Cardiovascular Flashcards
(87 cards)
1
Q
Arrhythmias - look at notes on onenote, includes pictures
ECGs: https://zerotofinals.com/medicine/cardiology/arrhythmias/
A
Abnormal heart rhythms
- Cardiac arrest rhythms
- Narrow complex tachycardia
- Broad complex tachycardia
- Atrial flutter
- Prolonged QT interval
- Ventricular ectopics
- Heart block
- Bradycardias
2
Q
Arrhythmia: Narrow Complex Tachycardia
A
Fast heart with QRS complex < 0.12s (3 small squares).
4 main differentials: sinus tachy, supraventricular tachy, AF, atrial flutter
3
Q
Arrhythmias: sinus tachycardia
A
Normal P waves, QRS complex and T waves
Not an arrhythmia but a response to underlying cause e.g. pain/sepsis
4
Q
Arrhythmia: supraventricular tachycardia
A
- QRS complex followed by T wave, P waves are buried in T waves
- Often no apperant cause
- Tx = vagal manoeuvres and adenosine
5
Q
Arrhythmia: atrial fibrillation
A
- Absent P waves and irregularly irregular ventricular rhythms
- Treat with rate and rhym control
6
Q
Arrhythmia: Atrial flutter
A
- Atrial rate of ~300 beats per minute, saw tooth pattern, usually two atrial contractions for every one ventricular contraction
- Due to re-entrant pathway and rhythm in either atriumresulting in self-peretuating loop
- Treat with rate and rhythm control e.g. anticoagulation based on CHA2DSVASc and radiofrequency ablation
7
Q
Arrhythmias: Broad Complex Tachycardia
A
Fast heart rate with QRS complex duration > 0.12s
- Ventricular tachycardia (tx IV amiodarone)
- Polymorphic ventricular tachycardia, such as torsades de pointes (tx IV magnesium)
- AF with BBB (tx as AF)
- Supraventricular tachycardia with BBB (tx as SVT)
8
Q
Arrhythmia: prolonged QT interval
A
- Start of QRS complex to end of T wave
- > 440 ms in men
- > 460ms in women
Tx: stop causative meds, correct electrolytes, beta blocker (not sotalol), pacemaker
9
Q
miss jasmine
Causes of prolonged QT
A
- Long QT syndrome
- Meds e.g. antipsychotics, citalopram, amidarone
- Electrolyte imbalances e.g. hypokalaemia, hypomagnesaemia and hypocalaemia
10
Q
Arrhythmia: ventricular ectopics
A
Premature ventricular beats caused by random electrical discharges outside the atria
Appears as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG
Bigeminy = every other beat is a ventricular ectopic
11
Q
Mx of ventricular ectopics
A
- Healthy and infrequent = reassurance
- Specialist advice if underlying heart disease, frequent/concerning symptoms, FHx of sudden death/heart disease
- Beta blockers
12
Q
Arrhythmia: Heart block (look at one note for ECG + more detail)
A
- First-degree heart block = delayed conduction through the AV node
- Second-degree heart block = Mobitz type 1 and 2
- Third-degree = complete heart block, no relationship between P waves and QRS complexes, significant asystole risk
13
Q
Asystole
A
Absence of electrical activity in the heart = cardiac arrest
Mx of asystole risk
- IV atropine (1st line) - inhibits parasympathetic nervous system
- Intotropes (e.g. adrenaline)
- Temp cardiac pacing e.g. transcutaneous or transvenous
- Pacemaker
14
Q
Chronic heart failure
A
When heart function is impaired, the LV is not as effective in pumping blood out of the heart and around the body > increased fluid in left atrium, pulmonary veins and lungs > pulmonary oedema
- HF with preserved ejection fraction > 50% = diastolic dysfunction with impaired LV filling
- HF with reduced ejection fraction < 50%
15
Q
Causes of chronic heart failure
A
- IHD
- Valvular heart disease (e.g. aortic stenosis)
- HTN
- Arrhythmia (e.g. AF)
16
Q
Clinical features of chronic HF
A
- SOB worse on exertion
- Cough + frothy white/pink sputum
- Orthopnoea (how many pillows?)
