15. Critical Care And ARDS Flashcards
Levophed
Blood pressure medication (increases)
Discuss the following vitals Some abdominal distension noted • Vitals: Febrile 38.9°C HR 109 BP 101/64 RR 22 SpO-93% • Labs: Hb 124 WBC 18.7 Plt 267
Temp: high HR: high BP: low RR: high SpO: normal Hb: WBC: Plt:
Discuss the following values
PC 22 PEEP 10 FiO2 0.55
- High level of support
- Machine is breathing for her (rate and depth)
PC
PEEP
FiO2
Midazolam
Sedation
Rocuronium
Paralysis (alpha 2 blocker)
Following surgery:
Hb 124. WBC 18.7. Plt 257.
Overnight:
Hb 102. WBC 25.6. Plt 154.
Why is there a decrease in Hb/Plt .
Diffusion effect form all the fluids she is receiving.
What is sepsis?
The presence of harmful bacteria and their toxins in tissue, through infection of wound.
ABG: PaO2 59, PaCO2 57, pH 7.21, HCO3 21
ABG suggest acidosis, why is HCO3 so low?
Due to sepsis
What does the following values indicate
PaO2/FiO2 = 73
Severe form of Acute Lung Injury (ALI) —> ARDS
What is ARDS?
Bilateral and diffuse alveolar damage due to an acute insult
- stiffening of alveolar walls
- no perfusion of oxygen
Risk factors for ARDS
Direct Risk:
- pneumonia
- aspiration of gastric contents
- pulmonary contusion
- inhalation injury
- near drowning
Indirect Risk
- Sepsis
- Non-thoracic trauma or hemorrhagic shock
- Pancreatitis
- Major Burn
- Drug overdose
- Transfusion of blood products
- Cardiopulmonary
Anatomical Changes to the lung in response to injury (exudative phase).
- Risk of what pathology?
- Increase of fluid due to what type of response?
- Response to injury
- Decreased surfactant = increased risk of atelectasis due to increased surface tension
- Exudative fluid
- Response
- Pulmonary capillary becomes engorged
- Increased permeability of alveolar-capillary membrane
- Interstitial and Intra-alveolar oedema
- Scattered areas of haemorrhaging alveolar consolidation
Anatomical Changes to the lung in response to injury (proliferation phase/week-days)
- Response
- Lung pathology that can develop
- Can lead to which lung disorder
- VQ matching
- Intra-alveolar walls thickened with hyaline membrane (fibrin, cellular debris)
- Intra-alveolar fibrosis (fibrin and exudative develop)
- Restrictive lung disease
- Worsened VQ matching - hypoxia, pulmonary hypertension
Physiological Changes to the lung in response to injury.
- Lungs become very stiff (decreased compliance) and therefore are difficult to ventilate
- Small areas of the lung are still functioning normally
What is non-cardiogenic pulmonary edema
- Pulmonary Capillary Wedge Pressure (PCWP) < 18mmHg
(pressure required to occlude the artery) - Acute hypoxaemic respiratory failure
- Leaking into the lungs is not due to the heart, stead due to sepsis or other external cause; nothing we do to the heart will improve oedema.
Managing ARDS until lungs start to improve
Manage symptoms
- support BP
- ABx to fight infection
- monitor skin integrity
- nutritional support
- Prisma/dialysis, if renal impairment is present
ARDS patient
- Hemodynamics
- Ventilators support
- ABGs
- Unstable
- simple turning can desaturated or cause hypotension
- will be on multiple drugs to support blood pressure (e.g. NE, E, vasopressin) - High Ventilators support (PC, PEEP, and FiO2)
- Poor ABG (permissive hypercapnia) due to low TV (6ml cf 10-12ml)
Best position for ARDS patients.
Prone with pillows on chest
- Abdomen freed to allow for expansion into lower lobes
- Increased VQ matching: Improved oxygenation, perfusion more evenly distributed
- No adverse effects on hemodynamic status
Adverse Effects of putting ARDS patients in prone
- facial oedema
- requires manpower (up to 8 people to turn/manage lines)
- difficult to manage lines/tubes
- not appropriate for all patients: orthopaedic, neurological
Compare the following ABG:
Before:
Ventilation: PC 24, PEEP 16, FiO2 0.8
ABG: PaO2 59, PaCO2 57, pH 7.21, HCO3 21
PaO2/FiO2 = 78
After:
Ventilation: PC 24, PEEP 14, FiO2 0.95
ABG: PaO2 48, PaCO2 51, pH 7.29, HCO3 22
PaO2/FiO2 = 50
What could be the main precipitating factor for this laparotomy patient?
- slight improvement in ventilation but still high level of dependence on ventilators support
- no significant improvement, uncompensated respiratory acidosis; septic and febrile
- lower the ratio, the worse the disease process = renal failure, multi-organ failure
- sepsis, non-cardigenic oedema
Ventilation: PC 24, PEEP 14, FiO2 0.95
ABG: PaO2 48, PaCO2 51, pH 7.29, HCO3 22
PaO2/FiO2 = 50
What is the main role of PT for this patient?
Very limited
- main roles:
1) Maintain ROM
2) Positioning - underlying issues of sepsis and non-cardiogenic oedema must be controlled as this is a precipitating factor
- Chest PT may worsen outcome as it is in inflammatory process
Compare the following:
Before
Ventilation: PC 24, PEEP 14, FiO2 0.95
ABG: PaO2 48, PaCO2 51, pH 7.29, HCO3 22
PaO2/FiO2 = 50
After
Ventilation: SIMV PC 20 PEEP 12 PiO2 0.65
ABG: PaO2 62, PaCO2 47, pH 7.36, HCO3 31
PaO2/FiO2 = 95
Patient is getting better
- SIMV = shared work between ventilator and patient: machine does most of the breathing, when pt takes breath it allows her to
- decreased dependence on ventilator
- ABG: compensated respiratory acidosis
- PaO2 = normalized
Ventilation: SIMV PC 20 PEEP 12 PiO2 0.65
ABG: PaO2 62, PaCO2 47, pH 7.36, HCO3 31
PaO2/FiO2 = 95
What is the main PT management for this patient
Still not able to do a whole lot of intervention possible
- Sit up in bed 30-40degrees
- PROM, especially ankles
- Positioning
- Check chest
ARDS Prognosis
Survivors are at high risk for
- cognitive decline
- depression
- PTSD
- persistent skeletal-muscle weakness
Return to work is very slow (less than half the first year)
