1
Q
what is VQ mismatch
A
- ventilation-perfusion mismatch
- normally, the volume of blood perfusing the lungs and the amount of gas reaching the avleoli are almost identical
- d/t secretions or mucus plug: this will either block blood flow or block air flow.
- low V/Q mismatch: d/t shunt and alveoli is perfused but not ventilated
- high V/Q mismatch: d/t deadspace and alveoli are ventilated, but not perfused
2
Q
what is ARDS
A
- sudden and progressive form of ARF in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid.
- non-cardiogenic pulmonary edema (pulmonary edema is caused by either indirect or direct injury
- Widespread inflammation (usually inflammation causes little inflammatory cells to travel the blood stream and when that blood reaches the lungs to get rid of CO2 and gain O2, those inflammatory cells damage the capillary cells of the alveoli in the lungs, which causes them to be more permeable and essentially leak)
- ARDs has a HIGH mortality rate (greater than 50%) (mortality is 70-90% in pts w/ septic shock and ARDs).
3
Q
etiology of ARDS
A
There are many predisposing conditions of ARDs.
- widespread inflammation after physiologic insults:
> systemic inflammatory response, SEPSIS, trauma, gut ischemia, lung injury, or as a consequence of multiple organ dysfunction syndrome (MODS).
4
Q
What is the most common cause of ARDS
A
sepsis
5
Q
what is the berlin cirteria for ARDS
A
- Timing: 1 week of clinical insult or worsening resp symptoms
- Chest X-ray: bilateral “opacities”-whiteout
- Oxygenation: P/F ratio-mild less than 300; moderate less than 200; severe less than 100;
All w/ PEEP or CPAP=greater than 5cmH2O
6
Q
risk factor for ARDS: indirect injury
A
- develops d/t a problem somewhere else in the body NOT in the lungs
- SEPSIS (esp. gram negative infection)
- Severe massive trauma
- severe TBI
- shock states (hypovolemic, cardiogenic, septic)
- burns
- DIC
- cardiopulmonary bypass
Other:
- acute pancreatitis
- cardiopulmonary bypass
- disseminated intravascular coagulation
- opioid drug overdose (heroin)
- transfusion-related acute lung injury (multiple blood transfusions)
- urosepsis
7
Q
risk factor for ARDS: Direct injury to lungs
A
The pathogen comes into contact w/ the tissue of the lung!
- aspiration of gastric contents or other substances
- bacterial or viral PNA
- sepsis (infection in the lung)
Other:
- Chest trauma (blunt or penetrating-pulmonary contusions)
- Embolism: fat, air, amniotic fluid, thrombus
- inhalation of toxic substances
- near-drowning
- O2 toxicity
- radiation pneumonitis
8
Q
Injury to alveolar-capillary membrane d/t damaged alveolar cell-
A
- damaged type II alveolar cell
- decreases surfactant production
- decreased alveolar compliance and recoil (harder to keep from collapsing!)
- atelectasis (alveoli collapse after gas exchange)
- Hyaline membrane formation
- decreased lung compliance and impaired gas exchange
= ARDs
9
Q
injury to alveolar-capillary membrane d/t release of inflammatory mediators-
A
- release of inflammatory mediators (bronchoconstriction and then impaired gas exchanged OR vascular narrowing and obstruction and then impaired gas exchange)
- increased alveolar capillary membrane permeability
- outward migration of blood cells and fluids from capillaries
- pulmonary edema
- impaired gas exchange
=ARDs
10
Q
What are the three phases of ARDs?
A
- injury phase or exudative phase
- proliferation phase
- fibrotic phase
11
Q
Exudative or injury phase:
A
- occurs 24-72 hrs after the insult
- generally lasts up to 7 days
- increase interstitial pulmonary edema (more of the blood is pass through the capillary membrane into the alveoli)
- intrapulmonary shunt: fluid moves into the alveolar space-type 1 and 2 alveolar cells are damaged, which leads to decreased surfactant (alveolar collapse after exhalation-atelectasis) and protein accumulation (pulmonary edema-interstitial and alveolar edema)
= severe atelectasis and decreased lung compliance
12
Q
What are the primary pathophysiologic changes that occur during the exudative phase?