- Paroxysmal nocturnal dyspnoea (waking with sudden cough, SOB, wheeze)
- Peripheral oedema
Signs:
- Tachycardia + tachypnoea, HTN, murmur (VHD), bilateral basal crackles (wet = pulmonary oedema), raised JVP, peripheral oedema (ankle, legs and sacrum)
17
Q
Ix chronic heart failure
A
- Clinical asessment
- N-terminal pro-B-type natruretic peptide (NT-proBNP) blood test
- ECG
- Echo
Refer to cardiology depending NT-proBNP
- 400 - 2000ng/L = echo within 6 weeks
- > 2000ng/L = echo within 2 weeks
18
Q
New York Heart Association Classification for heart failure
A
- Class I: No limitation on activity
- Class II: Comfortable at rest but symptomatic with ordinary activities
- Class III: Comfortable at rest but symptomatic with any activity
- Class IV: Symptomatic at rest
19
Q
Management of chronic heart failure
A
ABAL
- ACEi/ARB (ramipril/candesartan) - renal function, hyperkalaemia
- Beta blocker (e.g. bisoprolol)
- Aldosterone antagonist if above ineffective (e.g. spironolactone) - renal function, hyperkalaemia
- Loop diuretic (e.g. furosemide) - monitor U+Es
Surgery - implantable cardioverter defibrillators
ARB = Angiotensin receptor blocker
20
Q
Atrial Fibrillation (AF)
A
Condition where the electrical activity in the atria becomes disorganised. Choatic electrial activity in the atria overrides regular, organised electrical activity from SA node.
-Irreguarly irregular pulse
- Tachycardia
- Heart failure due to impaired filling of the ventricles during diastole
- Increased risk of stroke (x5)
21
Q
Common causes of AF
A
SMITH
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension
Alcohol and caffeine too
22
Q
Presentation of AF
A
- Often asymptomatic, could be dx after stroke
- Palpitations
- Shortness of breath
- Dizziness or syncope (loss of consciousness)
- Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
23
Q
Key examination finding in AF
A
Irregularly irregular pulse.
Consider ventricular ectopics as differential - VE disappear above certain HR, normal HR during exerise indicate VE
24
Q
Investigations for AF
A
ECG:
- Absent P waves
- Narrow QRS complex tachycardia
- Irregularly irregular ventricular rhythm
25
Paroxysmal AF
Episodes of AF that occur spontaneously and resolve back to sinus rhythm
- 24-hr ambulatory RCG (Holter monitor)
- Cardiac event recorder for 1 - 2 weeks
26
Management of AF
- Rate or rhythm control
- Anticoagulation to prevent strokes
- Rate control is first-line*
## Footnote
* Unless reversible cause of AF, new onset (within 48hrs), HF caused by AF, rate control ineffective
27
AF: options for rate control
1st line: beta blockers e.g. bisoprolol
1st line anticoagulation: DOAC (e.g. apixaban), warfarin as alternative
| Remember most patients treated with bisprolol and DOAC for anticoag.
28
AF: options for rhythm control
Cadioversion
- Immediate (<48hrs, life-threatening haem instability): electrical or pharmacological with flecainide/amiodarone (structual heart disease)
- Delayed (>48 hrs, stable): electrical - anticoagulation 3 weeks before.
Long-term = 1st line beta-blockers
29
AF: when is ablation considered?
When rate and rhythm control not effective
- Left atrial ablation - identifying areas of abnormal signals and destroying them
- Atrioventricular node ablation and a permanent pacemaker
30
CHA2DS2-VASC
Stroke risk score for patient with AF, and whether to start anticoagulation.
C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)
- 0 – no anticoagulation
- 1 – consider anticoagulation in men (women automatically score 1)
- 2 or more – offer anticoagulation
Aspirin alone is not used for stroke prevention in AF.
31
AF: Orbit score
Assesses risk of major bleeding in patients with AF taking anticoagulation:
O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication
## Footnote
Most pts with AF = risk of stroke with no anticoag. > bleeding risk on anticoag.
