart as well as pace it) and can respond to increased demand (by monitoring temperature, CO2, lactate etc) Pacemakers have a 3 letter code (1st = paced chamber, 2nd = sensed, 3rd = action) A = atria, V = ventricle, D – dual (= both), I = inhibit pacemaker, T = trigger VVI – AF / complete heart block (V sensed, V paced) DDD – Sick sinus syndrome (both sensed, both paced) CVS 24 Acute myocardial infarction • Describe the typical history of AMI. Sudden onset Crushing central chest pain Radiating down left arm / shoulder / neck Assoc with nausea, vomiting, sweating, SOB Can be history of angina / cardiac problems • Describe the clinical examination features of a patient with AMI. Distress, anxiety, pallor Sweaty Tachypnoea +/- subjective dyspnoea Increased/decreased pulse & BP 4th heart sound Can be signs of heart failure or pansystolic murmer • Discuss the differential diagnosis of AMI. Angina – Shorter duration, relieved by GTN, Pericarditis Myocarditis Aortic Dissection –Tearing central chest pain, loss of limb pulses and renal function as dissection progresses. PE – Haemoptysis, inspiratory pain, radiation to shoulder if diaphragm involved. Oesophageal reflux – worse after meals and lying down, burning pain. • Describe the causes, morphology and pathological consequences of AMI distinguishing between full thickness and partial thickness (subendocardial) patterns of infarction Causes Atherosclerosis and thrombus, (most common – 25% due to superficial ulceration of endothelium over a plaque. 75% due to plaque fissuring resulting in a deep cleft à thrombus / bleeding into plaque Also - embolus, vasopasm of coronary arteries (cocaine), trauma and hypoperfusion Morphology Regional MI (90% of cases) one section of the ventrical wall affected. Thrombus formation on an atheromatous plaque Full thickness = persisting occlusion Partial thickness = thrombolysis / collateral supply Circumferential (10% of cases) Subendocardial zone of ventricle Due to hypoperfusion of main arteries Pathological Consequences 0-12 hrs = ischaemia 12-24 hrs = intracellular oedema 24-72 hrs = acute inflammatory response with neutrophils infiltrating 3-10 days = organisation and vascular granulation tissue forms weeks à = collagenous scar • Describe the investigation of AMI and the sequential changes in cardiac enzymes after heart muscle damage. ECG – See previous section CVS 25 Immediate = tall T waves, ST elevation or new BBB Later = T wave inversion & pathological Q waves CXR Cardiomegaly Pulmonary oedema Widened mediastinum (aortic dissection) Bloods FBC, U&E Glucose – increases Lipids – decrease CK – increased by MI, trauma, prolonged exercise, hypothermia, hypothyroidism Trop T – only increased by cardiac muscle damage. Can be used prognostically. Peaks at 12-24hrs, elevated for over 7 days • Describe the management of AMI ABC – high flow O2, IV access (for bloods) Brief assessment for contraindications for thrombolysis à Thrombolysis Aspirin 300mg Morphine 5-10mg IV + antiemetic GTN – symptomatic relief B blocker (unless asthma / Left ventricular failure) CXR If Diabetic à glucose, insulin & K+ DVT prophylaxis Seek cause and treat (also manage all risk factors) • Discuss the indications and contraindications for thrombolysis. Of greatest benefit <12hrs (can be used upto 24hrs) Indications (within 12 hrs) • ST elevation >2mm in > chest leads • ST elevation >1mm in > limb leads • Posterior infarct (dominant R & ST depression in V1-V3) • New LBBB • Continuing chest pain or ST elevation (12-24hrs) Contraindications • Internal bleeding (inc prolonged CPR) • Suspected aortic dissection • Previous allergic reaction • Heavy PV bleed / Pregnant / <18 weeks PN • Acute Pancreatitis • Severe lung disease / active lung disease with cavitation • Oesophageal varices • Recent trauma/surgery (<2 weeks) • Cerebral neoplasm • Severe hypertension (>200/120 Relative contraindications • Peptic ulcer • History of CVA • Bleeding diathesis CVS 26 • • Anticoagulated Describe the complications of AMI and describe their presentation: Immediate • Arrhythmias particularly ventricular tachycardia and fibrillation & heart block (à bradycardia) - due to damage to conduction pathways • Cardiac arrest & cardiogenic shock Short term • Left ventricular failure à Pulmonary Oedema & Cardiogenic shock due to large infarct à dilatation of ventricle wall • Valve incompetence – due to ruptured chordae tendinae • Rupture of ventricular wall (2-10 days) à haemopericardium = cardiac tamponade or VSD à Là R shunt Long term • Heart Failure – due to loss of ventricular muscle • Ventricular Aneurysm – due to fibrous scar à dilation à thrombus (but embolus uncommon) • Dressler’s Syndrome – immune mediated pericarditis. High ESR • Describe pharmacological methods of secondary prevention including aspirin, betablockers, ACE inhibitors and lipid lowering therapy. Secondary prevention lowers risk