Exam 2 Critical Care

What are the 3 Shunts

Anatomic

Capillary

Absolute

What is an anatomic shunt?

Blood bypasses alveoli

Ex. Hole in the heart

Perfusion Issue

High VQ

What is a Capillary shunt?

Blood passes unventilated alveoli

Ex. Pneumonia

Ventilation Issue

Low VQ

What is an Absolute shunt? 

Combination of Anatomic and Capillary

Occurs in ARDS

% of Cardiac Output that flows from right heart to left heart without undergoing adequate pulmonary gas exchange or achieving normal PaO2

What is a False shunt?

At least a few alveoli still working, but inefficiently

“Shunt-like” conditions

O2 SAT will improve if oxygen is applied unlike true shunts

Ex. Bronchospasm, Hypoventilation, Pooling of secretions, Mild Inflammatory Process

What is dead space?

Occurs when the alveoli are shrinking because there is no gas exchange - leads to dead space

Can happen from a ventilation or perfusion issue

Shunt Assessment Methods: 100% Oxygen Test

100% Oxygen Test (true shunt if O2 doesn’t move)

Oxygen for 15-20 minutes

Normal Response = PaO2 300-500mmHg

PaO2 <300 = significant shunt presence

Shunt Assessment Methods: V/Q Scan

Nuclear medicine study using inhaled and injected radioactive tracers to visualize ventilation and perfusion patterns separately, identifying mismatch regions

Explain how the Number of Alveoli (Surface Area for Diffusion) impacts gas diffusion

Increased surface area enhances the rate of diffusion according to Fick’s Law, which states that diffusion is proportional to surface area and concentration gradient.

Diseases like emphysema reduce alveolar number and surface area, impairing gas exchange

Explain how the Surfactant (Reducing Surface Tension) impacts gas diffusion

reduces surface tension within alveoli, preventing collapse (atelectasis) and allowing them to remain open for gas exchange

Improves lung compliance

Deficiency, as seen in neonatal respiratory distress syndrome (NRDS), leads to alveolar collapse and impaired diffusion

Explain how the Alveolar-Capillary Membrane (Thickness and Permeability) impacts gas diffusion

This membrane is the interface between alveolar air and capillary blood

thicker membranes (d/t pulmonary edema, fibrosis, or inflammation) slow diffusion by increasing the distance gases must travel

Which type of a diffusion issue is occurring with ARDS?

surfactant dysfunction + membrane thickening

Which type of a diffusion issue is occurring with COPD/emphysema?

alveolar destruction

Which type of a diffusion issue is occurring with Pulmonary fibrosis?

thickened alveolar-capillary barrier

How do alterations in compliance affect the patient? Why?

Decreased lung compliance = stiff and do not expand, hard to breathe in

Increased lung compliance = floppy, overinflated - hard to breathe out

Criteria for identifying “acute respiratory failure”

Type 1: Oxygenation Failure

PaO2 <60mmHg with normal to decreased CO2 levels (V/Q mismatch)

Type 2: Ventilation Failure

PaCO2 >50mmHg with or without hypoxemia (inadequate ventilation)

What is PaO2 and what are normal parameters?

Oxygenation Staus

80-100

<80=hypoxemia

What is PaCO2 and what are normal parameters?

Partial Pressure of Carbon Dioxide - how well are the lungs releasing carbon dioxide

35-45

>45=hypercapnia

What is HCO3 and what are normal parameters?

Metabolic component (bicarbonate buffer - base)

22-26

What is the normal range for pH?

7.35-7.45

<7.35=acidic

>7.45=alkaline

What is SaO2 and what is its normal range and what to do if out of range?

% of hemoglobin saturated with O₂

95-100%

What is PIP and what is its normal range and what to do if out of range?

Peak inspiratory Pressure

<40

If greater than 40 - check biting (needs more sedation), kinks, physical obstruction like sputum

If not any of these - lungs could be worsening (assess airway and contact provider)

What is PEEP and what is its normal range and what to do if out of range?

Positive End Expiratory Pressure (prevents alveoli from collapse)

8-10

Rupture/Barotrauma/Pneumothorax are concerns

S/S include absent lung sounds, decreased O2, decreased BP d/t physical pressure on the heart, compensating high heart rate

What is f and what is its normal range on a vent and what to do if out of range?

Respiratory Rate

8-12/min

Low=Acidosis

High=Alkalosis, because you are blowing out more CO2 (carbon dioxide makes you more acidic)

Ex. If f is set at 4 (low) and patient is in acidosis, increase it

What is fiO2 and what is its normal range and what to do if out of range?

Fraction of Inspired Oxygen—the percentage of oxygen a patient breathes in (oxygen concentration)

21-60%, >60%=fiO2 toxicity

One of the last settings we decrease

What is Tidal Volume (VT) and what is normal?

Tidal Volume is the total volume of oxygen being inhaled and exhaled in one breath (too high can cause barotrauma/pneumothorax)

500mL/kg Avg Adult

OR

7-9mL/kg by weight

What is ARDS?

