PE
Source:http://academiclifeinem.blogspot.com/2011/06/paucis-verbis-pulmonary-embolism.html
Friday, June 24, 2011
UGIB
Source:http://academiclifeinem.blogspot.com/2011/06/paucis-verbis-upper-gi-bleeding.html#comments
Did you know that it takes at least 100 cc of blood in the upper GI tract to produce melena?
A BUN-to-Creatinine ratio of ≥ 36 predicts an upper GI bleeding(sensitivity 90-95%)..assuming no h/o renal failure
Wednesday, June 22, 2011
Tuesday, June 21, 2011
A-a O2 Gradient
A-a gradient = PAO2 − PaO2[2]
Where:
PAO2 = alveolar PO2 (calculated from the alveolar gas equation)
PaO2 = arterial PO2 (measured in arterial blood A-a gradient)
In general the A-a gradient can be calculated by:
Aa Gradient = [FiO2*(Patm-PH2O)-(PaCO2/0.8) ] - PaO2
On Room air ( 21 % ) and at sea level, a simplified version of the equation is:
Aa Gradient = (150 - 5/4(PCO2)) - PaO2
Read more...
Permissive hypercapnia
Source:wikipedia
Permissive hypercapnia is hypercapnia, (i.e. high concentration of carbon dioxide in blood), in respiratory insufficient patients in which oxygenation has become so difficult that the optimal mode of mechanical ventilation (with oxygenation in mind) is not capable of exchanging enough carbon dioxide. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs.
In acute respiratory distress syndrome (ARDS), decreasing the tidal volume on the ventilator (usually 8-12 mL/kg) to 4-6 mL/kg may decrease barotrauma by decreasing ventilatory peak airway pressures and leads to improved respiratory recovery. Hypercapnia (increased pCO2) sometimes needs to be tolerated in order to achieve these lower tidal volumes. The permissive hypercapnia leads to respiratory acidosis which might have negative side effects, but given that the patient is in ARDS, improving ventilatory function is more important.
Since hypoxemia is a major life threatening condition and hypercapnia is not, one might choose to accept the latter. Hence the term, "permissive hypercapnia."
Altogether, the negative side effects of permissive hypercapnia may outweigh the benefits. For that reason, the implementation of extracorporeal CO2 removal (iLA Membrane Ventilator, Novalung) at an early stage of ARDS, has become a well established standard to allow for protective ventilation and avoid respiratory acidosis.
Symptoms
Symptoms of early hypercapnia (i.e. where PaCO2 is elevated but not extremely so) include flushed skin, full pulse, extrasystoles, muscle twitches, hand flaps, and possibly a raised blood pressure. In severe hypercapnia (generally PaCO2 greater than 10 kPa or 75 mmHg), symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death. other discription about permissive hypercapnia in ARDS patient Mechanical ventilation using high tidal volume (VT) and transpulmonary pressure can damage the lung, causing ventilator-induced lung injury. Permissive hypercapnia, a ventilatory strategy for acute respiratory failure in which the lungs are ventilated with a low inspiratory volume and pressure, has been accepted progressively in critical care for adult, pediatric, and neonatal patients requiring mechanical ventilation and is one of the central components of current protective ventilatory strategies.
Permissive hypercapnic ventilation (PHV)
Source:http://www.uptodate.com/contents/permissive-hypercapnic-ventilation
INTRODUCTION
Read more...
Permissive hypercapnic ventilation (PHV) is a strategy of mechanical ventilation that accepts deliberate alveolar hypoventilation [1]. Its primary purpose is to allow ventilator changes that reduce alveolar pressure and its associated risks, such as pulmonary barotrauma, ventilator-associated lung injury, and hypotension. Hypercapnic acidosis is a consequence of this strategy and not a goal.
Patient selection, efficacy, and potential harms of PHV are discussed in this topic. In addition, the strategy itself is described. Use of PHV in patients with acute respiratory distress syndrome and asthma is reviewed separately. (See "Mechanical ventilation in acute respiratory distress syndrome" and "Mechanical ventilation in adults with acute exacerbations of asthma".)
PATIENT SELECTION
Selecting patients for PHV requires careful consideration of the indications and contraindications, which are discussed in this section.