factors to prevent further events. Aspirin 75mg prevents clots, may consider clopidogrel especially if thrombolysis or stenting was used. B-blocker - HR <60 for minimum 1 year, but can give lifelong, longer term decreases mortality further ACE-I should continue for 1-2 years minimum in all patients Statin, even if normal level of cholesterol • Outline the principles of cardiac rehabilitation including advice given regarding driving and employment. Pharmocological Management Dietary Advice – Oily fish, fruit veg and fibre, low saturated fats Exercise – Regular exercise, low intensity building up NO SEX for 1/12 NO FLIGHTS 2/12 NO WORK 2/12 longer if heavy manual labour, not at all for divers, pilots etc Driving MI / ACS – cease for 4 weeks Unstable angina – cease until stable Stable angina – drive if well Angioplasty – 1 week Pacemaker – 1 week & notify DVLA CABG – 4 weeks & notify DVLA Incapacitating arrhythmias – 4 weeks after controlled and notify DVLA CVS 27 Non-q wave infarction / Unstable angina • Understand the spectrum of the acute coronary syndromes ACS = STEMI, NSTEMI or Unstable Angina – requires 2/3 of typical hx, ECG chages and cardiac enzyme changes STEMI will have classic ECG findings. – see earlier. ACS presents with new onset pain, pain at rest or worsening angina, may have atypical features instead, (indigestion etc) ECG may be normal in ACS but ST depression and T wave inversion likely, but no new LBB or ST elevation (unless Prinzmetels) If cardiac enzymes are elevated and no ECG changes then NSTEMI, if enzymes normal then angina. • Be able to recognise the ECG, cardiac enzyme and plasma troponin changes that allow a diagnosis of the different syndromes to be established. ECG – ST elevation = STEMI, NSTEMI and angina have either no change or ST depression, occasionally with pathological Q waves. ECG is definitive. Troponins will follow a similar pattern in STEMI and NSTEMI but a significant rise should NOT be seen in unstable angina • Describe the difference in treatment between acute (Q-wave) myocardial infarction and other acute coronary syndromes (no thrombolysis, heparin, intravenous nitrates, antiplatelet agents). Rx similar in aspects of MONA and Heparin, Iv nitrates can be given for either in prolonged pain. NO THROMBOLYSIS if ACS, unless diagnosed as a posterior AMI. • Understand the difference in prognosis between AMI (high early death rate, relatively good prognosis) and unstable angina/acute coronary syndromes (patients with elevated CK or troponin have a low early death rate but a high risk of death or AMI in the next three months). AMI carries a high risk of myocardial rupture, arrhythmia and cardiogenic shock during the first few weeks after the event. Outside of the first month there is a good survival rate. NSTEMI and unstable angina are harder to treat, and mopre likely to recur, doing small amounts of damge until AMI occurs. The heart is already weakened and the risks of early complications and therefore death are increased. • Outline the indications for early angiography with a view to PTCA or CABG (persistent pain, early positive exercise test). Ideally all patients would undergo early angiography and PTCA following AMI. Balloon angioplasty and stenting has better outcomes than TPA treatment, with less risk of haemorrhage etc. Due to costs generally only used where TPA or streptokinase has failed or is contraindicated. Continuing pain or unresolving ST elevation, or an ETT showing severe ischaemic changes would be considered indications for stenting. CABG is rarely considered as an emergency procedure, it is a definitive treatment for narrowed coronary vessels, but there are great risks in undergoing heart surgery. Indications are the same, but choice depends on risks and the amount of narrowing – in certain cases angioplasty is not possible. CVS 28 Stable Angina • Define stable and unstable angina Stable angina – existing, no change in severity, duration or frequency. Predictable based on activities Unstable angina – new onset or existing with change in severity, duration or frequency • Describe the typical history of a patient with angina Classical Heavy / tight / gripping pain – central or retrosternal, radiating to arm/neck, ranging from mild ache to severe pain Provoked by exertion, after meals, cold weather, anger or excitement Decubitus Occurs on lying down Assoc with impaired left ventricular function Nocturnal Occurs at night, waking patient from sleep Provoked by vivid dreams Occurs with critical CAD and vasospasm Variant (Prinzmetal) Coronary artery spasm Occurs without provacation Can get arrhythmias with it Cardiac Syndrome X History of angina and +ve exercise test but with normal arteries More common in women Good prognosis but difficult to treat • Discuss the underlying causes of angina including coronary artery disease, valvular heart disease, cardiomyopathy and anaemia