A
- interstitial and alveolar edema (increased capillary permeability) and atelectasis (decreased surfactant)
- significant V/Q mismatch: increasing shunt bc the alveoli fill with fluid
- Refractory hypoxemia: hypoxemia unresponsive to increasing concentrations of oxygen delivered by our supplemental devices (blood in the capillary network cannot be oxygenated)
13
Q
Initial findings that occur during exudative phase:
A
- increase RR
- decrease tidal volume
- hyperventilation increases CO2 excretion
- leading to respiratory alkalosis
- CO increases in response to hypoxemia, a compensatory effort to increase pulmonary blood flow; however, as atelectasis, pulmonary edema, and pulmonary shunt increase, compensation fails and hypoventilation, decreased O2, and decreased tissue O2 perfusion occur.
14
Q
Hyaline membrane during exudative phase:
A
- a hyaline membrane occurs during exudative phase
- necrotic cells, protein, and fibrin form a hyaline membrane that line the inside of each aveolus.
- these thick hyaline membranes contribute to the development of fibrosis and atelectasis, leading to a further decrease in gas exchange capability and reduced lung compliance.
15
Q
Refractory hypoxemia during exudative phase:
A
- severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of oxygen=refractory hypoxemia
- despite receiving higher concentrations of oxygen, the pts condition does not improve but continues to get worse
- this causes a diffusion limitation, caused by hyaline membrane formation, contributes to and worsens hypoxemia
- as the lungs become less compliant bc of decreased surfactant, pulmonary edema, and atelectasis, the pt must generate higher airway pressures to inflate “stiff” lungs.
- reduced lung compliance increases the pts WOB
16
Q
Reparative or proliferative phase:
A
- begins 1-2 weeks after the initial lung injury
- there continues to be an influx of neutrophils, monocytes, lymphocytes, and fibroblasts as part of the inflammatory response
- increased pulmonary vascular resistance and pulmonary hypertension may occur bc the fibroblasts and inflammatory cells destroy the pulmonary vasculature
- lung compliance continues to decrease d/t interstitial fibrosis
- hypoxemia worsens bc of the thickened alveolar membrane-> V/Q mismatch, diffusion limitation and shunting
- airway resistance is severely increases from fluid in the lungs and secretions in the airways
- this phase is complete when the diseased lung is replaced by dense, fibrous tissue
- persistence: widespread fibrosis results
- stops: lesions will resolve
17
Q
Short form of proliferation phase:
A
- occurs 1-2 weeks post injury
- inflammatory process continues!
- result: increase vascular resistance and pulmonary hypertension
- decreased lung compliance: r/t interstitial fibrosis
- completed phase: characterized by dense fibrotic tissue
- if we can stop the process: lesions will resolve
- Hypoxemia: worsens!!