Indications — PHV is indicated in situations where decreasing the minute ventilation (ie, lowering the tidal volume or respiratory rate) may be beneficial. It is most commonly utilized in patients with acute lung injury or acute respiratory distress syndrome (collectively referred to as ARDS in this review), an acute exacerbation of asthma, or an acute exacerbation of chronic obstructive pulmonary disease (COPD).
- ARDS — Low tidal volume ventilation improves important clinical outcomes in patients with ARDS. The respiratory rate is routinely increased during low tidal volume ventilation in an effort to maintain an adequate minute ventilation. However, the increased respiratory rate may be insufficient to compensate for the low tidal volumes and hypercapnic acidosis may develop. PHV is indicated in this situation, rather than abandoning low tidal volume ventilation. (See "Mechanical ventilation in acute respiratory distress syndrome", section on 'Low tidal volume ventilation'.)
- Asthma — Widespread bronchoconstriction reduces expiratory airflow during an asthma exacerbation. Auto-PEEP will develop if the expiratory airflow is reduced to such a degree that the next breath is initiated prior to the completion of expiration. The expiratory time should be prolonged in this situation, which can be accomplished by increasing the inspiratory flow rate, decreasing the tidal volume, or decreasing the respiratory rate. Lowering the tidal volume or respiratory rate will decrease the minute ventilation and may result in hypercapnic acidosis. PHV is indicated in this situation, rather than accepting significant auto-PEEP. (See "Mechanical ventilation in adults with acute exacerbations of asthma".)
- COPD — Patients with COPD are similarly at risk for auto-PEEP during mechanical ventilation. PHV is indicated if efforts to reduce auto-PEEP result in hypercapnic acidosis, as described above for patients with an asthma exacerbation. (See "Positive end-expiratory pressure (PEEP)", section on 'Auto (intrinsic) PEEP'.)
PEEP
Source:http://www.uptodate.com/contents/positive-end-expiratory-pressure-peep?source=see_link&anchor=H9#H9
Positive end-expiratory pressure (PEEP) is the alveolar pressure above atmospheric pressure that exists at the end of expiration. There are two types of PEEP:
PEEP that is provided by a mechanical ventilator is referred to as applied PEEP (also called extrinsic PEEP)
PEEP that is secondary to incomplete expiration is referred to as auto-PEEP (also called intrinsic PEEP).
Clinical aspects of PEEP are discussed in this topic review. The strategy of high PEEP that has been investigated in patients with acute lung injury or acute respiratory distress syndrome is described separately. (See "Mechanical ventilation in acute respiratory distress syndrome", section on 'High PEEP'.)
APPLIED (EXTRINSIC) PEEP
Applied PEEP is usually one of the first ventilator settings chosen when mechanical ventilation is initiated. It is set directly on the ventilator. (See "Overview of mechanical ventilation", section on 'Initiation'.)
Indications — A small amount of applied PEEP (3 to 5 cmH2O) is indicated for most patients undergoing mechanical ventilation because it mitigates end-expiratory alveolar collapse, a consequence of the endotracheal tube bypassing the glottic apparatus [1]. Such low levels of applied PEEP are occasionally referred to as physiologic PEEP, while higher levels are called supraphysiologic PEEP
Basics Ventilator Setting
Oxygenation(02)=> FiO2 and PEEP
Ventilation (CO2)=> TV (tidal volume)and RR (resp.rate)
Minute Ventilation=> TV x RR (normal 5-8L/min)
CPAP
BiPAP
initial:IPAP= 10-12 cmH2O
EPAP= 5-7 cmH2o
then adjust IPAP to 15-20 cmH2O
PAW=airway pressure
PIP= Peak aiway pressure (normal <45 cmH20 )
Pplat= Plateu pressure (normal 30-35 cmH20)
Recommendation:
initial:
CMV...for paralysed patient
AC...for paralysed patient
AC is preferred the CMV
SIMV..for non paralysed patient
PSV...for mild-moderate respiratoy failure and non paralyses patient
TV= 7-8ml/kg
RR=10-12
PEEP= 2-5 cmH20
What is the Plateau Pressure?