Inadequate oxygen delivery to myocardium à ischaemia Coronary artery disease – Concentric plaques are less likely to respond to vasodilators than eccentric Anaemia – normal flow but decreased oxygen Arteritis – reduced lumen Fissuring of plaques – abrupt disruption in flow • Describe relevant examination features Commonly have hypertension Can be 4th heart sound Signs of anaemia, thyrotoxicosis or hyperlipidaemia (xanthelasmata, tendon xanthoma) May have aortic stenosis (possible direct cause) • List recognised risk factors for coronary artery disease and describe the pathology of coronary arteries in patients presenting with angina Non Modifiable Age, Male gender Family history (genetic predisposition) High fibrinogen levels Homocysteinaemia Modifiable CVS 29 Hyperlipidaemia (give statin & diet) Smoking Hypertension DM (improve control) COCP Lack of exercise Obesity Gout (may be association rather than risk) Heavy alcohol intake • Describe the investigation of a patient with suspected angina including FBC, cholesterol, ECG and exercise testing Bloods – FBC (anaemia), lipids (for monitoring), TFTs (exclude poss cause) Resting & exercise ECGs Myocardial perfusion scan Echo Angiogram • Describe the management of stable angina Lifestyle alterations – stop smoking, exercise, weight loss Modify risk factors – DM, HT B-Blocker Sx treatment. 50-100mg unless contraindicated (asthma, COPD, bradycardia) -ve ionotropic and chronotropic effects à reduce work & rate à increase diastole à increases time for coronary blood flow Aspirin – 75mg reduces mortality by 34% Nitrates Sx treatment given as GTN spray or sublingual tablets upto every ½ hr Prophylaxis – Isosorbide Mononitrate 10-30mg bd. ENSURE a nitrate free period overnight or tolerance will develop Act by v/d à reduce preload & by increasing coronary flow Ca2+ antagonists – amilodipine / diltiazem = NON dihydropyridine drugs. NB: the dihydropyridine Ca2+ antagonists (amilodipine, felodipine) are –ve chronotropes (as are B–blockers and should NEVER be given together) Verapamil is a strong –ve ionotrope and can be used in angina BUT NEVER with Bblockers Statin - If total cholesterol > 4mmol/L K+ channel activator – if resistant CVS 30 Oedema • Define the term oncotic (colloid osmotic) pressure and state how it is conferred to plasma. Oncotic pressure is the force exerted by proteins within the blood which causes influx of fluid into the vascular compartment from the tissue fluid. Capillaries • Have no smooth muscle in their walls • Can be continuous, fenestrated (kidney) or discontinuous (liver) • Don’t have uniform flow velocity (0-8mm/s, average 1mm/s) • Don’t have uniform transfer across the BM – depends on type of tissue, diffusion (Ficks Law), filtration (0.06ml/min/100g tissue, determines ECF & Plasma distribution) and pinocytosis • Describe starlings law & factors altering the outcome Rate of fluid movement = Kf [ (Pc - pI) – (pc + Pi) ] Kf = filtration constant which depends on permeability and surface area If Pc > pc there is net filtration p If c > Pc there is net reabsorption Filtration favoured by • Capillary hydrostatic pressure (Pc) Depends on pre/post capillary resistances & pressures Pre capillary constriction à lower hydrostatic pressure Post capillary constriction à higher hydrostatic pressure Increased Pc à increased filtration Decreases across a capillary bed (32mmHg à 12mmHg) • Interstitial fluid colloid osmotic pressure (pi) – usually negligible Depends on protein in interstitium & protein permeability Reabsorption favoured by • Capillary (plasma) colloid osmotic pressure (pc) Depends on synthesis & breakdown of proteins (liver), capillary permeability to protein and abnormal loss of protein (kidney damage) Increased pc à increased reabsorption Remains constant across capillary bed • Interstitial fluid hydrostatic pressure (Pi) – usually negligible Depends on interstitial fluid vol, organ compliance, & effective drainage. Lymphatics drain excess fluid & proteins via valved vessels. 2-4 litres / day • Define the term oedema. Oedema = excessive tissue fluid formation resulting in swelling Pre capillary V/C à decreased Pc à increased reabsorption Increased venous pressure (e.g. heart failure) à increased Pc à increased filtration Hypoproteinaemia à decreased pc à decreased reabsorption Increased capillary permeability à decreased pc à decreased reabsorption Obstructed lymph drainage à increased Pi à some increased reabsorption CVS 31 Cardiac failure • Define, in one sentence, the term myocardial failure A compromised state of the myocardium in which flow is inadequate to meet the needs of the circulation. An increase in filling pressure (EDV) fails to cause an increase in stroke volume (starlings curve no longer applies) A manifestation of the body’s response to an inadequate circulation. A collection of symptoms and physical signs Causes of cardiac failure • Ischaemia / Infarction à decreased contractility à decreased force (rapid onset) • Valve dysfunction – stenosis / incompetence à affects afterload • Pressure overload – high BP à increased afterload (slow onset) • Infection / Bacteria – affects cells or valves • Drugs • List the signs and symptoms most commonly associated with chronic congestive heart failure. Give reasons for these. Right ventricular failure • Raised end diastolic pressure • Raised right atrial pressure & JVP • Raised central venous pressure à liver distension à ascited & discomfort à increased interstitial fluid formation (peripheral oedema) à swollen ankles & feet Left ventricular failure • Raised end diastolic pressure • Raised left atrial pressure • Raised pulmonary capillary pressure à reduced area for gas exchange & increased interstitial fluid formation (pulmonary oedema) à breathlessness – esp when lying flat Congestive heart failure • Breathless – pulmonary oedema • Ankle swelling – peripheral oedema • Distended neck veins – raised JVP • Abdominal discomfort – liver distension due to raised venous pressure • Ischaemic (angina) pain – poor coronary perfusion Compensatory mechanisms ê myocardial contractility é central venous pressure ê ADH release (pituitary) ê H2O excretion (kidney) ê Cardiac output ê renal blood flow é rennin secretion (kidney) é angiotension II (circulation) é aldosterone (adrenal) ê Na+ excretion (kidney) FLUID RETENTION & OEDEMA Increasing load on failing heart CVS 32 V1 receptors é sympathetic actitvity NA release (Baro reflex) AT receptors A adrenoceptors VASOCONSTRICTION Increasing TPR & afterload on failing heart Classification of Heart Failure Class I – no limitation of physical activity Class II – Slight limitation of activity (breathless/fatigue with moderate exercise) Class III – Marked limitation (breathless with minimal exercise) Class IV – Severe limitation (symptoms at rest) • State what is meant by the term positive inotropic drug. Ionotropes change cardiac contractility, positive increases, negative decreases. Chronotropes change cardiac rate, positive increases, negative decreases. • Describe the treatment of heart failure Aims are to: Reduce Na+ and Water retention Diuretics (e.g. frusemide) – can lower K+, which affects digoxin Angiotensin converting enzyme inhibitors (e.g. Captopril) – inhibit conversion of angiotensin I (inactive) to II (active) preventing production of aldosterone à reduces Na+ reabsorption. Also cause some vasodilatation Dopamine agonists (e.g. ibopamine) – renal vasodilatation à increases flow à increased sodium & water excretion Reduce Afterload & Preload ACE inhibitors (e.g. captopril) – reduce circulating angiotensin II à reduce vasoconstriction Vascular smooth muscle relaxants (e.g. Hydrallazine (arterial), GTN (venous)) – variety of mechanisms including increasing cGMP Phosphodiesterase inhibitors (e.g. Amrione) – theoretically could cause Badrenoceptor mediated dilatation Dopamine agonists (e.g. Ibopamine) – possible B-adrenoceptor / Dopamine receptor mediated reaxation Improving Contractility – Positive Inotrophic Drugs B-adrenoceptor agonist (e.g. Dobutamine) – mimic the action of of NA to increase force (& rate). Used in short term cardiac failure – e.g. septic shock Dopamine Agonists (e.g. Ibopamine) – act on B-adrenoceptors to increase force, also vasodilate kidney Phosphodiesterase Inhibitor (e.g. Amrinone) – inhibit cAMP breakdown to augment NA at B-adrenoceptors, also cause vasodilatation. BUT increase mortality due to arrhythmia (short term use only) Cardiac Glycosides (e.g. Digoxin, Ouabain) – inhibit Na/K/ATPase à increased intracellular Na à reduce Na/Ca exchange à reduce Ca expulsion from cell à increase intracellular Ca à increase contractility. • State simplistically the currently accepted mechanism of action of digoxin. DIGOXIN - from foxglove (digitalis). Increases force of contraction, reduces HR, slows/blocks AV conduction ( can à heartblock). Poisons AV node this can have a rate limiting effect in AF. NARROW therapeutic range. Effects worsened by low K (NB: beware if used with diuretic). Excreted by kidney (Ouabain eliminated by liver) CVS 33 Acute pulmonary oedema • Describe the typical history of pulmonary oedema • • • • • • Describe the typical clinical features • • • • • • • • • • Increased fluid in alveolar wall à alveolar spaces à pulmonary stiffness à sense of dyspneoa Capillary rupture à red cells in interstitium Macrophages phagocytose & accumulate pigment à heart failure cells Discuss the differential diagnosis including chest infection, pulmonary embolism and adult respiratory distress syndrome. • • • • • • Left ventricular failure Mitral stenosis Malignant hypertension ARDS (trauma, malaria, aspirin OD, glue sniffing) Fluid overload Head injury Describe the morphology and histological changes of the lungs in pulmonary oedema • • • • • Cough with