today I'll be talking about an approach to the patient with acute dyspnea also known as shortness of breath arbitrarily define acute as an onset over the course of anywhere between seconds to about a week but keep in mind that a patient with any classic cause of chronic progressive dyspnea can occasionally present after just a few days of symptom onset so consider checking out the approach to chronic dyspnea video as well regarding a diagnostic framework for dyspnea either acute or chronic as with most symptoms it's common to categorize causative diagnoses based upon organ systems for example grouping pneumonia pulmonary embolism and a pleural effusion under the heading of lung heart failure and ischemia under heart and so on and so forth that's perfectly fine to do and this is what I do for the chronic just me a video but for acute dyspnea both for a variety and because I actually think it's more instructive I'll construct the framework around the pathophysiologic mechanisms that can lead to the dyspnea sensation the most clear-cut physiologic trigger for dis neo is input from peripheral chemoreceptors in the carotid and a or tech bodies that the person is experiencing hypoxemia hypercapnia or acidemia so let's start with those categories focusing first on hypoxemia the most common causes of acute hypoxemia include pulmonary edema either cardiogenic or non cardiogenic pneumonia pulmonary embolism pleural effusion and a COPD exacerbation less common causes include interstitial lung disease pneumothorax atelectasis which is collapsed a part of a lung and mucous plugging which is when a large airway literally gets abruptly obstructed with mucus moving on from isolated hypoxemia another general trigger for increasing ventilation is hypercapnia this can be from obstructive lung disease either COPD or severe asthma exacerbations or hypercapnia can be from acute neurologic and neuromuscular disease such as acute attacks of myasthenia gravis transverse myelitis and guillain-barre syndrome while generally speaking central hypoventilation from either drug overdose or obesity hypoventilation syndrome can leave the hypercapnia these causes of hypercapnia they don't cause dyspnea regarding acidemia shhhhh triggering of dyspnea this works synergistically with a dyspnea triggered by hypercapnia since hypercapnia necessarily lowers pH however acidemia can also occur in the absence of hypercapnia as seen with metabolic acidosis in this circumstance the body's natural response to the lowering of serum pH is so called respiratory compensation in which respiratory drive increases with the goal of lowering arterial co2 below normal and partially normalizing pH the causes of a metabolic acidosis that are most likely to cause dis mia via this mechanism are ketoacidosis and lactic acidosis beyond those three main peripheral chemoreceptors mediated triggers for dyspnea there are a few more to consider for oxygen delivery to peripheral tissues as a consequence of factors other than hypoxemia also can lead to dis BIA if you recall that oxygen delivery is proportional to both the hemoglobin concentration and to the cardiac output you will quickly deduce this category includes anemia low output heart failure and obstructive shock such as that seen from massive Pease tamponade and tension pneumothorax under miscellaneous causes there is myocardial ischemia which in some patients particularly the elderly and diabetics this can occur in the absence of chest pain exertional symptoms other than chest pain which are due to myocardial ischemia are often referred to as an engine equivalent because the approach to its diagnosis and management is the same as it would be for ischemic pain people can also present with acute dyspnea in the setting of upper airway obstruction as can be seen in anaphylaxis angioedema and various infections such as epiglottitis and retro pharyngeal abscesses people can get acutely disconnect from anxiety or panic attacks and last acute pain can lead to dyspnea in some individual this diagnostic framework is not perfect there are patients with heart failure pease pneumonia pleural effusions and obstructive lung disease who can present with dyspnea before the onset of hypoxemia or hypercapnia this can occur through a variety of mechanisms including mechanical loading of the respiratory system decreased respiratory compliance and incompletely characterized sensory receptors within the lungs themselves before leaving the framework you'll notice that there's one diagnosis I have not mentioned lung cancer how could I leave off something so important and relatively common well put simply it's because a tumor mass in the lung rarely causes dystiny itself instead is the other problems that lung cancer causes which lead to dis Nia such as malignant pleural effusions post obstructive pneumonia Pease tamponade and niimi of chronic disease or chemotherapy side-effects either direct toxicity or opportunistic infections in the setting of immunosuppression now what is a practical approach to diagnosis in a patient with acute dyspnea obviously one will take a history of the patient's presenting illness and past medical problems the most important objective data will be the vital signs a good examination of the lungs heart including jbp and extremities and a chest x-ray this is the minimum data set for a patient presenting with dyspnea depending on the situation additional data could include more exam components CBC chemistry panel d-dimer BNP procalcitonin serum lactate and ketones an ABG ECG a focused bedside ultrasound or a formal echocardiogram and/or a CT scan of the chest but starting off with just the focused history vitals focused physical exam and chest x-ray one of several combinations of findings will be apparent focal crackles and a focal opacity on x-ray suggests pneumonia additional the features include the presence of cough fever leukocytosis and an elevated procalcitonin for additional workup consider blood cultures plus or minus sputum cultures though these will be more helpful to tailor antibiotic therapy than they will be to make the initial diagnosis diffuse coarse crackles and diffuse alveolar opacities on chest x-ray suggest pulmonary edema additional features specifically suggestive of a cardiogenic etiology of pulmonary edema include known cardiovascular risk factors and elevated jbp an s3 symmetric leg swelling a dilated IBC and low LV systolic function on bedside ultrasound a significantly elevated BNP and either a significant arrhythmia and/or LVH seen on ECG there are also a few radiographic clues on the chest x-ray such as current pleural effusions cardiomegaly and curly B lines all of which are more commonly seen with cardiogenic edema diffuse fine crackles and diffuse interstitial opacities on chest x-ray suggest