Source::http://www.ccmtutorials.com/rs/mv/platpres.htm
The plateau pressure is the pressure applied (in positive pressure ventilation) to the small airways and alveoli. It is believed that control of the plateau pressure is important, as excessive stretch of alveoli has been implicated as the cause of ventilator induced lung injury. The peak pressure is the pressure measured by the ventilator in the major airways, and it strongly reflects airways resistance. For example, in acute severe asthma, there is a large gradient between the peak pressure (high) and the plateau pressure (normal).
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In pressure controlled ventilation, the pressure limit is (usually) the plateau pressure due to the dispersion of gas in inspiration. In volume control, the pressure measured (the PAW) by the ventilator is the peak airway pressure, which is really the pressure at the level of the major airways. To know the real airway pressure, the plateau pressure which is applied at alveolar level, the volume breath must be made to simulate a pressure breath. An inspiratory hold (0.5 to 1 second) is applied, and the airway pressure, from the initial peak, drops down to a plateau. The hold represents a position of no flow.
The figure above is a waveform of a patient on volume control ventilation with a 0.8 second inspiratory hold.
Overview of Mechanical Ventilation
Source:http://www.merckmanuals.com/professional/sec06/ch065/ch065b.html Mechanical ventilation can be noninvasive, involving various types of face masks, or invasive, involving endotracheal intubation. Selection and use of appropriate techniques require an understanding of respiratory mechanics. Indications: There are numerous indications for endotracheal intubation and mechanical ventilation (see Table 1: Respiratory Arrest: Situations Requiring Airway Control Respiratory Mechanics Normal inspiration generates negative intrapleural pressure, which creates a pressure gradient between the atmosphere and the alveoli, resulting in air inflow. In mechanical ventilation, the pressure gradient is the result of increased (positive) pressure of the air source. Peak airway pressure is measured at the airway opening (Pao) and is routinely displayed by mechanical ventilators. It represents the total pressure needed to push a volume of gas into the lung and is composed of pressures resulting from inspiratory flow resistance (resistive pressure), the elastic recoil of the lung and chest wall (elastic pressure), and the alveolar pressure present at the beginning of the breath (positive end-expiratory pressure [PEEP]—see also Fig. 1: Respiratory Failure and Mechanical Ventilation: Components of airway pressure during mechanical ventilation, illustrated by an inspiratory-hold maneuver. Resistive pressure is the product of circuit resistance and airflow. In the mechanically ventilated patient, resistance to airflow occurs in the ventilator circuit, the endotracheal tube, and most importantly, the patient's airways. Note that even when these factors are constant, an increase in airflow increases resistive pressure. Fig. 1 Components of airway pressure during mechanical ventilation, illustrated by an inspiratory-hold maneuver. PEEP = positive end-expiratory pressure. Elastic pressure is the product of the elastic recoil of the lungs and chest wall (elastance) and the volume of gas delivered. For a given volume, elastic pressure is increased by increased lung stiffness (as in pulmonary fibrosis) or restricted excursion of the chest wall or diaphragm (eg, tense ascites, massive obesity). Because elastance is the inverse of compliance, high elastance is the same as low compliance. End-expiratory pressure in the alveoli is normally the same as atmospheric pressure. However, when the alveoli fail to empty completely because of airway obstruction, airflow limitation, or shortened expiratory time, end-expiratory pressure may be positive relative to the atmosphere. This pressure is called intrinsic PEEP or autoPEEP to differentiate it from externally applied (therapeutic) PEEP, which is set by adjusting the mechanical ventilator or by adding a mask to the airway that applies positive pressure throughout the respiratory cycle. Any elevation in peak airway pressure (eg, > 25 cm H2O) should prompt measurement of the end-inspiratory pressure (plateau pressure) by an end-inspiratory hold maneuver to determine the relative contributions of resistive and elastic pressures. The maneuver keeps the exhalation valve closed for an additional 0.3 to 0.5 sec after inspiration, delaying exhalation. During this time, airway pressure falls from its peak value as airflow ceases. The resulting end-inspiratory pressure represents the elastic pressure once PEEP is subtracted (assuming the patient is not making active inspiratory or expiratory muscle contractions at the time of