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PULMONARY EMBOLISM
(PE)
ALOK HRIDAY MISHRA
MD 7A1
TOPICS TO COVER
• GENERAL WORDS
• DEFINITION
• EPIDEMIOLOGY
• TYPES
• CONCEPT BOOSTER
• PATHOGENESIS
• CLINICAL FEATURE
• DIAGNOSIS
• TREATMENT
GENERAL WORDS
PE is among those Five critical condtion of lung
which is associated with cough and(+- dyspnea)
1. Obstructive lung disease
2. Restrictive lung disease
3. Pulmonary vascular abnormality
4. Infection
5. Malignancy
PE fall under the category of pulmonary
vascular abnormality
DEFINITION
The sudden blockage of pulmonary artery or its
branches by an embolus.
Types of embolus:-
1. Air (gas)
2. Viscous fluid (e.g. amniotic fluid)
3. Fat
4. Thrombus
5. Septic embolus
Among these types thrombus is much common that causes PE
This embolus blocks the blood supply to the affected area of
lung parenchyma, thus leads to cough, dyspnea and other
clinical features.
IT COULD BE EVEN FATAL
EPIDEMIOLOGY
• Most common preventable cause of death in
hospitalized patients.
• PE is 3rd most common cardiovascular cause of
death. 1st is Ischemic heart disease
2nd is stroke
• 1 out of 10 patients with PE die within the first
hour.
• Death rate of men by PE is 20-30% more than
females
TYPES OF PULMONARY EMBOLISM
CONCEPT BOOSTER
• Thrombus in deep veins is called
DEEP VENOUS THROMBUS (DVT)
• DVT PE
• These deep veins can be from different veins of
lower or even upper extremity, most common by
1. Popliteal vein
2. Femoral veins
• Stasis of blood (varicose veins, comatose patients,
immobile limb)
• Hypercoagubility,(nephrotic syndrome) leads to
release of many coagulant in urine such as protein
C and Protein S as well as Antithrombin III
• Hypertension:- high BP in long run starts to
damage endothelial lining this coould be the
reason of male fatality rate is higher than female
• Not only thrombus;
But also,
1. fat embolus ----------> fracture of long bone
2. Air embolus---------- > needle stick injury
3. Amniotic embolus--- > pregnancy
4. Setic embolus --------> infected bolus of
bacterial colony
PATIENT MUST BE TAKEN INTO CONSIDERATION
PATHOGENESIS
• Deep veins of lower leg
• Femoral veins
• Thrombus dislodges
• Embolus
• Blocks pulmonary vessels
• Ventilation without perfusion
• V/Q reaches infinity
• V/Q mismatch
• Deadspace physiology
• Decreased O2 in Pulmonary artery
• Hypoxaemia
• Hypoxia
• Compensatory reflexes activated
• Vaso contriction
• Loss of function of type II pneumocyte
• Loss of surfactant
• ATELECTASIS
Also as the blood supply to lung decreases
• Ischemia
• Infarction
Pulmonary artery radius decreases due to vasoconstriction
• Increase vascular resistance
• Pulmonary hypertension
• Increase work load on RV
Lung parenchyma is highly distensible,
So you can occlude upto 50% of vessel in lung before the RV begin to suffer.
In case of massive PE,
• Increased pressure on RV
• RV dysfucntion
• RV failure
• NO blood/ less blood pumped in lung
• NO blood/ less blood return back to LA
• Less to no blood in LV
• Sudden ischemia
• DEATH
CLINICAL FEATURE
• SYMPTOMS:
a. Dyspnea
b. Chest pain
c. Hemoptysis due to pulmonary hypertension
d. Productive cough
• SIGNS:
a. Tachypnea
b. Tachycardia
c. Respiratory distress
DIAGNOSIS
First we check for DVT and then PE
• WELL’s criteria for DVT
• WELL’s criteria for PE
If well’s criteria for DVT yields:-
• Low probability--------------------------------------------- > D-dimer
• Intermediate to High probability ------------------------- > compression
Ultrasound of leg
• High probability for DVT + US show No clot-------------> CT-PA
(non invasive)
• If patient is obese, allergic to contrast or haverenal failure then
V/Q scan (non- invasive)
• Even if PE is not clear then PULMONARY ANGIOGRAPHY (invasive)
WELL’s criteria for DVT
WELL’s criteria for PE
CONCLUSION
TREATMENT
Fatality rate is high and time is a crucial factor in saving
person’s life
TREATMENT MUST BE AGGRESSIVE
1. Supportive therapy:-
for everyone
asses vitals and secure ABCs
if hypoxic give ……. O2 supplement
If hypotensive give……IV bolus fluid
If bradycardic give……DOBUTAMINE
2. ANTICOAGULANT THERAPY:
• heparin:-
i. UH (unfractionated heparin)
ii. LMWH
 Enoxaparin
 Dalteparin
 Tinzaparin
• Warfarin
• Others
i. Factors Xa inhibitors (ApiXabar)
ii. Direct thrombin inhibitor
(argatroban)
3. FIBRINOLYTIC THERAPY:-
For hemodynamic unstable patients
(in case of MASSIVE EMBOLUS)
TISSUE PLASMINOGEN INHIBITOR (tpA)
• ALTEPLASE
• RETEPLASE
• TENECTEPLASE
4.SURGERY:-
• THROMBECTOMY
• EMBOLECTOMY
For PE ------------------ > HEPARIN
For massive PE --------> tpA
Everything about Pulmonary embolism- PPT

