Dyspnea, Respiratory failure and mechanical ventilation
Dyspnea (shortness of breath)
It is a symptom, the subjective feeling of difficult, uncomfortable, or labored breathing. In most patients, the cause of dyspnea is cardiac, or pulmonary (common causes of dyspnea are asthma, chronic obstructive pulmonary disease-COPD, pneumonia, bronchitis, congestive heart failure, cardiac ischemia pulmonary embolism and less common causes upper airway obstruction, pneumothorax, a large pleural effusion, postoperative atelectasis, cardiac tamponade). There are also other non-cardiopulmonary causes such as anxiety (panic attack), anemia, massive ascites. An initial assessment of a patient complaining of dyspnea should include an observation of the patient's general appearance and vital signs to form an impression about the emergency of the situation. Does the patient look comfortable or does he look distressed? Signs of significant distress that should alert the physician to the possibility of an acute severe cause of dyspnea are the following: Tachypnea, tachycardia, difficulty in speaking due to breathlessness, use of accessory respiratory muscles, stridor, altered mental status (lethargy, or agitation). In the presence of such signs, the administration of oxygen must be started immediately, an intravenous catheter should be placed and diagnostic evaluation and treatment should be prompt and focused. The usual evaluation in acute cases includes a focused history and physical examination, pulse oximetry, arterial blood gasses (ABGs) analysis, an ECG, a chest X-ray and blood tests : complete blood count, basic biochemical tests such as glucose, urea, creatinine, electrolytes, creatine phosphokinase- (CPK), transaminases, etc and depending on suspected diagnosis, cardiac troponin, D-dimers, natriuretic peptide (BNP or NT-proBNP) and c-reactive protein (CRP) may be helpful. It should be emphasized, that the history and physical examination are the most useful guides to diagnosis.
With pulse oximetry a resting hemoglobin oxygen saturation< 95 % is abnormal (normal levels 95-100%).
Normal levels of arterial blood gases are the following: pH (7.35-7.45)
PaO2 (75-100 mmHg)
PaCO2 (35-45 mmHg)
HCO3 (22-26 meq/L)
SaO2 (95-100%)
Oxygen administration should start early in case of a patient with acute dyspnea, even before completing the history and physical examination. An important general goal, that we should keep in mind, is to maintain an oxygen saturation of hemoglobin > 90%, or a partial oxygen pressure in the arterial blood, PaO2 > 60 mmHg. In patients with a long-standing severe pulmonary disease, such as severe COPD, lower goals are appropriate, provided that the patient's dyspnea improves and clinical condition stabilizes. Apart from oxygen administration, further treatment of the patient with dyspnea is directed to the underlying disease, therefore we need a correct diagnosis.The history is important and especially a previous history of cardiac or pulmonary disease, because the most common cause of dyspnea in patients with chronic cardiac or pulmonary disease is exacerbation (worsening) of this disease. However acute dyspnea can also be caused by another condition different from their chronic disorder.
A patient with dyspnea, cough and fever. Diagnosis ?
With pulse oximetry a resting hemoglobin oxygen saturation< 95 % is abnormal (normal levels 95-100%).
Normal levels of arterial blood gases are the following: pH (7.35-7.45)
PaO2 (75-100 mmHg)
PaCO2 (35-45 mmHg)
HCO3 (22-26 meq/L)
SaO2 (95-100%)
Oxygen administration should start early in case of a patient with acute dyspnea, even before completing the history and physical examination. An important general goal, that we should keep in mind, is to maintain an oxygen saturation of hemoglobin > 90%, or a partial oxygen pressure in the arterial blood, PaO2 > 60 mmHg. In patients with a long-standing severe pulmonary disease, such as severe COPD, lower goals are appropriate, provided that the patient's dyspnea improves and clinical condition stabilizes. Apart from oxygen administration, further treatment of the patient with dyspnea is directed to the underlying disease, therefore we need a correct diagnosis.The history is important and especially a previous history of cardiac or pulmonary disease, because the most common cause of dyspnea in patients with chronic cardiac or pulmonary disease is exacerbation (worsening) of this disease. However acute dyspnea can also be caused by another condition different from their chronic disorder.
ANSWER
Pneumonia of the right upper lobe. The patient has typical symptoms and typical radiological features of pneumonia. A consolidation (white area) can be seen, with air bronchogram (bronchi containing air appearing as black tubular structures within the area of consolidation). The radiological picture of lobar pneumonia is not specific for a certain micro-organism. The most common cause is Streptococcus pneumoniae. Other causative organisms that may cause such a pattern are: Klebsiella pneumoniae, Legionella pneumophila, Haemophilus influenzae, and Mycobacterium tuberculosis.
For explanations about the chest X ray in pneumonia also watch this video: LINK https://www.youtube.com/watch?v=uhRIu8bDYA0
from the you tube channel hammadshams
Physical examination of the patient with dyspnea
The respiratory rate is important. A low rate < 12/minute suggests a depression of the respiratory center of the central nervous system, due to a stroke, drug overdose (e.g. opioids, tricyclic antidepressants, sedatives), or respiratory muscle fatigue.An elevated respiratory rate (e.g.>20/min in adults) suggests hypoxia ( due to pulmonary embolism, pulmonary edema, ARDS, pneumonia, COPD exacerbation, asthmatic attack, etc), anxiety, or pain.
[ The respiratory rate is determined by counting how many times the chest rises per minute. Normal limits are approximate: Normal respiratory rate at rest for adults is 12-18/ minute. In children normal respiratory rate is higher: 0-5 months 25-50/min, 6 months- 5years 20-30/min, 6-12 years 12-20/min, older children approximately like adults].
The heart rate is often elevated (usually sinus tachycardia) in patients with severe hypoxia or fever, because of stimulation of the sympathetic nervous system.
Body temperature is also one of the vital signs. Fever usually suggests an infection as a cause of dyspnea (such as pneumonia, or bronchitis), but it can also be present with pulmonary embolism.
Blood pressure can also provide some clues. Hypotension with dyspnea can be caused by tension pneumothorax, cardiac tamponade, severe congestive heart failure or cardiogenic shock, or septic shock.
