Cardio and vasc Flashcards
Clinical presentation of lymphedema
• Non-pitting edema • Feeling of heaviness or fullness, aching pain in limb • Impaired mobility • Skin changes in advanced cases ○ Discolotation ○ Hyperkeraosis ○ Verrucous hyperplasia ○ Papillomatosis ○ Deformity (elephantiasis)
Causes of lymphedema
Primary (congenital)
○ Milroy’s syndrome (congenital hereditary lymphedema)
Secondary ○ Infection § Filariasis (#1 cause worldwide, developing nations) § Post-op infection ○ Malignant infiltration § Axillary, groin, intrapelvic ○ Radiation/surgery (#1 cause in developed world) § Axillary, groin lymph node removal
Treatment lymphedema
Compression bandages and sleves
Gentle exercise
Massage and manual lymph drainage therapy
Skin care (moisturisers, topical/systemic treatment of fungal and bacterial infections)
Risk factors for venous thrombi embolism
THROMBOSIS ○ Trauma, Travel ○ Hypercoagulable state, history of previous VTE ○ Recreational drugs (IVDU) ○ Old age >60 ○ Malignancy ○ Birth control pill (OCP) ○ Obesity, obstetrics ○ Surgery, smoking ○ Immobilisation ○ Sickness (CHF, MI, nephrotic syndrome, vasculitis)
PERC
Old Age Tachycardia O2 saturation Prior history VTE Recent trauma/surgery Hemoptysis Exogenous oestrogen clinical signs of VTE
If all are negative, can rule out PE. If any one is positive, must move onto Wells.
Treatment for VTE
Anticoagulant: LMWH or Heparin if in renal failure; start Warfarin at same time. Stop LMWH/Hep when INR in therapeutic range for 2 days.
If haemodynamically unstable: thrombolyse
If anticoag CI: IVC filter of surgical thrombectomy
Long-term Warfarin or NOAC (3-6mo or lifelong if recurrent)
Causes of thrombophilia
Genetic
- overactivity of pro-coag factors (Factor V leiden and prothrombin mutation)
- Deficiency of anti-coag factors (anti-thrombin III, protein C and S)
Acquired
- Antiphospholipid syndrome (lupus anticoagulant, anticardiolipin, anti PLD antibody)
- Heparin induced thrombocytopenia (immune reaction against heparin)
- Sickle cell disease (prothrombotic state induced by hyper viscous blood)
Investigating DVT
- Well’s
- D-dimer: if neg and wells shows low pretest probability, exclude DVT
- USS of leg id D-dimer >0.5 and/or high pre-test probability
- Bloods
- FBE, coag studies +/- thrombophilia screen
Investigating PE
- PERC. If none are positive, can rule out PE. If 1 + are positive, calculate Well’s.
- Well’s criteria
- D-dimer: if negative, along with low- pretest probability, PE can be excluded. Otherwise do CTPA
- CTPA first line diagnostic
CXR, ECG, ABG, FBE, blood film, procoag screen
Classic PE ECG changes
Sinus tachycardia
T wave inversion leads V1-V4 +/- II, III, aVF
RV strain pattern
Non specific ST segment changes or T wave changes
S1Q3T3: S wave lead 1, Q wave and T wave inversion in lead III
RBBB (complete or incomplete)
R axis deviation
Classic presentation and investigation results for polymyalgia rheumatica
Old (>50) white female with morning stiffness and pain (worse in evening) of shoulder, arms, hip girdle and neck and began relatively suddenly. + general malaise, fatigue, weight loss. Family HX.
Raised ESR
What condition is assoc in polymyalgia rheumatic?
Temporal arteritis
Treatment polymyalgia rheumatica
Low dose corticosteroids
2 large vessel vasculitides and their treatment
Giant cell arteritis
Takayasu’s arteritis
Steroids
2 medium vessel vasculitides and their treatment
Polyarteritis nodosa
Kawasaki disease
Treatment is steroids + IV cyclophosphamide
an example of p-anca associated small vessel vasculitis + treatment
Churg-strauss syndrome.