- thick dense membranes=causing diffusion limitations and shunting
18
Q
Fibrotic phase:
A
- occurs 2-3 weeks after the initial lung injury
- not all pts who have ARDs will enter this phase
- the lung tissue completely remodels by collagenous and fibrous tissues
- diffuse scarring of the lungs, interstitial fibrosis and alveolar duct fibrosis result in decreased lung compliance (hypoxemia and hypercapnia)
- this reduces the surface area for gas exchange bc the interstitial is fibrotic, and hypoxemia continues
- varying degrees of pulmonary hypertension may result from pulmonary vascular destruction and fibrosis
- systemic dysfunction: result of decreased ventilation/oxygenation
- mechanical ventilation
- poor survival at this point
19
Q
Initial clinical manifestations of ARDs:
A
- SOB
- dyspnea
- tachypnea
- cough
- restlessness
- clear or mild crackles
- chest xray: mild infiltrates; these findings usually lag behind clinical presentation by about a day (24hrs)
- respiratory alkalosis caused by hyperventilation (increased RR)
- mild hypoxemia (normal or decreased CO2 despite complicated presentation)
20
Q
Progressive or worsening clinical manifestations of ARDs:
A
- Resp: increased WOB, chest retractions (skin is basically pulling over the ribs, making them more visible indicating the pt wants more air)
- Lungs: diffuse coarse crackles on expiration, rhonchi, productive cough
- non-cardiogenic pulmonary edema
- CXR: consolidation diffuse infiltrates (whiteout)
- systemic s/s of worsening hypoxemia
- ABGs: first resp alkalosis, but then turns to respiratory acidosis=muscle fatigue and hypoventilation
- finally metabolic acidosis
- hallmark sign: hypoxemia despite increased FiO2
- hypercapnia signifies that respiratory muscle fatigue and hypoventilation have severely affected gas exchange, and respiratory failure is imminent
other: - tachycardia, diaphoresis, changes in mental status, cyanosis, pallor
21
Q
Diagnostic findings of ARDs:
A
- timing: within 1 week of clinical insult or worsening condition
- Chest X-ray: bilateral infiltrates (whiteout or snow screen)
22
Q
Oxygenation using PaO2/FiO2 Ratio (p/f ratio): mild ARDS:
A
p/f is greater than 200-300 w/ PEEP or CPAP greater than 5cmH2O
23
Q
Oxygenation using PaO2/FiO2 Ratio (p/f ratio): MODERATE ARDS
A
p/f is less than or equal to 100-200 w/ PEEP or CPAP greater than 5cmH2O
24
Q
Oxygenation using PaO2/FiO2 Ratio (p/f ratio): severe ards
A
p/f is less than 100 w/ PEEP or CPAP greater than 5cm H2O
25
What labs do we use to diagnose ARDs?
- ABG
- serum lactate: increased, increased lactate=anaerobic metabolism
- CBC: lesss than 4 or 10-12
- sputum, blood, urine cultures
- coags
- electrolytes
- liver/renal function tests
- progression from ARDs to MODs
26
ARDs progressive clinical manifestations:
- profound respiratory distress
- pleural effusions
- severe hypoxemia
- hypercapnia: endotracheal intubation, PPV mechanical ventilation
- metabolic acidosis
- organ dysfunction
27
Intrapulmonary shunt:
- blood leavs the heart but has not participated in gas exchange
- result: decrease oxygenation ventilation
- extreme V/Q mismatch
- Qs/Qt ratio (CO shunted/total CO)
Normal: less than 5%
ARDs= greater than 30%
28
Hemodynamic clinical manifestations:
Hemodynamic changes:
- central or arterial based monitoring usually required: APCO arterial pressured based CO
- decreased CO
- decreased MAP
Pulmonary capillary wedge pressure (PCWP)
- normal PCWP: 4-12mmHg
- in ARDS: wedge pressure is less than 18
- PCWP less than 18: reflects non-cardiogenic pulmonary edema. No evidence of inc L heart pressure
- this device is rarely used this time
- dont just rely on PCWP! Chest xray can also confirm.
- PaO2/FiO2 ratio: determines severity
29
What are cardiovascular complications in ARDs?
- hypotension
- mottled skin and altered microcirculation
- increased lactate levels (in septic shock)
- altered echocardiography variables
- decreased CO
- decreased MAP
- dysrhythmia
30
What complications occur in the Hepatic system bc of ARDS?
- increased bilirubin levels
| - increased enzymes
31
What complications occur in the renal system bc of ARDS?
- oliguria
- increased serum creatinine
- increased blood urea nitrogen
- increased biomarkers
32
What complications occur in the neurological system bc of ARDS?
- altered mentation
- confusion
- disorientation
- agitation
- delirium
- PICs
33
What complications occur in the respiratory system bc of ARDS?