Hypertension with acute severe dyspnea is often present in patients with acute pulmonary edema due to congestive heart failure caused by left ventricular diastolic or systolic dysfunction).
Pulsus paradoxus is a fall of the systolic blood pressure in inspiration by more than 10 mmHg and can occur in cardiac tamponade and in an asthmatic attack.
Central cyanosis (a bluish color of the lips, the tongue, and the ears) suggests significant hypoxemia, with consequent hemoglobin desaturation. However, if there is anemia, cyanosis does not usually occur even with severe hypoxia. Cyanosis is a helpful clue only when it is present, but its absence cannot exclude hypoxemia.
Inspection of the jugular veins is usually performed with the upper part of the patient's body elevated at a 45 degree angle. Jugular venous distention in a patient with dyspnea can suggest heart failure, tension pneumothorax, or cardiac tamponade. Jugular venous distention on expiration can occur in patients with asthma or COPD exacerbation.
Examination of the respiratory system includes:
Checking if the trachea is in the midline (deviation of the trachea from the midline can be noted in a large pleural effusion or pneumothorax and it is towards the opposite side),
The symmetry of breath sounds (diminished or absent breath sounds over one area can occur in pleural effusion, pneumothorax, or pneumonia and diffuse reduction of the intensity of breath sounds in emphysema.
Crackles can be present in pneumonia (usually unilaterally), or in pulmonary edema (bilaterally).
Rhonchi and wheezing are musical sounds suggesting stenosis of bronchi due to asthma or COPD.
Stridor suggests upper (extrathoracic) airway obstruction, due to a foreign body, acute allergic reaction (anaphylaxis), angioedema, epiglottitis, vocal cord dysfunction, etc. It is a high-pitched, musical sound produced by the turbulent flow of air through a narrowed segment of the upper respiratory tract. It is often heard without the aid of a stethoscope, because of its intensity.
Stridor suggests upper (extrathoracic) airway obstruction, due to a foreign body, acute allergic reaction (anaphylaxis), angioedema, epiglottitis, vocal cord dysfunction, etc. It is a high-pitched, musical sound produced by the turbulent flow of air through a narrowed segment of the upper respiratory tract. It is often heard without the aid of a stethoscope, because of its intensity.
For a clear and concise explanation of lung sounds see this LINK
NEJM blog-Now@NEJM- LUNG AUSCULTATION
I also RECOMMEND this VIDEO which allows you to listen clearly to the pathological respiratory sounds (from the youtube channel RegisteredNurseRN)
LINK Listen to abnormal respiratory sounds
Dullness to percussion indicates pleural fluid or pneumonia and hyperresonance to percussion suggests pneumothorax.
Heart sounds should be auscultated noting any extra heart sounds (e.g an S3 gallop is suggestive of heart failure), muffled heart sounds (in a large pericardial effusion, lung emphysema, or left tension pneumothorax), or a cardiac murmur (suggestive of valvular heart disease.
The legs and presacral area should be palpated for pitting edema (which suggests heart failure).
Heart sounds should be auscultated noting any extra heart sounds (e.g an S3 gallop is suggestive of heart failure), muffled heart sounds (in a large pericardial effusion, lung emphysema, or left tension pneumothorax), or a cardiac murmur (suggestive of valvular heart disease.
The legs and presacral area should be palpated for pitting edema (which suggests heart failure).
Respiratory failure
Respiratory failure is a severe impairment of pulmonary gas exchange, categorized into two types:Type 1 respiratory failure or Hypoxemic respiratory failure occurs when a patient’s partial oxygen pressure in the arterial blood, PaO2 is reduced to such a level, that it is life-threatening or has serious adverse physiologic effects: PaO2 < 60 mm Hg.
A PaO2 of 55 mm Hg corresponds to a reduced arterial hemoglobin saturation of about 88%. The oxygen -hemoglobin dissociation curve, shows that further decrements in PaO2 from this level will result in steep, linear falls in arterial hemoglobin O2 saturation and thus in arterial O2 content.
Type 1 (hypoxic) respiratory failure is usually caused by diseases directly impairing the function of alveoli, such as pulmonary edema, acute respiratory distress syndrome (ARDS), extensive pneumonia, fibrosing alveolitis. The main feature of this type of respiratory failure is hypoxemia (reduced PaO2 ),which initially leads to hyperventilation, resulting in an initially low PaCO2 (partial pressure of carbon dioxide in the arterial blood). At a later stage PaCO2 can rise, because of fatigue of the respiratory muscles. Patients cannot maintain hyperventilation indefinitely.
Appart from respiratory muscle fatigue, another consequence of hyperventilation is an increased work of breathing with an increased oxygen consumption by the respiratory muscles. This oxygen cost reduces the benefit of hyperventilation as a mechanism of increasing blood oxygenation. In fact, this"oxygen cost" is often greater than the improvement in oxygenation from hyperventilation.
Without effective treatment, the exhaustion of the respiratory muscles can lead to rapid decompensation and progressive worsening can eventually result in respiratory arrest.
Type 2 respiratory failure or Hypercapnic respiratory failure is the inability to sustain a sufficient rate of carbon dioxide elimination to maintain a stable pH without mechanical assistance of ventilation, intolerable dyspnea, or respiratory muscle fatigue. Hypercapnic respiratory failure, i.e. failure to maintain adequate alveolar ventilation usually is characterized by carbon dioxide retention (PaCO2 > 50 mm Hg suggests respiratory failure) and consequent acidosis (lowering of the blood pH, as measured with an arterial blood gasses test). The elevated PaCO2 is also usually accompanied by hypoxemia (reduced PaO2 ). Type 2 (hypercapnic) respiratory failure results from a severe reduction in alveolar ventilation. An impairment of ventilation can be caused by chronic obstructive pulmonary disease (COPD) and especially when there is an exacerbation of the disease. This is the most common cause. Other causes are the following: a severe attack of bronchial asthma, upper airway obstuction, reduced respiratory drive from the central nervous system (CNS), neuromuscular disorders causing an impairment of the function of the respiratory muscles, severe deformities or severe trauma of the chest wall (e.g. flail chest).