• Granulomatous inflammation of vessels with hypereosinophilia and eosinophilic tissue infiltration
(often lung involvement)
Treatment is steroids + IV cyclophosphamide
an example of C-anca associated small vessel vasculitis + treatment
Wegener’s granulomatosis
- Granulomatous inflammation of vessels of resp tract, lungs and kidneys
Treatment is steroids + IV cyclophosphamide
An example of small vessel ANCA negative vasculitis +treatment
Henoch-Schonlein purpura
Treatment is steroids + IV cyclophosphamide
Mainstays of diagnosing vasculitis?
Angiography
Biopsy of affected vessel
Always do ANCA as well.
What does an isolated systolic HTN reflect generally?
High pulse pressure, seen in aged and stiff arteries
Difference between primary and secondary HTN, which is more common?
Primary HTN - no specific cause identified (95%)
Secondary HTN - specific cause identified (5%). Treatable but more severe than primary.
What are some of the causes of secondary hypertension?
Chronic Renal disease (Polycystic kidneys, diabetic glomerulosclerosis, glomerulonephritis)
Vascular - Renal artery stenosis and coarctation of aorta
Endocrine - Adrenal tumours secreting aldosterone, cortisol, ACTH, catecholamines (pheochromocytoma); cushing’s
Sleep apnoea
Meds (steroids, high oestrogen states such as OCP, HRT, pregnancy)
NOT atherosclerosis (except in case of renal artery stenosis)
In what patients with HTN do you investigate for a secondary cause?
Young patients (<30 years)
Resistant HTN
Presence of certain SX
Examples of renal causes of secondary HTN
Diabetic glomerulosclerosis
Polycystic kidneys
Glomerulonephritis
Medications that can cause secondary HTN
Corticosteroids
High oestrogen states(OCP, HRT, pregnancy)
Vascular complications of HTN
- Worsens Arteriosclerosis
- Worsens Atherosclerosis -> aneurism / dissection
- Hyaline arteriolosclerosis
- Berry aneurysm
- Acute plaque event -> thrombus formation, thromboembolism
Cardiac complications of HTN
- IHD and infarct
- LV concentric hypertrophy
- Cardiac failure
Kidney complications of HTN
- Benign nephrosclerosis (elevated BP transmitted to glomeruli which respond with tubular fibrosis, sclerosis and atrophy & hyaline arteriolosclerosis -> kidney ischaemia)
Brain complications of HTN
Ischaemic Strokes (atherosclerotic TE)
Haemmhoragic stroke (due to hyaline arteriolosclerosis in basal ganglia or SA haemmhorage due to ruptured berry aneurysm)
Eye complications of HTN
Hypertensive retinopathy
(hyalinised retinal vessels are weak and leaky, can bleed or lead to ischaemia).
What factors determine the treatment of HTN?
Degree of HTN (stage 1 SBP 140-179 & DBP 90-109; severe SBP>180 & DBP>110)
Presence of CV risk factors
Evidence of end organ damage (cardiac, arteries, kidneys)
How is the treatment protocol (pharm vs lifestyle modification) for different categories for HTN divided up?
Stage 1 SBP 140-179 & DBP 90-109 with NO CV RFs: life style modification (pharm treatment if still high after 6 months)
Stage 1 SBP 140-179 & DBP 90-109 WITH CV RFs or end-organ damage: start pharmacological treatment
Severe HTN SBP>180 & DBP>110: start pharmacological treatment
Pharm. treatment (order of use) for HTN
Step 1:
If <55yo, ACE inhibitor (or AT1Rantag)
If >55yo or afro-carribbean origin - Ca channel blocker
if >65yo - low dose thiazide
Step 2:
ACE inhibitor + Ca channel blocker
Step 3:
Add thiazide diuretic (or beta blocker only if patient has IHD and heart failure)
If BP still elevated after step 3 = RESISTANT HTN
Step 4: Refer. Consider further diuretic (thiazide-like or spironolactone) or beta or alpha blocker
When NOT to use Ca channel blocker in HTN
If patient has heart failure
When NOT to use ACE inhibitor in HTN
In severe renal impairment and pregnancy
What drug combinations to avoid in HTN and why? (3)
- Ace inhibitor + K-sparing diuretic (spironolactone) - risk of hyperkalaemia
- Ca channel blocker + beta blocker - risk of heart block
- ACEi + AT1R antag - not shown to be clinically effective
LONG-TERM Treatment protocol for CHF
- Lifestyle modification
Smoking and alcohol cessation
Na and fluid restriction
