Patient With Respiratory Failure

1. A 55 year old Bahamian male with a long history of smoking presents to the Emergency Department in severe respiratory distress. An aterial blood gas shows a PO2 of 50 mm Hg and a PCO2 of 80 mm Hg. What type of respiratory failure does he have?

Hypoxemic

Hypercapnic

Hyperoxic

Hypocapnic

Respiratory FailureClassifications:

Hypoxemic respiratory failure (type I)
PaO2 Low or normal PaCO2
Hypercapnic respiratory failure (type II)
PaCO2>50 mmHg
Usually PaO2
****Hypercapnic failure includes hypoxemia, but not the opposite*****

Hypercapnia is generally defined as a blood gas carbon dioxide level over 45 mmHg. Since carbon dioxide is in equilibrium with bicarbonate in the blood, hypercapnia can also result in a high serum bicarbonate (HCO3−) concentration, driving pH up and creating an alkalosis. Normal bicarbonate concentrations vary from 22 to 28 milligrams per deciliter.
Hypercapnia is generally caused by hypoventilation, lung disease, or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide (usually due to volcanic or geothermal causes), or by rebreathing exhaled carbon dioxide. It can also be an initial effect of administering supplemental oxygen on a patient with sleep apnea. In this situation the hypercapnia can also be accompanied by respiratory acidosis.

Explanation

Respiratory FailureClassifications:

Hypoxemic respiratory failure (type I)
PaO2 Low or normal PaCO2
Hypercapnic respiratory failure (type II)
PaCO2>50 mmHg
Usually PaO2
****Hypercapnic failure includes hypoxemia, but not the opposite*****

Hypercapnia is generally defined as a blood gas carbon dioxide level over 45 mmHg. Since carbon dioxide is in equilibrium with bicarbonate in the blood, hypercapnia can also result in a high serum bicarbonate (HCO3−) concentration, driving pH up and creating an alkalosis. Normal bicarbonate concentrations vary from 22 to 28 milligrams per deciliter.
Hypercapnia is generally caused by hypoventilation, lung disease, or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide (usually due to volcanic or geothermal causes), or by rebreathing exhaled carbon dioxide. It can also be an initial effect of administering supplemental oxygen on a patient with sleep apnea. In this situation the hypercapnia can also be accompanied by respiratory acidosis.

2. A 55 year old Bahamian male with a long history of smoking presents to the Emergency Department in severe respiratory distress. An aterial blood gas shows a PO2 of 50 mm Hg and a PCO2 of 80 mm Hg. Your treatment of the above patient should concentrate on

Supplemental O2

Increased ventilation

Decreased ventilation

Immediate intubation because of the severity of the hypoxemia

Treatment:

Assurance of adequate airway
Support gas exchange
Hypoxemia  supplemental oxygen
Hypercapnea  increase ventilation
Correct underlying cause !

Explanation

Treatment:

Assurance of adequate airway
Support gas exchange
Hypoxemia  supplemental oxygen
Hypercapnea  increase ventilation
Correct underlying cause !

3. The chest x-ray of a 56 year-old female with pancreatitis and respiratory failure shows patchy, wide spread infiltrates without evidence of heart enlargement or congestion. The decision is made to intubate and mechanically ventilate this patient. The most important ventilator setting to consider in this patient is:

High levels of positive end expiratory pressure (PEEP)

High oxygen levels

Low tidal volumes

Low minute ventilation

Continuous positive airway pressure (CPAP)

ARDS Treatment:
Lung protective ventilation = Low tidal volume ventilation
Normal tidal volume 10 ml/kg
Reduce to 8-6 ml/kg
Increase respirator rate to meet minute ventilation

Explanation

ARDS Treatment:
Lung protective ventilation = Low tidal volume ventilation
Normal tidal volume 10 ml/kg
Reduce to 8-6 ml/kg
Increase respirator rate to meet minute ventilation

4. Following a vehicular accident with blood loss leading to prolonged, severe hypotension, a 30-year-old man is intubated and placed on a mechanical ventilator. He has progressively decreasing oxygen saturations despite increasing PEEP and FiO₂ of 100%. He remains afebrile and dies 3 days later. The microscopic appearance of the lungs is shown. Which of the following pulmonary diseases most likely complicated his course?