Some patients with COPD develop a reduced sensitivity of the respiratory center of the brain to carbon dioxide, so that increases in PaCO2 produce only a small or even no increase in ventilation. These patients rely predominantly or entirely on the hypoxic stimulus (reduced PaO2 ) as a respiratory drive, to stimulate the respiratory center. Thus, prolonged oxygen administration in high concentrations can be dangerous in a small proportion of patiens with COPD, by depressing the respiratory center.
In severe type 2 respiratory failure, a progressive increase in PaCO2 can occur and without the appropriate treatment to improve minute ventilation of the lungs, it can potentially lead to carbon dioxide narcosis and respiratory arrest.
A PaO2 of 55 mm Hg corresponds to a reduced arterial hemoglobin saturation of about 88%. The oxygen -hemoglobin dissociation curve, shows that further decrements in PaO2 from this level will result in steep, linear falls in arterial hemoglobin O2 saturation and thus in arterial O2 content.
Type 1 (hypoxic) respiratory failure is usually caused by diseases directly impairing the function of alveoli, such as pulmonary edema, acute respiratory distress syndrome (ARDS), extensive pneumonia, fibrosing alveolitis. The main feature of this type of respiratory failure is hypoxemia (reduced PaO2 ),which initially leads to hyperventilation, resulting in an initially low PaCO2 (partial pressure of carbon dioxide in the arterial blood). At a later stage PaCO2 can rise, because of fatigue of the respiratory muscles. Patients cannot maintain hyperventilation indefinitely.
Appart from respiratory muscle fatigue, another consequence of hyperventilation is an increased work of breathing with an increased oxygen consumption by the respiratory muscles. This oxygen cost reduces the benefit of hyperventilation as a mechanism of increasing blood oxygenation. In fact, this"oxygen cost" is often greater than the improvement in oxygenation from hyperventilation.
Without effective treatment, the exhaustion of the respiratory muscles can lead to rapid decompensation and progressive worsening can eventually result in respiratory arrest.
Type 2 respiratory failure or Hypercapnic respiratory failure is the inability to sustain a sufficient rate of carbon dioxide elimination to maintain a stable pH without mechanical assistance of ventilation, intolerable dyspnea, or respiratory muscle fatigue. Hypercapnic respiratory failure, i.e. failure to maintain adequate alveolar ventilation usually is characterized by carbon dioxide retention (PaCO2 > 50 mm Hg suggests respiratory failure) and consequent acidosis (lowering of the blood pH, as measured with an arterial blood gasses test). The elevated PaCO2 is also usually accompanied by hypoxemia (reduced PaO2 ). Type 2 (hypercapnic) respiratory failure results from a severe reduction in alveolar ventilation. An impairment of ventilation can be caused by chronic obstructive pulmonary disease (COPD) and especially when there is an exacerbation of the disease. This is the most common cause. Other causes are the following: a severe attack of bronchial asthma, upper airway obstuction, reduced respiratory drive from the central nervous system (CNS), neuromuscular disorders causing an impairment of the function of the respiratory muscles, severe deformities or severe trauma of the chest wall (e.g. flail chest).
Some patients with COPD develop a reduced sensitivity of the respiratory center of the brain to carbon dioxide, so that increases in PaCO2 produce only a small or even no increase in ventilation. These patients rely predominantly or entirely on the hypoxic stimulus (reduced PaO2 ) as a respiratory drive, to stimulate the respiratory center. Thus, prolonged oxygen administration in high concentrations can be dangerous in a small proportion of patiens with COPD, by depressing the respiratory center.
In severe type 2 respiratory failure, a progressive increase in PaCO2 can occur and without the appropriate treatment to improve minute ventilation of the lungs, it can potentially lead to carbon dioxide narcosis and respiratory arrest.
Components of the respiratory system and their dysfunction in respiratory failure
The respiratory system has four functional and structural components:(1) The central nervous system (CNS) component (chemoreceptors, the respiratory center in the medulla, which controls the respiratory system, and CNS efferents)
(2) The chest bellows component (composed of the peripheral nervous system, respiratory muscles, and the chest wall and soft tissues surrounding the lung)
(3) The airways (trachea, bronchi, bronchioles) through which the air passes
(4) The alveoli (the site of gas exchange in the lungs).
Respiratory failure can result from severe impairment of the function of one or more of these components of the respiratory system. Finding the cause of acute dyspnea, or acute respiratory failure is important because it guides specific treatment.
For pneumonia diagnosis and treatment see Pneumonia
Acute respiratory failure due to an impaired CNS drive
It can be caused by drugs that can depress the central nervous system (CNS) and hence CNS respiratory drive. Such drugs are opioids, sedatives and tricyclic antidepressants and their effect can be augmented in cases of overdose, or synergistic drug interactions, or altered drug metabolism (hepatic or renal failure).Other causes that may lead to a depression of the respiratory center include head injury, raised intracranial pressure and brain infection (meningitis, encephalitis).
Treatment, if the cause is a drug, includes reversing the CNS depression by giving an antidote if there is one available. An example is intravenous naloxone for opioids. However, many drugs that depress the respiratory center, do not have antidotes.
In cases where there is no available antidote, or when the depression of the respiratory center is caused by conditions that cannot be rapidly reversed, the patient should be intubated, in order to provide mechanical ventilation and to protect from aspiration of gastric contents (because the gag reflex is usually depressed or absent).
Acute respiratory failure due to an impairment of the mechanical function of the chest
It can be the result of:Respiratory muscle weakness due to disorders such as cervical spinal cord injury involving the phrenic motor neurons (C3–5), Guillain-Barré syndrome (acute demyelinating polyneuropathy), dysfunction of the neuromuscular junction (myasthenia gravis, organophosphorus poisoning, muscle relaxants, botulism), severe muscular dystrophy.
Disorders of the thoracic cage and subdiaphragmatic tissues can cause respiratory failure or can contribute to its development. Such disorders are multiple rib fractures and especially flail chest with severe pain during breathing, certain postoperative states (after multiple rib thoracoplasty), severe kyphoscoliosis. There are also some other conditions having an adverse effect on lung expansion (e.g. abdominal distension due to increased intra-abdominal pressure as a result of a tense ascites, or intra-abdominal hemorrhage). Morbid obesity can also adversely influence the function of the chest wall and of the diaphragm.