ARDS is a form of acute respiratory failure caused by widespread inflammation and injury to the alveolar-capillary membrane, leading to non-cardiogenic pulmonary edema, severe hypoxemia, and decreased lung compliance

Symptoms of ARDS and how to determine if Mild/Moderate/Severe

Acute onset within 1 week, bilateral pulmonary opacities, non-cardiogenic pulmonary edema, impaired PaO2/FiO2 ratio

Divide the PaO2 by the FiO2 

Mild ARDS=201-300mmHg

Moderate ARDS=101-200mmHg

Severe ARDS=< or equal to 100mmHg

What are the phases of ARDS

Exudative Phase (0-72hrs)

Uncontrolled inflammation, Neutrophil Activation, Increased Capillary Permeability

Proliferative Phase (1-3 weeks)

Edema resolves, hyaline membrane forms, progressive hypoxemia

Fibrotic Phase (2-3 weeks)

Fibrosis of lung tissue, decreased lung capacity, severe right to left shunting

A/C Mode

🫁 1. Assist-Control (A/C)

What it is:

• A full-support mode where every breath is either patient-triggered or machine-triggered, but the ventilator delivers a preset tidal volume or pressure every time.

Key features:

• Patient can initiate breaths, but each breath gets full support.

• If the patient doesn’t breathe, the ventilator delivers breaths at a set rate.

Clinical implications:

• Great for patients with minimal respiratory effort (e.g., sedation, ARDS).

• Risk of respiratory alkalosis if patient over-breathes.

• Can lead to barotrauma if not carefully monitored.

Used for sedated or critically ill!

SIMV Mode

2. Synchronized Intermittent Mandatory Ventilation (SIMV)

What it is:

• A hybrid mode: the ventilator delivers mandatory breaths at a set rate, but allows the patient to take spontaneous breaths in between—which are not fully supported unless paired with pressure support.

Key features:

• Synchronizes with patient effort to avoid breath-stacking.

• Spontaneous breaths can be pressure-supported (SIMV + PSV). PSV=extra boost

Clinical implications:

• Useful for weaning—encourages patient effort.

• Less risk of over-ventilation compared to A/C.

• May increase work of breathing if spontaneous breaths aren’t supported.

Why is decreased cardiac output sometimes an early complication of intubation?

Increased pressure on the heart

Explain cuff pressure and risks to intubated client

What Is Cuff Pressure?

When a patient is intubated, the endotracheal tube (ETT) has a small inflatable balloon (cuff) near its tip.

• Cuff pressure refers to the amount of pressure inside that balloon, which seals the airway to:

  • Prevent air leaks during mechanical ventilation

  • Minimize aspiration of secretions

  • Ensure effective oxygen delivery

Risks of Improper Cuff Pressure🔻 Too Low (<20 cm H₂O)

• Air leak → inadequate ventilation, low tidal volumes

• Aspiration risk → gastric contents or secretions enter lungs → pneumonia

• Poor oxygenation → especially dangerous in ARDS or high FiO₂ settings

🔺 Too High (>30 cm H₂O)

• Tracheal mucosal ischemia → pressure cuts off blood flow

• Ulceration, necrosis, or tracheal stenosis

• Long-term complications → tracheoesophageal fistula, vocal cord damage

20-30=normal

Chest X Ray is Gold Standard to check placement, auscultate lungs, stomach - removal if ventilation heard in stomach, pull back slightly if only one side is being ventilated

Explain the different types of noninvasive ventilation

Oxygen - Start here for mild hypoxemia. Nasal cannula (1–6 L/min), simple face mask, or non-rebreather mask

High-Flow Nasal Cannula - Heated, humidified oxygen at up to 60 L/min.

CPAP - Delivers constant pressure to keep alveoli open

BIPAP - Bi-level positive airway pressure, supports both oxygenation and ventilation

Intubation

Ventilation

ROME

Compare CO2 to pH:

Respiratory Opposite

Metabolic Equal

Fully Compensated

pH=normal

Partially Compensated

Everything is abnormal

Uncompensated

One of CO2/CO3 is normal

If PaCO₂ is High (>45 mmHg) → Respiratory Acidosis

What do you do to the vent settings?

Goal: Improve ventilation to remove CO₂

Respiratory Rate (RR)

Tidal Volume (Vt) (if safe—watch for barotrauma)

If PaCO₂ is Low (<35 mmHg) → Respiratory Alkalosis (LOW=alkalosis)

What do you do to the vent settings? 

