Cardiology Flashcards
What are the causes of ST elevation?
Myocardial infarction
Pericarditis (saddle-shaped)
Normal variant (high take off)
Left ventricular aneurysm (persistent after MI)
Prinzmetal’s angina (Coronary artery spasm)
Rarely: Subarachnoid Haemorrhage
What are the causes of peaked T waves?
Myocardial ischaemia (Acute ischaemic change) Hyperkalaemia
What are some causes of inverted T waves?
Myocardial ischaemia Digoxin toxicity Subarachnoid haemorrhage (Deep) Arrhymogenic right ventricular cardiomopathy Brugada syndrome.
Causes of a prolonged PR interval?
Idiopathic (athletes) Ischaemic heart disease Digoxin toxicity Hypokalaemia Rheumatic fever Aortic root pathology Lyme disease Sarcoidosis Myotonic dystrophy
What is the criteria defining Stage 1 hypertension?
Clinic BP >140/90mmHg and subsequent ABPM or HBPM average BP >135/85mmHg
What is the criteria defining Stage 2 hypertension?
Clinc BP >160/100mmHg and subsequent ABPM or HBPM average BP >150/95mmHg
What is the criteria defining severe hypertension?
Clinic systolic BP>180mmHg or Clinic diastolic >110mmHg
Describe Atrial Fibrillation, it’s causes, signs and tests, and management
A chaotic irregular atrial rhythm with variable AV response causing an irregularly irregular pulse. May be split into fast and slow AF, Fast AF more than 100bpm, Slow considered less than 60bpm.
Causes: heart failure/ischaemia, IHD, MI, PE, Mitral Valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnesia
Symptoms: may be none or chest pain, palpitations, dyspnoea, faintness. May be acute, chronic or paroxysmal
Tests: ECG shows absent p waves and irregular QRS complexes. Blood tests; U+E, Troponin, TFTs to look for underlying cause, CXR
Management:
- haemodynamically unstable AF requires immediate DC cardioversion, if prolonged AF (more than 48h) TOE is needed to confirm that there is no evidence of left atrium thrombus.
- Haemodynamically stable, can be rate or rhythm controlled, younger patients or reversible causes should opt for rhythm control, elderly patients with chronic AF should opt for rate control
- Rate control includes beta-blocker (metoprolol, bisoprolol), or rate-limiting Ca-blocker e.g. Verapamil, diltiazem failing this digoxin can be used
- rhythm control, try amiodarone, or sotalol, if persisting for more than 48hr anticoagulation 3wks and cardioversion,
- paroxysmal AF can be dealt with pill in the pocket with flecainide or sotalol.
- Anticoagulation should be initiated in chronic and paroxysmal AF
Describe the CHADS-VASc score
Score of 1 or more consider oral anticoagulation, 2 or more warfarin.
C ongestive cardiac failure H ypertension A ge >75 (2 points) D iabetes S troke (2 points) V ascular disease A ge >65 Sc - Sex catergory female
Describe the HAAS-BLED score
Score of 3 or more indicates high risk of bleeding and alternatives to anticoagulation should be considered
H ypertension A lcohol abuse A bnormal renal or liver function S troke B leeding disorder or previous major bleed L abile INR E lderly >65 D rug abuse
What is a bounding pulse a sign of?
CO2 Retention, liver failure, sepsis
What is a small volume pulse a sign of?
Aortic stenosis, shock, pericardial effusion
What is a collapsing pulse a sign of?
Aortic regurgitation, AV malformation, patent ductus arteriosus
What is a slow rising pulse a sign of?
Aortic stenosis
What is a bisferiens pulse a sign of?
Combined Aortic stenosis and regurgitation
What is pulsus alternans a sign of?
suggests LVF, cardiomyopathy or aortic stenosis
What is a jerky pulse a sign of?
HOCM
What is pulsus paradoxus and what is it a sign of?
Systolic pressure drop in inspiration >10mmHg occurs in severe asthma, constrictive pericarditis or cardiac tamponade.
Describe the 1st heart sound (S1)
S1 represents the closure or mitral (M1) and tricuspid (T1) valves. splitting in inspiration may be heard and is normal.
What is a loud S1 a sign of?
Mitral stenosis
What is a soft S1 a sign of?
occurs if PR interval prolonged or mitral valve incompetent e.g. mitral regurgitation
Describe the 2nd heart sound S2
S2 represents the closure of the aortic (A2) and pulmonary (P2) valves.
