Oxygenation Kills: Part I
Hemodynamic Kills: Part 2
Alliteration aside, I have wondered for sometime why EMS in general has not adopted some of the scoring criteria for pulmonary embolism. Emergency medicine in general is very algorithm based and paramedics love algorithms. We are not doctors but we can act like them especially when we have a patient that we think might be having a PE. By utilized the 2 scores that we will discuss we can greatly improve patient treatment and continuing of care for our customers.
This week we will discuss all things PE. Make sure you listen to the PE podcasts so that you get some more details about the pathophysiology, treatment, recognition and ECG findings in PE.
So, the second you have a patient and the thought of PE crosses your nugget even for an instant, consider adding this to your assessment
There are many calculators to help you with this for example (Wells Criteria Calculator). What you are going to do is ask yourself and the patient these questions and score it. The traditional scoring method will lead you to prognostics.
Generally if the score is >3 than PE might still be in the cards. Look for other things such as ECG findings to help you which we will discuss in another post. If the score is ❤ AND your gut feeling tells you that the probability is low you can move onto the next scoring method.
PERC Rule (Pulmonary Rule Out Criteria) PERC Rule Calculator
Age < 50 years
Pulse < 100 bpm
SaO2 > 94%
No unilateral leg swelling
No recent trauma or surgery
No prior PE or DVT
No hormone use
If you assess your patient to have NONE of the above than you have essentially ruled out PE. A menumonic that I was taught in the past to remember this is HAD CLOTS: Hormone, Age >50, DVT/PE history, Coughing blood, Leg swelling, O2 >95%, Tachycardia 100+, Surgery/trauma <28 d.
Keeping this stuff in mind will help you manage your patient better and recognize treatment modalities and transport considerations.
Hello all! I sincerely apologize for being absent for so long but I have been extremely busy with my new job and some personal things going on in my life. But, I am going to start posting some material here in the next coming weeks.I am looking forward to getting this back up and running and I appreciate everyone’s patience. I am also going to be starting my podcasts again that should be available on Itunes shortly. Stay tuned…I promise it will be worth the wait.
This is a lecture we did on Respiratory for my medic students. It is gonna be a multi-part series and I hope you like it!
CORRECTION: (Thanks to the point from my student Post, awesome job man!!!!)
The part where preload is addressed is incorrect. During normal negative pressure ventilation, preload actually increases as opposed to PPV where preload will decrease. LVEDP will decrease during negative pressure ventilation but the net effect is an overall decrease.
Pressures in the right atrium and thoracic vena cava are very dependent on intrapleural pressure (Ppl ), which is the pressure within the thoracic space between the organs (lungs, heart, vena cava) and the chest wall. During inspiration, the chest wall expands and the diaphragm descends (see animated figure). This makes the Ppl become more negative, which leads to expansion of the lungs, cardiac chambers (right atrium [RA] and right ventricle [RV]), and the thoracic superior and inferior vena cava (SVC and IVC, respectively). This expansion causes the intravascular and intracardiac pressures (e.g., right atrial pressure) to fall. Because the pressure inside the cardiac chambers falls less than the Ppl, the transmural pressure (pressure inside the heart chamber minus the Ppl) increases, which leads to cardiac chamber expansion and an increase in cardiac preload and stroke volume through the Frank-Starling mechanism. Furthermore, as right atrial pressure falls during inspiration, the pressure gradient for venous return to the right ventricle increases. During expiration, the opposite occurs although the dynamics are such that the net effect of respiration is that increasing the rate and depth of ventilation facilitates venous return and ventricular stroke volume.
The left side of the heart responds differently to the respiratory cycle. During inspiration, expansion of the lungs and pulmonary tissues causes pulmonary blood volume to increase, which transiently decreases the flow of blood from the lungs to the left atrium. Therefore, left ventricular filling actually decreases during inspiration. In contrast, during expiration, lung deflation causes flow to increase from the lungs to the left atrium, which increases left ventricular filling. The net effect of increased rate and depth of respiration, however, is an increase in left ventricular stroke volume and cardiac output.
Tired of getting stopped on those ABG questions on the FP-C exam. Well watch this and then go to the following sites for practice and download the PDF! You will no doubt master ABG analysis once and for all!
Capnography is the monitoring of the concentration or partial pressure of carbon dioxide (CO2) in the respiratory gases. Its main development has been as a monitoring tool for use during anaesthesia and intensive care. It is usually presented as a graph of expiratory CO2 plotted against time, or, less commonly, but more usefully, expired volume. The plot may also show the inspired CO2, which is of interest when rebreathing systems are being used.
