1. What clinical findings support a diagnosis of ARDS?
There are a number of findings supporting a diagnosis of ARDS. Through physical examination, labs, and diagnostics including the patient's inability to breathe on her own, alteration in perfusion, and end-organ dysfunction (Urden, Stacy, & Lough, 2014, p. 522). There are multiple findings supporting a diagnosing of progressing ARDS to include the patient’s condition has worsened. The patient is sinus tachy with a heart rate of 120 BPM and decreased BP of 80/60’s evidence of alteration in perfusion. The patient is unable to breathe on her own. She is mechanically ventilated on FiO2 and is in the low 80s to high 90s on FiO2 of 80%. She has a PaO2:FiO2 ratio of 78. A PA02/Fi02 less than or …show more content…
What is the pathophysiology of acute lung injury and ARDS? There are three phases to progressive ARDS, which is the exudative, fibroproliferative and resolution phase. There is an injury or insult to the body causing an inflammatory immune system reaction. Cellular mediators release humoral mediators that damage alveolar capillary membranes. Alveolar start flooding, small airway diameter changes; there is pulmonary vasoconstriction, alveolar collapse, the patient forms pulmonary hypertension, V/Q mismatching and finally leading to hypoxemia (Urden et al., 2014, p. 521).
3. What is refractory hypoxemia and how would the nurse recognize it?
According to Urden, Stacy, & Lough (2014) in regards to refectory hypoxemia there will be “intra-alveolar atelectasis, increased shunt fraction, decreased diffusion, decreased functional residual capacity, interstitial fibrosis, and increased dead space ventilation” (p. 522). Refectory hypoxemia is due to pulmonary shunting. Pulmonary shunting can result in pneumothorax, atelectasis, and pulmonary edema (White, 2013, p. Resp12). The nurse would evaluate diagnostic tests and clinical notes in addition to assessing the patient for findings of pulmonary shunting indicative of refractory hypoxemia.
4. What is PEEP and what is its role in mechanical …show more content…
What are the benefits of rotational sleep surface therapy (or prone positioning)?
Benefits of rotational sleep therapy are to increase the oxygenation in patients up to 75% (White, 2013, p. Resp21).
9. Describe drug action, side effects and dosage requirements for norepinephrine and dexmedetomidine.
Dexmedetomidine Hydrochloride is a sedative used on intubated or mechanically ventilated patients. Side Effects include “Pain, infection, hypotension, bradicardia, atrial fibrillation, nausea, thirst, hypoxia pleural effusion, pulmonary edema, anemia, anemia, leukocytosis, and oliguria” Dosage for “Adults: IV 1 mcg/kg loading dose infused over 10 min, then continue with infusion of 0.2-0.7 mcg/kg/h for up to 24 h adjusted to maintain sedation” (Wilson, Shannon, & Shields, 2016, p. 455).
Norepinephrine is a sympathomimetic that causes vasoconstriction and cardiac stimulation. Side effects include “restlessness, hepatic necrosis, fatal arrhythmias, cerebral hemorrhage” Dosage: IV initial 8-12 mcg/min, titrate to response; maintenance dose usually 2-4 mcg/min” (Wilson, Shannon, & Shields, 2016, p. 455).
References
Urden, S., Stacy, K. & Lough, M. (2014). Critical Care Nursing: Diagnosis
There are a number of findings supporting a diagnosis of ARDS. Through physical examination, labs, and diagnostics including the patient's inability to breathe on her own, alteration in perfusion, and end-organ dysfunction (Urden, Stacy, & Lough, 2014, p. 522). There are multiple findings supporting a diagnosing of progressing ARDS to include the patient’s condition has worsened. The patient is sinus tachy with a heart rate of 120 BPM and decreased BP of 80/60’s evidence of alteration in perfusion. The patient is unable to breathe on her own. She is mechanically ventilated on FiO2 and is in the low 80s to high 90s on FiO2 of 80%. She has a PaO2:FiO2 ratio of 78. A PA02/Fi02 less than or …show more content…
What is the pathophysiology of acute lung injury and ARDS? There are three phases to progressive ARDS, which is the exudative, fibroproliferative and resolution phase. There is an injury or insult to the body causing an inflammatory immune system reaction. Cellular mediators release humoral mediators that damage alveolar capillary membranes. Alveolar start flooding, small airway diameter changes; there is pulmonary vasoconstriction, alveolar collapse, the patient forms pulmonary hypertension, V/Q mismatching and finally leading to hypoxemia (Urden et al., 2014, p. 521).
3. What is refractory hypoxemia and how would the nurse recognize it?
According to Urden, Stacy, & Lough (2014) in regards to refectory hypoxemia there will be “intra-alveolar atelectasis, increased shunt fraction, decreased diffusion, decreased functional residual capacity, interstitial fibrosis, and increased dead space ventilation” (p. 522). Refectory hypoxemia is due to pulmonary shunting. Pulmonary shunting can result in pneumothorax, atelectasis, and pulmonary edema (White, 2013, p. Resp12). The nurse would evaluate diagnostic tests and clinical notes in addition to assessing the patient for findings of pulmonary shunting indicative of refractory hypoxemia.
4. What is PEEP and what is its role in mechanical …show more content…
What are the benefits of rotational sleep surface therapy (or prone positioning)?
Benefits of rotational sleep therapy are to increase the oxygenation in patients up to 75% (White, 2013, p. Resp21).
9. Describe drug action, side effects and dosage requirements for norepinephrine and dexmedetomidine.
Dexmedetomidine Hydrochloride is a sedative used on intubated or mechanically ventilated patients. Side Effects include “Pain, infection, hypotension, bradicardia, atrial fibrillation, nausea, thirst, hypoxia pleural effusion, pulmonary edema, anemia, anemia, leukocytosis, and oliguria” Dosage for “Adults: IV 1 mcg/kg loading dose infused over 10 min, then continue with infusion of 0.2-0.7 mcg/kg/h for up to 24 h adjusted to maintain sedation” (Wilson, Shannon, & Shields, 2016, p. 455).
Norepinephrine is a sympathomimetic that causes vasoconstriction and cardiac stimulation. Side effects include “restlessness, hepatic necrosis, fatal arrhythmias, cerebral hemorrhage” Dosage: IV initial 8-12 mcg/min, titrate to response; maintenance dose usually 2-4 mcg/min” (Wilson, Shannon, & Shields, 2016, p. 455).
References
Urden, S., Stacy, K. & Lough, M. (2014). Critical Care Nursing: Diagnosis