Diet and exercise (weight control) - Treat underlying cause and aggravating factors (valvular disease/arrhythmia; thyroid, infection, anaemia, HTN)
- Meds
ACE inhibitor/ARB (slows progression, improves survival)
+ Beta blocker (slows progression, improves survival)
+/- aldosterone antag*(spironolactone) if severe and symptomatic
+/- diuretic (furosemide) if fluid overloaded
+/- digoxin (SX control only)
+/- antiarrhythmic (if AF)
+/- Warfarin (if AF, prior TE or LV thrombus on echo)
*mortality benefit
ACUTE treatment of CHF (Acute pulmonary oedema)
LMNOPP
Lasix (furosemide) Morphine IV Nitroglycerin (GTN) O2 (if hypoxaemic) Positive airway pressure (CPAP/BiPAP) Position
Treat underlying cause (MI/ischaemia/arrhythmia etc)
Precipitants/exacerbaters of heart failure
MADHATTER: MI/ischaemia Anaemia Drugs (NSAIDs, steroids, non-compliance) HTN Arrhythmias Thyroid Toxic (infection) Endocarditis/embolus Renal failure
Signs/Symptoms of Heart failure
Systolic (fwds) dysfunction: S3 Displaced apex beat Mitral/tricuspid regard fatigue syncope systemic hypotension cool extremities and slow cap refill w peripheral cyanosis
Diastolic (backwards) dysfunction:
Dyspnoea, orthopnoea, PND
Cough
Crackles
Peripheral edema
Incr JVP
Hepatomegaly, pulsatile liver
Pathophysiology of heart failure
Incr preload leads to incr work (septal defect or regurg)
Decr strength/contractility (IHD/cardiomyopathy)
Incr resistance leads to incr work (HTN, stenosis)
What conditions does IHD encompass?
- Stable angina
- Unstable angina
- MI (STEMI or NON-STEMI)
- Sudden cardiac death
Stable angina vs unstable angina
Stable:
- pain comes on w exercise, cold, stress and is relieved by stress. REPRODUCIBLE.
- due to atherosclerotic narrowing
Unstable:
- new onset pain or pain at rest
- accelerating pattern of pain
- pain post MI or post-procedure
- due to acute plaque event (plaque rupture, acute thrombus formation, partially occludes vessel)
STEMI vs non-STEMI
STEMI: Criteria for MI + ST elevation or new BBB
NON-STEMI: Criteria for MI WITHOUT ST elevation or new BBB
WHO Criteria for MI
2 of the following:
- Classic SX of MI
- Elevated troponin, CK
- Typical ECG pattern (ST segment changes, T wave changes, new BBB, development of Q waves)
What conditions does ACS encompass and what is the underlying pathophys?
Acute plaque event (plaque rupture)
Unstable angina (ruptured plaque partially occludes coronary artery)
NSTEMI + STEMI (ruptured plaque completely occludes coronary artery)
ACUTE Management of STEMI
Percutaneous therapy (PCI) i.e. stent or balloon angioplasty (preferred) within 60 door to balloon time
OR Thrombolysis/Fibrinolysis (if early presentation or PCI contraindicated) with stress test before discharge
O2 Morphine IV PRN Aspirin (+/- clopidogrel if high risk or PCI) Unfractioned heparin GTN IV \+/- metaclopramide
ACUTE Management of NSTEMI or UA
DO NOT THROMBOLYSE!
If high risk -> PCI immediately.
If low risk with no recurrent CP -> Stress testing -> positive result -> PCI, otherwise conservative treatment (RF modification and long-term anti anginal therapy)
O2 Morphine IV PRN Aspirin (+ clopidogrel if high risk or PCI) LMWH GTN sublingual \+/- metaclopramide
Long-term management of IHD post-acute ACS event (8)
- Dual anti-platelets (aspirin + clopidogrel)
- Beta blockers (Ca channel blocker second line)
- ACE inhibitors (prevent remodelling)
- Nitrates (GTN) PRN for symptom relief
- Statin (irrespective of cholesterol levels for plaque stabilisation)
- Modify lifestyle (exercise, diet, cease smoking, weight control, alcohol, stress)
- Modify CV Risk Factors (diabetes, cholesterol, HTN)
- Review (1 month then 6 mo thereafter)
Complications of MI
Electrical instability -> Arrhythmias
Pericardial inflammation -> Pericarditis
Tissue necrosis ->
- Cardiac tamponade or VSD (wall rupture);
- Congestive heart failure (papillary muscle infarct -> MR)
- Aneurysm
Impaired contractility ->
- CHF;
- Cardiogenic shock (hypotension -> decr perfusion)
- Stroke, PE, DVT, organ ischaemia or infarct (ventricular thrombus -> embolism)
Investigations for all patients w HTN
FBC UEC Fasting glucose Lipid profile 12 lead ECG Urinalysis
What tests do you order if investigating endocrine cause of HTN?