measurement). The difference between peak and plateau pressure is the resistive pressure. Elevated resistive pressure (eg, > 10 cm H2O) suggests the endotracheal tube has been kinked or plugged with secretions or the presence of an intraluminal mass, increased intraluminal secretions, or bronchospasm. An increase in elastic pressure (eg, > 10 cm H2O) suggests decreased lung compliance from edema, fibrosis, or lobar atelectasis; large pleural effusions, pneumothorax or fibrothorax; extrapulmonary restriction as may arise from circumferential burns or other chest wall deformity, ascites, pregnancy, or massive obesity; or a tidal volume too large for the amount of lung being ventilated (eg, a normal tidal volume being delivered to a single lung because of malpositioning of the endotracheal tube). Intrinsic PEEP can be measured in the passive patient through an end-expiratory hold maneuver. Immediately before a breath, the expiratory port is closed for 2 sec. Flow ceases, eliminating resistive pressure; the resulting pressure reflects alveolar pressure at the end of expiration (intrinsic PEEP). A nonquantitative method of identifying intrinsic PEEP is to inspect the expiratory flow tracing. If expiratory flow continues until the next breath, or the patient's chest fails to come to rest before the next breath, intrinsic PEEP is present. The consequences of elevated intrinsic PEEP include increased inspiratory work of breathing and decreased venous return, which may result in decreased cardiac output and hypotension. The demonstration of intrinsic PEEP should prompt a search for causes of airflow obstruction (eg, airway secretions, bronchospasm); however, a high minute ventilation (>20 L/min) alone can result in intrinsic PEEP in a patient with no airflow obstruction. If the cause is airflow limitation, intrinsic PEEP can be reduced by shortening inspiratory time (ie, increasing inspiratory flow) or reducing the respiratory rate, thereby allowing a greater fraction of the respiratory cycle to be spent in exhalation. Means and Modes of Mechanical Ventilation Mechanical ventilators are typically volume or pressure cycled; some newer models combine features of both. Because pressures and volumes are directly linked by the pressure-volume curve, any given volume will correspond to a specific pressure, and vice versa, regardless of whether the ventilator is pressure or volume cycled. Adjustable ventilator settings differ with mode but include respiratory rate, tidal volume, trigger sensitivity, flow rate, waveform, and inspiratory/expiratory (I/E) ratio. Volume-cycled ventilation: In this mode, which includes assist-control (A/C) and synchronized intermittent mandatory ventilation (SIMV), the ventilator delivers a set tidal volume. The resultant airway pressure is not fixed but varies with the resistance and elastance of the respiratory system and with the flow rate selected. A/C ventilation is the simplest and most effective means of providing full mechanical ventilation. In this mode, each inspiratory effort beyond the set sensitivity threshold triggers delivery of the fixed tidal volume. If the patient does not trigger the ventilator frequently enough, the ventilator initiates a breath, ensuring the desired minimum respiratory rate. SIMV also delivers breaths at a set rate and volume that is synchronized to the patient's efforts. In contrast to A/C, however, patient efforts above the set respiratory rate are unassisted, although the intake valve opens to allow the breath. This mode remains popular, despite the fact that it neither provides full ventilator support as does A/C nor facilitates liberating the patient from mechanical ventilation. Pressure-cycled ventilation: This form of mechanical ventilation includes pressure control ventilation (PCV), pressure support ventilation (PSV), and several noninvasive modalities applied via a tight-fitting face mask. In all of these, the ventilator delivers a set inspiratory pressure. Hence, tidal volume varies depending on the resistance and elastance of the respiratory system. In this mode, changes in respiratory system mechanics can result in unrecognized changes in minute ventilation. Because it limits the distending pressure of the lung, this mode can theoretically benefit patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS); however, no clear clinical advantage over A/C has been shown. Pressure control ventilation is similar to A/C; each inspiratory effort beyond the set sensitivity threshold delivers full pressure support maintained for a fixed inspiratory time. A minimum respiratory rate is maintained. In pressure support ventilation, a minimum rate is not set; all breaths are triggered by the patient. Pressure is typically cut off when back-pressure causes flow to drop below a certain point. Thus, a longer or deeper inspiratory effort by the patient results in a larger