Patient With Respiratory Failure

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

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

Explanation
Respiratory FailureClassifications:

Hypoxemic respiratory failure (type I)
PaO250 mmHg
Usually PaO2< 60 mmHg as well

****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
Treatment:

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

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

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

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

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

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

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.