plasma aldosterone and renin
What tests do you order if investigating pheochromocytoma as cause of HTN?
24hour urine catecholamines
Treatment for myocarditis
Supportive treatment
○ Bed rest, treat CHF, treat arrhythmias
Anticoagulation
Treat underlying cause
What is the prognosis/outlook/comlpications for myocarditis
- Usually self-limiting -> Full recovery
- Progression to dilated cardiomyopathy (systolic heart failure)
- Sudden death in young adults
Causes of myocarditis
Idiopathic in 50%
Viral (coxsackie B, echovirus, poliovirus, HIV, mumps, flu)
Bacterial (s aureus, clostridia etc), protozoal, fungal Drugs Toxins Vasculitis, SLE, RA, sarcoid Acute rheumatic fever (strep)
Complications of acute pericarditis
- Recurrence
- Atrial arrhythmias
- Pericardial effusion and tamponade
- Constrictive pericarditis
Management of acute pericarditis
NSAIDs
Treat the cause
Colchicine»_space; steroids if recurrent/continuing SX
ECG pattern of acute pericarditis
ECG: wide-spread saddle shaped ST elevation +/- depressed PR segment
Chest pain pattern of pericarditis
Central chest pain - worse on inspiration and when lying flat; relieved by leaning forwards
Standard Management of dyslipidaemia
Manage modifiable risk factors
- Smoking cessation
- Diet (reduce saturated fats and refined sugars, incr fruit veg and fibre)
- Reduce alcohol
- 150min mod-intense exercise/week
- Weight reduction
Medications
- Statins are 1st line mono therapy
- If severe, add Fibrates +/- fish oil
Monitoring/follow up (don’t need to know details)
- Monitor LFTs and CK at baseline then 6 weeks after starting statin (SEs)
- Fasting lipids at 3 mo, and if under control, monitor every 6-12 months thereafter.
Alternate medications to Statins, for control of dyslipidaemia
Fibrates
Bile acid resins/sequestrates
Ezetemibe
Niacin/vitamin B3/nicotinic acid
Fish oil
Mechanism of action - Fibrates
Lower TGLs by increasing synthesis of lipoprotein lipase which increases hydrolysis of TGL into FFAs which can then be taken up by tissues as an energy source
Mechanism of action - Bile acid resins
Lower blood LDLs by binding to bile acids in SI so they can’t be absorbed and must be excreted.
Increase expression of hepatic LDL Rs to further decr blood LDL (must resynthesises the bile acids you have excreted)
Mechanism of action - Ezetimibe
Lowers LDL by by inhibiting the cholesterol transporter in the small intestine to inhibit cholesterol absorption in gut
Mechanism of action - niacin/vitamin B3
Lowers risk of abnormal lipids; decr LDL and VLDL, decr TGL incr HDL and hepatic LDL receptors. Mechanism unclear.
What does hyperlipidaemia put you at risk of?
Atherosclerosis
IHD - MI, stroke
What is the screening protocol for hyperlipidameia?
Full fasting lipid profile every 3 years for
○ Males > 40
○ Females > 50 (or menopausal)
○ Anyone with other CAD risk factors
Secondary causes of hyperlipidaemia
Obesity Hypothyroid Diabetes mellitus Metabolic syndrome CKD Nephrotic syndrome Liver disease Alcoholism
Primary causes of hyperlipidaemia
genetics
What infectious agent is rheumatic fever caused by? What medical condition precedes it and by how long?
Strep progenies (group A beta haemolytic strep)
Pharyngeal infection precedes it 2-4 weeks earlier
What valves are mostly affected with Rheumatic heart disease?
Mitral (70%)»_space; Aortic (40%)»_space; Tricuspid (10%)
Treatment for Rheumatic fever
High dose steroids to shut down inflammatory response
Benzylpenicillin and penicillin
NSAIDs/aspirin for carditis-arthritis.