tidal volume. This mode is commonly used to liberate patients from mechanical ventilation by letting them assume more of the work of breathing. However, no studies indicate that this approach is more successful. Noninvasive positive pressure ventilation (NIPPV): NIPPV is the delivery of positive pressure ventilation via a tight-fitting mask that covers the nose or both the nose and mouth. Because of its use in spontaneously breathing patients, it is primarily applied as a form of PSV, although volume control can be used. NIPPV can be given in the form of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP). In CPAP, constant pressure is maintained throughout the respiratory cycle with no additional inspiratory support. With BIPAP, the physician sets both the expiratory positive airway pressure (EPAP) and the inspiratory positive airway pressure (IPAP), with respirations triggered by the patient. Because the airway is unprotected, aspiration is possible, so patients must have adequate mentation and airway protective reflexes and no imminent indication for surgery or transport off the floor for prolonged procedures. NIPPV should be avoided in patients who are hemodynamically unstable or those with evidence of impaired gastric emptying, such as occurs with ileus, bowel obstruction, or pregnancy. In such circumstances, the swallowing of large quantities of air may result in vomiting and life-threatening aspiration. Indications for conversion to endotracheal intubation and conventional mechanical ventilation include the development of shock or frequent arrhythmias, myocardial ischemia, and transport to a cardiac catheterization laboratory or surgical suite where control of the airway and full ventilatory support are desired. Obtunded patients and those with copious secretions are not good candidates. Also, IPAP must be set below esophageal opening pressure (20 cm H2O) to avoid gastric insufflation. NIPPV can be used in the outpatient setting. For example, CPAP is often used for patients with obstructive sleep apnea (see Sleep Apnea: Obstructive Sleep Apnea), whereas BIPAP can be used for those with concomitant central sleep apnea (see Sleep Apnea: Central Sleep Apnea) and obstructive sleep apnea or for chronic ventilation in patients with progressive neuromuscular diseases. Ventilator settings: Ventilator settings are tailored to the underlying condition, but the basic principles are as follows. Tidal volume and respiratory rate set the minute ventilation. Too high a volume risks overinflation; too low a volume risks atelectasis. Too high a rate risks hyperventilation and respiratory alkalosis along with inadequate expiratory time and autoPEEP; too low a rate risks inadequate minute ventilation and respiratory acidosis. A tidal volume of 8 to 10 mL/kg ideal body weight (see Respiratory Failure and Mechanical Ventilation: Initial Ventilator Management in ALI/ARDS Sensitivity adjusts the level of negative pressure required to trigger the ventilator. A typical setting is –2 cm H2O. Too high a setting will cause weak patients to be unable to trigger a breath. Too low a setting may lead to overventilation by causing the machine to auto-cycle. Patients with high levels of autoPEEP may have difficulty inhaling deeply enough to achieve a sufficiently negative intra-airway pressure. The ratio of the time spent in inhalation versus that spent in exhalation (I:E ratio) can be adjusted in some modes of ventilation. A normal setting for patients with normal mechanics is 1:3. Patients with asthma or COPD exacerbations should have ratios of 1:4 or even more to limit the degree of autoPEEP. The inspiratory flow rate can be adjusted in some modes of ventilation (ie, either the flow rate or the I:E ratio can be adjusted, not both). The inspiratory flow should generally be set at about 60 L/min but can be increased up to 120 L/min for patients with airflow limitation to facilitate having more time in exhalation, thereby limiting autoPEEP. Fio2 is initially set at 1.0 and is subsequently decreased to the lowest level necessary to maintain adequate oxygenation. PEEP can be applied in any ventilator mode. PEEP increases end-expired lung volume and reduces airspace closure at the end of expiration. Most patients undergoing mechanical ventilation may benefit from the application of PEEP at 5 cm H2O to limit the atelectasis that frequently accompanies endotracheal intubation, sedation, paralysis, and/or supine positioning. Higher levels of PEEP improve oxygenation in disorders such as cardiogenic pulmonary edema and ARDS. PEEP permits use of lower levels of Fio2 while preserving adequate arterial oxygenation. This may be important in limiting the lung injury that may result from prolonged exposure to a high Fio2 (≥ 0.6). PEEP increases intrathoracic pressure and thus may impede venous return, provoking hypotension in the hypovolemic patient, and