What is a soft A2 a sign of?
aortic stenosis
What is a loud P2 a sign of?
Pulmonary hypertension
What is a soft P2 a sign of?
Pulmonary stenosis
Describe the splitting of the second heart sounds under normal and abnormal conditions
In inspiration the sounds are normally split with A2 followed by P2 this is due to the variation of right heart venous return with respiration delaying the pulmonary component.
Wide splitting of the heart sounds occurs in RBBB, pulmonary stenosis, deep inspiration, mitral regurgitation and VSD.
Fixed wide splitting occurs in ASD
Reversed splitting P2 followed by A2 with splitting increasing on expiration occurs in LBBB, aortic stenosis, Patent ductus arteriosus.
Describe the 3rd heart sound
S3 may occur just after S2, it is low pitched and best heard with the bell. S3 is pathological over the age of 30.
What is a loud S3 a sign of?
Mitral regurgitation, VSD, Dilated cardiomyopathy, post MI.
Describe the 4th heart sound
S4 occurs just before S1, always abnormal. it represents atrial contraction against a stiff ventricle i.e. aortic stenosis, HOCM
What is an ejection systolic click a sign of?
heard early in systole with bicuspid aortic valves may be aortic stenosis
What is a mid-systolic click a sign of?
mitral valve prolapse
What is an opening snap a sign of?
precedes the mid-diastolic murmur of mitral and tricuspid regurgitation
What are the causes of an ejection-systolic murmur?
cresendo-decresendo murmur, may be due to aortic stenosis or sclerosis, pulmonary stenosis or HOCM
What are the causes of a pansystolic murmur?
monotoned murmur, and merges with S2. May be due to mitral or tricupsid regurgitation (also soft S1) or VSD.
What are the causes of a late-systolic murmur?
mitral valve prolapse may also have mid-systolic click
What are the causes of an early diastolic murmur?
high pitched murmur occurs in aortic and pulmonary (much rarer cause) regurgitation.
What is a Graham-Steell murmur
A early diastolic murmur due to pulmonary regurgitation because of pulmonary hypertension from a stenotic mitral valve.
What are the causes of a mid-diastolic murmur?
Low pitched and rumbling in nature. the occur in mitral stenosis, rheumatic fever, aortic regurgitation
What is a tapping apex beat a sign of?
Palpable first hearts sound indicative of Mitral Stenosis
What is Corrigan’s sign?
Cartoid pulsation may be seen in Aortic Regurgitation
What is Duroziez’s sign?
In severe Aortic Regurgitation, gradual pressure over the femoral artery leads to a systolic and diastolic bruit. The former heard with the bell of the stethoscope when the proximal femoral artery is compressed and the latter with the distal femoral artery.
What is de Musset’s sign?
Head nodding with each heart beat a sign of Aortic Regurgitation
What is Quincke’s sign?
Capillary pulsations in nail beds a sign of Aortic Regurgitation
What is Traube’s sign?
‘Pistol shot’ sound over femoral arteries a sign of Aortic Regurgitation
What is Austin Flint murmur?
A mid-diastolic murmur due to the fluttering of the anterior mitral valve cusp caused by the regurgitant stream of Aortic Regurgitation.
What are Osler nodes?
Painful pulp infarcts in fingers or toes which together with janeway lesions is pathognomic of IE. Due to immune complex deposition
What are janeway lesions?
Non-tender erythematous, haemorrhagic or pustular spots on the palms or soles, which together with Osler nodes are pathognomic of IE. Due to infective embolic phenomena
Describe bradycardia and its treatment
If asymptomatic and rate greater than 40bpm, no treatment is required. Look for a cause (drugs, sick sinus syndrome, hypothyroidism) and stop any drugs that may be contributing (Beta-blockers, digoxin).
If rate less than 40bpm or patient is symptomatic give atropine 0.6-1.2mg IV up to max of 3mg. If no response, insert a temporary acing wire. If necessary, start an isoprenaline infusion or use external cardiac pacing.
Describe sick-sinus syndrome, its causes, and its management.
Aka Tachy-Brady syndrome, sinus node dysfunction causes bradycardia +/- arrest, sinoatrial block or SVT or AF alternating with bradycardia/asystole.
Causes:
- Intrinsic e.g. Idiopathic Degenerative Fibrosis (Commonest), ischaemia, cardiomyopathy, sarcoidosis, haemochromatosis, congenital abnormalities.