32
Management of Paroxysmal Atrial Fibrillation
- "Pill-in-pocket" - take flecainide+ when symptoms start
- Anticoagulation based on CHA2DSVASc
## Footnote
* Risk of atrial flutter, 1:1 AV conduction to ventricles = high ventricular rate
33
Thoracic Aortic Aneurysms
Dilatation of the thoracic aorta, most commonly ascending aorta (normally < 4.5cm)
True aneursym = all three layers (intima, media and adventitia) intact, but dilated
False aneurysms: intima and media rupture and blood enters adventitia = dilation
34
Risk factors for thoracic aortic aneurysm
- Men affected when younger and more often than women
- Increased age
- Smoking
- HTN
- FHx
- Existing CVD
- Marfan symdrome
35
Presentation and diagnosis of thoracic aortic aneurysms
Usually asymptomatic, incidental finding on CXR, echo or CT
DIagnosis: echo, CT or MRI angiogram
36
Management of thoracic aortic aneurysm
Prevent progression by tx of modifiable RFs: stop smoking, healthy diet + exercise, optimise HTN, diabetes + hyperlipidaemia
Depends on size:
- Surveillance with regular imaging
- Thoracic endovascular aortic repair (TEVAR)
- Open surgery (midline sternotomy)
Complications: aortic dissection, rupture, aortic regurgitation
| TEVAR - stent via catheter via femoral artery to affected area of aorta
## Footnote
Open surgery - remove affected section and replace with sythetic graft
37
Rupture of thoracic aortic aneuysms
Bigger = increase risk of rupture
Bleeding into the mediastinum, oesophagus (haematemesis), lungs (haemoptysis), pericardial cavity (cardiac tamponade)
- Severe chest/back pain
- Haemodynamic instability
- Collapse
- Death (often patients do not reach hospital)
Tx = emergency open surgery
38
Abdominal aortic aneursym (AAA)
39
Management and prevention of AAA
- One USS screening for males aged 65
- Manage risk factors e.g. smoking and optimise HTN, diabets and hyperlipidaemia
- For large AAAs, surgery = endovascular repair (EVAR) or open surgery
40
Aortic dissection
Break or tear in the intima of the aorta, allowing blood to pool in between the intima and media = false lumen
41
Risk factors for aortic dissection
Same as PAD
- Increasing age
- Smoking
- HTN (weight lifting, coacine, primary)
- Poor diet
- Male
- Sedentary lifestyle
Conditions/surgery: bicuspid aortic valve, coarctation of aorta, aortic valve replacement, Marfan's
42
Presentation of aortic dissection
- Often missed, typically old man with PMHx of HTN with sudden "tearing" or "ripping" chest pain if ascending aorta or back if descending aorta
- Pain migrates, some pts don't have chest pain
- DIfference in BP of arms (>20mmHg)
- Radial pulse deficit
- Collapse
- Hypotension as dissection progresses
- Focal neuro deficits (e.g. limb weakness)
43
DIagnosis of aortic dissection
ECG and CXR to rule ddx
CT angiogram = 1st line to confirm dx
44
Management of aortic dissection
- Surgrical emergency with experienced seniors, vascular surgeons, anaesthetists, ICU team, high mortality
- Analgesia e.g. morphine
- Control BP and HR = beta blockers
- Surgical intervention: type A = open surgery, Type B = TEVAR (see thoracic aortic aneurysm for details)
45
46
Complications of aortic dissection
- Myocardial infarction
- Stroke
- Paraplegia (motor or sensory impairment in the legs)
- Cardiac tamponade
- Aortic valve regurgitation
- Death
47
Aortic stenosis
- Narrowing of aortic valve
- Most common valve pathology + replacement
- Ejection-systolic, high-pitched murmur, crescendo-decrescendo
- Causes LVH (pump harder to overcome narrowing)
- Causes: idiopathic age-related calcification (MC), bicuspid aortic valve
48
Aortic regurgitation
- Incompentent aortic valve, allowing blood to flow back from aorta into LV
- Causes: age-related, biscuspid, Marfans or Ehlers-Danlos
- Early diastolic, soft murmur or Austin-Flint murmur, "rumbling" at apex
- Collapsing/Water hammer pulse (forcefully appearing then disappearing radial pulse)
49
Arterial ulcers
