welcome to the third session in the ICU curriculum this session will cover acute respiratory failure in this session we will define hypoxemic and high per capita Crestor failure and provide examples of each form of respiratory distress identify which groups of patients with respiratory failure benefit from non-invasive positive pressure ventilation identify common reasons for intubation and mechanical ventilation and finally define the four major variables that can be controlled on the ventilator and how they relate to oxygenation and ventilation let's start with a case your team picks up a new admission in the morning the patient is a 55 year old man with COPD who initially presented with dyspnea his initial oxygen saturation was 72% on room air and he required three liters nasal cannula to maintain an oxygen saturation of greater than 90% chest x-ray showed no focal consolidation or opacities his respiratory viral panel returned positive for rhinovirus while you are pre rounding the nurse calls to tell you that the patient is working harder to breathe more tired appearing and requiring 10 liters nasal cannula to maintain an oxygen saturation greater than 90% he transferred the patient of the Mikki for further management his ABG on 10 liters nasal cannula on arrival of the makeu shows a pH of 7.15 pco2 of 65 and po2 of 52 how would you classify this patient's respiratory distress and more importantly what form of respiratory support should he receive and how do we go about making this decision in this session we want to help you to find the type of respiratory failure understand which patients benefit from which forms of respiratory support and recognize when intubation may be necessary first we need to define the two major types of respiratory failure we will use the diagram in the center of the screen to help us throughout the session the two major types of acute respiratory failure or hypoxemic respiratory failure also known as type 1 respiratory failure and hypercapnia respiratory failure known as type 2 respiratory failure hypoxemic respiratory failure is a problem of oxygenation and is defined as an oxygen saturation less than 90 percent or pao2 less than 60 millimeters of mercury on room air hypercapnia respiratory failure is a problem of ventilation as defined as a PA co2 greater than 45 millimeters of mercury plus an accompanying respiratory acidosis or pH less than 7.3 v now let's talk about both in more detail first acute hypoxemic respiratory failure as previously stated hypoxemic respiratory failure is defined by an oxygen saturation less than 90 percent or pao2 less than 60 millimeters of mercury on room air recall that there are five major causes of hypoxemia low inspired oxygen hypoventilation or decreased minute ventilation diffusion restriction shunt and VQ mismatch in the ICU the vast majority of causes of hypoxemia or due to VQ mismatch what is VQ mismatch VQ mismatch is a mismatch between ventilation and perfusion in the lung in the case of hypoxemia blood is moving through the pulmonary capillaries without picking up enough oxygen from the alveoli this is supposed to shunt and which blood is moving from the right side of the heart to the left side of the heart without picking up any oxygen VQ mismatch is often due to pathology resulting in alveolar or air space filling basically the alveoli fill with something that pushes out or impairs the usual movement of oxygen then the capillaries and red blood cells traversing those alveoli are unable to pick up as much oxygen as usual this leads to more deoxygenated blood and making its way to the left side of the heart and therefore out into the systemic circulation this creates hypoxemia an easy way then to construct a differential for acute hypoxemic respiratory failure is to go through the various things that can fill an alveolus the three most common causes are blood pus and water blood can be the result of diffuse alveolar hemorrhage due to any number of causes like a vasculitis bland hemorrhage from anticoagulation infection or a drug plus can be the result of pneumonia bacterial viral or fungal or a RDS water represents cardiogenic pulmonary edema or another manifestation of a RDS additional less common alveolar filling processes include cells eosinophils lymphocytes or cancer protein a disease called pulmonary alveolar protein OSIS fat or lipid a disease called like boyd pneumonia and calcium a rare entity called pulmonary kalsa gnosis finally pulmonary embolism also results in hypoxemia be a VQ mismatch in this case there is ventilation but no perfusion hypoxemic respiratory failure is best treated with nasal canula non rebreather heated High Flow nasal canula or invasive mechanical ventilation next we transition to acute hypercapnia respiratory failure as a reminder acute hypercapnia respiratory failure is defined by a pco2 greater than 45 millimeters of mercury plus an accompanying respiratory acidosis if hypercapnia is severe enough it will ultimately result in hypoxemia referring back to the five major causes of hypoxemia hypercapnia respiratory failure is due to hypoventilation or