Methods of entry for infective endocarditis
Blood stream
surgical and dental procedures
Infective agents for endocarditis
Staph aureus Strep viridian's Staph epidermis Enterococcus E coli
Classic signs and symptoms of infective endocarditis
Fever +/- new heart murmur
Clubbing
Anaemia
Splinter haemmhorages, osler’s nodes
ECG findings of Premature Ventricular or atrial complexes
Management
Premature complex followed by a pause, then normal beat.
May be every 2 or 3 beats (bigeminy or trigemini).
MX: beta blockers/Ca channel blockers if frequently symptomatic otherwise just reassure and cut down caffeine.
Risk factors for AF
CHADS2
CCF HTN Age >75 DM Stroke/TIA/Thromboembolus previously
Management of CHRONIC AF
- Evaluate stroke risk and manage -> score 0 gets aspirin; score >1 gets anticoagulation (warfarin or NOAC)
- Rate control if patient stable (beta blocker, diltiazem, verapamil or digoxin, or amiodarone last line)
Rhythm control (flecainide»_space;> amiodarone if in HF) if patient is symptomatic, CCF, younger, or presenting for 1st time with lone AF or AF from corrected precipitant.
Triggers of AF
Heart failure/ischaemia HTN MI PE Valvular disease (mitral) Hyperthyroid Caffeine/alcohol
Bloods when investigating AF
UEC
Cardiac enzymes
TFTs
Management of Acute AF (<48 hours)
If very ill or haemodynamically unstable:
- O2
- Emergency cardioversion (electrical or IV amiodarone if unavailable. Flecanide)
- Rate control (Verapamil or Bisoprolol = Ca channel or beta blocker; digoxin or amiodarone 2nd line)
- Anticoagulation (LMWH)
Treat any triggering illnesses (pneumonia, MI, PE etc)
Risk factors for PAD
Smoking Diabetes HTN Hypercholesterolaemia Family HX (hyperhomocysteinaemia)
SX and signs of PAD
SX:
Claudication
Rest pain
Signs:
Rubor
Ulcers, gangrene, cellulitis
Abnormal nails
What are the most common sites for narrowings in PAD?
in order of occurrence
80-90%: femoral and popliteal arteries (calf claudication, reduced popliteal, pedal pulses)
40-50%: tibial and peroneal vessels (pedal pulses absent)
30%: abdominal aorta and iliac arteries (claudication in butt, thigh, calf and reduced femoral and distal pulses)
Why might the ABI be raised or lower than normal?
Diabetics - increased ABI due to stiff calcified vessels that are incompressible
Low ABI - extremely stenosed vessel, there is no blood flow distally
what sized arteries is angiography good for? What is a draw back to this?
Good for large arteries (aortic, iliac,, femoral, popliteal), but requires contrast which is nephrotoxic.
Management of intermittent claudication
○ Diet and lifestyle ○ BP control ○ Aspirin ○ Statins ○ Smoking cessation ○ Exercise (improves fitness and general pump function as well as efficiency with using O2 delivered (if they stop walking to 'control symptoms' they will lose their legs)
○ Surgical
§ End-arterectomy for short segments
§ Angioplasty and stending for short segments
□ More for proximal arteries
§ Bypass for longer blocks
□ Bigger operation with more risks and longer recovery time
For critical limb ischaemia
○ HEPARIN IMMEDIATELY
○ Limb salvageable -> arteriography or duplex scanning -> endarctectomy or angioplasty
○ Limb NOT salvageable:
§ Palliation if patient unfit for surgery
§ Amputation if patient fit for surgery
How does carotid stensois present?
TIA or stroke
Amaurosis (temporary monocular blindness due to CRA embolic obstruction)
Asymptomatic
Risk factors for peripheral/chronic venous disease
old age family HX venous disease ligamentous laxity prolonged standing incr BMI Smoking Past DVT High estrogen states and pregnancy
What is venous disease caused by?