- Extrinsic e.g. Digoxin, beta-blockers, calcium-channel blockers, autonomic dysfunction, hypothyroidism, hyperkalemia
Management:
-Pace if symptomatic
Causes of sinus tachycardia
Rate>100 Causes:
- Anaemia
- Anxiety
- Exercise
- Pain
- Fever
- Sepsis
- hypovolaemia
- Heart failure
- PE
- Pregnacy
- Thyrotoxicosis
- Beriberi
- CO2 retention
- caffeine, adrenaline, nicotine
Define Narrow Complex Tachycardias, the types, and principles of management.
ECG shows rate of >100bpm and QRS complex duration of less than 120ms.
Types:
- sinus tachycardia
- Supraventricular tachycardia
- Atrial fibrillation
- atrial flutter
- multifocal atrial tachycardia
- junctional tachycardia
Management:
- if patient is compromised use DC cardio version
- otherwise identify rhythm and treat accordingly.
- generally vagal manoeuvres (carotid massage, Valsalva) attempted to correct/ unmask rhythm
- if unsuccessful adenosine 6mg IV bolus, if fails try 12mg and another 12mg.
Describe SVT and its management
Narrow complex tachycardia with ECG showing P waves absent or inverted after QRS complex.
Management:
- Vagal manoeuvres (breath-holding, vasalva, carotid massage) are 1st line
- IV adenosine is the drug of choice (6mg bolus)
- If adenosine fails use IV verapamil (5mg over 2mins)
- If drug therapy fails use DC cardioversion
Describe Junctional Tachycardia and its management
Narrow complex tachycardia with ECG showing rate of 150-250bpm, P wave either buried in QRS complex or occurring just after. There are 3 types of junctional tachycardia:
- AV nodal reentry tachycardia
- AV reentry tachycardia
- His bundle tachycardia
Management:
- Try vagal manoeuvres
- IV Adenosine will usually return to sinus rhythm
- If it re-occurs try amiodarone or beta-blocker
- Radiofrequency ablation is more frequently being used in AVRT and symptomatic AVNRT
Describe Wolff-Parkinson-White syndrome, the types, associations, features and management
Caused by congenital accessory conduction pathway between atria and ventricles. May preset as a tachyarrhythmia by the formation of a reentry circuit involving the accessory pathway termed Atrioventricular reentry tachycardias (AVRT).
Types:
- Type A which indicates a left sided accessory pathway, and show a dominant R wave in V1 and tall R waves and inverted T waves in V1-V3 mimicking right ventricular hypertrophy.
- Type B indicates a right sided accessory pathway, there is a dominant S wave in V1 and tall R waves and inverted T waves in inferior leads and V4-V6 mimicking left ventricular hypertrophy.
Associations: HOCM, Mitral valve prolapse, Ebstein’s Anomaly, Thyrotoxicosis, ASD (Ostium Secundum)
Features: Resting ECG shows short PR interval, Wide QRS complex (due to slurred upstroke or delta wave) and ST-T changes in opposite direction of major component of QRS complex
Management:
Refer to cardiologist for electrophysiology and ablation of accessory pathway
WPW with AF needs urgent treatment with DC Cardioversion as it can quickly deteriorate into VF, Digoxin is contradindicated in this scenario.
Define Broad Complex Tachycardia, the differentials and management
ECG shows rate of >100bpm and QRS complexes >120ms. If no clear QRS complexes, it is VF of asystole.
Differential Diagnosis:
- VT includes torsade de pointes
- VF
- SVT with bundle branch block/aberrant conduction
Management:
- if VF or pulseless VT use asynchronised DC shock
- if stable VT give high flow oxygen, obtain IV access, try B-blockers e.g. Sotalol, metoprolol, if fails or known LV Dysfunction try Amiodarone IVI, if fails consider DC shock
Define Torsades de pointes and its management
Looks like VF but is VT with varying axis. it is due to increased QT interval (a SE of antiarrhythmics)
Management:
- magnesium sulphate 2g IV over 10 mins
- look at drug chart for QT prolonging medications (Anti-psychotics)
Describe the Framingham criteria for congestive cardiac failure
Diagnosis of CCF requires the simultaneous presence of at least 2 major criteria or 1 major and 2 minor
Major criteria: •paroxysmal nocturnal dyspnoea •crepitations •S3 gallop •cardiomegaly •increased central venous pressure (>16cmH2O at right atrium) • weight loss >4.5kg in 5 days of treatment •neck vein distension •acute pulmonary oedema •hepatojugular reflux
Minor criteria: •bilateral ankle oedema •dyspnoea on ordinary exertion •tachycardia •nocturnal cough •decreased vital capacity by 1/3 of maximum recorded •hepatomegaly •pleural effusion
Describe the management of chronic heart failure
Conservative: Change lifestyle factors e.g stop smoking, eat less salt, optimise weight and nutrition, Treat exacerbating factors such as anaemia, thyroid disease, infection, hypertension Avoid exacerbating factors such as NSAIDs (cause fluid retention) and verapamil (-ve inotrope)
Pharmacological:
- ACE inhibitors: Consider in all with left ventricular systolic dysfunction, improves symptoms and prolongs life. If cough is a problem an angiotensin receptor blocker may be substituted
- Beta-blockers: e.g. carvedilol decreased mortality in heart failure. Use with caution start low and go slow.
