Non-Invasive Positive Pressure Ventilation

Case Presentation:

You are on CCU nights when the ED calls you regarding a 58yo M with a PMH of CAD, HFrEF (35% in an OSH), CKD II, DM, and OSA who presented for progressive swelling and dyspnea. He is saturating at 91% on 6L of nasal cannula but he is clearly in distress with labored breathing and a RR in the 30s. He is mildly tachycardic but otherwise hemodynamically stable. EKG shows sinus tachycardia in the 110s with notable Q waves in aVR and III as well as T wave inversions on V3-V5 (no comparison available). CXR shows bilateral interstitial opacities concerning for pulmonary edema (Figure 1). BNP is 30,000, Cr and BUN are notably elevated from baseline, Na is 134, HCO3 is 28, but otherwise electrolytes are unremarkable. Initial HS troponin was 50 with a subsequent level of 44. You accept the patient for acute decompensated heart failure. He has just gotten an IV dose of Lasix and you prepare to manage the rest of his care.

Ask Yourself:

How do I further manage his acute respiratory failure aside from waiting for the Lasix to kick in?

Background:

Respiratory distress can be viewed as a significant increase in the work of breathing, significant tachypnea, and potential accessory muscle use.

Respiratory failure on the other hand is characterized as either hypoxemia (when SpO2 less than 90% on room air or PaO2 < 60) and/or hypercapnia (when PaCO2 > 45).

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Pulmonary edema is the 2nd most frequent cause of respiratory failure (second only to pneumonia) of which acute cardiogenic pulmonary edema is a main contributor.

The pathophysiology of this presentation involves an increase in pulmonary capillary hydrostatic pressure secondary to acute left-sided heart failure, which eventually results in a net force of fluid filtration out of the vasculature. The buildup of interstitial fluid in the lung impedes proper gas exchange at the alveoli. The condition left unchecked may progress to shunting of deoxygenated blood to the left heart, increase in pulmonary dead space in scenarios where lung perfusion is reduced, and, ultimately, cardiopulmonary collapse. The rate of progression varies among individuals and/or clinical scenarios but can reach terrifying speeds such as with flash pulmonary edema. Therefore, quick evaluation is important to recognize and treat this pathology.

Diagnosis:

While physical exam is important because the patient may be in respiratory distress, have audible crackles, and an S3, CXR can also show increased pulmonary edema. Bedside POCUS of the lungs has been shown to be a very quick and sensitive method for assessing pulmonary edema, especially if there are 2+ B-lines on multiple lung zones bilaterally (Figure 2).

*Echocardiography and right heart catheterization will also show signs of elevated filling pressures but are not typically used as initial diagnostic measures.

Quick Lung POCUS Tips:

When performing an ultrasound of the lungs, it is important to get 6 views of the lung. Ideal views will be anterior, lateral, and posterior on both the right and left side (Figure 3). This will allow visualization of the lung lobes (Figure 4).

Normally, you should be able to visualize normal lung, as seen by horizontal A-lines and lung sliding (Figure 5a). An A-Line is a normal artifact seen on ultrasound caused by the insonation of an aerated lung. However, when patients have pulmonary vascular congestion, there is now fluid within the interlobular septa that causes artifacts known as B-lines (Figure 5b). Pleural effusions can be seen when looking at the posterior view. Specifically, you can see fluid between the patient’s diaphragm and lung (Figure 6).

Arterial Blood Gas (ABG) vs Venous Blood Gas (VBG):

Many times when patients are short of breath, we can order either an ABG or a VBG to help us understand the pathophysiology behind the shortness of breath and to manage the patient’s condition in front of us. While ABGs are significantly more accurate than VBGs as they give us an exact measurement of pH, oxygenation, CO2, and HCO3, they are technically more difficult to perform because they need to be drawn from an artery. In some cases, a VBG can be drawn instead and can give us the information we need despite it being less accurate than an ABG.

Any time a patient is clinically decompensating and is hypoxic, you must get an ABG so you can have as accurate information as possible. :

Conversions:

pH: For a VBG, add 0.03-0.04 to the pH to get a more accurate measurement

pO2: Cannot correlate

pCO2: If the pCO2 is less than 45 mmHG on a VBG, there is no hypercarbia. However, in cases when you must know an accurate pCO2, such as post cardiac arrest,get an ABG. Otherwise, a VBG should suffice. When patients are hypercarbic, the pH will help you determine whether or not the patient is compensated regardless of the test used.

HCO3: Correlates well between the two tests with differences usually being 0.52-1.5 mmol/L different (McCanny 2011, Kelly 2001). As a reminder, the bicarb on both an ABG and VBG is calculated and NOT measured. Therefore, if you want an accurate level, look at the serum chemistry.

ABG: pH / pO2 / pCO2 / HCO3

VBG: pH /pCO2 / HCO3

Pathophysiology of Positive Pressure Ventilation:

Adding positive pressure causes decreased venous return to the right side of the heart due to the increased intrathoracic pressure and leads to decreased preload (Figure 7, part A). Since the positive pressure causes increased pressure in the thorax, pulmonary vascular resistance increases, which causes increased afterload on the right side of the heart.

The increased intrathoracic positive pressure helps increase ventricular squeeze and push the blood outside the thorax. In other words, it helps to decrease the afterload on the left side of the heart (Figure 7, part B).