may overdistend portions of the lung, thereby causing ventilator-associated lung injury (VALI). By contrast, if PEEP is too low, it may result in cyclic airspace opening and closing, which in turn may also cause VALI from the resultant repetitive shear forces. Patient positioning: Mechanical ventilation is typically done with the patient in the semi-upright position. However, in patients with ALI/ARDS, prone positioning may result in better oxygenation primarily by creating more uniform ventilation. Uniform ventilation reduces the amount of lung that has no ventilation (ie, the amount of shunt), which is generally greatest in the dorsal and caudal lung regions, while having minimal effects on perfusion distribution. Although many investigators advocate a trial of prone positioning in patients with ALI/ARDS who require high levels of PEEP (eg, > 12 cm H2O) and Fio2 (eg, > 0.6), trials have not shown any improvement in mortality with this strategy. Prone positioning is contraindicated in patients with spinal instability or increased intracranial pressure. This position also requires concerted effort by the ICU staff to avoid complications, such as dislodgement of the endotracheal tube or intravascular lines. Sedation and comfort: Although some patients tolerate mechanical ventilation via endotracheal tube without sedatives, most require continuous IV administration of sedatives (eg, propofol Neuromuscular blocking agents are now rarely used in patients undergoing mechanical ventilation because of the risk of prolonged neuromuscular weakness and the need for continuous heavy sedation. Exceptions include failure to tolerate some of the more sophisticated and complicated modes of mechanical ventilation and to prevent shivering when cooling is used after cardiac arrest. Complications and safeguards: Complications can be divided into those resulting from endotracheal intubation, from mechanical ventilation itself, or from prolonged immobility and inability to eat normally. The presence of an endotracheal tube causes risk of sinusitis (which is rarely of clinical importance), ventilator-associated pneumonia (see Pneumonia: Hospital-Acquired Pneumonia), tracheal stenosis, vocal cord injury, and rarely tracheal-esophageal or tracheal-vascular fistula. Purulent tracheal aspirate in a febrile patient who has an elevated WBC count > 48 h after ventilation has begun suggests ventilator-associated pneumonia. Complications of ongoing mechanical ventilation itself include pneumothorax, O2 toxicity, hypotension, and VALI. If acute hypotension develops in the mechanically ventilated patient, particularly when accompanied by tachycardia and/or a sudden increase in peak inspiratory pressure, tension pneumothorax must always be considered; patients with such findings should immediately have a chest examination and a chest x-ray (or immediate treatment if examination is confirmatory). More commonly, however, hypotension is a result of sympathetic lysis from sedatives or opioids used to facilitate intubation and ventilation. Hypotension can also be caused by decreased venous return from high intrathoracic pressure in patients receiving high levels of PEEP or in those with high levels of intrinsic PEEP from asthma or COPD. If there are no physical findings suggestive of tension pneumothorax, and ventilation-related causes of hypotension are a possible etiology, pending a portable chest x-ray, the patient may be disconnected from the ventilator and gently bagged manually at 2 to 3 breaths/min with 100% O2 while fluids are infused (eg, 500 to 1000 mL of 0.9% saline in adults, 20 mL/kg in children). An immediate improvement suggests a ventilation-related cause, and ventilator settings should be adjusted accordingly. Relative immobility increases the risk of venous thromboembolic disease, skin breakdown, and atelectasis. Most hospitals have standardized protocols to reduce complications. Elevating the head of the bed to > 30° decreases risk of ventilator-associated pneumonia, and routine turning of the patient every 2 h decreases the risk of skin breakdown. All patients receiving mechanical ventilation should receive deep venous thrombosis prophylaxis, either heparin Last full review/revision August 2007 by Brian K. Gehlbach, MD; Jesse Hall, MD Content last modified August 2007
) but, in general, mechanical ventilation should be considered when there are clinical or laboratory signs that the patient cannot maintain an airway or adequate oxygenation or ventilation. Concerning findings include respiratory rate > 30/min, inability to maintain arterial O2saturation > 90% with fractional inspired O2 (Fio2) > 0.60, and PaCO2 of > 50 mm Hg with pH < 7.25. The decision to initiate mechanical ventilation should be based on clinical judgment that considers the entire clinical situation and should not be delayed until the patient is in extremis.