Due to insufficient blood supply to skin due to PAD
Features (to distinguish it from venous ulcer):
- DIstal, affecting the toes or dorsum of the foot
- Associated with PAD, with absent pulses, pallor and intermittent claudication
- Smaller than venous ulcers
- Deeper than venous ulcers
- Well defined borders
- “punched-out” appearance
- Pale colour due to poor blood supply
- Less likely to bleed
- Painful
-Pain worse at night (when lying horizontally)
- Pain worse on elevating and improved by lowering the leg (gravity helps the circulation)
50
Venous ulcer
- Gaiter area (between the top of the foot and bottom of the calf muscle)
- Are associated with chronic venous changes, such as hyperpigmentation, venous eczema and lipodermatosclerosis
- After minor injury to the leg
- Larger than arterial ulcers
- More superficial than arterial ulcers
- Irregular, gently sloping border
- More likely to bleed
- Less painful than arterial ulcers
- Pain relieved by elevation and worse on lowering the leg
51
Investigations for arterial/venous ulcers
- Ankle-brachial pressure index (ABPI)
- Bloods (FBC (infection/anaemia), CRP, HbA1c, Albumin (malnutrition))
- Charcoal swab (infection)
- Skin biopsy, 2WW to dermatology if skin skin cancer suspected
52
Management of arterial ulcers
- Same as PAD, urgent vascular sugery referral to consider surgical revascularisation
- If tx effective, ulcer should heal quickly
53
Management of venous ulcers
NICE CKS
Might need referral for:
- Vascular surgery if mixed/arterial ulcers suspected
- Tissue viability / specialist leg ulcer clinics in complex or non-healing ulcers
- Dermatology if skin cancer suspected
- Pain clinics if the pain is difficult to manage
- Diabetic ulcer services (for patients with diabetic ulcers)
- Wound care by experienced nurses: clean, debridment, dress
- Compression therapy
- Abx for infection
- Analgesia (not NSAIDs)
54
Deep vein thrombosis (DVT)
Called venous thromboembolism (VTE) together with pulmonary embolism.
Thrombi in the venous system = DVT
Heart defect e.g. ASD = clot travels to systemic circulation > stroke
Risk factors: hypercoagulability, venous stasis, endothelial injury e.g. immboility, recent surgery, active cancer, pregnanct, HRT, COCP, polycythaemia, lupus, thrombophilia*
## Footnote
*Antiphoslipid syndrome ,factor V Leiden etc.
55
DVT presentation
- Unilateral (if B?L think chronic venous insufficency/HF)
- Calf/leg swelling - measure below tibial tuberosity, > 3cm difference = significant
- Dilated superfical veins
- Calf tenderness, particularly ove rdeep vins
- Oedema
- Colour changes
Consider and exclude PE
56
Wells score
Predicts risk of DVT or PE
- Active cancer (tx within 6m)
- Bedrideen > 3 days, major surgery < 12 weeks
- Calf swelling > 3cm compared to other leg
- Collateral (non0varicose) superficial veins present
- Entire leg swollen
- Localised tenderness along the deep venous system
- Pitting oedema in affected leg
- Paralysis
- Previous DVT
- Alternative dx to DVT likely
57
Diagnosis of DVT
D-dimer is sensitive (95%) but not speific, good for excluding when low suspicion. But can be raised in pneumonia, malignanvy, HF, surgery, pregnancy
Diagnostic = doppler USS, repeat in 6-8 days if negative USS but postive D-dimer and high Well's
58
Management of DVT
- Prophylaxis (after surgery): compression stockings, LMWH e.g. enoxaparin
- Initial: apixaban/rivaroxaban, catheter-directed thrombolysis if iliofemoral DVT < 14 days
Long-term: DOACs, wafarin (antiphospholipid syndrome), LMWH (pregnancy)
- 3m if reversible, then review
- > 3m if unprovoked or recurrent
- 3 - 6m active cancer, then review
59
Investigations for unprovoked DVT
Review medical history, bloods, physical examination for cancer
If stopping anticoagulation after 3-6m, consider testing for antiphospholipid syndrome or hereditary thrombophilias (if 1st degree relative affected by DVT/PE)
60
Hypertension
90% essential
Secondary causes: ROPDED