Goal: Reduce ventilation to retain CO₂ Actions:

Reduce Respiratory Rate

Reduce Tidal Volume

Consider sedation if patient is over-breathing (e.g., anxiety, pain)

If PaO₂ is Low (<60 mmHg) → Hypoxemia

Goal: Improve oxygenation Actions:

FiO₂ (short-term fix)

PEEP (long-term strategy to recruit alveoli)

Consider prone positioning in ARDS

Avoid FiO₂ >60% for prolonged periods—risk of oxygen toxicity

If pH is Abnormal

pH <7.35 → Acidosis: check if respiratory (PaCO₂) or metabolic (HCO₃⁻)

pH >7.45 → Alkalosis: same approach

Adjust RR and Vt for respiratory causes

Treat underlying cause for metabolic issues (e.g., fluids, bicarbonate)

How do you evaluate blood gases?

1. Assess pH

2. Evaluate PaCO₂ (Respiratory Component)

↑ PaCO₂: Respiratory acidosis (hypoventilation)

↓ PaCO₂: Respiratory alkalosis (hyperventilation - blowing off CO2)

3. Evaluate HCO₃⁻ (Metabolic Component)

Normal: 22–26 mEq/L

↑ HCO₃⁻: Metabolic alkalosis

↓ HCO₃⁻: Metabolic acidosis

4. Check PaO₂ and SaO₂ (Oxygenation)

PaO₂ normal: 80–100 mmHg

SaO₂ normal: 95–100%

↓ PaO₂/SaO₂: Hypoxemia → assess FiO₂, PEEP, lung pathology

Causes of ABG changes

ABG Change	Possible Causes
Respiratory acidosis (↑ PaCO₂)	COPD, sedation, neuromuscular weakness, hypoventilation
Respiratory alkalosis (↓ PaCO₂)	Anxiety, pain, early sepsis, hypoxia-driven hyperventilation
Metabolic acidosis (↓ HCO₃⁻)	DKA, renal failure, lactic acidosis, diarrhea
Metabolic alkalosis (↑ HCO₃⁻)	Vomiting, diuretics, NG suction, compensation for chronic respiratory acidosis
Hypoxemia (↓ PaO₂)	ARDS, pneumonia, PE, atelectasis, low FiO₂

Client response to blood gas values

ABG Pattern	Clinical Signs
Acidosis (pH <7.35)	Confusion, lethargy, hypotension, Kussmaul respirations
Alkalosis (pH >7.45)	Irritability, muscle cramps, paresthesias, arrhythmias
Hypoxemia (PaO₂ <60 mmHg)	Dyspnea, cyanosis, restlessness, tachycardia
Hypercapnia (PaCO₂ >50 mmHg)	Headache, drowsiness, flushed skin, CO₂ narcosis

Change to values based on ventilator settings

ABG Issue	Vent Changes
↑ PaCO₂ (acidosis)	↑ RR or ↑ Vt to blow off CO₂
↓ PaCO₂ (alkalosis)	↓ RR or ↓ Vt to retain CO₂
↓ PaO₂ (hypoxemia)	↑ FiO₂ or ↑ PEEP to improve oxygenation
↑ PaO₂ (hyperoxia)	↓ FiO₂ to avoid oxygen toxicity
Metabolic acidosis	Treat underlying cause (fluids, insulin, dialysis)
Metabolic alkalosis	Correct volume status, stop diuretics, replace electrolytes

Anticipating ABG Changes

Post-intubation: expect transient respiratory alkalosis if over-ventilated

ARDS: progressive hypoxemia, possible permissive hypercapnia

COPD: chronic respiratory acidosis with metabolic compensation

Sepsis: early respiratory alkalosis → later metabolic acidosis

DKA: metabolic acidosis with compensatory low PaCO₂

Shift to the left

LEFT

Locked - O2 is locked to the hemoglobin and not going to tissues

aLkalosis

coLd

Low PaCO₂ = Oxygen to Lungs

ABG clues:

High pH, low PaCO₂, normal/high SaO₂, but patient may show signs of tissue hypoxia (e.g., confusion, lactic acidosis)

Shift to the right

RIGHT

Released - Hemoglobin releases O2 to tissues

SaO₂ may be lower, but tissue oxygenation is better

Acidosis (↓ pH)

Hyperthermia

Ramped up PaCO₂

ABG clues:

Low pH, high PaCO₂, lower SaO₂, but patient may tolerate it better if tissues are getting oxygen.

COPD is right shift due to 

ABG Patterns in Left and Right Shift

Parameter	Left Shift	Right Shift
PaO₂	Normal or ↑	Normal or ↓
SaO₂	Normal or ↑	↓ (but tissues get more O₂)
PaCO₂	↓ (alkalosis)	↑ (acidosis)
pH	↑ (alkalosis)	↓ (acidosis)
Tissue O₂ delivery	↓ (O₂ stuck to Hb)	↑ (O₂ released from Hb)

Think Low PaCO2 = aLkaLosis = Left

What would you do for a PaO2 <40mmHg?

This is severe hypoxemia

Escalate: high-flow O₂, BiPAP, prepare for intubationA

Acute respiratory decompensation interventions - what will you do if your patient starts to decline? Explain the medical and nursing management of the client experiencing respiratory failure