Acute respiratory failure AND PE.pptx DEEPIKA

Acute respiratory failure AND PE.pptx DEEPIKA

1. ACUTE RESPIRATORY FAILURE AND PULMONARY EMBOLISM

2. Respiratory failure results when one or both of these gas-exchanging functions are inadequate For Eg. , Inadequate O2 transferred to the blood. Inadequate CO2 is removed from the lungs. ACUTE RESPIRATORY FAILURE

3. Normal gas exchange unit in the lung.

4. Classification of respiratory failure

5. Type 1 Hypoxemic RF (oxygenation failure) PaO2 < 60 mmHg, decreased SaO2 Inadequate oxygen saturation of hemoglobin (1) Disorder that interfere with O2 transfer into the blood (2) Associated with acute diseases of the lung Pulmonary edema (Cardiogenic, noncardiogenic (ARDS), pneumonia, pulmonary hemorrhage, and collapse Type 2 Hypercapnic RF (ventilatory failure) Insufficient co2 removal PaCO2 > 45 mmHg Combination of acidosis PH <7.35 PaCO2 than the normal (1) Body inability to compensate increases acidosis (2), severe acid base imbalance. Common causes Drug overdose, neuromuscular disease, chest wall deformity, COPD, and Bronchial asthma

6. Distinction between Acute and Chronic RF • Acute RF • Develops over minutes to hours • ↓ pH quickly to <7.2 • Example; Pneumonia Chronic RF • Develops over days to weeks • ↑ in HCO3 • ↓ pH slightly • Polycythemia, Corpulmonale • Example; COPD

7. MECHANISM OF RESPIRATORY FAILURE I. Mechanisms of hypoxemic respiratory failure V/Q mismatch Shunt Alveolar hypoventilation Airway-Alveolar abnormalities Diffusion limitation Low FIO2 Low barometric pressure II. Hypercapnic respiratory failure CNS problems, Neuromuscular conditions, Chest wall abnormalities, and Problems affecting the airways and/or alveoli.

8. I . MECHANISMS OF HYPOXEMIC RESPIRATORY FAILURE V/Q Shunt Alveolar hypoventilation Airway-Alveolar abnormalities Diffusion limitation Low FIO2 Low barometric pressure

9. In normal lungs, the volume of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical. So, when you compare normal alveolar ventilation (4 to 6 L/min) to pulmonary blood flow (4 to 6 L/min), V/Q=1 (ventilation-perfusion mismatch )-1ml of air for 1 ml of blood flow i.e.., 1:1 Condition that alter V/Q (V/Q mismatch ) Increased secretion in airways-COPD Inc secretion in alveoli- pneumonia Limited airflow ventilation Bronchospasm- asthma but have no effect on blood flow Alveolar collapse- Atelectasis to the gas exchange units . Embolus. PATHOPHYSIOLOGY-V/Q

10. REGIONAL V/Q DIFFERENCES IN THE NORMAL LUNG

11. Range of ventilation to perfusion (V/Q) relationships.

12. SHUNTS Blood exits the heart without participated in gas exchange Two types : Anatomical and intrapulmonary shunts Anatomical shunts: e.g. VSD intrapulmonary shunts: ARDS , pneumonia, pulmonary edema (Alveoli filled with fluid prevent gas exchange)

13. Intra-pulmonary • Small airways occluded ( e.g asthma, chronic bronchitis) • Alveoli are filled with fluid ( e.g pulm edema , pneumonia) • Alveolar collapse ( e.g atelectasis) Perfusion without ventilation (shunting)

14. DIFFUSE LIMITATION Alveolar-capillary membrane Compromise become thicken or destroys the membrane Due to severe emphysema and pulmonary emboli that worsen pulmonary vascular bed Thickening of alveolar capillary membrane Fibrotic changes Slow gaseous exchange classic signs: hypoxemia during exercise but not at rest

15. Alveolar hypoventilation Decreased in ventilation due to increased PaCo2 and dec in PaO2 Various conditions that affect hypoventilation such as restrictive lung disease , CNS disease, chest wall dysfunction , asthma, neuromuscular failure Hypoxemia