The positive intra-alveolar pressure also helps improve the pulmonary edema by forcing the fluid back into the vasculature once it has overcome the increased hydrostatic pulmonary capillary pressure driving the patient’s edema (Figure 7, part C).

While non-invasive ventilation tends to cause decreased blood pressure and cardiac output, it has been shown to actually help patients with acute decompensated heart failure as the decreased right sided preload and left sided afterload actually helps to increase cardiac output since its putting less stress on the heart.

With the advent of Non-Invasive Ventilation (NIV), such as continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), and average volume-assured pressure support (AVAPS), we are better able to help our patients. CPAP helps with oxygenation, while BiPAP has the added benefit of helping with ventilation. Therefore, if a patient needs better oxygenation, for instance at night when patients have decreased respiratory drives and are thus not oxygenating well, CPAP should be chosen. However, when patients have increased work of breathing, such as with volume overload and pulmonary vascular congestion, you should put them on BiPAP as it helps with both oxygenation and ventilation.

Figure 8 shows how adding NIV helps increase the pressure within the system. Notably, PEEP is the amount of pressure added to the system, which is equal to the CPAP and EPAP. Unlike CPAP that just helps with oxygenation, BiPAP helps with ventilation by providing the IPAP.

Patients who are placed on NIV should be closely monitored to assess tolerability and response to treatment. In general, people who are not on NIV at home should be started at low pressures (i.e. CPAP of 5 or BiPAP of 10/4) and gradually increased as needed. Starting with high pressures may cause patient discomfort, desynchrony (in case of ventilator-driven modes), and air leakage. Calculate the tidal volume (ideal body weight x 7) and adjust the pressure to ensure the patient is comfortably taking in enough volume by looking at the inhaled volume on the machine.

Generally speaking, when patients with HFrEF or HFpEF develop acute respiratory failure, they tend to do worse than other patients who develop similar physiology but who have normal EF. That said, the patients with HFrEF and HFpEF tended to do better when they were put on NIV and had better mortality outcomes compared to those requiring intubation. Within the NIV group, around 1.5% failed therapy and required intubation and had higher in-hospital mortality. Of note, those who failed and ultimately required intubation still had better outcomes compared to those directly placed on mechanical ventilation. Thus, it is reasonable to trial NIV in patients who do not clearly require immediate intubation. Despite the conflicting research of mortality benefit, the Cardiology and Critical Care associations such as ATS, ESC, etc. recommend the use of NIV in such clinical scenarios

Right-sided heart failure is a rather nuanced topic of discussion with not much data with regards to NIV. Given the hemodynamic changes with positive pressure ventilation, it is reasonable to be weary of initiating interventions that would work against the right ventricle (preload reduction and afterload increase). It is important to understand, however, that right ventricular failure rarely occurs in isolation and that left-sided heart failure is actually the most common cause of right-sided heart failure. Such cases may still derive benefit when the original cause of right-sided heart failure is addressed. The same applies to right-sided heart failure secondary to different lung diseases, whether COPD, ILD, etc. It is good to think ahead about any hemodynamic compromise that may happen with right-sided heart failure in response to positive pressure ventilation (including intubation), specifically with the drop in preload and, thus, cardiac output, and be prepared with management strategies.

Back to the Case:

How do I further manage his acute respiratory failure aside from waiting for the Lasix to kick in?

Because the patient is in respiratory distress, starting him on BiPAP will help to not only recruit more alveoli and improve the pulmonary edema by forcing the fluid in the alveoli back into the vasculature, but it will also help with reducing preload and afterload and assisting with ventricular squeeze (via reducing transmural pressure gradient). Ultimately, these factors lead to more efficient gas exchange and increased cardiac output.

Further Learning:

Resident responsibilities:

Prompt patient evaluation with regards to degree of respiratory distress or respiratory failure
Mobilize respiratory technicians to assist you with setting up NIV; call airway team straight away if patient is too unstable for NIV or with clear contraindications
If a patient with concern for right-sided heart failure needs to be intubated, make sure you have vasopressors (such as norepinephrine) in the room prior to intubation to help assist with hypotension that may result due to the sudden drop in pre-load from the increased positive pressure.
After being placed on NIV, closely follow up on the patient’s hemodynamics and respiratory status in 15-30 minute intervals to assess response to your interventions and need to escalate further. Blood gases change quickly with therapy and can generally be reevaluated within 30 minutes.
Check tolerance to NIV: can adjust settings to patient comfort, consult RT to help with getting better fitting masks, consider changing to HFNC if intolerant to CPAP or BiPAP

High yield trials and resources for further reading:

ADHERE registry analysis: Patients in ADHF requiring respiratory support had lower mortality on NIV compared to those requiring immediate intubation. Of those who failed NIV requiring intubation, they still had lower mortality than those requiring immediate intubation. Mortality and length of hospital stay have been significantly reduced with patients on NIV.11
EAHFE registry analysis: The use of NIV to treat AHF patients in the emergency department was not found to be associated with improved mortality outcomes. It should be used with caution in the elderly patients and those with hypotension and ACS as those populations tended to have worse outcomes with NIV.10

European Society of Cardiology (ESC) 2021 guidelines give the use of NIV in acute pulmonary edema a class IIa recommendation with level B evidence.5

Remember that ANY type of continuous pressure ventilation, not just intubation, will require a proton pump inhibitor (PPI)! That means, if you have a patient on your service who is on continuous BIPAP or even high-flow, you MUST add a PPI!!

Resources

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