The general therapeutic approach includes positive-pressure mechanical ventilation via endotracheal intubation.
Alternatively, if there is no significant risk of aspiration, many patients can be managed effectively with non-invasive positive-pressure ventilation.
Non-invasive positive-pressure ventilation is delivered via a continuous positive airway pressure (CPAP) mask.
Impairment of the function of the airways
These causes of respiratory failure include status asthmaticus (acute severe asthma), acute decompensation of chronic obstructive pulmonary disease (COPD) and upper airway obstruction. In these cases, airway obstruction causes a reduction in minute ventilation.
Asthma is characterized by variable airways obstruction with one or more of the following symptoms: breathlessness, wheeze, chest tightness or cough, with reversible airways obstruction shown by diurnal variation in peak expiratory flow >25%.Acute asthma is diagnosed by worsening symptoms and signs and a reduction in the patient’s usual peak expiratory flow (PEF).
Treatment of asthma or COPD exacerbation:
Treatment of both asthma and COPD exacerbations includes supplemental oxygen, inhaled bronchodilators, and intravenous glucocorticosteroids. If a COPD exacerbation is suspected to be the result of a bacterial respiratory infection, antibiotics are added to the above treatment.
Nebulised beta adrenergic agonists (e.g. salbutamol 5mg) should be administered quickly. The dose can be repeated in 15- 30 minutes
An inhaled anticholinergic drug (ipratropium bromide (500 μgm /6 hours) is added to the treatment in patients with acute severe asthma, or with COPD exacerbation if initial response to salbutamol was not satisfactory.
Salbutamol and ipratropium are preferably given via a mask, but they can also be given as an inhaler. Corticosteroids should be given immediately to patients with asthma or COPD exacerbation [hydrocortisone 100mg x 4 times/day intravenously or intramuscularly, or prednisolone 40-50 mg orally (PO)/day]
Corticosteroids should be administered for a minimum
of 5 days. If they are given for less than 12 days they can be stopped without gradual dose reduction (tapering) but if they are given for longer periods, then dose reduction should be gradual.
In case of acute severe asthma with poor response to initial therapy, a single dose of magnesium sulfate (1.2-2g IV over 20min) can be administered.
Aminophylline may be considered in those with severe asthma or severe COPD exacerbation. A loading IV dose of 5mg/kg (omit if the patient is on oral aminophylline) is followed by an infusion of
0.5mg/kg/hour.
Consider transfer of the patient to the intensive care unit if there is worsening hypoxia, if hypercapnia or acidosis is evident or the patient shows signs of imminent respiratory exhaustion.
Although giving oxygen to patients with COPD exacerbation (who are non-intubated) can often cause worsening of hypercapnia, the physician should still aim to achieve adequate oxygenation in these patients, so oxygen administration is often necessary. If despite the above management life-threatening gas exchange and acid-base abnormalities develop, positive-pressure mechanical ventilation is indicated. In such cases, non-invasive ventilation should be attempted in most patients who are breathing spontaneously and can mobilize their respiratory secretions, because it is usually effective.When non-invasive ventilation is ineffective endotracheal intubation and conventional mechanical ventilation is indicated.
Causes are cardiogenic or noncardiogenic pulmonary edema (adult respiratory distress syndrome-ARDS), diffuse pulmonary hemorrhage, or extensive pneumonia. Hypoxemic respiratory failure can also be caused by acute pulmonary embolism, but in this case, respiratory failure is not due to flooded alveoli but to the blocked blood supply to a large part of the lung and thus to a very large number of alveoli. For the diagnosis and treatment of acute pulmonary embolism click on the link, to see the chapter of the online book: Pulmonary Embolism
Generally, therapy includes oxygen administration (in high concentrations) and treatment directed to the cause: e.g. intravenous antibiotics for bacterial pneumonia, diuretics, nitrates and morphine for acute cardiogenic pulmonary edema, therapeutic anticoagulation and/or thrombolysis for acute pulmonary embolism.
In severe cases, mechanical ventilation is needed to achieve safe levels of arterial oxygenation, until the causative treatment can begin to show results.
Treatment of cardiogenic pulmonary edema
Apart from the administration of oxygen with a target to keep hemoglobin oxygen saturation > 90%, treatment of cardiogenic pulmonary edema focuses on 3 main goals: (1) reduction of pulmonary venous return (preload reduction), (2) reduction of systemic vascular resistance (afterload reduction), and, in some cases, (3) inotropic support (augmentation of the force of myocardial contraction). Preload reduction decreases pulmonary capillary hydrostatic pressure and this leads to a reduction in fluid transudation into the interstitium and alveoli of the lungs. Afterload reduction increases cardiac output and improves renal perfusion, which facilitates diuresis in patients with fluid overload.
Preload reduction is mainly achieved by the administration of nitroglycerin (sublingually or with an intravenous infusion) and the administration (intravenously-IV) of the loop diuretic furosemide (usually a starting dose of 40-80 mg of furosemide IV).
Afterload reduction can be achieved by the administration of an angiotensin converting enzyme inhibitor (ACE-inh), or IV nitroprusside. Both are contraindicated in hypotensive patiens.
ACE inhibitors apart from being the cornerstone of treatment of chronic heart failure with a reduced ejection fraction , are also beneficial in the setting of acute heart failure (provided there is no hypotension). The administration of enalapril 1.25 mg IV or captopril 25 mg sublingually provides hemodynamic improvement as well as improvement of symptoms within 10 minutes. Oral (PO) administration of ACE-inh is also beneficial, but the result occurs much more slowly.