16. Hypercarbia   • Hypercarbia is always a reflection of inadequate ventilation & ventilatory failure PaCO2 is Directly related to CO2 production Inversely related to alveolar ventilation PaCO2 = k x VCO2 / VA  When CO2 production increases, ventilation increases rapidly to maintain normal PaCO2 • Alveolar ventilation is only a fraction of total ventilation VA = VE – VD • Increased dead space or low V/Q areas may adversely effect CO2 removal

17. II . HYPERCAPNIC RESPIRATORY FAILURE ventilatory failure, Many conditions can cause impaired ventilation. This often occurs from an increase in CO2 production or a decrease in alveolar ventilation. Hypercapnic respiratory failure can be acute or chronic. 4 categories: (1) CNS problems, (2) neuromuscular conditions, (3) chest wall abnormalities, and (4) problems affecting the airways and/or alveoli.

18. Abnormalities of airway Central nervous system abnormalities Chest wall abnormalities Neuromuscular conditions 4 categories involved in Hypercapnic RF

19. 1.AIRWAY AND ALVEOLI ABNORMALITIES Asthma, COPD, cystic fibrosis , are high risk for hypercapnic RF ,due to airflow obstruction Respiratory muscle fatigue Ventilatory failure PATHOPHYSIOLOGY

20. PATHOPHYSIOLOGY 2.CNS Abnormalities Various CNS may supress the drive to breathe Overdose of res dep drugs e.g.., opioids, benzodiazepines It dec O2 reactivity in brain Arterial CO2 levels rise Brainstem infarction and head injury may also interfere Normal function of resp centre in the medulla

21. PATHOPHYSIOLOGY 3.Chest wall abnormalities Due to flail chest ,fractures Difficulty in expanding lungs due to pain , muscle spasm , mechanical restriction and due to kyphoscoliosis Change in spinal configuration Compress the lungs and it prevents normal expansion Develop risk of respiratory failure Because of limitation in lung expansion

22. 4. DUE TO NEUROMUSCULAR CONDITION Due to Guillain-Barre syndrome ,muscular dystrophy , myasthenia gravis(acute exacerbation) or multiple sclerosis Respiratory muscles are weakened or paralyzed Risk for respiratory failure

23. CAUSES:1-CNS Depression of the neural drive to breath Brain stem tumors or vascular abnormality Overdose of a narcotic, sedative Myxedema, chronic metabolic alkalosis Acute or chronic hypoventilation and hypercapnia Causes

24. 2 - Disorders of peripheral nervous system, Respiratory dysfunction in multiple sclerosis • Inability to maintain a level of minute ventilation appropriate for the rate of CO2 production • Guillain-Barre syndrome, muscular dystrophy, myasthenia gravis, Kyphoscoliosis, morbid obesity • Hypoxemia and hypercapnia CAUSES

25. 3-Abnormities of the airways Upper airways • Acute epiglottitis • Tracheal tumours Lower airway • COPD, Asthma, cystic fibrosis • Acute and chronic hypercapnia causes

26. 4 - Abnormities of the alveoli Diffuse alveolar filling hypoxemic RF Cardiogenic and noncardiogenic pulmonary edema Aspiration pneumonia Pulmonary hemorrhage Associate with Intrapulmonary shunt and increase work of breathing causes

27. CLINICAL MANIFESTATION Hypoxemia respiratory failure Respiratory system Dyspnoea Tachypnoea Prolonged expiration (I:E 1:3, 1:4) Intercostal muscle retraction Use of accessory muscles in respiration SpO2, (<80%) Paradoxic chest/abdominal wall movement with respiratory cycle (late) Cyanosis (late)

28. CLINICAL MANIFESTATION Cerebral Agitation Delirium Confusion. Coma (late) Cardiac. Tachycardia Skin cool, clammy, and diaphoretic Other Fatigue Unable to speak in complete sentences without pausing to breathe

29. CLINICAL MANIFESTATION Hypercapnia respiratory failure Respiratory Dyspnoea Respiratory rate or rapid rate with shallow respirations Tidal volume Minute ventilation Cerebral Morning headache Progressive somnolence Disorientation• Coma (late). Cardiac Dysrhythmias. Tachycardia Hypertension Bounding pulse Neuromuscular Muscle weakness Tremor, seizures (late) Deep tendon reflexes,

30. OTHER STUDIES CBC Sr.Electrolytes Gram stain Culture and sensitivity Capnometry BLUE PROTOCOLS(bedside lung ultrasound in emergency) DIAGNOSIS OF RF