frothy, blood tinged sputum Increased HR & RR Peripheral circulation shutdown Increased JVP Gallop Rhythm Crackles (esp basal) & Wheeze throughout the chest Decreased PaO2 Initial decreased PaCO2, then later increases Diffuse haze on CXR (can be unilateral) List the common causes of pulmonary oedema. • • • • • • • Dyspnoea – which may first occur at night as PND Orthopnoea Wheezing Anxious Sweaty Asthma COPD Pneumonia PE ARDS Outline the general principles of management of pulmonary oedema including drugs used in treatment, their route of administration and mechanism of action. NB: begin treatment before investigations • Monitor BP, HR, RR, JVP, ABG, UO, Cyanosis • Sit patient upright • Give 100% O2 • IV Access & monitor ECG – treat any arrhythmias CVS 34 • • • • • • Frusemide (& catheter) à diuresis to offload fluid ACEi – shown to reduce mortality. Use sartan if ACEi not suitable B-Blocker – start low-go slow but shown to reduce mortality Spironlactone – if Sx despite all the above Digoxin – even if in sinus à improved outcomes Vasodilators - GTN (if systolic BP > 90mmHg), Start Nitrate if >100mmHg, Diamorphine (monitor RR closely) – will à vasodilatation à reduce preload • If resistant / contraindications to drugs / severe à ITU and arrange CPAP to force the fluid back into the circulation If due to cardiogenic shock can try an Intra Aortic Balloon Pump (IABP) – inflates during diastole à forces fluid forward to body and backwards into coronary arteries • • Outline the investigations used in acute pulmonary oedema including ECG, CXR, cardiac enzymes and echocardiography. • • • • • CXR – cardiomegaly, pulmonary oedema, fluid in costophrenic angles & fissures ECG – signs of MI, AF, LV hypertrophy, Tamponade, rhythm changes U&E – ensure checked esp if planning to use spironolactone (can à raised K+) Cardiac enzymes - to check for MI ECHO – will assess heart function. Normal LVF = 50%, < 30% = poor X-ray changes of left ventricular failure A – Alveolar oedema (bats wings shadowing) B – Kerley B lines (interstitial oedema) C – Cardiomegaly D – Dilated prominent upper lobe vessels E – Pleural effusion CVS 35 Congestive cardiac failure (CCF) • Define heart failure and classify common causes Heart Failure – CO & BP are inadequate for the body’s requirements Common Causes Pump failure • Heart muscle disease (IHD, Cardiomyopathy) • Restrictive filling (tamponade) • Inadequate HR (B-blockers, heart blodk, MI) • Negative inotrophic drugs Excessive preload • Mitral regurgitation • Fluid overload Chronic excessive overload • Aortic stenosis • Hypertension • Describe the typical history of a patient with CCF • • • Describe the typical clinical examination features of a patient including tachycardia, raised internal venous pressure, tender hepatomegaly, peripheral oedema and ascites • • • Coronary artery disease Loss of ventricular muscle (post MI) Ischaemia Hypertension Valvular disease Congenital heart disease Infective endocarditis Describe the morphology and histological changes of the lungs and liver in heart failure • • • LHF – Cardiomegaly, displaced apex beat, tachycardia, gallop rhythm, mitral regurgitation, crackles at lung bases RHF – raised JVP, smooth tender hepatomegaly, dependent pitting oedema, development of free abdominal fluid (ascites), pleural trasudates List the common causes of CCF • • • • • • • • LHF – fatigue, exertional dyspnoea, dyspnoea, orthopnoea, PND RHF – fatigue, anorexia, nausea, swollen feet & ankles Heart failure cells & low protein fluid in lungs Nutmeg lever due to venous congestion Outline the general management principles for CCF including a description of the common drugs used in treatment, their route of administration and mechanism of action. Lifestyle advice • Education • Diet & weight control (salt & water restrict if severe) • Smoking cessation • Increase physical activity • Vaccination (increased risk of flu etc) CVS 36 Monitoring • Functional capacity • Fluid status • Cardiac rhythm MDT • Diet, opthalmologist etc Pharmacological • Frusemide (& catheter) à diuresis to offload fluid • ACEi – shown to reduce mortality. Use sartan if ACEi not suitable • B-Blocker – start low-go slow but shown to reduce mortality • Spironlactone – if Sx despite all the above • Digoxin – even if in sinus à improved outcomes • Vasodilators - GTN (if systolic BP > 90mmHg), Start Nitrate if >100mmHg, Diamorphine (monitor RR closely) – will à vasodilatation à reduce preload If resistant / contraindications to drugs / severe à ITU and arrange CPAP to force the fluid back into the circulation Surgical options • AIBP = If due to cardiogenic shock can try an Intra Aortic Balloon Pump (IABP) – inflates during diastole à forces fluid forward to body and backwards into coronary arteries • Valve replacement • Angio / stent / bypass if IHD • < 65yrs – transplant • LVAT – mechanical pump if no transplant available • Outline