Nitroprusside causes relaxation of the vascular smooth muscle resulting in simultaneous preload and afterload reduction. Its effect on afterload reduction is more marked and results in an increased cardiac output. Initial infusion rate: 0.3 mcg/kg/min (micrograms/kilogram body weight/minute). Evaluate blood pressure for at least 5 minutes before titrating to a higher or lower dose according to the BP. Increments (titration) of the dose must be gradual and with close monitoring of the BP. Maximum dose is 10 mcg/kg/min but in practice the reduction of BP often happens in smaller doses and if so, such a high dose is not used. Nitroprusside is used only in critically ill patients in the intensive care unit (ICU) with continuous blood pressure monitoring. Its action is potent with rapid onset and also rapid offset (when the infusion is terminated). If nitroprusside is administered, it is desirable to convert therapy to an oral vasodilator as soon as possible, because prolonged high-dose administration of nitroprusside may cause thiocyanate toxicity, particularly in patients with significant hepatic or renal dysfunction.
Inotropic support in a patient with acute cadiogenic pulmonary edema is used when preload and afterload reduction does not achieve adequate improvement of the patient's clinical condition or when there is hypotension. Inotropic agents include catecholamine agents (dobutamine, dopamine, norepinephrine-see chapter about circulatory shock) and phosphodiesterase inhibitors (milrinone).
All known IV inotropic drugs are associated with an increased long-term mortality compared with placebo. Therefore, they should be reserved for patients with acute heart failure with a markedly depressed cardiac index and stroke volume.
Another class of inotropic drugs used in acute heart failure are calcium sensitizers (levosimendan). Levosimendan increases myocardial contractility and also causes peripheral arterial and venous dilatation. Its most common adverse effects are hypotension and headache. The randomized clinical study SURVIVE (the Survival of Patients With Acute Heart Failure in Need of Intravenous Inotropic Support ) did not demonstrate a mortality benefit from levosimendan in comparison with dobutamine in patients with acute heart failure.
Acute respiratory distress syndrome (ARDS) is any acute diffuse
parenchymal infiltration of the lungs associated with severe hypoxemia and not attributable to cardiogenic (hydrostatic) pulmonary edema. In general terms, ARDS is acute noncardiogenic pulmonary edema with certain characteristic features:
There is a brief delay between the precipitating event and
rapidly developing dyspnea, markedly reduced aerated lung volume, impaired compliance of the lungs, hypoxemia refractory to modest levels of inspired oxygen and PEEP and delayed resolution.
In all forms of ARDS there is an injury to the alveolar-capillary membrane resulting in increased permeability of the membrane. This causes protein rich fluid to enter the interstitial and alveolar spaces. The fluid causes impairment of gas exchange and of lung compliance and also inhibits surfactant, leading to widespread microatelectasis. The injury can occur either from the gas side of the alveolar-capillary membrane (e.g., smoke inhalation, aspiration of gastric acid) or from the blood side (e.g., sepsis, fat embolism). In contrast to cardiogenic pulmonary edema, in ARDS the pulmonary edema is not the result of increased hydrostatic pressure in the capillaries and so in ARDS the pulmonary capillary wedge pressure (PCWP) is normal. In ARDS pulmonary edema is due to the increased permeability of the capillaries.
Etiology of ARDS:
Sepsis (severe systemic bacterial infection),trauma, with or without pulmonary contusion, fractures (multiple fractures and long bone fractures causing fat embolism), burns, pancreatitis, massive transfusion, drug overdose, postperfusion injury after cardiopulmonary by-pass, aspiration, pneumonia, near drowning.
ARDS is initially treated with high flows of oxygen (70 to 100% O2) by a nonrebreather face mask. If O2 saturation > 90% is not achieved by the administration of high flow of O2, then mechanical ventilation is instituted. For patients with the acute respiratory distress syndrome (ARDS), it is beneficial to add PEEP during mechanical ventilation. PEEP (positive end-expiratory pressure) is present when the pressure in the lungs (alveolar pressure) is maintained above atmospheric pressure (the pressure outside of the body) at the end of expiration. PEEP is one of the ventilator settings that can be chosen when mechanical ventilation is initiated. A small amount of PEEP (4 to 5 cmH2O) is chosen in most mechanically ventilated patients to avoid end-expiratory alveolar collapse. A higher level of applied PEEP (>5 cmH2O) is used to improve hypoxemia in the acute respiratory distress syndrome (ARDS), or other forms of hypoxemic respiratory failure. Moreover treatment of the underlying cause of ARDS should be instituded. Asthma is characterized by variable airways obstruction with one or more of the following symptoms: breathlessness, wheeze, chest tightness or cough, with reversible airways obstruction shown by diurnal variation in peak expiratory flow >25%.Acute asthma is diagnosed by worsening symptoms and signs and a reduction in the patient’s usual peak expiratory flow (PEF).
Treatment of asthma or COPD exacerbation:
Treatment of both asthma and COPD exacerbations includes supplemental oxygen, inhaled bronchodilators, and intravenous glucocorticosteroids. If a COPD exacerbation is suspected to be the result of a bacterial respiratory infection, antibiotics are added to the above treatment.
Nebulised beta adrenergic agonists (e.g. salbutamol 5mg) should be administered quickly. The dose can be repeated in 15- 30 minutes
An inhaled anticholinergic drug (ipratropium bromide (500 μgm /6 hours) is added to the treatment in patients with acute severe asthma, or with COPD exacerbation if initial response to salbutamol was not satisfactory.
Salbutamol and ipratropium are preferably given via a mask, but they can also be given as an inhaler. Corticosteroids should be given immediately to patients with asthma or COPD exacerbation [hydrocortisone 100mg x 4 times/day intravenously or intramuscularly, or prednisolone 40-50 mg orally (PO)/day]
Corticosteroids should be administered for a minimum
of 5 days. If they are given for less than 12 days they can be stopped without gradual dose reduction (tapering) but if they are given for longer periods, then dose reduction should be gradual.
In case of acute severe asthma with poor response to initial therapy, a single dose of magnesium sulfate (1.2-2g IV over 20min) can be administered.
Aminophylline may be considered in those with severe asthma or severe COPD exacerbation. A loading IV dose of 5mg/kg (omit if the patient is on oral aminophylline) is followed by an infusion of
0.5mg/kg/hour.
Consider transfer of the patient to the intensive care unit if there is worsening hypoxia, if hypercapnia or acidosis is evident or the patient shows signs of imminent respiratory exhaustion.