decrease minute ventilation minute ventilation is equal to the tidal volume multiplied by the respiratory rate therefore decreasing out of the tidal volume or the respiratory rate will decrease the minute ventilation ventilation is how our body controls the level of carbon dioxide in the blood therefore as the minute ventilation decreases the pco2 will increase and the pH will decrease when constructing a differential diagnosis for acute hypercapnia respiratory failure it is easiest to think about pathology that causes either decrease in the tidal volume respiratory rate or both a good way to think about this is the won't breathe can't breathe and can't breathe enough schema this schema breaks down hypercapnia respiratory failure into CNS neuromuscular and pulmonary ideologies won't breathe represents central causes of high per capita Kress per Tori failure the mechanism is a decrease in the respiratory rate the best examples are sedative and narcotic overdoses can't breathe represents neuromuscular or diaphragmatic dysfunction in this scenario the patient is unable to activate the muscles of the diaphragm and chest wall and therefore cannot expand the lungs and get sufficient tidal volumes causes of neuromuscular dysfunction include guillain-barre a myasthenia gravis botulism and polio finally can't breathe enough represents the pulmonary causes of hypercapnia crest Batory failure this category is defined by impaired gas exchange with overwhelmed respiratory mechanics the two most common causes are COPD and asthma exacerbations but why do COPD and asthma exacerbations cause hypercapnia Crespo Torrey failure COPD exacerbation start with dynamic hyperinflation triggered by infection medication non-compliance PE etc dynamic hyperinflation leads to air trapping within the lung as air is trapped the lungs expand close to the total lung capacity lung expansion causes diaphragmatic flattening as the diaphragm flattens and the lungs expand more effort is required to expand the lungs further and contract the diaphragm more increased effort and hyper expanded lungs will lead to smaller tidal volumes recall the minute ventilation equation from earlier in the session smaller tidal volumes will cause the pco2 to increase and the pH to decrease in addition smaller tidal volumes will only make the dynamic hyperinflation worse this is the vicious cycle of COPD and asthma exacerbations for a good way to represent this physically go ahead and take a deep breath in and hold that breath now without exhaling try and take another breath on top of that the difficulty and increased effort required to pull the next breath while the lungs are already expanded is similar to the discomfort patients with COPD feel in the midst of an acute exacerbation so how do we go about breaking the vicious cycle of a COPD or asthma exacerbation the answer non-invasive positive pressure ventilation non-invasive positive pressure ventilation includes both CPAP and BiPAP no BiPAP is actually a brand name and the general term is bi-level positive airway pressure in CPAP a continuous positive pressure is delivered throughout the entirety of the respiratory cycle for example five centimeters of water in BiPAP both an inspiratory pressure the eye PAP and an expert Ori pressure the e PAP are set at the bottom is a picture of non-invasive ventilation from 1995 on the right is a current image to show face mass that we utilize today but why does non-invasive positive pressure ventilation help in the midst of a COPD exacerbation on the screen we are again showing the vicious cycle of the COPD or asthma exacerbation non-invasive positive pressure ventilations stents open the obstructed Airways as these Airways are stented open they are allowed to empty during exhalation therefore the lungs deflate and the diaphragm and chest wall returned to a more normal and physiologic position as these muscles of respiration return to their normal position the patient could then take a larger breath with less effort again recall the minute ventilation equation from earlier in the session a larger breath or larger tidal volume will cause the pco2 to decrease and the pH to increased in addition larger breaths with less effort reduced the respiratory rate and the patient's dyspnea as long as the patient is wearing non invasive this cycle will continue while the inhaled bronchodilators and systemic steroids are allowed to work data supports the use of non-invasive positive pressure ventilation for acute COPD exacerbation one of the first landmark studies was from Bruce shard at all on the New England Journal of Medicine in 1995 in their trial non-invasive was associated with a lower intubation rate decreased length of stay and lower mortality rate than standard care how has this trial held up over the years a Cochrane review and 2017 found that use of non-invasive and COPD exacerbations decreases mortality reduces risk of intubation and reduces length of hospital stay the benefit of non-invasive in asthma is extrapolated from the affirmation data in COPD another somewhat unexpected group of patients that benefit from non-invasive