The capnogram is a direct monitor of the inhaled and exhaled concentration or partial pressure of CO2, and an indirect monitor of the CO2 partial pressure in the arterial blood. In healthy individuals, the difference between arterial blood and expired gas CO2 partial pressures is very small. In the presence of most forms of lung disease, and some forms of congenital heart disease (the cyanotic lesions) the difference between arterial blood and expired gas increases and can exceed 1 kPa.
During anaesthesia, there is interplay between two components: the patient and the anaesthesia administration device (which is usually a breathing circuit and a ventilator). The critical connection between the two components is either an endotracheal tube or a mask, and CO2 is typically monitored at this junction. Capnography directly reflects the elimination of CO2 by the lungs to the anaesthesia device. Indirectly, it reflects the production of CO2 by tissues and the circulatory transport of CO2 to the lungs.
When expired CO2 is related to expired volume rather than time, the area beneath the curve represents the volume of CO2 in the breath, and thus over the course of a minute, this method can yield the CO2 minute elimination, an important measure of metabolism. Sudden changes in CO2 elimination during lung or heart surgery usually imply important changes in cardiorespiratory function.
Capnographs usually work on the principle that CO2 absorbs infra-red radiation. A beam of infra-red light is passed across the gas sample to fall on a sensor. The presence of CO2 in the gas leads to a reduction in the amount of light falling on the sensor, which changes the voltage in a circuit. The analysis is rapid and accurate, but the presence of nitrous oxide in the gas mix changes the infra-red absorption via the phenomenon of collision broadening. This must be corrected for. Measuring the CO2 in human breath by measuring its infra-red absorptive power was established as a reliable technique by John Tyndall in 1864, though 19th and early 20th century devices were too cumbersome for everyday clinical use.
Anaphylaxis is defined as “a serious allergic reaction that is rapid in onset and may cause death”. It typically results in a number of symptoms including throat swelling, an itchy rash, and low blood pressure. Common causes include insect bites, foods, and medications.
On a pathophysiologic level, anaphylaxis is due to the release of mediators from certain types of white blood cells triggered either by immunologic or non-immunologic mechanisms. It is diagnosed based on the presenting symptoms and signs. The primary treatment is injection of epinephrine, with other measures being complementary.
Acute Asthma (CLICK HERE)
An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness. While these are the primary symptoms of asthma, some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.
Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. A blue color of the skin and nails may occur from lack of oxygen.
In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best. Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best. Insufficient levels of vitamin D are linked with severe asthma attacks.
Airway management is the most important skill for an emergency practitioner to master because failure to secure an adequate airway can quickly lead to death or disability. Endotracheal intubation using rapid sequence intubation (RSI) is the cornerstone of emergency airway management.
The decision to intubate is sometimes difficult; clinical experience is required to recognize signs of impending respiratory failure. Patients who require intubation have at least one of the following 5 indications: 1) inability to maintain airway patency, 2) inability to protect the airway against aspiration, 3) ventilatory compromise, 4) failure to adequately oxygenate pulmonary capillary blood, 5) anticipation of a deteriorating course that will eventually lead to the inability to maintain airway patency or protection.
RSI is the preferred method of endotracheal intubation in the emergency department (ED) because it results in rapid unconsciousness (induction) and neuromuscular blockade (paralysis). This is important in patients who have not fasted and are at much greater risk for vomiting and aspiration. To this end, the goal of RSI is to intubate the trachea without having to use bag-valve-mask (BVM) ventilation, which is often necessary when attempting to achieve intubating conditions with sedative agents alone (eg, midazolam, diazepam). Instead of titrating to effect, RSI involves administration of weight-based doses of an induction agent (eg, etomidate) immediately followed by a paralytic agent (eg, succinylcholine, rocuronium) to render the patient unconscious and paralyzed within 1 minute. This method has been proven safe and effective in EDs over the past 2 decades, and it is considered the standard of care.
The class is determined by looking at the oral cavity as the patient protrudes the tongue, and tongue size is described relative to oropharyngeal size. The test is conducted with the patient in the tongue wide open and relaxed and protruding to the maximum. The subsequent classification is based on the pharyngeal structures that are visible.
Scoring is as follows:
Class 1: Full visibility of tonsils, uvula, and soft palate.
Class 2: Visibility of hard and soft palate, upper portion of tonsils, and uvula.
Class 3: Soft and hard palate and base of the uvula are visible.
Class 4: Only hard palate visible.