Although giving oxygen to patients with COPD exacerbation (who are non-intubated) can often cause worsening of hypercapnia, the physician should still aim to achieve adequate oxygenation in these patients, so oxygen administration is often necessary. If despite the above management life-threatening gas exchange and acid-base abnormalities develop, positive-pressure mechanical ventilation is indicated. In such cases, non-invasive ventilation should be attempted in most patients who are breathing spontaneously and can mobilize their respiratory secretions, because it is usually effective.When non-invasive ventilation is ineffective endotracheal intubation and conventional mechanical ventilation is indicated.
Disorders of the alveolar component of the respiratory system
These disorders are due to diffuse flooding of the alveoli with fluid (causing abnormalities in gas exchange) and primarily result in hypoxemic respiratory failure, but they can also cause hypercapnia.Causes are cardiogenic or noncardiogenic pulmonary edema (adult respiratory distress syndrome-ARDS), diffuse pulmonary hemorrhage, or extensive pneumonia. Hypoxemic respiratory failure can also be caused by acute pulmonary embolism, but in this case, respiratory failure is not due to flooded alveoli but to the blocked blood supply to a large part of the lung and thus to a very large number of alveoli. For the diagnosis and treatment of acute pulmonary embolism click on the link, to see the chapter of the online book: Pulmonary Embolism
Generally, therapy includes oxygen administration (in high concentrations) and treatment directed to the cause: e.g. intravenous antibiotics for bacterial pneumonia, diuretics, nitrates and morphine for acute cardiogenic pulmonary edema, therapeutic anticoagulation and/or thrombolysis for acute pulmonary embolism.
In severe cases, mechanical ventilation is needed to achieve safe levels of arterial oxygenation, until the causative treatment can begin to show results.
Treatment of cardiogenic pulmonary edema
Apart from the administration of oxygen with a target to keep hemoglobin oxygen saturation > 90%, treatment of cardiogenic pulmonary edema focuses on 3 main goals: (1) reduction of pulmonary venous return (preload reduction), (2) reduction of systemic vascular resistance (afterload reduction), and, in some cases, (3) inotropic support (augmentation of the force of myocardial contraction). Preload reduction decreases pulmonary capillary hydrostatic pressure and this leads to a reduction in fluid transudation into the interstitium and alveoli of the lungs. Afterload reduction increases cardiac output and improves renal perfusion, which facilitates diuresis in patients with fluid overload.
Preload reduction is mainly achieved by the administration of nitroglycerin (sublingually or with an intravenous infusion) and the administration (intravenously-IV) of the loop diuretic furosemide (usually a starting dose of 40-80 mg of furosemide IV).
Afterload reduction can be achieved by the administration of an angiotensin converting enzyme inhibitor (ACE-inh), or IV nitroprusside. Both are contraindicated in hypotensive patiens.
ACE inhibitors apart from being the cornerstone of treatment of chronic heart failure with a reduced ejection fraction , are also beneficial in the setting of acute heart failure (provided there is no hypotension). The administration of enalapril 1.25 mg IV or captopril 25 mg sublingually provides hemodynamic improvement as well as improvement of symptoms within 10 minutes. Oral (PO) administration of ACE-inh is also beneficial, but the result occurs much more slowly.
Nitroprusside causes relaxation of the vascular smooth muscle resulting in simultaneous preload and afterload reduction. Its effect on afterload reduction is more marked and results in an increased cardiac output. Initial infusion rate: 0.3 mcg/kg/min (micrograms/kilogram body weight/minute). Evaluate blood pressure for at least 5 minutes before titrating to a higher or lower dose according to the BP. Increments (titration) of the dose must be gradual and with close monitoring of the BP. Maximum dose is 10 mcg/kg/min but in practice the reduction of BP often happens in smaller doses and if so, such a high dose is not used. Nitroprusside is used only in critically ill patients in the intensive care unit (ICU) with continuous blood pressure monitoring. Its action is potent with rapid onset and also rapid offset (when the infusion is terminated). If nitroprusside is administered, it is desirable to convert therapy to an oral vasodilator as soon as possible, because prolonged high-dose administration of nitroprusside may cause thiocyanate toxicity, particularly in patients with significant hepatic or renal dysfunction.
Inotropic support in a patient with acute cadiogenic pulmonary edema is used when preload and afterload reduction does not achieve adequate improvement of the patient's clinical condition or when there is hypotension. Inotropic agents include catecholamine agents (dobutamine, dopamine, norepinephrine-see chapter about circulatory shock) and phosphodiesterase inhibitors (milrinone).
All known IV inotropic drugs are associated with an increased long-term mortality compared with placebo. Therefore, they should be reserved for patients with acute heart failure with a markedly depressed cardiac index and stroke volume.
Another class of inotropic drugs used in acute heart failure are calcium sensitizers (levosimendan). Levosimendan increases myocardial contractility and also causes peripheral arterial and venous dilatation. Its most common adverse effects are hypotension and headache. The randomized clinical study SURVIVE (the Survival of Patients With Acute Heart Failure in Need of Intravenous Inotropic Support ) did not demonstrate a mortality benefit from levosimendan in comparison with dobutamine in patients with acute heart failure.
Acute respiratory distress syndrome (ARDS) is any acute diffuse
parenchymal infiltration of the lungs associated with severe hypoxemia and not attributable to cardiogenic (hydrostatic) pulmonary edema. In general terms, ARDS is acute noncardiogenic pulmonary edema with certain characteristic features:
There is a brief delay between the precipitating event and
rapidly developing dyspnea, markedly reduced aerated lung volume, impaired compliance of the lungs, hypoxemia refractory to modest levels of inspired oxygen and PEEP and delayed resolution.
In all forms of ARDS there is an injury to the alveolar-capillary membrane resulting in increased permeability of the membrane. This causes protein rich fluid to enter the interstitial and alveolar spaces. The fluid causes impairment of gas exchange and of lung compliance and also inhibits surfactant, leading to widespread microatelectasis. The injury can occur either from the gas side of the alveolar-capillary membrane (e.g., smoke inhalation, aspiration of gastric acid) or from the blood side (e.g., sepsis, fat embolism). In contrast to cardiogenic pulmonary edema, in ARDS the pulmonary edema is not the result of increased hydrostatic pressure in the capillaries and so in ARDS the pulmonary capillary wedge pressure (PCWP) is normal. In ARDS pulmonary edema is due to the increased permeability of the capillaries.