- Diuretics e.g. Frusemide can reduce the risk of death and worsening heart failure.
- Ivabradine can be used it acts by reducing the heart rate via specific inhibition of the funny channel, it is contraindicated in sick-sinus syndrome and should not be used with verapamil or diltiazem
- Spironolactone decreased mortality by 30% when added to conventional therapy. Use in those still symptomatic despite above treatment.
- Digoxin helps symptoms even in those with sinus rhythm and should be considered in those with LVSD HF who have signs or symptoms of heart failure whilst receiving standard therapy or those with concurrent AF
- hydralazine and isosorbide mononitrate symptomatic, not often used now.
Surgical: Symptomatic patients with maximum pharmacological management and LVEF less than 35% may benefit from implantable devices.
- If narrow QRS complex Implantable Cardioverter defibrillators (ICD) may be indicated.
- If broad QRS complex cardiac desynchronisation therapy with defibrillators (CRT-D)
Describe the types of hypertension
Isolated systolic hypertension - the most common form of hypertension in the UK. Affects >50% of over-60s. It results from stiffening of the arteries. Doubles the risk of MI, triples the risk of CVA.
‘Malignant’ or accelerated phase hypertension - refers to a rapid rise in BP leading to vascular damage. Hypertension is usually severe (systolic >200, diastolic >130) + bilateral retinal haemorrhages. Symptoms are common e.g. visual disturbance and headache. It is more common in younger patients and in black patients.
Essential hypertension - cause unknown
Secondary hypertension - due to renal disease, endocrine disease (cushing’s, conn’s, phaeochromocytoma), coarctation, pregnancy, steroids, the pill
Describe the management of hypertension.
Treatment goal: ideally less than 140/90mmHg, less than 130/80mmHg in diabetics, 150/90 if older than 80. Reduce slowly.
Lifestyle changes: stop smoking, low fat diet, reduce alcohol and salt intake, increase excercise and reduce weight if obese.
Drug therapy:
- Monotherapy if older than 55 and/or Afro-carribean 1st line is Ca channel blocker e.g. Amlodopine. Otherwise ACE-i e.g. Ramipril is first line also first in diabetics.
- Dual therapy, both Ca channel blocker and ACE-i
- If this fails add diuretic
- if this fails and potassium less than 4.5mmol/L add spironolactone if K+ high dose diuretic. If further diuretic therapy not tolerated or ineffective consider alpha or beta blocker.
Describe Acute Coronary Syndrome, its risk factors, symptoms, and tests.
ACS includes unstable angina, and evolving MI. MI can be further divided into STEMI or new onset LBBB, and NSTEMI.
Risk factors: age, male, family history, smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use.
Symptoms: Acute central chest pain, lasting >20min, often associated with nausea, sweatiness, dyspnoea, palpitations. May present without chest pain e.g. in the elderly or diabetics, in which syncope, pulmonary oedema, epigastric pain, vomiting, post-op hypotension, oliguria, acute confusional state.
Tests: ECG (in 20% ECG may be normal at first repeat ECG!)
-STEMI: Classically hyperacute (tall) t waves, ST elevation or new LBBB, T wave inversion and pathological Q waves follow over hours-days.
-NSTEMI: ST depression, t-wave inversion, non-specific changes.
CXR,Bloods, cardiac enxymes. Troponin elevated after 3-12h of onset if normal 6h after onset chance of missing MI is small.