Bronchopneumonia

Adult respiratory distress syndrome

Bronchiectasis

Viral pneumonia

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS);
also known as Diffuse Alveolar Damage (DAD)

-Diffuse alveolar capillary damage
-Life-threatening resp. isufficiency, cyanosis and severe arterial hypoxemia –may progress to multi-organ -failure; resistant to O2 therapy –50% mortality
-Severe pulmonary edema,hyaline membranes
-Severe infections, 02 toxicity, gastric aspiration, septic shock, severe, esp. head trauma, assoc. with shock, burns, DIC

Explanation

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS);
also known as Diffuse Alveolar Damage (DAD)

-Diffuse alveolar capillary damage
-Life-threatening resp. isufficiency, cyanosis and severe arterial hypoxemia –may progress to multi-organ -failure; resistant to O2 therapy –50% mortality
-Severe pulmonary edema,hyaline membranes
-Severe infections, 02 toxicity, gastric aspiration, septic shock, severe, esp. head trauma, assoc. with shock, burns, DIC

5. A 47-year-old man is admitted to the hospital with an acute necrotizing pancreatitis. In two days he develops respiratory failure and expires on the 9^th day after admission. Postmortem examination reveals the shown lung changes.

Which of the following is the most likely diagnosis?

Bronchopneumonia

Brown induration of the lungs

Idiopathic interstitial pulmonary fibrosis

Adult respiratory distress syndrome

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS);
also known as Diffuse Alveolar Damage (DAD)

-Diffuse alveolar capillary damage
-Life-threatening resp. isufficiency, cyanosis and severe arterial hypoxemia –may progress to multi-organ -failure; resistant to O2 therapy –50% mortality
-Severe pulmonary edema,hyaline membranes
-Severe infections, 02 toxicity, gastric aspiration, septic shock, severe, esp. head trauma, assoc. with shock, burns, DIC

ANYTHING THAT CAN PROVOKE INfLAMMATION TO THE ALVEOLI CAN CAUSE IT. THE LUNGS ARE PARTICULARLY SUSCEPTIBLE TO INFLMAMATORY MEDIATORS GENERATED ELSE WHERE IN THE BODY AS THE ENTIRE CARDIAC OUTPUT GOIES THROUGH THE LUNGS. Thus a distant inflammatory conditions such as severe pancreatitis can trigger ARDS. THESE DISEASE STATE RELEASE INFLAMMATORY MEDIATORS THAT PRODUCE DIFFUSE ALVEOLAR DAMAGE

Explanation

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS);
also known as Diffuse Alveolar Damage (DAD)

-Diffuse alveolar capillary damage
-Life-threatening resp. isufficiency, cyanosis and severe arterial hypoxemia –may progress to multi-organ -failure; resistant to O2 therapy –50% mortality
-Severe pulmonary edema,hyaline membranes
-Severe infections, 02 toxicity, gastric aspiration, septic shock, severe, esp. head trauma, assoc. with shock, burns, DIC

ANYTHING THAT CAN PROVOKE INfLAMMATION TO THE ALVEOLI CAN CAUSE IT. THE LUNGS ARE PARTICULARLY SUSCEPTIBLE TO INFLMAMATORY MEDIATORS GENERATED ELSE WHERE IN THE BODY AS THE ENTIRE CARDIAC OUTPUT GOIES THROUGH THE LUNGS. Thus a distant inflammatory conditions such as severe pancreatitis can trigger ARDS. THESE DISEASE STATE RELEASE INFLAMMATORY MEDIATORS THAT PRODUCE DIFFUSE ALVEOLAR DAMAGE

6. 59 year old female presents to the clinic with severe dyspnea at rest associated with fever and a productive cough. Chest x-ray shows a consolidation in the right middle lobe. On exam the patient appears to be in respiratory distress and central cyanosis is noted. Her vitals are: T 101.2F (38.4C) BP 140/88 P 100 bpm RR 26 bpm O₂ saturation on room air = 73% Which of the following is the best choice for providing supplemental oxygen in this patient?

Nasal cannula

Simple face mask

Non-rebreather mask

Bag-valve mask

Venturi mask

•Non-rebreather mask◦Ideally 100% Oxygen, in reality it’s closer to 80%
◦Best we can do passively

•Before an NRB is placed on the patient, the reservoir bag is inflated to greater than two-thirds full of oxygen, at a rate of 15 liters per minute (lpm)[1]. Approximately ¹⁄₃ of the air from the reservoir is depleted as the patient inhales, and it is then replaced by the flow from the O2 supply. If the bag becomes completely deflated, the patient will no longer have a source of air to breathe.