Etiology of ARDS:
Sepsis (severe systemic bacterial infection),trauma, with or without pulmonary contusion, fractures (multiple fractures and long bone fractures causing fat embolism), burns, pancreatitis, massive transfusion, drug overdose, postperfusion injury after cardiopulmonary by-pass, aspiration, pneumonia, near drowning.
Mechanical ventilation
Ventilators used in current practice are called positive pressure ventilators because they apply positive pressure to the airways and lungs. Positive-pressure ventilation can be applied through an endotracheal tube, a tracheostomy, or a tight-fitting mask. When positive pressure ventilation is applied through a mask, this treatment is called noninvasive ventilation .
Some basic terms, necessary to understand the principles of assisted ventilation are the tidal volume and the air flow.
The tidal volume is the amount (volume) of air delivered with each breath, i.e. the volume of air that enters the lungs during an inspiration. The appropriate tidal volume depends on the disease for which the patient requires mechanical ventilation and also on the patient's body size (ideal body weight).
Air flow is the volume of air passing through the airway per minute and it depends on pressure and airway resistance. The following equation holds during inspiration:
∆Pairways=Pprox-Palv =R(airways)×flow
where ∆Pairways is the pressure difference across the airways during inspiration (this is the driving force for the air to move into the lungs), Pprox is the pressure at the proximal end of the artificial airway during inspiration, Palv is the alveolar pressure during inspiration and R(airways) is the airway resistance.
Air flow is the volume of air passing through the airway per minute and it depends on pressure and airway resistance. The following equation holds during inspiration:
∆Pairways=Pprox-Palv =R(airways)×flow
where ∆Pairways is the pressure difference across the airways during inspiration (this is the driving force for the air to move into the lungs), Pprox is the pressure at the proximal end of the artificial airway during inspiration, Palv is the alveolar pressure during inspiration and R(airways) is the airway resistance.
Basic Elements of a mechanical ventilator
Basic Elements of a mechanical ventilator are the inspiratory tubing, the humidifier, the expiratory tubing, the exhalation valve and the main unit of the ventilator (the machine). During inspiration, the main unit of the ventilator delivers a volume of air (tidal volume) via the inspiratory tubing and humidifier to the lungs. The exhalation valve is closed during inspiration. At the onset of exhalation, the exhalatory valve opens and the expired air exits the circuit via the expiratory tubing (through which the expired air reenters the ventilator to monitor its volume). |
| 1.ventilator machine 2. inspiratory tubing or inspiratory circuit 3.expiratory tubing or expiratory circuit 4.humidifier 5.Y piece or Y connection 6. endotracheal tube |
Modes of mechanical ventilation
Modes of mechanical ventilation are generally divided into volume-controlled or pressure-controlled modes.
In volume-controlled ventilation, the desired tidal volume and respiratory rate are set by the physician, and the airway pressure varies (it is the dependent variable). The airway pressure depends on the mechanical properties of the patient’s respiratory system (airway resistance, pulmonary compliance) and on the ventilator’s flow settings.
In pressure-controlled ventilation, the pressure applied to the airways when a breath is delivered and the respiratory rate are set by the physician, and the tidal volume is the dependent variable (it is not preset, and so it can vary).
Here are some basic modes of ventilation, that ventilators can provide:
· Controlled mandatory ventilation (CMV)
· Assist/control (A/C) mode,
· Pressure support (PS) mode,
· Intermittent mandatory ventilation (IMV) mode.
In the CMV mode, the patient is ventilated at a preset tidal volume and respiratory rate. Therefore, the tidal volume delivered is constant, but the peak airway pressure required to deliver this volume varies. This mode is suitable for patients who are not making any respiratory effort (e.g. heavily sedated and /or paralysed patients). It is not indicated for patients who are attempting spontaneous breaths.
The peak pressure depends on other ventilator settings and the patient’s pulmonary compliance.
Thus, a disadvantage of volume controlled modes of ventilation is that in some cases high peak airway pressures may occur and this can lead to lung damage (barotrauma).
In the A/C mode the ventilator can detect a patient’s inspiratory effort (by detecting a negative pressure deflection from baseline in the inspiratory circuit or by detecting the beginning of air flow initiated by the patient). When the patient's spontaneous inspiratory effort exceeds a certain threshold and so it is detected by the ventilator, this triggers the ventilator to deliver the preset inspiratory tidal volume. The timing of the start of the next inspiration is defined by the set respiratory rate or by the patient’s spontaneous
rate, whichever is higher. For example, if the preset rate is 10 breaths/min, the ventilator gives a tidal volume every 6 seconds unless it detects the patient’s spontaneous inspiratory effort earlier. If this happens, the ventilator starts to deliver the tidal volume at that time and resets the start of the next ventilator-initiated breath to be 6 seconds after the start of the patient-initiated breath.
The pressure support (PS) mode of ventilation, unlike A/C does not deliver a preset tidal volume. Instead, PS delivers a preset pressure. When the ventilator detects that the patient is starting a spontaneous inhalation, it provides a certain level of pressure to the inspiratory circuit. This results in the delivery of a synchronized inspiratory pressure “boost” that assists the patient’s own respiratory effort. This will augment the patient’s spontaneous tidal volume and will also unload the patient’s respiratory muscles. The delivery of the pressure boost stops when the ventilator detects that inspiratory flow has decreased to a certain degree.
The level of pressure support (PS) is set in order to achieve a certain tidal volume during the patient’s spontaneous respiratory efforts, often with a trial-and-error approach. The respiratory rate is the patient’s spontaneous respiratory rate. Modern ventilators have a backup minute ventilation, which is a safety feature, in case the patient stops or slows breathing or if tidal volumes fall because of changes in lung mechanical properties.
