Respiratory VI (P. Hypertension; PE Flashcards
Define what is meant by pulmonary hypertension [1]
Pulmonary hypertension is defined as a mean pulmonary arterial pressure of more than 25 mmHg at rest when assessed with right heart catheterization
Pulmonary hypertension is an umbrella term for many different diseases which lead to increased pressure in the pulmonary arteries
Describe the general pathophysiology of pulmonary hypertension
In general, pulmonary hypertension occurs when the pulmonary arteries become narrowed due to hypoxic pulmonary vasoconstriction or thrombosis, thickened or damaged causing increased pressure in the vessels.
This causes strain on the right side of the heart. And can causes right ventricular hypertrophy
The causes of pulmonary hypertension can be classified into five groups.
What are they? [5]
Group 1 Idiopathic pulmonary hypertension or connective tissue disease (e.g., systemic lupus erythematous)
Group 2 – Left heart failure, usually due to myocardial infarction or systemic hypertension
Group 3 – Chronic lung disease (e.g., COPD or pulmonary fibrosis)
Group 4 – Pulmonary vascular disease (e.g., pulmonary embolism)
Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorder
What ECG changes would you expect to see of someone with pulmonary hypertension? [4]
All indicate right sided heart strain:
P pulmonale: peaked P waves
Right ventricular hypertrophy (tall R waves in V1 and V2 and deep S waves in V5 and V6)
Right axis deviation
Right bundle branch block
What blood test might indicate pulmonary hypertension? [1]
Raised NT‑proBNP blood test result indicates right ventricular failure
What imaging would you use to investigate pulmonary artery pressure? [1]
Echocardiogram can be used to estimate the pulmonary artery pressure
Name and state the drug classes used to treat idiopathic pulmonary hypertension [4]
Idiopathic pulmonary hypertension may be treated with:
Calcium channel blockers
Intravenous prostaglandins e.g., epoprostenol
Endothelin receptor antagonists e.g., macitentan
Phosphodiesterase-5 inhibitors e.g., sildenafil
Which inherited disorders increase the risk of PE? [5]
Factor V Leiden mutation:
- Normally used for blood clotting: helps enzyme reaction to form fibrin in blood clot
- Once the coagulation process is turned on in people with factor V Leiden, it turns off more slowly than in people with normal factor V
Antithrombin deficiency
- Normally anti-thrombin acts as the inhibitory component to thrombin formation
Prothrombin deficiency
Protein C & S deficiencies
Antiphospholiipid syndrome
Which type of hormone therapy increases the risk of PE? [1]
Hormone therapy with oestrogen (e.g., combined oral contraceptive pill or hormone replacement therapy)
What is important to note about symptoms of dysopnea in PE? [1]
Symptoms of PE usually come on acutely rather than gradually.
Explain what is meant by the PERC rule
The pulmonary embolism rule-out criteria (PERC) are recommended by the NICE guidelines (2020) when the clinician estimates less than a 15% probability of a pulmonary embolism to decide whether further investigations for a PE are needed. If all the criteria are met, further investigations for a PE are not required.
Describe the investigations you would conduct for a ptx suspected with PE
computed tomographic pulmonary angiography (CTPA)
- preferred investigation for definitive confirmation of PE
echocardiography:
- presence of any signs of right ventricular (RV) dysfunction is sufficiently suggestive of PE to confirm the diagnosis and justify urgent reperfusion treatment
- used if CTPA not immediately available / contraindicated
D-dimer:
- Elevated
- Used if Wells Score < 4.
ECG:
- An ECG is not diagnostic of PE but can be useful to support the diagnosis of PE or rule out other causes.
- S1Q3T3 pattern
urea and electrolytes:
- guides CTPA use
Why might a CTPA be contraindicated for PE investigation? [2]
The contrast dye used in CTPA for the evaluation of PE may cause nephropathy.
Radiation from CT is considered to be a risk factor for certain cancers.