Explanation

•Non-rebreather mask◦Ideally 100% Oxygen, in reality it’s closer to 80%
◦Best we can do passively

•Before an NRB is placed on the patient, the reservoir bag is inflated to greater than two-thirds full of oxygen, at a rate of 15 liters per minute (lpm)[1]. Approximately ¹⁄₃ of the air from the reservoir is depleted as the patient inhales, and it is then replaced by the flow from the O2 supply. If the bag becomes completely deflated, the patient will no longer have a source of air to breathe.

7. 36 hours following admission to the hospital, despite supplemental oxygenation the patient's respiratory status continued to worsen. An ABG shows pH 7.3, PO₂ 55 mmHg, PCO₂38 mmHg. His chest x-ray is shown below. The decision for intubation and mechanical ventilation is made. What is the most important consideration when placing this patient on the ventilator?

Low oxygen concentration

Increased ventilation

Low tidal volumes

High levels of PEEP (Positive End Expiratory Pressure)

ARDS Treatment:
Lung protective ventilation **** Low tidal volume ventilation*****
Normal tidal volume 10 ml/kg
Reduce to 8-6 ml/kg
Increase respirator rate to meet minute ventilation

Explanation

ARDS Treatment:
Lung protective ventilation **** Low tidal volume ventilation*****
Normal tidal volume 10 ml/kg
Reduce to 8-6 ml/kg
Increase respirator rate to meet minute ventilation

8. A 28 year-old presents with dyspnea at rest and is begun on oxygen supplementation via nasal cannula set at 4 L/min. Which of the following is the best estimate of the amount of oxygen this patient is receiving?

21%

37%

45%

57%

83%

Supplemental Oxygen
•Nasal cannula◦Up to 6 L/min
◦Each L/min provides an additional 4% of oxygen
◦Remember room air contains 21% oxygen

•2L/min provides a total of 29% oxygen 6L/min provides a total of 45% oxygen
•Good for people with mild hypoxia ie 92-94% sat, MIs
•Only delivers oxygen to the nose so not good for the mouth breathers

Explanation

Supplemental Oxygen
•Nasal cannula◦Up to 6 L/min
◦Each L/min provides an additional 4% of oxygen
◦Remember room air contains 21% oxygen

•2L/min provides a total of 29% oxygen 6L/min provides a total of 45% oxygen
•Good for people with mild hypoxia ie 92-94% sat, MIs
•Only delivers oxygen to the nose so not good for the mouth breathers

9. An 80-year-old male with a history of COPD and who is managed as an outpatient with supplemental oxygen, presents to his pulmonologist with the complaint of worsening dyspnea on exertion. Following his evaluation, the pulmonologist recommends increasing the patient's supplemental oxygen from 38% to 42% F_iO₂. Which of the following is the best oxygen supplementation device to achieve this goal?

Non-rebreather mask

Venturi mask

Nasal cannula

Non invasive CPAP

Simple face mask

•Venturi mask
•Uses venturi effect to regulate flow
•Precise
•Helpful in COPD

Explanation

•Venturi mask
•Uses venturi effect to regulate flow
•Precise
•Helpful in COPD

10. A 30-year-old Asian woman presents to the Emergency Department with the sudden onset of pleuritic chest pain and shortness of breath. Past history is remarkable for 4 first trimester pregnancy losses. On physical examination she is afebrile but has a respiratory rate of 32/min. Her heart rate is 120 bpm and her blood pressure is 142/80. An accentuated (loud) S₂is heard on heart auscultation. Lung examination and chest x-ray are normal. Arterial blood analysis shows a PCO₂of 30 mm Hg and a PO₂ of 58 mm Hg. Which of the following is the most appropriate next diagnostic step?

Ventilation perfusion scan

Transthoracic echocardiogram

D-dimer assay

Venous Doppler studies

Imaging studies are used to diagnose DVT. Ultrasound on the veins is the most common method, and the two standard options include proximal compression ultrasound or whole-leg ultrasound

PMH:
may have a history of neoplasm or other hypercoagulable state such as Factor V Leiden, Antithrombin III deficiency, or Lupus anticoagulant. BEWARE OF A HISTORY OF FREQUENT MISCARRIAGES in a woman - she may have anti phospholipid antibody syndrome, a risk factor for hypercoagulability and PE.

