L17 Respiratory Failure

-V and Q are matched due to hypoxic vasoconstriction

• Under normal physiologic conditions (pH):
• -minute ventilation varies to target PCO2 of 40 

• Under abnormal conditions (abnormal pH):
• -minute ventilation varies to target a normal pH (pH trumps CO2 for respiratory drive)
• -metabolic acidosis → ↑ ventilation until pH >7.35
• -metabolic alkalosis → inhibit ventilation until pH <7.45 

• Acute Respiratory Acidosis:
• -pH <7.35
• -increased PCO2 (relative to their normal) (hypercabic)

-PaO2 on 100% FiO2 is ~ 660 mmHg under ideal conditions

-if PaO2 on 100% FiO2 is < 200 mmHg SHUNT is present

• Hypoxemic Respiratory Failure = PaO2 < 60 mmHg
• -end organs are vulnerable to regional hypoxic injury
• -triggers hyperventilation reflex

-Tells you if there is derangement in oxygenation

• -Gradient = [(760 - 47 xFiO2) -(pCO2/0.8)] -(PaO2)
• -Normal gradient should ~ (age/4) + 4

-Hypoventilation is the only cause of hypoxemia without A-a gradient

-inability of the respiratory system to maintain adequate gas exchange

• -arterial PO2 < 60 mmHg
• OR
• -PCO2 > 50 mmHg

In patients with preexisting lung disease these numbers may be normal, therefore, acute respiratory failure is a significant change from the patient's baseline gase exchange status

**pH can help distinguish if the CO2 retention is acute or chronic

• 1. Hypoxemic (with normal or low PCO2): PaO2 < 60 mmHg
• -pt NOT displaying signs of respiratory distress
• -mainly occurs due to shunt physiology

• 2. Hypercapnic/hypercarbic: pH <7.35 with ↑ pCO2
• -pt working hard to breath
• -most common cause of respiratory arrest

• 3. Failure to protect or maintain airway patency
• -Central: decreased mental status; at risk for airway obstruction
• -Anatomical narrowing of the airway → stridor

• -Acute drop in PaO2 < 60
• -PCO2 normal or even low

• Causes: Sudden decrease or absent ventilation to an area with preserved perfusion
• 1. Pneumonia (localized diseases of the pulmonary parenchyma)
• 2. ARDS (increase of fluid within alveolar spaces)

• Symptoms:
• -confusion, agitation WITHOUT dramatic dyspnea
• -tachycardia

• Common Causes (Lecture):
• -Pneumonia (often intubate)
• -Bronchospasm - (tx: steroids, beta agonists)
• -Cardiogenic Pulmonary Edema (rarely have to intubate)
• -Gastric Aspiration (large volume aspiration)
• -Non-cardiogenic pulmonary edema
• -PE

• Tx:
• -V/Q mismatch: responds to increased FiO2
• -Shunt (V=0): poor response to increased FiO2

• Lecture: pH <7.35 and elevated PCO2 (relative to pH)
• -pH becomes driving force for ventilation
• -metabolic acidosis with pH 7.26 should drive ventilation to a PCO2 ~26

• -PCO2 > 50 mmHg
• **pH < 7.35 (to show absent/incomplete metabolic compensation)
• -decreased PaO2 (due to hypoventilation and sometimes V/Q mismatch)

• Causes: Inadequate ventilation = inadequate CO2 removal
• 1. Depression of CNS ventilatory control
• 2. Disease of respiratory bellows (chest wall/neuromuscular)
• 3. Chronic obstructive lung disease

*patients often have preexisting disease that makes them more vulnerable to an acute problem --> acute on chronic respiratory failure

• Symptoms:
• -Acidosis: dramatic dyspnea, increased work of breathing
• -progressive decrease in pH causes loss of vascular tone (hypotension, tachyarrhythmia)
• -Narcosis: ↑PCO2 → obtundation

• 1. Dyspnea
• 2. Impaired mental status
• 3. HA (hypercapnia)
• 4. Tachycardia
• 5. Papilledema (hypercapnia --> cerebral vessel dilation)
• 6. Lung findings depend on underlying disease
• 7. Cyanosis (severe hypoxemia)

• Causes of Hypoxemia
• 1. VQ Mismatch
• -Ventilation in some regions limited
• -Prefusion normal
• *responds to 100% O2

• 2. Shunt
• -Ventilation is completely absent
• -Perfusion normal
• *does NOT respond to 100% O2

**CO2 eliminate is normally adequate b/c patients are able to maintain alveolar ventilation (compensate by increasing minute ventilation)

• -gradual drop in PaO2 <60 (typically >55)
• Causes:
• -heterogenous lung disease
• -VQ mismatch (typically obstructive)
• -hypoventilation

• Symptoms:
• -mild cognitive impairement
• -exercise limited by ventilation

-tx with O2 to prevent cardiac complications and risk of sudden death (not exercise intolerance)

• OPTIMIZE O2 TRANSPORT TO TISSUES:
• 1. Arterial O2 Saturation
• -Target O2 Sat >90% (PO2 >60 without hypocarbia)
• *lecture says >95% (buffer zone in case pt isn't on the 'normal' dissociation curve)
• *may need to intubate if can't achieve PO2 >60
• 2. Acceptable Hg level
• -Target > 10 g/dL
• 3. Normal-near normal Cardiac Output
• 4. PEEP for ARDS

• MAINTAIN CO2 ELIMINATION:
• -maintain an acceptable pH rather than a normal PCO2
• -may need to ventilate if PaCO2 rises enough to cause pH < 7.3 or impaired mental status

• REDUCE WORK OF BREATHING:
• -mechanical ventilation
• -rests respiratory muscles

• -Hb is approximately 90% saturated at PO2 of 60
• -PO2 much beyond this point does not provide much benefit
• -"margin of safety": maintain PO2 of 65 where Hb is 95% saturated and pH will remain normal (if not can get an ABG to check pH)

• 
• Patients at risk for hypoxic respiratory arrest get 100% FiO2:
• -extreme V/Q mismatch
• -hypoxemia despite O2 4-6 L/min
• **may lead to increased CO2 (~6mmHg) retention in COPD patients but avoiding hypoxic respiratory arrest is more important!