Renal disease, Obesity, Pregnancy-induced or Pre-eclampsia, Endocrine, Drugs (alcohol, steroids, NSAIDs, oestrogen and liquorice)
61
Complications of hypertension
- Ischaemic heart disease
- Cerebrovascular accident
- Vascular disease (PAD, aortic dissection, aortic aneurysms)
- Hpyertensive retino/nephropathy
- LVH
- HF
62
Dignosis of hypertension
Screen BP every 5 years, more often if borderline every year in type 2 diabetes
Clinic BP 140/90 to 180/120 = 24-hr ambulatory BP or home readings
White coat syndrome: > 20/10 difference in clinic and home readings
New HTN dx:
- Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
- Bloods: HbA1c, renal function and lipids
- Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities e.g. LVH
- QRISK > 10% = offer statin (atorvastatin 20mg)
63
Management of essential hypertension
-Lifestyle advice - stop smoking, lose weight, reduce alcohol, exercise
Medications:
- A – ACE inhibitor (e.g., ramipril)
- B – Beta blocker (e.g., bisoprolol)
- C – Calcium channel blocker (e.g., amlodipine)
- D – Thiazide-like diuretic (e.g., indapamide)
- ARB – Angiotensin II receptor blocker (e.g., candesartan)
64
Hypertenstion stepwise medical management
- Step 1: under 55 or type 2 diabetic of any age and any family origin = A. Over 55 or black = C
- Step 2: A + C, or A+D, C+D
- Step 3: A+C+D
- Step 4: A+C+D+4th
If K ≤4.5 = K-sparing diuretic e.g. spironolactone, > 4.6 = alpha blocker (doxazosin) or beta blocker (e.g. bisoprolol)
Check adherence, specialist mx if uncontrolled
65
Hypertensive emergency/accelerated hypertension/malignant hypertension
> 180/20 with retinal haemorrhages or papiloedema on fundoscopy
Same-day referral
IV meds in hypertensive emergency (experienced specialist) - sodium nitroprusside, labetalol, glyceryl trinitrate, nicardipine
66
Bowel ischaemia
- Acute meseneric ischaemia (AMI) - embolism > occlusion small bowel artery (e.g. superior mesenteric artery) > urgent surgery, poor prognosis
- Chronic mesenteric ischaemia (CMI) - rare, colickly intermittent abdo pain (non-speicfic) "intestinal angina"
- Ischaemic colitis (IC) - acute, transient blood flow distruption to large bowel > inflammation, ulceration + haemorrhage > "thumbprinting" abdo x-ray = oedema/haemorrhage > supportive mx, surgery if peritonitis, peforation or persistant haemorrhage
67
Risk factors for bowel ischaemia
- Age
- AF (espeically mesenteric ischaemia) - Endocarditis (emboli)
- Malignancy (emboli)
- CVD RFs e.g. smoking, HTN, diabetes
- Cocaine - consider IC if coacine use
68
Common features of bowel ischaemia + investigation
- Abdo pain - sudden, severe and disportionate to findings in AMI
- Rectal bleeding
- Diarrhoea
- Fever
- Bloods = ↑WBC, lactic acidosis
- Diagnostic = CT abdo
69
Ischaemic heart disease
Most commonly caused by atherosclerotic plaque build-up = chronic inflammation of medium and large arteries + immune system activation > lipid plaques > stiffening, stenosis and plaque rupture
70
Risk factors for IHD
Non-modifiable risk factors:
- Older age
- FHx
- Male
Modifiable risk factors:
- Raised cholesterol
- Smoking
- Alcohol
- Poor diet/sleep
- Sedentary
- Obesity
- Stress
- Co-mobidities: diabetes, HTN, CKD, inflammatory conditions e.g. RA, atpyical antipsychotics
| Consider + ask RFs when taking Hx from pt with suspected IHD
71
Primary prevention of CVD/IHD
Prevention of CVD for patients that never had a dx of CVD
- Diet + exercise
- QRISK3 - risk of having stroke or MI in next 10 years, > 10% or CKD (eGFR < 60)/T1DM = atorvastatin
- Review in 3m, aim >40% ↓ non-HDL cholesterol
- LFTs = ↑ ALT+AST, continue if < 3x normal
| Statin inhibit HMG CoA reductase = ↓cholesterol production in liver
72
What are some rare but sigificant side effects of statins?
- Myopathy (muscle weakness + pain)
- Rhabdomyolysis (CK levels if muscle pain)
- T2DM
- Interaction with macrolide abx, stop statins during course
73
Secondary prevention of CVD/IHD
4As!