Physical exam
o Vitals: tachycardia, tachypnea, hypoxia, possibly hypotension in large PEs, secondary to reduced blood return to the left heart.
o Lung: clear lung sounds.
o Extremities: possibly signs of DVT, though many PEs embolize from the pelvic veins and sometimes from the upper extremities.

Studies
o EKG: sinus tachycardia with right axis deviation and S1Q3T3 pattern (prominent S wave in lead I, prominent Q wave in lead III, inverted T wave in lead III). This is an uncommon finding, though pretty specific for PE. Nonspecific ST and T wave changes are common EKG findings in PE but are not specific.

o CXR: normal.

o D-dimer (sometimes referred to as fibrin split products): elevated, due to the body’s attempt to break down the clot by fibrinolysis. A negative d-dimer can be very useful for ruling out PE (it is very sensitive), but is not useful at all for ruling it in (poor specificity).

o Arterial blood gas (ABG): A-a (alveolar-arterial) gradient elevated.

o Ventilation/Perfusion (V/Q) scan: a nuclear medicine test using radioactive isotopes to visualize the air passage and blood passage though the lungs. Read as high, moderate, or low probability. PE will show up as an area that is being ventilated but not perfused.

o CT Pulmonary Angiogram: a special protocol CT scan done to show the pulmonary arteries, better for central clots.

Treatment
o Resuscitation and stabilization (ABCs).
o Oxygen
o Anticoagulation: heparin and warfarin.
o Thrombolytics: in cases with unstable vital signs, or signs of significant right heart strain, somewhat controversial.
o Inferior vena cava (IVC) filter: if recurrent clots from the lower extremity, or if unable to anticoagulate.

Imaging studies are used to diagnose DVT. Ultrasound on the veins is the most common method, and the two standard options include proximal compression ultrasound or whole-leg ultrasound

Explanation

Imaging studies are used to diagnose DVT. Ultrasound on the veins is the most common method, and the two standard options include proximal compression ultrasound or whole-leg ultrasound

PMH:
may have a history of neoplasm or other hypercoagulable state such as Factor V Leiden, Antithrombin III deficiency, or Lupus anticoagulant. BEWARE OF A HISTORY OF FREQUENT MISCARRIAGES in a woman - she may have anti phospholipid antibody syndrome, a risk factor for hypercoagulability and PE.

Physical exam
o Vitals: tachycardia, tachypnea, hypoxia, possibly hypotension in large PEs, secondary to reduced blood return to the left heart.
o Lung: clear lung sounds.
o Extremities: possibly signs of DVT, though many PEs embolize from the pelvic veins and sometimes from the upper extremities.

Studies
o EKG: sinus tachycardia with right axis deviation and S1Q3T3 pattern (prominent S wave in lead I, prominent Q wave in lead III, inverted T wave in lead III). This is an uncommon finding, though pretty specific for PE. Nonspecific ST and T wave changes are common EKG findings in PE but are not specific.

o CXR: normal.

o D-dimer (sometimes referred to as fibrin split products): elevated, due to the body’s attempt to break down the clot by fibrinolysis. A negative d-dimer can be very useful for ruling out PE (it is very sensitive), but is not useful at all for ruling it in (poor specificity).

o Arterial blood gas (ABG): A-a (alveolar-arterial) gradient elevated.

o Ventilation/Perfusion (V/Q) scan: a nuclear medicine test using radioactive isotopes to visualize the air passage and blood passage though the lungs. Read as high, moderate, or low probability. PE will show up as an area that is being ventilated but not perfused.

o CT Pulmonary Angiogram: a special protocol CT scan done to show the pulmonary arteries, better for central clots.

Treatment
o Resuscitation and stabilization (ABCs).
o Oxygen
o Anticoagulation: heparin and warfarin.
o Thrombolytics: in cases with unstable vital signs, or signs of significant right heart strain, somewhat controversial.
o Inferior vena cava (IVC) filter: if recurrent clots from the lower extremity, or if unable to anticoagulate.

Imaging studies are used to diagnose DVT. Ultrasound on the veins is the most common method, and the two standard options include proximal compression ultrasound or whole-leg ultrasound