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Everything about Pulmonary embolism- PPT

  • 2. TOPICS TO COVER • GENERAL WORDS • DEFINITION • EPIDEMIOLOGY • TYPES • CONCEPT BOOSTER • PATHOGENESIS • CLINICAL FEATURE • DIAGNOSIS • TREATMENT
  • 3. GENERAL WORDS PE is among those Five critical condtion of lung which is associated with cough and(+- dyspnea) 1. Obstructive lung disease 2. Restrictive lung disease 3. Pulmonary vascular abnormality 4. Infection 5. Malignancy PE fall under the category of pulmonary vascular abnormality
  • 4. DEFINITION The sudden blockage of pulmonary artery or its branches by an embolus. Types of embolus:- 1. Air (gas) 2. Viscous fluid (e.g. amniotic fluid) 3. Fat 4. Thrombus 5. Septic embolus Among these types thrombus is much common that causes PE This embolus blocks the blood supply to the affected area of lung parenchyma, thus leads to cough, dyspnea and other clinical features. IT COULD BE EVEN FATAL
  • 5. EPIDEMIOLOGY • Most common preventable cause of death in hospitalized patients. • PE is 3rd most common cardiovascular cause of death. 1st is Ischemic heart disease 2nd is stroke • 1 out of 10 patients with PE die within the first hour. • Death rate of men by PE is 20-30% more than females
  • 8. • Thrombus in deep veins is called DEEP VENOUS THROMBUS (DVT) • DVT PE • These deep veins can be from different veins of lower or even upper extremity, most common by 1. Popliteal vein 2. Femoral veins • Stasis of blood (varicose veins, comatose patients, immobile limb) • Hypercoagubility,(nephrotic syndrome) leads to release of many coagulant in urine such as protein C and Protein S as well as Antithrombin III • Hypertension:- high BP in long run starts to damage endothelial lining this coould be the reason of male fatality rate is higher than female
  • 9.
  • 10. • Not only thrombus; But also, 1. fat embolus ----------> fracture of long bone 2. Air embolus---------- > needle stick injury 3. Amniotic embolus--- > pregnancy 4. Setic embolus --------> infected bolus of bacterial colony PATIENT MUST BE TAKEN INTO CONSIDERATION
  • 11. PATHOGENESIS • Deep veins of lower leg • Femoral veins • Thrombus dislodges • Embolus • Blocks pulmonary vessels • Ventilation without perfusion • V/Q reaches infinity • V/Q mismatch • Deadspace physiology • Decreased O2 in Pulmonary artery • Hypoxaemia • Hypoxia • Compensatory reflexes activated • Vaso contriction • Loss of function of type II pneumocyte • Loss of surfactant • ATELECTASIS
  • 12. Also as the blood supply to lung decreases • Ischemia • Infarction Pulmonary artery radius decreases due to vasoconstriction • Increase vascular resistance • Pulmonary hypertension • Increase work load on RV Lung parenchyma is highly distensible, So you can occlude upto 50% of vessel in lung before the RV begin to suffer. In case of massive PE, • Increased pressure on RV • RV dysfucntion • RV failure • NO blood/ less blood pumped in lung • NO blood/ less blood return back to LA • Less to no blood in LV • Sudden ischemia • DEATH
  • 13. CLINICAL FEATURE • SYMPTOMS: a. Dyspnea b. Chest pain c. Hemoptysis due to pulmonary hypertension d. Productive cough • SIGNS: a. Tachypnea b. Tachycardia c. Respiratory distress
  • 14. DIAGNOSIS First we check for DVT and then PE • WELL’s criteria for DVT • WELL’s criteria for PE If well’s criteria for DVT yields:- • Low probability--------------------------------------------- > D-dimer • Intermediate to High probability ------------------------- > compression Ultrasound of leg • High probability for DVT + US show No clot-------------> CT-PA (non invasive) • If patient is obese, allergic to contrast or haverenal failure then V/Q scan (non- invasive) • Even if PE is not clear then PULMONARY ANGIOGRAPHY (invasive)
  • 17.
  • 19. TREATMENT Fatality rate is high and time is a crucial factor in saving person’s life TREATMENT MUST BE AGGRESSIVE 1. Supportive therapy:- for everyone asses vitals and secure ABCs if hypoxic give ……. O2 supplement If hypotensive give……IV bolus fluid If bradycardic give……DOBUTAMINE
  • 20. 2. ANTICOAGULANT THERAPY: • heparin:- i. UH (unfractionated heparin) ii. LMWH  Enoxaparin  Dalteparin  Tinzaparin • Warfarin • Others i. Factors Xa inhibitors (ApiXabar) ii. Direct thrombin inhibitor (argatroban)
  • 21. 3. FIBRINOLYTIC THERAPY:- For hemodynamic unstable patients (in case of MASSIVE EMBOLUS) TISSUE PLASMINOGEN INHIBITOR (tpA) • ALTEPLASE • RETEPLASE • TENECTEPLASE 4.SURGERY:- • THROMBECTOMY • EMBOLECTOMY For PE ------------------ > HEPARIN For massive PE --------> tpA