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Transcript
Pulmonary Hypertension and Right Heart Failure
Pulmonary venous hypertension (Cardiac)
• LVF-ischaemic
• Mitral Regurgitation / Stenosis
• Cardiomyopathy-eg alchohol ,viral
Pulmonary arterial hypertension
• Hypoxic – COPD , OSA , Fibr Alveolitis
• Multiple Po Emboli
• Po vasculitis –eg SLE , PAN ,Systemic Sclerosis
• Drugs –eg appetite suppressants
• Cardiac Left to right shunt – ASD , VSD
• Primary pulmonary hypertension (only after excluding all of above)
Clinical Signs of Pulmonary Hypertension
and Right Heart Failure
• Central cyanosis if hypoxic
• Dependent oedema
• Raised JVP with V waves (due to secondary
tricuspid regurg)
• Right ventricular heave at left parasternal edge
• Murmur of tricuspid regurgitation
• Load P2
• Enlarged liver (pulsatile )
Investigation of Pulmonary
Hypertension
•
•
•
•
•
•
•
•
ECG
CXR
SaO2 and arterial blood gases
Pulmonary function
Echocardiogram / Cardiac Catheterisation
D dimers and VQ scan if PE suspected
CT Pulmonary Angiogram
Auto-antibodies if vasculitis suspected
Primary pulmonary hypertension
• Diagnosis by exclusion of other secondary causes
• Progressive SOBOE and signs of right heart
failure
• Pharmacologic Treatment
-prophylactic anticoagulation [warfarin]
-O2 if hypoxic
-Po Vasodilators :Endothelin antagonist (Oral
Bosentan) , PDE5-inhibitor (Oral Sildenafil), iv
Epoprostenol
THROMBOEMBOLIC LUNG DISEASE
• Pulmonary infarction
-in situ
-venous emboli
• Virchow’s Triad
-Stasis
-Vessel wall damage
-Hypercoagulablity
RISK FACTORS FOR DVT AND PE #1
•Thrombophilia- FH,freq,site,age
•Contraceptive pill ,HRT
•Pregnancy
•Pelvic obstruction-eg uterus,ovary,lymph nodes
•Trauma-eg RTA
RISK FACTORS FOR DVT AND PE #2
• Surgery- eg pelvic,hip,knee
• Immobility-eg bed rest,long haul flights
• Malignancy
• Myocardial infarction
• Po hypertension/vasculitis
DVT
• Proximal (Ileofemoral)
-most likely to embolise
-most likely to lead to chronic venous
insufficiency and venous leg ulcers
• Distal (Polpiteal)
-least likely to embolise
Clinical presentation of DVT
• Whole leg or calf involved depending on
site
• Swollen,hot,red,tender
• Differential:Popliteal synovial
rupture[Bakers cyst],Superficial
thrombophlebitis,Calf cellulitis
Investigation of DVT
• Ultrasound Doppler leg scan(1st line)
-Non invasive
-Exclude popliteal cyst, pelvic mass
• CT scan of ileofemoral veins,IVC and pelvis
• Constrast venography
-Invasive,contrast(irritant,allergy)
-Rarely indicated
Pulmonary Emboli
• Predisposing DVT may be silent
• Clinical presentation depends on size:
• Large-cardiovascular shock,low BP,central
cyanosis,sudden death
• Medium-pleuritic pain,haemoptysis,breathless
• Small recurrent-progressive dyspnoea,
pulmonary hypertension and right heart failure
Diagnosis of PE #1
• Clinical SignsTachycardia,Tachypnoea,Cyanosis,Fever
Low BP,Crackles, Rub, Pleural effusion
• Arterial blood gases-PaO2,Sao2
(Type 1 resp failure:PaCO2 normal or low)
• CXR-Normal early on before infarction
-Basal atelectesis,Consolidation ,
Pleural effusion after infarction
Diagnosis of PE #2
Investigations
• ECG :Acute Rt heart strain pattern
(S1,Q3,T3 , T inv in V1-3)
• D-dimers usually raised
• Isotope lung scan (Ventilation/Perfusion)
• Perfusion defect before infarction