positive pressure ventilation is patient with acute cardiogenic pulmonary edema these patients have an alveolar filling process water and are not hypercapnia why then do they benefit from non-invasive non-invasive positive pressure ventilation and positive pressure in general increases intrathoracic pressure increased intrathoracic pressure decreases venous return to the heart and therefore decreases preload second positive pressure decreases after load and thereby improves forward flow how does it do this there are multiple components of cardiac afterload one of which is the transmural pressure of the left ventricle the transmural pressure is the pressure the left ventricle must generate in order to eject the stroke volume the transmural pressure is the difference between the left ventricular systolic pressure the pressure inside the LV and the plural or intrathoracic pressure the pressure outside the LV normal inspiration produces negative intrathoracic pressure or negative pressure across the pleura and throughout the thoracic cavity therefore during normal inspiration the transmural pressure will equal a systolic blood pressure minus a negative intrathoracic pressure therefore for a normal person this will produce a higher transmural pressure basically the heart has to overcome a force that is trying to pull the left ventricular walls outward the negative intrathoracic pressure when positive pressure is applied the transmural pressure and therefore the after load is decreased because you are now subtracting a positive pressure therefore the LV no longer has to overcome an additional negative pressure but rather is assisted in its mission by the inward positive pressure of positive pressure ventilation a simplistic way to think about this positive pressure provides an extra push during systole to help get blood out of the heart finally positive pressure pushes fluid within the alveoli back into the interstitial where it can be cleared you're about to put your patient on non-invasive for acute hyper cabining respiratory failure or acute cardiogenic pulmonary edema what are some things you always need to think about before putting the mask on their face what are the major contraindications to non-invasive positive pressure ventilation things to consider include whether there are copious world secretions as positive pressure could lead to aspiration and worse in their respiratory distress altered Mental Status inability to protect the airway facial trauma and hemodynamic instability or shock note that the majority of these contraindications deal with the CNS head and neck so patients with COPD and asthma exacerbations as well as acute cardiogenic pulmonary edema benefit from non-invasive positive pressure ventilation once your patient is placed on non-invasive you know they are getting better because their respiratory rate and dyspnea improve and their pco2 decreases but what if they get worse the next step is intubation and mechanical ventilation it is easiest to think about indications for intubation in a head-to-toe fashion for the head and central nervous system alter Mental Status and an unprotected airway or indications for intubation as well as copious secretions airway edema and burns or smoke inhalation cardiac indications include cardiac arrest and cardiogenic pulmonary edema that has failed non-invasive pulmonary indications include failure of ni PPV or Heda high flow nasal canula ard s and massive from Optus s GI indications include massive hematemesis or facilitation of a procedure like an EGD and total body indications include shock shock represents type 4 respiratory failure why intubate for shock while in shock a patient's respiratory system will be unable to meet the metabolic demands of the body the ability to control the patient's ventilation allows for both improved management of metabolic acidosis and to minimize the work of the respiratory musculature and decrease the proportion of the cardiac output consumed the patient is now intubated and receiving mechanical ventilation on the right is an image of the hamilton ventilator interface while a patient is on the ventilator we can control both the oxygenation the pao2 and the ventilation the pH and paco2 what four major variables allow us to affect these numbers the variables that control oxygenation are the fio2 the fraction of inspired oxygen and the peep the positive end expiratory pressure the variables that control ventilation are the components of the minute ventilation equation referenced throughout this session the tidal volume and the respiratory rate in this session we defined hypoxemic and hypercapnia cress / Torrey failure and created a differential for each form of respiratory distress we then identified patients with hypercapnia respiratory failure namely COPD and asthma exacerbations plus acute cardiogenic pulmonary edema that benefit from non-invasive we then briefly discussed indications for intubation and mechanical ventilation and finally what four major variables we can control on the ventilator and how they relate to oxygenation and ventilation thank you for your participation