31. providing support with oxygenation and ventilation, Correction of Hypoxemia Correction of Hypercapnia and Respiratory Acidosis Ventilatory Support HFNC may be as effective as NIV in the management of AHRF, particularly in improving arterial pH, pCO2, and pO2, as well as preventing endotracheal intubation and mortality. MANAGEMENT-GOALS

32. Embolus derives from a Greek word meaning “plug” or “stopper.” Pulmonary Embolism refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart Most commonly due to blood clot or thrombus -HARI PRASATH. Pulmonary embolism (PE) is the blockage of 1 or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue - LEWIS PULMONARY EMBOLISM

33. A saddle embolus refers to a large thrombus lodged at an arterial bifurcation. Less common causes Fat emboli (from fractured long bones), Air emboli (from improperly administered IV therapy), Bacterial vegetation on heart valves, Amniotic fluid, and Cancer. SADDLE EMBOLUS

34. Virchow’s Triad criteria: Factors that contributed to thrombosis. Stasis of blood, Hypercoagulability, and Endothelial vessel wall injury Virchow’s Triad criteria:

35. RISK FACTORS Risk factors for pulmonary embolus: Venous stasis Prolonged immobilization Prolonged periods of sitting/traveling Varicose veins Spinal cord injury Hypercoagulability Injury Tumour (pancreatic, Gl , breast, lung) Increased platelet count ( polycythemia , splenectomy) Venous endothelial disease Thrombophlebitis Vascular disease Foreign bodies (IV/central venous catheters) Certain disease States (combination of stasis, coagulation alterations, and venous injury) Heart disease (especially heart failure). Trauma Postoperative state/postpartum period DM COPD

36. PREDISPOSING FACTORS Advanced age Obesity Pregnancy Oral contraceptive use History of previous thrombophlebitis, pulmonary embolism Constrictive clothing Smoking Hypertension

37. When a thrombus completely or partially obstructs a pulmonary artery or its branches, the alveolar dead space is increased continuing to be ventilated, receives little or no blood flow gas exchange is impaired or absent various substances are released from the clot and surrounding area that cause regional blood vessels and bronchioles to constrict. increase in pulmonary vascular resistance V./Q. Mismatch PATHOPHYSIOLOGY

38. Increased pulmonary vascular resistance due to the regional vasoconstriction and reduced size of the pulmonary vascular bed Increase in pulmonary arterial pressure Increase in right ventricular work to maintain pulmonary blood flow Right ventricular failure occurs Decrease in cardiac output followed by a decrease in systemic blood pressure Shock develop PATHOPHYSIOLOGY

39. Classic triad Dyspnea Chest pain Hemoptysis Common manifestation May be nonspecific , difficult to diagnose . Dyspnea, Pleuritic chest pain Crackles Fever Accentuation of pulmonic heart sounds Altered mental status Hypoxemia Syncope Hypotension Tachycardia Clinical manifestation

40. Collapse of patient with shock , pallor , severe dyspnea, hypoxemia , crushing chest pain Massive-do not have pain Pulse rapid and weak BP low ECG Indicates RT VENT strain Massive emboli

41. Pleuritic chest pain Dyspnea Slight fever Productive cough with blood streaked sputum Tachycardia Pleural friction rub SMALL EMBOLI Undetected or produce vague Transient symptoms Reduction in capillary bed pulmonary HT Rt vent hypertrophy Medium sized emboli

42. Ventilation perfusion lung scan D- dimer testing= measures the amount of cross-linked fibrin fragments. Pulmonary angiography Computed tomography ABG Analysis A spiral (helical) CT scan (also known as CT angiography or CTA) Diagnostic studies

43. The V/Q scan has 2 parts. Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation. Ventilation scanning involves inhalation of a radioactive gas, such as xenon. Scanning reflects the distribution of gas through the lung. CHEST X RAY= R/O Atelectasis, pleural effusion V/Q SCANNING

44. BNP >90 pg /ml N-terminal pro BNP >500 pg /ml Troponin I >0.4 ng/ml, or troponin T >0.1 ng/ml Electrocardiogram (ECG)=RT VENT STRAIN Transoesophageal echocardiography- specific Ultrasound for lower extremities Diagnostic studies