• Perfusion+Ventilation matched defect after
infarction
V/Q isotope scan in Recurrent Po emboli
Multiple filling defects (arrows) on perfusion (Q) scan
Mismatched to ventilation (V) scan
Dyspnoea ,Hypoxia,Cardiomegaly ,Po Hypertension and Large RV on
Echo , Restrictive Lung Vols with Low DLCO ,Hypoxia
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Diagnosis of PE #3
• CT pulmonary angiogram to image
pulmonary artery filling defect
• Leg and pelvic ultrasound to detect silent
DVT
• Echocardiogram to measure pulmonary
artery pressure and RV size
• Gas transfer factor (TLCO) to measure
perfusion defect
CT Po Angiogram in Acute Massive PE
Occluded Rt main Po Artery (arrow ) and filling defect Lt Po artery
Acute Dyspnoea ,Hypoxia ,Low BP , Acute Rt Heart Strain on ECG
Raised D dimers .No clot seen in IVC or ileofemoral veins
Treated with Thrombolysis and Low MW Heparin

Investigation of underlying cause of PE
• If no obvious underlying cause –eg surgery
/pregnancy /malignancy /immobility
• Look for underlying Ca – Clin exam
,CXR,PSA,CA125,CEA,Pelvic USS
• Autoantibodies (SLE) – Antinuclear ,AntiCardiolipin
• Coagulation factor screen – Antithrombin3,Protein C/S, Factor 5/8
Prevention of DVT
•
•
•
•
Early post-op mobilisation
TED compression stockings
Calf muscle exercises
Subcutaneous low dose low mol wt heparin
perioperatively
• Dabigatran - direct thrombin inhibitor
Rivaroxaban - direct inhibitor of activated
factor X- both given orally for prophylaxis of
venous thromboembolism in adults after hip or
knee replacement surgery
Treatment of DVT/PE #1
• Anticoagulation prevents clot
propagation-tips balance to thrombolysisbody dissolves clot
• Initiate with parenteral heparin-fast
acting-via antithrombin-3
• Usually therapeutic dose of s/c low mol wt
heparin ( Dalteparin “Fragmin”)
Treatment of DVT/PE #2
• Low mol wt heparin –once daily injection
,no monitoring –no hassle
• IV infusion unfractionated heparin -more
hassle-need to monitor clotting, increased
bleeding risk- rarely used nowadays
Treatment of DVT/PE #3
• Start concurrent oral warfarin-takes 3
days-antagonises vit K1 dependent
prothrombin
• After 3-5 days stop heparin-when INR>2
• Need to monitor APTT with unfractionated
-but not with low mol wt heparin
Treatment of DVT/PE #4
• Continue Warfarin for 3-6 months
• Monitor Warfarin with INR-Target range 2.53.5
• Interactions which increase anticoagulation
-Alcohol,Antibiotics ,Aspirin,NSAIDs,
Amiodarone, Cimetidine,Omeprazole ,etc etc
• Look in BNF for possible interactions
Treatment of DVT/PE #5
• Thrombolysis-Streptokinase or TPA
• Only for large life threatening PE-ie low BP
and severe hypoxaemia due to main pulmonary
artery occlusion
• IVC filter to prevent embolisation from large
ileofemoral/IVC clot - for recurrent PE’s
• Thrombo-embolectomy –rarely indicated
• Aspirin –no role – anti-platelet
Overanticoagulation
• Address underlying cause-eg drug
interaction,chronic liver disease,CHF
• If bleeding then stop anticoagulant and reverse
effect
• Low MW Heparin has a long half life
• Warfarin has a long half life
• May need cover with prothrombin complex
concentrate or fresh frozen plasma
• Reverse warfarin with vitamin K1(especially if
chronic liver disease)
• Reverse heparin with protamine