The intermittent mandatory ventilation (IMV) or synchronised intermittent mandatory ventilation (SIMV) mode consists of two types of ventilation. The first type is identical to that in A/C mode, providing breaths with a set tidal volume, at a preset respiratory rate. These IMV breaths are synchronized with the patient’s spontaneous breaths. In IMV, the second type of ventilation allows the patient to breathe spontaneously from the ventilator’s demand valve. A low level of pressure support (5 -8 cm H2O) is often added to aid these spontaneous breaths, in order to compensate for the airway resistance of the artificial airway.
Thus, in IMV mode the operator must set the IMV rate and tidal volume and the level of pressure support to spontaneous breaths.
Typical initial ventilator settings
On adjusting the ventilator settings, primary goals are: adequate oxygenation and adequate ventilation, reduced work of breathing, synchrony of the ventilator and patient, and avoidance of high peak pressures. The current trend is to use ventilation modes which allow and support spontaneous respiratory effort.
Some typical initial ventilator settings are the following:
Mode: A/C (assist control) This mode is used for patients not breathing spontaneously, but also for starting assisted ventilation.
Respiratory rate: usually is set at 8-14 BPM (breaths per minute) and the range is 5-35 BPM.
For patients without spontaneous breathing efforts, the respiratory rate is set to achieve the desired PaCO2 , using the measurement of the arterial blood gasses (ABGs) as a guide.
For spontaneously breathing patients in A/C or IMV (intermittent mandatory ventilation) mode, the respiratory rate is set 2-3 BPM below the patient's spontaneous rate.
Tidal volume: is usually set at 400-600 ml (these are initial settings for an adult with a body weight of about 70 kg). /Range of tidal volume: 400-800 ml, or (better): 6 -10 ml/ kg of ideal body weight.
As a general rule, in patients without lung disease,
a tidal volume of 8 ml/kg of ideal body weight is used provided the Pplat (end-inspiratory airway plateau pressure) remains <30 cm H2O. For patients with ARDS lower tidal volumes of 6 ml/kg of ideal body weight are recommended. In patients with obstructive lung disease (asthma, COPD) a tidal volume ≤ 8 ml/kg is recommended. (Limiting tidal volume decreases expiratory time).
Tidal volume: is usually set at 400-600 ml (these are initial settings for an adult with a body weight of about 70 kg). /Range of tidal volume: 400-800 ml, or (better): 6 -10 ml/ kg of ideal body weight.
As a general rule, in patients without lung disease,
a tidal volume of 8 ml/kg of ideal body weight is used provided the Pplat (end-inspiratory airway plateau pressure) remains <30 cm H2O. For patients with ARDS lower tidal volumes of 6 ml/kg of ideal body weight are recommended. In patients with obstructive lung disease (asthma, COPD) a tidal volume ≤ 8 ml/kg is recommended. (Limiting tidal volume decreases expiratory time).
FiO2 , the fractional concentration of oxygen in the inspired air, initially is set at 1 (100% oxygen), but it is gradually reduced (tapered) as guided by SaO2 (hemoglobin oxygen saturation) or the PaO2 .(The range for FiO2 is 0.21-1.0).
Inspiratory flow rate is usually initially set at 60-70 L/min (liters per minute). The range of this parameter is 50-100 L/min. The flow rate is generally set at a high value when the patient has a high respiratory rate ("air hunger").
I:E ratio is the ratio of inspiratory time to expiratory time ( 1:2, with a range from 2:1 to 1:4, but usually it is a derived, not a preset, parameter).
Peak airway pressure is usually set to 35 cm H2O (this parameter is important, in order to avoid a form of injury to the lungs).
Positive end expiratory pressure (PEEP) is usually initially set at 5 -10 cm H2O. PEEP is relatively contraindicated in patients with asthma and emphysema.
Pressure support : When this mode is used, it is usually set to 15-20 cm H2O
Pressure support : When this mode is used, it is usually set to 15-20 cm H2O
Positive end-expiratory pressure (PEEP) is a feature that can be combined with most ventilatory modes is the
level of the end-expiratory pressure. It is used in patients with diffuse pulmonary diseases affecting the alveoli , such as pulmonary edema or ARDS. The benefits are that it reopens (recruits) collapsed alveolar regions and small airways and maintains them in a recruited state, it increases functional residual capacity, and redistributes ventilation to dependent regions. These effects improve the matching of ventilation to perfusion, resulting in improved oxygenation and allowing the FiO2 to be reduced. Disadvantages of PEEP are that when it is set to high levels it may increase dead space by overdistending alveoli, and it can also reduce venous return to the heart (this can worsen hypotension in some patients).
PEEP can also be used in cases of non-invasive ventilation, in spontaneously breathing patients by a technique termed continuous positive airway pressure (CPAP). In patients with exacerbations of chronic obstructive pulmonary disease (COPD), PEEP and CPAP can be helpful to minimize the work of breathing, but the magnitude of the PEEP must be low enough, so that it does not cause additional hyperinflation of the lungs.
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LINK: Emergency medicine book-Table of contents
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Bibliography and Links
Merck Manual Proffesional Version: DYSPNEA
LINK https://www.merckmanuals.com/professional/pulmonary-disorders/symptoms-of-pulmonary-disorders/dyspnea
Kevin E J Gunning. Pathophysiology of Respiratory Failure and Indications for Respiratory Support. LINK http://jpck.zju.edu.cn/jcyxjp/files/ge/04/MT/0453.pdf
Pratter MR, Curley FJ, Dubois J, et al. The spectrum and frequency of causes of dyspnea. Arch Intern Med 1989;149:2277–2282
LINK https://www.merckmanuals.com/professional/pulmonary-disorders/symptoms-of-pulmonary-disorders/dyspnea
Kevin E J Gunning. Pathophysiology of Respiratory Failure and Indications for Respiratory Support. LINK http://jpck.zju.edu.cn/jcyxjp/files/ge/04/MT/0453.pdf
Pratter MR, Curley FJ, Dubois J, et al. The spectrum and frequency of causes of dyspnea. Arch Intern Med 1989;149:2277–2282
Girard TD, Bernard GR. Mechanical ventilation in ARDS. Chest 2007;131:921.
A power point presentation of mechanical ventilation: LINK: https://www.slideshare.net/bibinibaby5/mechanical-ventilation-ppt
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