the common investigations used to define the cause of CCF including ECG, CXR, and echocardiography. • Bloods – FBC, LFTs, U&E, Cardiac Enzymes • CXR • ECG • Naturetic peptide – if normal excludes heart failure • ECHO – show ventricular impairment • Nuclear cardiology / Cardiac MRI / PET CVS 37 Intracardiac defects • State the effects on pressures within the heart and major blood vessels of Pulmonary stenosis Back pressure on right ventricle and right atrium. Venous pressure rises due to reduced ejection fraction in right ventricle Aortic stenosis. Left Ventricle has to generate greater pressures, back pressure on left atrium and pulmonary circulation. Systemic pressure initially slight fall then rises as heart hypertrophies. • Describe the term juxtductal coarctation and state its effects on arterial blood pressures and collateral blood flow. • • • • • • • The duct referred to is the ductus arteriosus. The ligamentum arteriosus remains. The Arch of the aorta is narrowed between the brachiocephalic and left common carotid. There is a radio-radial delay due to the coarctation. There is a raised pressure in the right arm and to the right carotid arteries. If the coarctation is below the left subclavian there is a bilateral ABPI difference. Notching of the ribs is seen due to the internal thoracic artery dilating as a collateral circulation Explain the effects of the following on pressures, direction of blood flow and oxygen saturations in the cardiac chambers and major blood vessels. Ventricular septal defect VSD gives an increase to the pressures in the right ventricle and the pulmonary circulation. Flow is Left to Right Eismengers involves a shunt reverse due to pulmonary hypertension, this means that deoxygenated blood flows into the aterial circulation and cyanosis develops Atrial septal defect Flow is left to right, as above can be reversed. Increases pressure on R due to increased filling. Persistent ductus arteriosus Reduced filling of L heart due to escape of blood into Aorta. Increased pressure on R heart due to pumping against systemic arterial pressures. Tetralogy of Fallot. Right heart is under greater pressure, left heart pressure lower because there is an escape to the right heart. Pulmonary circulation under higher pressure. • List the changes in the cardiovascular system occurring during/after birth Closure of Umbilical Vessels Due to - Mechanical clamping, Trauma, Cold, Catecholamines Effect – Increase in peripheral resistance for fetus à increase BP in neonate. Decrease in venous return. Partial asphyxia (causes stimulus to breath) Closure of Foramen Ovale Due to – Decrease in venous return – from closure of umbilical vessels Partial asphyxia à stimulates breathing à reduces pulmonary vascular resistance à increases pulmonary venous return à increases LA pressure Increase in peripheral resistance (due to closure of umbilical vessels) à increased LV pressure à increases LA pressure CVS 38 Effect – left & right hearts no longer connected, now work in series Reduction in Pulmonary Vascular Resistance Due to – Partial asphyxia & cooling à stimulates respiratory system à gaseous distension of lungs à pulmonary vasodilatation Effect Fall in pulmonary arterial pressure (approx 50%) Reverse of flow through ductus arteriosus (aorta à pulmonary trunk) Closure of ductus arteriosus (à ligamentum arteriosus) Constriction – hours Closure – days (due to pO2, catecholamines, bradykinin, PG) Fibrosis – weeks Closure of ductus venosus Liver bypass closes CVS 39 Haemorrhage and shock • Define the term hypotensive shock and give three possible causes. Hypotensive shock occurs when the blood pressure is insufficient to perfuse the tissue beds. Can be due to hypovolaemic, cardiogenic or neuropgenic causes. • Summarize the cardiovascular reflexes elicited following the sudden loss of 1 litre of blood Haemorrhage ê Cardiac Output ê BP à Baro Reflex é HR & Str Vol Venocontriction é Sympathetic activity é Angiotensin é Aldosterone é Vasopressin (ADH) é Cardiac Output Vasoconstriction é Blood Pressure é TPR Long term Intense Constriction Impaired perfusion Accumulation of metabolites é Cap’ Permeability Loss of circulating fluid Other Causes of Shock • Cardiogenic • Endotoxic (septic) • Anaphylactic (CO2, K, H, Adenosine, Histamine, 5HT) Vasodilatation ê Cardiac Output ê Blood Pressure HYPOTENSIVE SHOCK ê Cerebral & Coronary Blood Flow CVS 40 Cardiac surgery • Outline the difference between open and closed heart surgery and outline the principles involved in cardio-pulmonary bypass. Open-heart surgery technically means any procedure where a heart chamber is cut open, but in modern use means a procedure where the heart lung bypass machine is used. In cardio-pulmonary bypass, the venous inflow to the heart and arterial outflow from the heart are replaced with cannulae and the blood is pumped around the body and oxygenated by the