- hypoxemia
- decreased PaO2/FiO2 ratio
- abnormal lung function
- VAP
- barotrauma/volutrauma
- O2 toxicity
- PE
- endotracheal: laryngeal ulceration, tracheal injury
34
Abnormal lung function:
- complication of ARDs
- most pts recover from ARDs within six months
- sometimes abnormal lung function can persist for years
- the severity of scarring and changes within the lungs are key factors
> contributing factors to the scarring (duration of time mechanically ventilated, use of extracorpeal life support)
s/s:
- extreme tiredness, chest pain, SOB after minimal activity, persistent dyspnea post ARDs
35
Ventilator associated PNA:
- complication of ARDS
D/T:
- impaired host defenses, invasive monitoring devices, aspiration of GI contents (especially in pts receiving enteral nutrition), prolonged mechanical ventilation
treatment:
- implement a ventilator bundle protocol
- HOB 30-45 degrees
- strict infection control measures (hand washing, sterile technique during endotracheal suctioning)
- frequent oral care
36
Barotrauma:
- complication of ARDS
- fragile alveoli are over-distended w/ excess pressure during mechanical ventilation
- the high peak airway pressures needed to ventilate the lungs predispose pts w/ ARDs to this complication
- alveolar air escapes ruptured alveoli=
Leads to:
- pulmonary interstitial edema
- pneumothorax
- SQ emphysema
- phemopericardum
- tension pneumothorax
37
Stress ulcers:
- at high risk bc of blood being diverted from the GI to respiratory system to help meet the body's demand for O2
Treatment:
- correct hypotension, shock, and acidosis
- prophylactic management includes anti-ulcer drugs, such as PPIs,, H2 blockers, mucosal protecting drugs (sucralfate)
- early initiation of enteral nutrition helps prevent mucosal damage
38
Venous thromboembolism (VTE):
- at risk for DVT and pulmonary emboli
Prophylactic management may include:
- intermittent pneumatic compression stockings
- anticoagulation (low-molecular weight heparin)
- early ambulation (when possible)
39
Acute Kidney Injury:
- occur d/t decreased renal perfusion and subsequent decreaed delivery of O2 to the kidneys
- occurs in ARDS bc of hypotension in septic shock
- may result from hypoxemia or nephrotoxic drugs (vancomyocin) used to treat ARDS related infections
Management:
- careful monitoring I/Os, daily creatinine and urea levels, and when needed, dialysis therapy
- CRRT is often used
- these pts are hemodynamically unstable, so they need vasopressors or inotropes to maintain HR and BP
- bc these pts cant tolerate large volumes of fluid that would be removed during traditional HD, CRRT is slow, gentle and continuous
- they can receive CRRT 24hrs a day
40
Psychological issues:
- anxiety
- issues w/ memory and attention
- inability to focus
- nightmares
- depression
- PTSD
41
heme issues
- anemia, DIC, thrombocytopenia
42
infection
- clauti, clabsi, sepsis
43
Where should we focus our interventions for pts with ARDS?
- what is the underlying cause??
| - Resp focus: promoted adequate oxygenation and ventilation
44
Interventions:
1. O2 administration- supplemental oxygenation
> goal is to correct hypoxemia
2. **Ventilation
> PPV w/ PEEP
> lung protective strategies: permissive hypercapnia, low vT
3. low vT ventilation (too high vT into stiff lungs is associated w/ volutrauma and barotrauma, so keep low to reduce risk)
4. permissive hypercapnia: (d/t low vT, PaCO2 levels will slowly rise above normal limits, body is able to compensate slowly)
5. PEEP
6. prone positioning
7. extracorporeal membrane oxygenation (ECMO): a large vessel is cannulated and a catheter is inserted-allows the blood to exit the pt and pass across a gas-exchanging membrane outside the body and oxygenated blood is returned back to the pt
45
What is prone positioning?
> early phases of ARDs, fluid moves freely throughout the lung
> bc of gravity the fluid pools in the dependent regions of the lung
> as a result, some alveoli are fluid filled (depdent areas), while others are air filled (nondepedent areas)
> when pt is supine, the heart and mediastinal contents place added pressure on the lungs, which predisposes pts to atelectasis
> prone positioning is option for pts with refractory hypoxemia who do not respond to other strategies to increase PaO2
> by turning the pt prone, perfusion may be better matched to ventilation
> air-filled alveoli in the anterior part of the lung become dependent
> alveoli in the posterior part of the lungs are recruited (given the opportunity to re-expand), improving oxygenation.