). Thus:
) is usually appropriate, although some patients with normal lung mechanics (particularly those with neuromuscular disease) benefit from tidal volumes on the high end of this range to prevent atelectasis, whereas patients with ALI/ARDS or acute exacerbations of COPD or asthma may require lower volumes (seeRespiratory Failure and Mechanical Ventilation: Mechanical ventilation in ALI/ARDS). Ideal body weight (IBW) rather than actual body weight is used to determine the appropriate tidal volume for patients with lung disease receiving mechanical ventilation:
, lorazepam
, midazolam
) and analgesics (eg, morphine
,fentanyl
) to minimize stress and anxiety. These drugs also can reduce energy expenditure to some extent, thereby reducing CO2 production and O2 consumption. Doses should be titrated to the desired effect, guided by standard sedation/analgesia scoring systems. Patients undergoing mechanical ventilation for ALI/ARDS typically require higher levels of sedation and analgesia. The use of propofol
for longer than 24 to 48 h requires periodic monitoring of serum triglyceride levels.
5000 units sc bid to tid or low molecular heparin
or, if heparin
is contraindicated, sequential compression devices. To prevent GI bleeding, patients should receive an H2blocker (eg, famotidine
20 mg enterally or IV bid) or sucralfate
(1 g enterally qid). Proton pump inhibitors should be reserved for patients with a preexisting indication or active bleeding. Routine nutritional evaluations are mandatory, and enteral tube feedings should be initiated if ongoing mechanical ventilation is anticipated. Finally, the most effective way to reduce complications of mechanical ventilation is to limit its duration. Daily “sedation vacations” and spontaneous breathing trials help determine the earliest point at which the patient may be liberated from mechanical support.
ARDS-Ventilator
new england journal of medicine, 2000. study on ARDS: low tidal volume ventilation vs traditional ventilation in ARDS by ARDS Network group.
- The one strategy that has proven effective in reducing the duration of mechanical ventilation and improving survival is the use of low tidal volume
ventilation.
- This strategy employs ventilator-delivered tidal volumes of 6 mL per kilogram of predicted body weight, with an additional goal of maintaining plateauairway pressures < 30 cm H2O.
- Part of this protocol dictates the use of certain combinations of inspired oxygen (FiO2) and PEEP.
- Because use of this protocol has been shown to improve outcomes for ALI/ARDS patients, it should be employed whenever possible in treating these
patients.- Therefore, these FiO2/PEEP combinations should be used to achieve adequate oxygenation:
PaO2/FiO2
PaO2/FiO2:
-Another tool for estimation of oxygenation,
-Normal is 500-600.
-Levels <300 suggest ALI, <200 suggest ARDS
A-a gradient :Formula
It is a useful tool in evaluating how well a patient is oxygenating.
A-a gradient = PAO2 – PaO2 (mmHg)
={(760-47)FiO2 - PaCO2/0.8}-PaO2
* Normal = 10-20 mmHg
Or Normal =age/4 + 4
Elevated A-a gradient is caused by:
V/Q mismatch (eg. Pneumonia, CHF, ARDS)
R-L shunt (eg. PE)
Diffusion abnormalities (eg. Interstitial lung dz)
The 5 Causes of Hypoxemia, #1-3 have an elevated A-a Gradient:
V/Q Mismatch (ex: PNA, CHF, ARDS, atelectasis, etc)
Shunt (ex: PFO, ASD, PE, pulmonary AVMs)
Alveolar Hypoventilation (ex: interstitial lung dz, environmental lung dz, PCP PNA)
Hypoventilation (ex: COPD, CNS d/o, neuromuscular dz, etc)
Low FiO2 (ex: high altitude)
Creatine Clearance:Formula
Creatine Clearance=
(140-Age) x Kg x constant (M=1.23,F=1.04) / serum creatine (umol/l)
Classification of Pelvic Fractures :Young – Burgess System (1987)
-differentiates fractures patterns due to trauma based on mechanism of injury and direction of causative force. Incidence of complications (i.e., urogenital and vascular) is correlated with the fracture pattern
Lateral compression (LC)
Anterior-post. Compression ( APC)
Vertical shear (VS
Monday, June 20, 2011
Early Stroke(CT Finding)
STROKEN
SHIFT-midline shift
THROMBOSIS- ischemic(infarct)
RIBBON-Loss of the insular ribbon
O-obliterated internal capsule
K
NORMAL
tPA Inclusion and Exclusion Criteria
Source:http://www.acep.org/content.aspx?id=29936
tPA Inclusion and Exclusion Criteria
tPA Indications
These statements must be true in order to consider tPA administration:
Ischemic stroke onset within 3 hours of drug administration.