Venous HTN and venous insufficiency
causes of venous HTN
- inadequate muscle pump function
- incompetent venous valves -> reflux
- venous thrombus or obstruction
Venous HTN leads to vein dilatation, skin changes and or ulceration
Clinical presentation of chronic venous disease
Hyperpigmentation and haemosiderin staining
Brawny pitting oedema
Lipodermatosclerosis
Varicose veins
Ulcers
Leg heaviness, ache and fatigue at end of day
Venous eczema: Pruritis, pain, swelling, erythema, recurrent cellulitis
LEg elevation, compression alleviates pain
How do you diagnose PVD?
Clinical diagnosis (typical symptoms) confirmed by DUPLEX ULTRASOUND revealing venous reflux
Treatment of PVD
Initial conservative
§ Leg elevation - improves O2 delivery and reduces oedema
§ Compression - compresses dilated veins and reduces oedema; helps heal ulcers
§ Exercise - improves O2 delivery
§ Topical dermatological agents for stasis dermatitis
Vein ablation - surgical excision, sclerotherapy, thermal ablation
§ Requires a minimum of 3 months conservative therapy before proceeding w ablation.
Venous reconstruction (translocation of vein segments, transplantation of vein segments, substitution)
Where are varicose veins commonly located?
Superficial veins of legs
Signs and SX of varicose veins
Visibly dilated tortuous veins in legs, more obvious upon standing
Painful when standing, relieved by walking
Haemosiderin staining near affected veins
Leg cramps
Over time can lead to leg swelling and venous eczema
Lipodermatosclerosis (inverted champagne bottle legs)
Ulceration
What is lipodermatosclerosis and what is it commonly caused by?
Skin thickening
Inverted champagne bottle legs - tapering of legs above ankle with reddish brown discoloration distally.
Pathophys of varicose veins
Caused by incompetent venous valves -> valves fail to close so blood falls back down and pools in leg veins which accelerates valves stretching and failing, and causes veins to become dilated and tortuous due to extra blood.
What causes a varicocoele?
What does it look like?
L testicular v drains into the L renal vein (must return blood at a 90deg angle which is hard to get through and so blood backs up around testicle, causing enlargement of testicular vein)
Looks like “bag of worms” which becomes larger when standing and smaller when lying flat
What is a potential complication of a varicocoele?
Warm stagnant venous blood causes testicular temp to rise
-> Testicular atrophy and infertility (poor quality sperm)
Investigations for varicose veins
Lower limb venous ultrasound to check for venous incompetence
DDX for varicose veins
Telangiectasis
Recticular veins
both have no evidence of reflux on venous ultrasound
Treatment varicose veins
Compression stockings Leg elevation Injection sclerotherapy Surgery - vein removal (Stripping, ligation) Vein ablation
Complications of varicose veins
- Superficial thrombophlebitis
- Venous eczema
- Venous ulceration
- Lipodermatosclerosis
- Bleeding varicose vein
Characteristics of venous ulcers
Commonly found in gaiter region - medial aspect of calf/ankle
Large, flat/shallow
Irregular edges
Granulomatous base (pink/beefy red)
Mild pain
Pedal pulses present
Characteristics of arterial ulcers
VERY PAINFUL
Often on foot pressure point areas
Small size
Deep with punched out appearance
Regular margins
Sloughy/necrotic base
Absent pedal pulses
Neuropathic ulcer characteristics
Often very large but size and shape varies
NOT PAINFUL
Appearance: Prominent hypertrophied squamous rind around edge
Often on feet -pressure point areas
Describing ulcers
○ Shape ○ Site ○ Size ○ Edges ○ Base description (colour, slough? Etc) ○ Surrounding tissues ○ Lymph nodes
MX of arterial ulcer
Feel pulses - absent/faint indicates arterial cause
USS + ABI to confirm (ABI <0.7 indicates PAD)
Wound debridement
Wound dressing
Angiography and revascularisation
How to intensify the MR murmur
get patients to roll onto L side and inspire
How to intensify the AS murmur
Patient leans forwards and expires
What is the quality of MR?
Pansystolic, blowing
What is the quality of AS?
Crescendo Decrescendo ejection systolic
What is AS commonly caused by?
Post RHD
Congenital Bicuspid valve
Calcification
What is MR commonly caused by
Congenital Consequence of: ◊ rheumatic heart disease ◊ Marked LV dilatation ◊ Acute infective endocarditis ◊ Papillary muscle dysfunction secondary to MI
ECG anomalies associated w syncope (3)
Sinus bradycardia
Conduction block
Wolff Parkinson white syndrome