46
What is the supportive care for ARDS?
Identify and treat the underlying cause:
- infection-sepsis (Pan culture, causative rx: antibiotics)
- corticosteroids (treat the inflammation-treat the inflammatory cells that are affecting the alveoli capillary membrane)
- hydration
- hemodynamic monitoring
- nutritional therapy (within 24-72 hours of ventilator)
- no specific treatment or drug
- identify those at risk for ARDs
- culture: suspicious wounds, secretions
47
Intervention: maintain adequate oxygenation:
Goal: PaO2 of 60mmHg; FiO2 less than 60%
Goal: adequate ventilation-maintain normal pH
Goal: SaO2 saturation greater than 90%
- Mechanical ventilation almost always necessary
- ECMO or ECCO as necessary
- PRBC transfusion if needed
- HgB as low as 7 before transfusion
48
Intervention: maintain adequate PERFUSION pressures:
- adequate BP, MAP, CO
- CO, BP, SV, SVV
> SV-stroke volume SVV stroke volume variance
- monitor volume status
- UOP, weight, I/Os
- Labs
49
intervention: IV fluids:
- crystalloid, colloids, blood products
50
Intervention: medications:
- inotropic vasopressor drugs (dopamine, norepinephrine, vasopressin, dobutamine, milrinone)
- corticosteroids
- meds to reduce oxidative stress: vitamin C
- nitric oxide, surfactant
51
Intervention: maintain adequate fluid and nutrition balance
Monitor fluid status:
- fluid balance is difficult d/t "leaky" pulmonary capillaries and third spacing
- crystalloids, diuretics used depending on fluid status
- use of colloids controversial d/t leakage into the pulmonary interstitium
Nutrition:
- maintain protein and energy stores: loss of muscle mass can prolong mechanical ventilation, decrease mobility and set pt up for pressure ulcers, VTE, increase LOS
- enteral feeding
- parenteral feeding
52
Respiratory care:
Positive pressure ventilation:
- non-invasive (NIVPP): partial support
- invasive endotracheal intubation: artificial airway w/ mechanical ventilation, full respiratory support
Goal of mechanical ventilation:
- maintain alveolar ventilation appropriate for pts metabolic needs
- correct hypoxemia in order to maximize O2 transport
53
Endotracheal Intubation:
* indications for mechanical ventilation
- acute respiratory or ventilatory failure
- PaCO2 greater than 50mmHg
- pH: 7.3
- respiratory less than 8 or greater than 40
- diminished or absent breath sounds
- unprotected airway
54
ARDS: other treatment:
- high dose steroid therapy
- prone positioning
- surfactant therapy
- high-frequency oscillatory ventilation (HFOV)
- extracorporeal lung support (ECMO/ECCO)
- nitric oxide
- neuromuscular blocking agents (NMBA)
55
Definition of RF
- Failure in Gas Exchange
- Either oxygenation or ventilation (CO2 removal)
- Many risks or causes
- Life threatening with high mortality risk
56
definition of ARDS
Direct or indirect lung injury
| Progressive hypoxemia, infiltration, and fibrosis of lung tissue
57
Hypoxemic RF:
PaO2 < 60mmHg and normal PaCO2
58
Hypercapnic RF:
Respiratory acidosis; PaCO2 > 50 and pH less than 7.35
59
mani of RF
- Hypercapnia: HA, confusion, decreased LOC, tachycardia, tachypnea, flushed skin,
- Hypoxemia: increased HR, RR, BP
- Plus all the symptoms of the underlying cause
60
early signs of RF
Tachycardia, increased BP (compensatory)
Dyspnea
Restlessness, Anxiety
Fatigue
61
late signs of RF
Cyanosis
Decreased BP
Agonal respiration
Coma
62
RF dx
ABG, Chemistry, CBC, Coags, Chest Xray, Chest CT, Sputum Cx, and very importantly History and Physical Exam
63
care for RF
- Monitor: Pulse Oximetry: keep SpO2>94
| - Normalize ABG and Hbg
64
Onset of ards
Less than 7 days
complex care 2
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