CPB machine. A separate circuit may be established to perfuse the coronary circulation to prevent the heart for beating, while still preserving myocardial function. Closed heart surgery is performed on a still beating heart and does not involve bypass. • Describe the main incisions for cardiac surgery • • • Median Sternotomy – Midline incision through sternum Lateral Thoracotomy – Divided anterior or posterior, may involve removal of whole of or part of a rib. Outline the surgical principles involved in the treatment of coronary artery disease Take non-essential vessels including Left and right Internal Mammary Arteries and the long saphenous veins, these are used to bridge around the narrowing and / or to provide a fresh flow of arterial blood to the heart. Operation is usually done on CPB but can now performed without if necessary. Vein grafts are always reversed to make sure there is no problem with valves. • Outline the surgical management of valvular heart disease including a simple classification of prosthetic valves (mechanical and tissue prostheses). Describe how to anticoagulate a patient and be aware of the pitfalls. 3 Main Types of mechanical valve – Ball and cage, tilting disc and bileaflet. Tissue prostheses can be pure pig or tissue leaflet on metal ring often from bovine pericardium Anticoagulation is very important – Warfarin is standard, INR 2-3. Start with loading does 996 over three days then re-check INR. Must use heparin until warfarin is in therapeutic range. Beware polypharmacy, diet and haemorrhage risks. If severe risk of bleeding can use clopidogrel instead. • Classify cardiac trauma (penetrating and non-penetrating). Recognise acute cardiac tamponade and outline the principles involved in aspirating the pericardial sac. • • • Outline the clinical presentation and treatment of the most common myocardial tumour, a myxoma. • • Acute cardiac tamponade Sx. – Shock and a raised JVP Needle 45 degrees below left xiphisternum, aim for tip of left scapula. Aspirate continuously. Watch for ECG changes as may indicate cardiac muscle damage Tumour of cardiac muscle. Benign. Presents either like endocarditis (fever, weight loss, clubbing, raised ESR) or mitraL stenosis (atrial obstruction, emboli, AF) Outline the principles involved in the surgical treatment of constrictive pericarditis. • Pericardiotomy – splitting of pericardium, removes constriction. CVS 41 Heart valve disease • Classify the causes of valvular heart disease • congenital (bicuspid aortic valve) • rheumatic • ischaemic (mitral regurgitation) • infective (endocarditis). • Outline the common symptoms of patients with valvular heart disease. Related to outcome (e.g. aortic stenosis à LHF à symptoms) • Outline the non-invasive tests (ECG, CXR and Echo) used to assess heart valves. CXR – size of heart, calcified valves, pulmonary HT ECG – shows muscle mass pattern & conduction pattern ECHO – demonstrate dilatation of chambers, use Doppler for velocity & direction • Outline the reasons for performing right and left heart catheterisation. Catheterisation of the right heart is performed to get a measure of CVP, to assess pressure gradient across the tricuspid valve. Left heart is to assess CO, to look at ventricular wall motility, pressure gradient across the mitral and aortic valves. • Outline the indications for medical or surgical treatment of valvular heart disease affecting the aortic and mitral valves. Indications are based on symptoms, not on clinical findings. Medical treatment of valvular disease relies on not treating aggressively with antihypertensives as this may compromise cardiac output. Surgical management should only be considered when the VHD is debilitating. CVS 42 Infective endocarditis • Define what bacterial endocarditis is and who is at risk. Overgrowth of bacteria on the valves of the heart 2 factors required – bacteraemia & abnormal endocardium Risk factors • Poor dental hygiene / dental treatment • IV drug use (in or out of hospital) – esp central line • Cardiac surgery • Pacemaker • Artificial heart valves • Any cardiac malformation • Describe the typical clinical examination features of a patient with bacterial endocarditis • • • • • • • • • List common infecting bacteria. • • • • • • Acute illness (95% malaise, 90% pyrexia, 25% arthralgia) New / changing murmer (90%) Haematuria (70%) Petechiae (50%) Splenomegally (40%) Oslers Nodes (15%) Splinter Haemorrhage / Clubbing (10%) Janeway Lesions / Roth Spots (5%) Dental procedures A-haemolytic viridans strep (mutans, sanguis, oralis, milleri) Valve (within 60 days) S.Aureus / S.Epidermidis Valve (after 60 days) S.Viridans / S.Aureus IVDU / Catheters S.Aureus / Candida Others Enterociccus, S.Bovis, HAKEC, Culture negative Describe the morphology and histological changes seen on an affected heart valve Infection à valvulitis à exposure of valve collagen à thrombus deposition = thrombotic vegetations à organisation & collagen scarring à mechanical & functional abnormality Mitral & aortic are most commonly affected Acute infective endocarditis – virulent organism can collonise a normal valve Subacute infective endocarditis – occurs on abnormal valves • Describe the pathological complications of infective endocarditis • • • • Small emboli à systemic circulation à infarcts (kidney, brain, spleen) Gradual destruction of valve cusps à valve incompetence à cardiac failure Immune complexes trap in small vessels à skin signs, roth spots and glomerulonephritis Outline important investigations including blood cultures, FBC, ESR, renal function tests and echocardiography. • Blood cultures X3 (speak to lab b4 sending) • FBC – often anaemia & leucocytosis CVS 43 • • • • U&E – check for renal dysfunction – correct any ion imbalance LFTs – often increased Alk Phos CRP & ESR – CRP will respond faster Urine – haematuria / proteinuria • Outline the common antibiotic regimen used to treat endocarditis • Benzylpenicillin IV 1.2g every four hours plus Gentamicin IV 80 mg BD • Amoxicillin and or Vancomyin instead of Ben Pen if not viridans strep • Understand the indications and justify the need for antibiotic prophylaxis in patients with pre-existing heart valve disease. If patients have existing vegitations (rheumatic fever) or replacement valves then risk of colonisation is greater. Prophylaxis for dental work, any surgery and after open wounds. CVS 44 Venous thrombo-embolic disease • Identify the usual initial anatomic location of deep venous thrombosis. • • • Describe the risk factors for venous thrombosis. • • • • • • • • • • Increasing age Pregnancy Synthetic oestrogen (Pill / HRT) Surgery (esp pelvis / othopaedic) Past DVT Malignancy Obesity Immobility Thrombophilia Describe the clinical features of a deep venous thrombosis • • • • Can occur in any vein of leg Most common in calf (65% are asymptomatic) Calf warmth / tenderness / swelling Mild fever Pitting oedema Describe the pathophysiology of chronic venous insufficiency and the post-phlebitic syndrome. Venous insufficiency Veins fail to drain blood adequately (due to absence / damage to valves) Increased venous pressure affects capillaries à low flow à leucocyte trapping à damage to BM à leaking plasma proteins to form a “cuff” à oedema & decreased O2 to tissues à inflammation & necrosis à varicose veins & discomfort à non-healing ulcers à leg oedema à lipodermatosclerosis (fat necrosis & fibrosis à red/brown colour) Post phlebitic syndrome Complications occurring post DVT - All result from the impaired return of blood through the veins of the lower leg to the heart. Features include: Persistent oedema (swelling), pain, purpura (bleeding into the skin), increased skin pigmentation, eczematoid (eczema-like) dermatitis, pruritus (itchiness), ulceration, and cellulitis (bacterial infection just below the skin). • Outline the invasive (venogram) and non-invasive tests (ultrasound and MRI) available for investigating a suspected DVT. • D-dimer (negative result excludes DVT) • Compression US / Doppler • Venography – inject contrast to foot & observe progress CVS 45 • Discuss the treatment of a proven DVT, the methods of administering appropriate anticoagulants and how anticoagulation is monitored. • • • • • • • Start with Warfarin and Heparin. Heparin alone will NOT stop the evolving clot, it ill only prevent new clots. Warfarin will stop the clot growing. It takes three days for warfarin to work so 72 hours of Heparin is needed. Clexane is normally used. Clexane can be monitored using APPT if necessary, warfarin uses INR / PTT Describe the range of clinical presentation and associated pathology of pulmonary embolic disease depending on clot size and cardiopulmonary haemodynamics. • • • • • • • • Acute breathlessness Pleuritic chest pain Haemoptysis Dizzy / syncope Pyrexia Cyanosis Tachypnoea & tachycardia Increased JVP MASSIVE = if 60% pulmonary vasculature blocked à EMD / PEA MAJOR = middle size artery à SOB & haemoptysis MINOR = small peripheral vessels à minor symptoms • Outline the available radiological techniques for diagnosing pulmonary emboli and discuss the limitations of ventilation-perfusion scanning in the diagnosis of pulmonary emboli. • CTPA vs VQ scan. • CTPA is better for small vascular defects, central is easier to see. • VQ is good for large peripheral wedge infacts but not in so good for central infarcts as may be masked. • VQ not good if already has significant lung pathology, but CTPA not tolerated in some due to problems with the contrast medium. • Outline the indication and contraindications for anticoagulation. Indication is that there is increased risk of DVT, Stroke or PE, HX of those or AF, stent & prosthetic heart valves. Contraindications – Bleeding disorders, endocarditis, current bleeding, recent haemorrhagic stroke etc. CVS 46