Explain a specific sign seen on echocardiogram that would indicate a PE [1]
60/60 sign :a combination of
- pulmonary acceleration time (PAT) less than 60 milliseconds
and
- tricuspid regurgitation (TR) jet gradient of less than 60 mmHg
What is the McConnell sign? [1]
What does it indicate? [1]
reduced contractility of the RV free wall compared with the RV apex
indicates PE
Typically this looks as if the apex of the RV is a trampoline bouncing up and down while the rest of the RV remains still
Ty
What ABG results would indicate PE? [1]
Explain your answer [1]
TOM TIP: Patients with a pulmonary embolism often have respiratory alkalosis on an ABG.
Hypoxia causes a raised respiratory rate.
Breathing fast means they “blow off” extra CO2.
A low CO2 means the blood becomes alkalotic.
What are the two causes of respiratory alkolosis in an ABG? [2]
How do you differentiate between them? [2]
PE
and
Hyperventilation syndrome.
Patients with PE will have a low pO2
Patients with hyperventilation syndrome will have a high pO2.
A V/Q scan is of limited use in patients with which co-morbidities? [3]
A V/Q scan is of limited use in patients with:
* significant underlying lung disease
* left ventricular failure
* congestive cardiac failure
What is the leading cause of death for patients with massive PE? [1]
The leading cause of death in patients with high-risk (massive) PE is acute right ventricular (RV) failure with resulting hypotension.[65]
Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically unstable [4]
First line:
- heparin: 10,000 units intravenously as a loading dose initially, followed by 18 units/kg/hour intravenous infusion
PLUS: thrombolysis: (involves injecting a fibrinolytic (breaks down fibrin) medication that rapidly dissolves clot)
- Alteplase or
- Streptokinase or
- Urokinase
PLUS:
- anticoagulation with unfractionated heparin (UFH) for several hours after the end of thrombolysis before: switching to apixaban or rivaroxaban; low molecular weight heparin (LMWH) is an alternative if these are unsuitable - this is preferable
CONSIDER: vasoactive drug if SBP < 90 mmHG after thrombolysis
- noradrenaline or
- dobutamine
-
Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically stable [4]
Stable, no renal impairment or co-morbidities: offer apixaban/rivaroxaban. If not-suitable, LWMH for 5 days then offer edoxaban/warfarin*
First line: anticoagulation:
- apixaban or
- rivaroxaban
OR
- UFH / LMWH / Fondaparinux lead AND warfarin
- Target INR 2-3 then stop heparin
Describe the long term managment of PE for:
- most people [4]
- patients suffering from antiphospholipid syndrome [1]
- pregnant people [1]
DOACs: most people
- apixaban
- rivaroxaban
- edoxaban
- dabigatran
Warfarin: for antiphospholipid syndrome patients
LMWH for pregnant people
How long would you continue treatment for patients:
- with a reversible cause [1]
- unprovoked PE [1]
- with cancer p1[
Treatment time:
* 3 months with a reversible cause (then review)
- Beyond 3 months with unprovoked PE, recurrent VTE or an irreversible underlying cause (e.g., thrombophilia)
- 3-6 months in active cancer (then review)
All patients of PE should have anticoagulation for at least [] months
All patients of PE should have anticoagulation for at least 3 months
State 4 acute complications of PE
Right ventricular failure:
Cardiogenic shock:
Arrhythmias
Respiratory failure
Describe the clinical consequence of PE causing right ventricular failure [2]
Large or multiple emboli can cause acute right ventricular (RV) dilata hypertrophy strain, leading to RV dysfunction and failure.
This may result in systemic hypotension, shock, and even sudden cardiac death.
Describe how massive PE causes hemodyanmic collapse [7]
Describe how PE can cause cardiogenic shock [2]
Cardiogenic shock
- Severe PE may lead to decreased cardiac output, causing systemic hypotension, impaired end-organ perfusion, and ultimately cardiogenic shock.
Which arrythmias can PE lead to [3]
Arrhythmias: PE can provoke supraventricular and ventricular arrhythmias, such as:
- atrial fibrillation
- ventricular tachycardia
- ventricular fibrillation
which can further compromise hemodynamics.