45. European Respiratory Society released the new guidelines for the diagnosis and management of Pulmonary embolism

46. Emergency management (cardiopulmonary support)=ECMO General management Anticoagulation therapy Thrombolytic therapy Surgical management Nursing management MANAGEMENT

47. EMERGENCY MANAGEMENT Stabilize the cardiopulmonary system O2 administration Iv lines Hemodynamic measurements, perfusion scan , ABG, helical CT , pulmonary angiography Treat hypotension-dobutamine infusion Monitor ECG-find dysarrthmias , rt vent failure Intubation , mechanical ventilation Small doses of morphine , sedatives

48. GENERAL MANAGEMENT- DRUG THERAPY Fibrinolytic agent Unfractionated heparin IV Low-molecular-weight heparin (e.g., enoxaparin [ Lovenox ]) Warfarin (Coumadin) for long-term therapy Analgesia

49. ANTICOAGULANT THERAPY ( at least 3-6 month) HEPARIN: 5000 to 10000 units bolus followed by 18U/Kg per hour not to exceed 1600 U /Hour. PTT: 1.5 TO 2.5 times normal or 46 to 70 sec Administered 5 TO 7 DAYS LMWH: usually cont. 3 to 6 month maintain INR 2.0 To 3.0 THROMBOLYTIC THERAPY GENERAL MANAGEMENT- DRUG THERAPY

50. Thrombolytic therapy with recombinant tissue plasminogen activator ( Activase ) or other thrombolytic agents like kabikinase ( Streptase ) are used in treating massive PE, Before thrombolytic therapy is started, INR, partial thromboplastin time (PTT), hematocrit, and platelet counts are obtained. An anticoagulant is stopped prior to administration of a thrombolytic agent. .During therapy, all but essential invasive procedures are avoided because of potential bleeding. If necessary, fresh whole blood, packed red cells, cryoprecipitate, or frozen plasma is given to replace blood loss and reverse the bleeding tendency. After the thrombolytic infusion is completed (which varies in duration according to the agent used), maintenance anticoagulation therapy is initiated Thrombolytic Therapy

51. Systemic routes of administration of thrombolytic drugs Drug name Loading dose Infusion dose Administration time Streptokinase 250000 IU, 30 min 100000 IU/h 24 h Urokinase 4400 IU, 10 min 4400 IU/kg/h 12 h Alteplase (rt-PA) Not needed 50 mg/h * 2 h Reteplase Not needed 10 U IV bolus, twice with 30-min interval Tenecteplase Not needed 10000 U bolus single dose in 5–10 seconds **

52. Tissue plasminogen activator (t-pa) infusion of 50–100 mg intravenously (IV) over 1–2 hours Infusing t-pa at a rate of 0.5–1 mg/h under ultrasound or fluoroscopic guidance Systemic thrombolysis catheter-directed thrombolysis(CDT)

53. EMBOLECTOMY APPLICATION OF TEFLON CLIPS TO THE INFERIOR VENA CAVA FILTER INSERTION ( Inferior vena cava filter ) NURSING MANAGEMENT Minimizing the Risk of Pulmonary Embolism Preventing Thrombus Formation Assessing Potential for Pulmonary Embolism Monitoring Thrombolytic Therapy Managing Pain prophylaxis of VTE SURGICAL MANAGEMENT

54. Massive or submissive PE with any of the following: Contraindication to thrombolytic therapy History of intracranial hemorrhage - Intracranial malignancy, mass, or aneurysm - Cerebrovascular accident with the past 3 months - Major surgery within the past 1 month - Brain or spinal surgery within the past 2 months Failed thrombolytic therapy Patent foramen ovale Pregnancy Right heart failure or cardiogenic shock Thrombus-in-transit within the right sided heart chambers EMBOLECTOMY-INDICATION

55. Managing Oxygen Therapy Relieving Anxiety Monitoring for Complications Providing Postoperative Nursing Care Promoting Home, Community-Based, and Transitional Care NURSING MANAGEMENT

56. Long-term anticoagulant therapy is essential. Anticoagulant therapy continues for at least 3 months. INR levels are drawn at intervals and warfarin dosage is adjusted. Preventing worsening of the condition and avoiding complications and recurrence. Reinforce the need for the patient to return to the hcp for regular follow-up examinations PATIENT TEACHING

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