Describe acute pericarditis, its features, tests and treatment
Inflamation of pericardium it may be idiopathic or secondary due to infection, MI, drugs (procainamide, hydralazine, penicillin, isoniazid), uraemia, RA, SLE, sarcoidosis, radiotherapy.
Features: central chest pain worse on inspiration or lying flat and relieved by sitting forward. A pericardial friction rub may be heard. look for evidence of pericardial effusion or cardiac tamponade. Fever may occur.
Tests: ECG classically shows saddle-shaped ST elevation, but can be normal. Troponin may be raised. Cardiomegaly on CXR may indicate pericardial effusion.
Treatment:
-NSAIDs are first line, ICAP study suggests that Colchicine and Aspirin reduce the risk of recurrent pericarditis.
Describe cardiac tamponade, its causes, signs, and management.
Fluid in the pericardial sac leads to increased pericardial pressure and poor ventricular filling and fall in cardiac output. Beck’s triad, falling BP, rising JVP (distended neck veins), muffled heart sounds. Fast/Echo is diagnostic.
Causes: Trauma (usually penetrating), any cause of pericarditis, aortic dissection, haemodialysis, warfarin, transeptal puncture at cardiac catheterisation, post cardiac biopsy.
Signs: increased PR, decreasing BP, pulsus paradoxus, increased JVP, kussmaul’s sign, muffled heart sounds.
Management:
- ABCDE
- seek expert help
- FAST scan if in ED
- If patient deteriorates consider pericardiocentesis
- If cardiac arrest emergency thoracotomy is needed
- if stable contact cardiothoracic surgeion as effusions need to be drained.
Describe SVC obstruction, its causes, signs and symptoms, investigation, and management
SVC obstruction is not an emergency unless there is tracheal compression with airway compromise.
Causes: malignancy account for >90%, 3/4 of which are lung cancer. rare causes include mediastinal enlargement, thymus malignancy, mediastinal lymphadenopathy (sarcoid, lymphoma).
Signs + symptoms: dyspnoea, orthopnoea, plethora/cyanosis, swollen face and arm, cough, headache, engorged veins.
Investigations: urgent contrast enhanced CT
Management: biopsy if cause unknown, dexamethasone PO 8-16mg/d. Consider balloon venoplasty and SVC stenting for rapid relief of symptoms
Describe Mitral stenosis its causes, symptoms, signs, tests and management
Causes: Rheumatic, congenital, carcinoid, prosthetic valve.
Symptoms: Dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis, chronic bronchitis-like picture
Signs: malar flush on cheeks (due to decreased cardiac output), low-volume pulse, AF, tapping non-displaced apex beat (palpable S1). On auscultation, loud S1, opening snap, rumbling mid-diastolic murmur heard best in expiration with the patient on the left side.
Tests: ECG may show AF, P-mitrale, RVH, Progressive RAD. Echo is diagnostic.
Management:
If AF rate control and warfarin.
Diuretics decreased preload and pulmonary venous congestion. May need valve replacement most can be managed with Percutaneous balloon mitral valvotomy unless they have contraindications such as
-Moderate to severe mitral regurgitation
-left atrial thrombus
-heavily calcified mitral Valve
-concomitant coronary artery or other valve disease requiring surgery
In these cases patients should undergo mitral valve replacement.
Describe mitral regurgitation its causes, symptom, signs, tests, and management
Causes: functional (LV dilatation), annular calcification (elderly), rheumatic fever, infective endocarditis, mitral valve prolapse, ruptured chordae tendinae, papillary muscle dysfunction, congenital, connective tissue disorders, cardiomyopathy
Symptoms: dyspnoea, fatigue, palpitation, signs of infective endocarditis
Signs: AF, displaced hyperdynamic apex, RV heave, soft S1, Loud P2 (due to pulmonary hypertension), pansystolic murmur at apex radiating to axilla.
Tests: ECG may show AF +/- P-mitrale, LVH, Echo is diagnostic looking at mitral valve function, degree of LVH, and degree of pulmonary HTN.
Management:
- rate control AF and warfarin
- diuretics improve symptoms
- valve replacement/repair ultimate treatment (metallic valves require INR 3-4)
- mitraclip less invasive, for patients that cannot tolerate open heart surgery, still in research phase
Describe mitral valve prolapse, its symptoms, signs, complications, tests and management.