- A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
- A – Atorvastatin 80mg
- A – Atenolol (or bisoprolol)*
- A – ACE inhibitor (commonly ramipril)*
| * titrated to the maximum tolerated dose
74
Familial hypercholesterolaemia
- Autosomal dominant
- Heterozgous
- Homozygous = extremely high cholesterol (>13mmol/L), early CVD
- Simon Broom/Dutch Lipid Clinic Network Criteria for clinical dx: **FHx (e.g. MI < 60 in 1st degree), very high cholesterol (> 7.5mmol/L), tendon xanthomata**
- Mx: specialist for genetic tests + statins
75
Mitral valve disease: mitral stenosis
- Narrowed mitral valve = restricted blood flow from LA > LV
- Mid-diastolic, low-pitched "rumbling" MURMUR
- Palpable tapping apex beat, malar flush (upper cheeks+nose, rise in CO2 + vasodilation), AF
- Causes: infective endocarditis, rheumatic fever
76
Mitral valve disease: mitral regurgitation
- Incompetent mitral valve = backflow of blood from LV to LA during systole > reduce EF and backlog waiting to be pumped through left heart > congestive HF
- Pan-systolic, high-pitched whistling murmur radiating to left axilla
- Thrill in mitral area on palpation
- HF+ pulmonary oedema
- AF
Causes: age-related, IHD, infective endocarditis, rheumatic heart disease, Marfans
77
Myocarditis
Inflammation of myocardium
Causes:
- Viral: coxsackie B, HIV
- Bacteria: diphtheria, clostridia
- Spirochaetes: Lyme disease
- Protozoa: toxoplasmosis
- Autoimmune
78
Presentation + investigations of myocarditis
Usually young patient with acute history, chest pain, dyspnoea and arrhythmias
Investigations: bloods: ↑CRP 99%, ↑ cardiac enzymes, ↑ BNP
ECGs: tachy, ST-segment elevation and T-wave inversion
79
Management of myocarditis
Tx of cause e.g. abx, methyprednisolone for autoimmune
Supportive for HF or arrhythmia
Complications: HF, arrhythmia > sudden death, dilated cardiomyopathy
80
Pericarditis
Inflammation of pericardium. membrane around the heart - two layers, < 50ml fluid = lubrication. Potential space: pericardial cavity
Causes: idiopathic, infection (TB, HIV, coxsackievirus, EBV), autoimmune (SLE, RA), injury (MI), cancer, methotrexate
81
Key presenting features of pericarditis
- Chest pain: central/anterior sharp, pleuritic (worse on inspiration), wose on lying down, relieved by sitting forward
- Low-grade fever
- Pericardial friction rub on exam
82
Investigations for pericarditis
- Bloods: ↑inflammatory markers (WCC, CRP, ESR)
- ECG changes
- Echo diagnostic of pericardial effusion
83
Management of pericarditis
- 1st line: NSAIDs (aspirin or ibuprofen
- Long-term: colchicine 3m reduce recurrence
- 2nd line: steroids in recurrent cases or inflammatory conditions
- Tx underlying causes
- Pericardiocentesis: remove fluid surrounding heart if pericardial effusion or tamponade
84
Pericardial (cardiac) tamponade
In pericarditis, pericardial cavity can fill with fluid = pericardial effusion = pressure on heart, reduce expansion during diastole
Tamponade = effusion large enough to ↑intra-pericardial pressure, emergency, drainage of effusion to relieve pressure
85
Tricuspid regurgitation
Incompetent tricuspid valve, blood back flow from RV to RA in systole
- Pan-systolic murmur
- Thrill in tricuspid area
- Raised JVP with giant C-V waves (Lancisi's sign)
- Peripheral oedema
- Ascites
86
Causes of tricuspid regurgitation
- Pressure to due LHF or pulmonary HTN
- Infective endocarditis
- Marfan syndrome
- Ebstein's anomaly
87
Pulmonary stenosis
Narrowed pulmonary valve, restricted blood flow from RV to pulmonary arteries
- Ejection systolic murmur, pulmonary area deep inspiration
- Thrill
- Raised JVP giant A waves
- Peripheral oedema
- Ascites
Congential: tetralogy of Fallot