interstitial lung disease determining the specific cause of ILD will initially require reviewing the patient's medications occupational environmental and animal exposures and the chest CT looking for specific radiographic patterns which aren't discernible on plain films unilaterally decreased breath sounds and a pleural effusion on x-ray is of course diagnostic of that condition determining the etiology of pleural effusions often but not always requires a diagnostic thoracentesis remember that there may or may not be in additional pathology hiding beneath that effusion unilaterally decreased breath sounds and a pneumothorax on x-ray is diagnostic of that additional diagnostic workup for a first-time primary spontaneous pneumothorax is usually not necessary bilaterally decreased breath sounds wheezing and an x-ray without any opacities suggests the possibility of an asthma exacerbation or particularly in heavy smokers a COPD exacerbation although COPD can occur in non-smokers as well additional supportive features include a previously established diagnosis of asthma or COPD hypercapnia on ABG and hyperinflation on the chest x-ray asthma and COPD exacerbation czar so-called clinical diagnosis which means there are no specific diagnostic tests that rule them in or out definitively but rather a diagnosis is based upon a combination of history exam measures a peak expiratory flow for asthma specifically and the exclusion of alternative explanations sometimes bronchodilators and steroids will be prescribed empirically as part of a diagnostic trial however a number of other causes of dyspnea can also respond to this therapy now what to do if the lung exam and chest x-ray are both normal but the patient is hypoxemic the main consideration here is a pulmonary embolism particularly if the disc is accompanied by pleuritic chest pain risk factors for PE such as cancer recent hospitalization or prior venous thromboembolism or science of a deep vein thrombosis on either exam or ultrasound the possibility of a PE can be further evaluated with either a serum d-dimer or a CT angiogram of the thorax depending upon the clinical suspicion and a specific clinical prediction rule called the well score the dislocation was a totally normal exam including normal Oh two sets and a normal chest x-ray represents a diagnostic challenge and will require casting a wider net so to speak if you have not already done so this is when to consider looking at the CBC metabolic panel troponin ABG or vbg either a d-dimer or CT angiogram of the thorax the ECG and consider checking pulsus paradoxus particularly if the patient has a history of cancer or other reason to have a park cardial effusion if a CTA shows a PE that's the diagnosis if the ECG shows unexplained ST and t-pain jiz or if the patient has cardiovascular risk factors consider whether this could be in angina equivalent as a presentation of acute coronary syndrome and if the patient warrants an ischemia evaluation although anemia is uncommon lis a cause of acute dyspnea a simple CBC will rule it in or out very quickly and anemia has its own completely separate diagnostic approach one should check a chem-7 and either in arterial or venous blood gas to ensure that the patient doesn't have in metabolic acidosis a blood gas would also pick up the respiratory acidosis from hypoventilation that might suggest the possibility of neuro or neuromuscular disease in elevated pulsus paradoxus should prompt an evaluation for a pericardial effusion which might get missed on a chest x-ray if the effusion is relatively small and finally anxiety disorders including panic attacks can only be diagnosed by rolling out all alternative explanations given how dangerous many causes of acute dyspnea can be one should never jump to the conclusion that anxiety is the cause irrespective of how young and otherwise healthy a person may be and irrespective of whether the person subjectively looks anxious because any cause of dyspnea can make one look and feel anxious to beyond the algorithm there are a few other clues to think about when trying to determine the etiology of acute dystonia the first is precisely how acute its onset really was if the onset was over just a few minutes I would be thinking a PE acute MI or pneumothorax attack arrhythmia leading to the very abrupt onset of cardiogenic pulmonary edema would be another consideration coincidentally these are also the handful of diagnoses most likely to be associated with chest pain though pain can also be seen with pneumonia and asthma attacks too another clue is the respiratory pattern rapid and unusually shallow respirations are typical of COPD asthma and anxiety unusually deep respirations of either and elevated rates or a surprisingly normal rate are typical of the respiratory compensation for metabolic acidosis best described in diabetic ketoacidosis and known by the eponym of Kussmaul respirations you may have noticed that the presence or absence of hypoxemia is only a minor factor in our diagnostic algorithm that may have been surprising since it was a significant part of our framework but it turns out to be minimally diagnostically helpful since most causes of dyspnea can present either with or without hypoxemia you should never be saying to yourself this patient can't have such and such diagnosis because their Oh too sad is normal that is a common and dangerous fallacy however the opposite can be true where some diagnoses can be ruled out because they do not cause the low to sat's that are observed for instance anemia metabolic acidosis and of course anxiety finally keep in mind that acute dismay up is one of a handful of symptoms that always warrants emergent evaluation because of the significant frequency of imminently life-threatening diagnoses which are most notably a PE MI pneumothorax and tamponade so in summary ideologies of acute dyspnea can be categorized either by organ system in which case the lungs and heart are the most common general categories or by pathophysiologic mechanism in which case hypoxemia is the most common all patients presenting with acute dyspnea warrant assessment of their vitals a thorough cardiac pulmonary and extremity exam and the chest x-ray most but not all will also need some basic blood tests an ECG and the bedside ultrasound of the heart if available less frequently required tests include a CT scan either a conventional CT thorax looking for ILD or a CT angiogram if looking for a pulmonary embolism despite it being the most common mechanism leading to dis Nia the presence or absence of hypoxemia usually has minimal impact on the differential diagnosis and imminently life-threatening diagnoses that frequently present with acute dyspnea most notably include PE and an acute MI but also includes tamponade and a pneumothorax you