Most common valvular abnormality (prevalence ~5%), occurs alone or with ASD, patent ductus arteriosus, cardiomyopathy, turner’s syndrome, marfans syndrome, osteogenesis imperfecta, WPW
Symptoms: asymptomatic or atypical chest pain and palpitations.
Signs: mid-diastolic click
Complications: mitral regurgitation, cerebral emboli, arrhythmias, sudden death
Tests: Echo is diagnostic, ECG may show inferior T-wave inversion
Management: beta-blockers may help palpitations and chest pain, surgery needed if progressive to MR
Describe aortic stenosis its causes, symptoms, signs, tests and management
Causes: Senile calcification is the commonest, congeitial (bicuspid valve, williams syndrome), rheumatic heart disease.
Symptoms: The classic triad includes angina, syncope and heart failure. May also have dyspnoea, dizziness, faints
Signs: slow-rising pulse with narrow pulse pressure, heaving non-displaced apex beat, LV heave, aortic thrill, ejection systolic murmur heard best at the base, left sternal edge and aortic area and radiates to the carotids.
Tests: ECG shows P-mitrale, LVH with strain pattern, LAD poor R wave progession LBBB or complete AV block. Echo is diagnostic severe stenosis can be more accurately invgestiaged with cardiac cauterisation and coronary angiography especially if severe (peak gradient over 50mmHg, valve area less than 1cm3, aortic jet velocity is more than 4m/s, Indexed aortic valve area less than 0.6cm2/m2, velocity ratio less than 0.25)
Management:
- Indications for AVR:
- Patients with severe high-gradient AS who have symptoms by history or on exercise testing
- For asymptomatic patients with severe AS and left ventricular ejection fraction less than 50%
- For patients with severe AS when undergoing other cardiac surgery
- For asymptomatic patients with very severe AS and low surgical risk.
- For asymptomatic patients with severe AS and decrease exercise tolerance or fall in systemic blood pressure with exercise
- For symptomatic patients with low-flow/low gradient severe as with reduced LVEF with a low-dose dobutamine stress study that shows aortic velocity over 4.0m/s or mean pressure gradient over 50mmHg with a valve area less than 1.0cm2 at any dobutamine dose.
- For symptomatic normotensive patients with low-flow/low-gradient severe AS with LVEF over 50%, if clinical, haemodynamic and anatomical data support valve obstruction as the most likely cause of symptoms.
- if patients cannot tolerate AVR, Transcatheter Aortic Valve Implantation (TAVI) is an option
Describe aortic regurgitation its causes, symptoms, signs, tests and management
Causes:
- Acute = IE, ascending aortic dissection, chest trauma
- Chronic = congenital, connective tissue disorders, rheumatic fever, takayasu arteritis, RA, SLE, hypertension,
Symptoms: Exertional dyspnoea, orthopnoea, PND, palpitations, angina, syncope, CCF.
Signs: collapsing ‘water-hammer’ pulse, wide pulse pressure, displaced hyperdynamic apex beat.
high pitched early diastolic murmur best heard in expiration with patient sitting forward.
Also corrigan’s sign, de Musset’s sign, duroziez’s sign, quincke’s sign and traube’s sign.
Tests: ECG shows LVH. Echo is diagnostic.
Management:
- Reduce systolic hypertension, ACE-i are helpful.
- surgery should be considered in asymptomatic patients with resting election reaction less than 50% with severe LV Dilatation (LVEDD over 70mm or LVESD over 50mm) and all symptomatic patients
Describe tricuspid regurgitation, its causes symptoms and signs, management
Causes: functional (RV dilatation), rheumatic fever, infective endocarditis (IV drug user), carcinoid syndrome, congenital (e.g. ASD).
Symptoms: Fatigue, hepatic pain on exertion, ascites, oedema. If the cause if LV failure orthopnoea and dyspnoea
Signs: Giant V waves, and prominent y descent in JVP. RV heave, pansystolic murmur heard best at lower sternal edge in inspiration, pulsatile hepatomegaly, jaundice ascites.
Management: Treat underlying cause. Diuretics, ACE-i, valve replacement.
Describe tricuspid stenosis, its causes, symptoms, signs and treatment.
Causes: main cause is rheumatic fever, which almost always occurs with mitral or aortic valve disease. rarer causes congenital, infective endocarditis
Symptoms: fatigue, ascites, oedema
Signs: giant a wave and slow y descent in JVP. opening snap, early diastolic murmur heard best at the left sternal edge in inspiration. AF can also occur.
Treatment is with diuretics and surgical repair.
