279 - DVT and Pulmonary Embolism

Question 1

Classical presentation of PE

Answer 1

• Sudden onset pleuritic chest pain
• Breathlessness
• Haemoptysis
• Postural giddiness
• Syncope

Massive PE may present as cardiac arrest or shock

Suspect in all patients with risk factors of DVT

Question 2

Atypical presentation of PE

Answer 2

• Unexplained breathlessness
• Unexplained hypotension
• Syncope only

Question 3

Signs of PE

Answer 3

• Fever (often mild)
• Tachycardia
• Tachypnoea
• Postural hypotension
• Cyanosis (large PE)
• Pleural rub or effusion
• Signs of DVT or thrombophlebitis

Features of Cor Pulmonale
- JVP prominent “a” wave
- TR: pansystolic murmur over tricuspid
- Parasternal heave
- S3
- Loud P2 with wide splitting
- PR: diastolic murmur over pulmonary

Question 4

Post-pulmonary embolism syndrome

Answer 4

Persistent dyspnoea
Fatigue
Reduced effort tolerance
Persistent right ventricular dysfunction on echocardiogram

Risk of developing chronic thromboembolic pulmonary hypertension

Question 5

Describe the pathophysiology of formation of VTE

Answer 5

1. Predisposing Factors
   A. Risk factors: cancer, obesity, smoking, hypertension, COPD, CKD, long distance travel, air pollution, OCP, pregnancy, hormonal replacement, surgery, trauma, sedentary lifestyle
   (Watching TV each 2H per day increases 40% likelihood of fatal PE)

B. Prothrombic state
- Autosomal dominant mutations: Factor V leiden, prothrombin gene mutation
- ATIII, protein C, protein S deficiency
- ALPS

2. Precipitating Factors (acute events)
   - Inflammation: UC/Crohns’, RA, psoriasis, atherosclerosis, pneumonia, ACS, stroke, sepsis, erythropoietin, transfusion, cancer
3. Virchow’s triad leads to recruitment of activated platelets
   A. Endothelial injury from inflammation
   (arterial plaque -> endothelial injury and inflammation ->x2 likely to get VTE, and conversely VTE x2 to get CVS diseases)
   B. Hypercoagulability state
   C. Venous stasis
4. Activated platelets
   - Activated platelets release proinflammatory mediators, bind to neutrophils and stimulate neutrophil extracellular traps
   - Histones stimulate platelet aggregation and platelet-dependent thrombin generation
   - Venous thrombi form and fluorish furhter in stasis, low oxygen tension and proinflammatory states
5. Embolisation
   - DVT detach from site of formation
   PE: -> vena cava -> RA/RV -> pulmonary circulation
   Stroke: PFO or ASD -> left heart circulation -> brain

Question 6

Describe the pathophysiology of pulmonary embolism

Answer 6

1. Increased dead space -> gas exchange abnormalities (hypoxaemia and increased alveolar-arterial O2 tension gradient)
   - Anatomical dead space: breathed gas does not enter gas exhcange units of lung
   - Physiological dead space: ventilation to gas exchange units exceed venous blood flow through pulmonary capillaries
2. Increased pulmonary vascular resistance (obstruction or vasoconstriction)
   - Vascular obstruction or platelet secretion of vasoconstricting neurohumoral agents (serotonin)
   -> ventilation-perfusion mismatch, even remote from embolus
   (explains discordance between small PE and large gradient)
3. Impaired gas exchange
   - Increased alveolar dead space from vascular obstruction, hypoxaemia from hypoventilation relative to perfusion of non-obstructed lung, right to left shunting
   - Impaired carbon monoxide transfer
4. Alveolar hyperventilation
   - Reflex stimulation of irritant receptors
5. Increased airway resistance
   - Constriction of airways distal to bronchi
6. Reduced pulmonary compliance
   - Lung oedema, haemorrhage or loss of surfactant
7. RV dysfunction and microinfarcts -> pulmonary hypertension
   - PA obstruction and neurohumoral mediators increases pulmonary arterial pressure and vascular resistance
   - RV wall tension rises, dilates RV and causes dysfunction
   - Release of cardiac biomarkers (troponin, BNP)
   - Interventricular septum bulging and compresses LV and right coronary artery
   - Diastolic LV dysfunction -> impaires LV filling and reduced CO, hypotension -> circulatory collapse
   - Right coronary artery ischaemia -> RV microinfarct, further releasing cardiac biomarkers

Question 7

Multiple whammy in resuscitation of massive PE
- Fluid resuscitation
- Intubation
- Inotropes
- ECMO

Answer 7

1. Fluid resuscitation - judicious, replete with +/- 500mL
   - Excessive fluid resuscitation exacerbates RV wall stress, more profound RV ischaemia, interventricular septal compression on LV worsens LV compliance and filling.
   -> Worsened hypotension and cardiac output
2. Intubation - trial BiPAP preferred first (drowsy/low GCS unable to maintain airway)
   - Pre/post-intubation medication causes profound hypotension further worsening circulation
   - Intubation and positive airway pressure increases intrathroacic pressure, reduces venous return -> hypotension
   - May lead to pericardiac/cardiac arrest
3. Inotrope - noradrenaline and dobutamine preferred
   - NA: increases RV inotropy and blood pressure, restores coronary perfusion gradient
   - Dobutamine: increases RV inotrophy, BUT lowers filling pressure and hypotension (must be used in conjunction with another vasopressor)
4. Consider ECMO as bridge to thrombolysis or embolectomy