• -in patients with chronic hypercapnia (due to underling lung disease) supplemental O2 may further increase PCO2
• -NOT due to inhibition of drive
• -due to inhibition of hypoxic vasoconstriction --> ventilation of relatively unperfused units(????????????? seems to show perfusion of relatively unventilated regions)
• -of little clinical significance
• 
• 

• 
• Pink Puffers will increase their respiratory rate to reduce the amount of CO2 retained

They will complain of dyspnea but won't retain more CO2 and develop acidosis

• MECHANISMS OF HYPERCAPNIA:
• -patients are unable to maintain a level of alveolar ventilation sufficient to eliminate CO2

• Mechanisms of Insufficient Ventilation:
• 1. decreased minute ventilation
• 2. decreased effectiveness of ventilation (increased V_D/V_T)

V_D/V_T: relative amount of alveolar vs dead space ventilation (increased dead space)

• Stages Affected:
• 1. Respiratory Generator in the CNS
• -Drugs
• -hypothyroidism
• -metabolic alkalosi
• -structural lesions

• 2. Chest wall/Neuromuscular system
• -Kyphoscoliosis
• -Myasthenia Gravis
• -Guillian Barre
• -ALS
• -Polymyositis
• -Cervical cord injury
• -obesity
• -electrolyte abnormalities

• 3. Lungs/Airways
• -COPD
• -LVF
• -Severe ARDS
• -Severe Asthma

• MECHANISMS OF HYPOXEMIA:
• 1. Hypoventilation
• 2. V/Q mismatch

• **rarely see shunt --> most respond to 100% O2
• **BUT O2 can lead to a further increase in PaCO2!!!!

• Patients who are acidotic have dramatic sx (dyspnea, hypotension, tachyarrhythmia)

• 1. CO2 Narcosis
• -sleepy to obtundation

• 2. Acidosis
• -dyspnea
• -hypotension
• -tachyarrhythmias
• -PEA arrest if pH < 7.15

• 1. Obstructive lung diseases (most common)
• 2. Restrictive lung diseases (late in fibrosis)
• 3. Hypoventilation syndromes

Patients are typically dyspneic with an increased work of breathing

• Causes:
• 1. Acute respiratory tract infection (usually viral)
• 2. Drugs that suppress the respiratory center (sedatives, narcotics)
• 3. CHF
• 4. Less Common: PE, environmental pollutants

• 
• Normal:
• -Elevated PaCO2
• -slight respiratory acidosis

• 
• COPD Exacerbation:
• -increase RR
• -use accessory muscles
• -increase PaCO2
• -worsen respiratory acidosis

• 
• COPD Exacerbation:
• -can no longer maintain RR --> 8
• -PaCO2 significantly increases
• -severe acute respiratory acidosis
• -obtundation (CO2 narcosis)

• 
• COPD:
• -increased RR (22)
• -pH normal
• -PaCO2 only slightly elevated

• 
• COPD Exacerbation:
• -increase RR (26)
• -use of accessory muscles
• -PaCO2?? (should decrease)
• -pH decrease

• 
• COPD Exacerbation:
• -can no longer maintain RR --> 8
• -breathing is shallow and ineffective
• -PaCO2 significantly increases
• -acute respiratory acidosis
• -CO2 Narcosis (PaCO2 much less than BB --> obtundation is a relative phenomenon)

• 
• Normal Patient: ie Diabetic

• 
• Metabolic Acidosis (DKA)
• -hyperventilation (RR 30)
• -PaCO2 decreases
• -pH decreases
• ***want to intubate here

• 
• -hyperventilation (RR40)
• -accessory muscle use
• -further decrease in PaCO2
• -further decrease in pH
• ***Don't intubate here! Can't move as much air as they can

• 
• -Hyperventilation (RR 45)
• -shallow and ineffective
• -acute respiratory acidosis
• -slight increase in PaCO2
• -pH decreases

• 
• PEA arrest from acidosis
• -PaCO2 never went over 40!

1. BiPAP (only CI: altered mental status or secretions)

2. Tx underlying cause

• 1. Central
• -commonly from respiratory depressants
• -obtunded
• -at risk for gastric aspiration, oral aspiration, mucus plugging

• 2. Airway Obstruction (anatomic narrowing)
• -extreme dyspnea
• -anxiety
• -increased work of breathing
• -stridor if obstruction is extrathoracic

• 1. CNS Depression
• -drugs
• -encephalopathy

• 2. Intrinsic decreased sensitivity to CO2
• -obesity hypoventilation
• -myxedema coma

• 3. CNS Disease
• -brain stem tumors

Often detected as an O2 desat in sleeping patient

• Symptoms:
• -minimal dyspnea
• -normal to diminished respiratory effort
• -sleep to obtunded mental status

• Treatment:
• -tx underlying condition
• -must protect airway: DO NOT USE BiPAP
• -Intubation

• 1. Allergic reaction
• 2. Postop swelling
• 3. Oropharyngeal abscess
• 4. Viral infection

• Treatment:
• -intubation can be difficult due to swelling (preemptive intubation)

• -any combination of parenchymal disease, acid load and drive
• -COPD + Bowel Ischemia
• -COPD + Bowel Ischemia + Narcotics for abdominal pain