Describe three subacute complications of PE
Infarction and lung necrosis
- PE can cause ischemic injury to the lung parenchyma, leading to pulmonary infarction, haemorrhage, or lung necrosis.
Pleural effusion:
- Inflammatory processes triggered by PE may cause pleural effusion, which may be exudative or hemorrhagic.
Pneumothorax:
- Rarely, PE-induced lung infarction may lead to pneumothorax due to the rupture of a bulla or necrotic lung tissue
Describe a chronic complication of PE [1]
Chronic thromboembolic pulmonary hypertension (CTEPH):
- CTEPH is a rare but serious complication characterized by unresolved thrombotic occlusions in the pulmonary arterial system, turning into fibrotic tissue leading to increased pulmonary vascular resistance, pulmonary hypertension, and eventually right heart failure.
What is the most appropriate next step in the investigation of suspected pulmonary embolism if D-dimer negative?
Stop anticoagulation and consider an alternative diagnosis
What is the most appropriate next step in the investigation of suspected pulmonary embolism if medium-high (> 15%) pre-test probability of PE? [1]
A 2-level PE Wells score should be performed:
Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less
What is the most appropriate next step in the investigation of suspected pulmonary embolism if CTPA negative? [1]
Consider the possibility of DVT and arrange proximal leg vein ultrasound if suspected
PE would cause change to axis deviation? [1]
Right axis deviation
Describe if lung tissue becomes infarcted during a PE
May infarct if not perfused by PE. But oxygen continues to be supplied by the bronchial circulation and airways
State 3 respiratory and 4 CVS differential diagnoses for PE
Respiratory:
- Pneumothorax
- Pneumonia
- Acute exaerbation of resp disease
CV:
- MI
- Pericarditis
- Aortic dissection
- Cardiac tampondade
What ECG findings would a PE cause? [6]
Sinus tachycardia
New onset AF
Right axis deviation
RBBB
T wave inversion
P pulmonale
S1Q3T3
Describe the S1Q3T3 ECG changes in PE [3]
deep S wave in lead I
Q wave in III
inverted T wave in III (20%)
Which drug is contraindicated in pregnancy, but safe with breastfeeding? [1]
Warfarin
State 4 invasive procedures used to treat PE if needed
- Embolectomy
- Mechanical fragmentation with R heart angiography
- Pulmonary thombro-endarterectomy
- IVC filter
Which of the following is used to treat chronic PEs unresolved after 3 months
- Embolectomy
- Mechanical fragmentation with R heart angiography
- Pulmonary thombro-endarterectomy
- IVC filter
Pulmonary thombro-endarterectomy (PTE)
Name a risk [1] and benefits [2] of using unfractionated heparin in treating PE [4]
Risks:
- Heparin induced thrombocytopenia (HIT)
Benefits:
- Rapid reversal possible
- More rapid anticoagulation
What is an IVC filter? [1]
When is it used? [3]
Traps fragmented thrombemboli on the way to pulmonary circulation
Used if:
- patient is contraindicated to anticoagulation in proximal PE/DVT
- Recurrent VTE despite anticoagulation tx
- Only temporary
What level of thrombophilia should make sure that you screen a patient? [2]
< 50 & recurrent unprovoked VTE or strong FHx
What ECHO findings might you find in acute PE? [6]
Direct visualization of
thromboemboli in the RT heart
and PA.
RV dilatation.
RV dysfunction.
Normal or hyper dynamic LV.
Septal flattening.
PA dilatation
Describe the different bridging times for LMWH if using:
- Warfarin
- Dabigatran or edoxaban
- Rivaroxaban or apixaban
Warfarin:
- Start LMWH and initiate warfarin at same time then after 5-10 days change to just warfarin
Dabigatran or edoxaban
- 5 days of LMWH with both then switch to doac same day
Rivaroxaban or apixaban
- No bridge - only use them
a prolonged PR interval
Hepatotoxicity
Optic neuritis
Gout
Type IV
Describe the diagnostic pathway for PEs