Measurable deficit on NIH Stroke Scale examination.
Patient's computed tomography (CT) does not show hemorrhage or nonstroke cause of deficit.
Patient's age is >18 years.
tPA Contraindications
Do NOT administer tPA if any of these statements are true:
Patient's symptoms are minor or rapidly improving.
Patient had seizure at onset of stroke.
Patient has had another stroke or serious head trauma within the past 3 months.
Patient had major surgery within the last 14 days.
Patient has known history of intracranial hemorrhage.
Patient has sustained systolic blood pressure >185 mmHg.
Patient has sustained diastolic blood pressure >110 mmHg.
Aggressive treatment is necessary to lower the patient's blood pressure.
Patient has symptoms suggestive of subarachnoid hemorrhage.
Patient has had gastrointestinal or urinary tract hemorrhage within the last 21 days.
Patient has had arterial puncture at noncompressible site within the last 7 days.
Patient has received heparin with the last 48 hours and has elevated PTT.
Patient's prothrombin time (PT) is >15 seconds.
Patient's platelet count is <100,000 uL.
Patient's serum glucose is <50 mg/dL or >400 mg/dL.
tPA Relative Contraindications
If either of the following statements is true, use tPA with caution:
Patient has a large stroke with NIH Stroke Scale score >22.
Patient's CT shows evidence of large middle cerebral artery (MCA) territory infarction (sulcal effacement or blurring of gray-white junction in greater than 1/3 of MCA territory).
TOAST-STROKE
The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).[2][17]
LMN Lesion
A lower motor neuron lesion is a lesion which affects nerve fibers traveling from the anterior horn of the spinal cord to the relevant muscle(s) -- the lower motor neuron.[1]
One major characteristic used to identify a lower motor neuron lesion is flaccid paralysis - paralysis accompanied by muscle loss. This is in contrast to a upper motor neuron lesion, which often presents with spastic paralysis - paralysis accompanied by severe hypertonia.
Symptoms
Muscle paresis or paralysis
fibrillations
fasciculations
hypotonia or atonia- Tone is not velocity dependent.
Areflexia or hyporeflexia -Along with deep reflexes even cutaneous reflexes are also decreased or absent
Strength -weakness is limited to segmental or focal pattern, Root innervated pattern
The extensor Babinski reflex is usually absent. Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are usually seen immediately following an insult. Muscle wasting, fasciculations and fibrillations are typically signs of end-stage muscle denervation and are seen over a longer time period. Another feature is the segmentation of symptoms - only muscles innervated by the damaged nerves will be symptomatic.
Etiology
Most common causes of lower motor neuron injuries are trauma to peripheral nerves that sever the axons and poliomyelitis - a virus that selectively attacks ventral horn cells. Disuse atrophy of the muscle occurs i.e,shrinkage of muscle fibre finally replaced by fibrous tissue(fibrous muscle) Other causes include Guillain-Barré syndrome, botulism and cauda equina syndrome.
Differential Diagnosis
Myasthenia gravis - synaptic transmission at motor end-plate is impaired
Muscular dystrophy - contraction of muscle is impaired due to a cellular defect
UMN
An upper motor neuron starts in the motor cortex of the brain and terminates within the medulla (another part of the brain) or within the spinal cord. So, an UMN disorder would include injury, disease or disturbance within this pathway from or within the brain and to the spinal cord (Photo 6). Some examples of diagnoses of UMN disorders are: Spinal Cord Injury, Multiple Sclerosis, Stroke and Primary Muscle Disease. UMN disorders involve various degrees of spasticity and synergy patterns. The synergistic pattern will be an extensor or flexor synergy pattern.UPPER MOTOR NEURON DISORDERS (UMN)
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