medic001918

I believe the book is called The Missing Protocol and they have a website. www.themissingprotocol.com I have read the book, and while being a dry read there is some good information to be had in it. Shane NREMT-P

+1 on the risk of diving injury. You're not supposed to fly for 24 hours after diving due to the build up of gases in the body. The sudden change in pressure with going to different elevations is enough to bring on a case of the bends, or decompression sickness. So please, tell us more about his vacation... Shane NREMT-P

Using your example of an overdose, charcoal is not the universal antidote for all overdoses. And secondly, while it's in my protocol I have to contact medical control for it for some reason. Being that I work in a city, most of the overdoses I do that would warrant it are too close to the hosptial and I can have them in the ED before I can get a doc on the phone. These patients are usually ambulatory and scene times are pretty short (<5min on avg). It's not always as easy as just reaching for the medication on the shelf. Make sure you're doing the most appropriate thing for your patient. Local protocols will dictate many treatments...both minimums and maximums. Shane NREMT-P

Truely a great site. Good find Rid. We can all benefit from sites like that being brought to our attention. Shane NREMT-P

This is a pretty easy and straight forward question. I am responsible for my aspects of prehospital care as I am the one making the decisions. I can't blame anyone else for what I do on a scene provided that I have worked within my protocols to the best of my ability. I'm not sure how many people you'll find willing to admit they should blame someone else for what they have done on a scene. Shane NREMT-P

Great post Marty. It's nice to see that someone was willing to post the entire story for us to see before passing judgement. I agree 100% with your feelings on the matter. Couldn't have said it better myself. Shane NREMT-P

Quality is important, and based on that I would like to think that a paramedic is a higher level of care and with that comes a higher quality of service through increased training and standards. The paramedic vs. EMT horse has been beaten to death repeatedly. The search function will yield many results to this topic of education. Also, let's not forget that the general public doesn't know much of the difference between an EMT and a paramedic, but as professionals we are familiar with the intricate differences. On top of that, I would reasonably expect that anyone coming to handle my emergency situation is going to be trained in the fundamentals of education, those include basic reading, writing and math disciplines. These are critical building blocks of a foundation for a long educational career. With those fundamentals in place, a more complex understanding of many issues can be achieved. And that is a higher standard that we should all adhere to. Shane NREMT-P

Nice work PRPG, the similarities of the two are what I was going for by putting them together in the same thread. Strong work my friend. Shane NRMET-P

I'm curious about something. You found out that he was carrying a weapon, but you never stated if he was doing so legally or illegally? I carry sometimes (legally), and if I'm involved in some kind of medical event as a patient, don't expect me to tell you about it until we're somewhere where there aren't a ton of people around as that just might cause more of an alarm than not saying anything at all. Once you are told about it, it will be happily surrendered to a police officer ONLY and noone else (and that does include a uniformed security person with a CCW). It sounds like your employer doesn't really want you to have the full limited capabilities of being an EMT-B in the first place since they limit how you can perform your assessments. Sounds like a sticky situation to be in that might hold some increased liability since you're hired to be an EMT, but not allowed to practice fully by the casino. While the firearm was present, it doesn't sound as though he had any intent on using it so you probably weren't in as much danger as you thought you were. Looking at it that way, do you ever know how safe or unsafe you really are? At work or not? You never know who might be standing next to you carrying a gun, holding a knife, etc. I know I've done a few calls where it hasn't been an "inner city" guy that used a weapon in a violent manner; just as I've done plenty of calls where it was the "inner city" guy that had an act of violence performed against him. Like I mentioned, I carry sometimes and I usually dress in jeans that fit properly and a button down or t-shirt. You'd never know I had a firearm on me. That's part of the whole "concealed carry" issue. If it's concealed properly, noone is supposed to know you have it. Maybe this call is a good reason to push for some protocol change and allow a little more hands on assessment? Or at least a search for the safety of the employees and the patrons of the casino.

The classic triad as it applies to ectopic pregnancy. While the triad is only about 100% reliable (something that I learned by looking it up again for this thread), prehospitally this could be useful to provide a potentital differential diagnosis. Great information on the first two Ace. Strong work as usual. *The part about the triad is highlighted in bold* Ectopic pregnancy presents a major health problem for women of childbearing age. It is the result of a flaw in human reproductive physiology that allows the conceptus to implant and mature outside the endometrial cavity, which ultimately ends in death of the fetus. Without timely diagnosis and treatment, ectopic pregnancy can become a life-threatening situation. Ectopic pregnancy currently is the leading cause of pregnancy-related death during the first trimester in the United States, accounting for 9% of all pregnancy-related deaths. In addition to the immediate morbidity caused by ectopic pregnancy, the woman's future ability to reproduce may be adversely affected as well. History of the Procedure: Ectopic pregnancy was first described in the 11th century, and, until the middle of the 18th century, it was usually fatal. John Bard reported the first successful surgical intervention to treat an ectopic pregnancy in New York City in 1759. The survival rate in the early 19th century was dismal. One report demonstrated only 5 patients of 30 surviving the abdominal operation. Interestingly, the survival rate in patients who were left untreated was 1 of 3. In the beginning of the 20th century, great improvements in anesthesia, antibiotics, and blood transfusion contributed to the decrease in the maternal mortality rate. In the early half of the 20th century, 200-400 deaths per 10,000 cases were attributed to ectopic pregnancy. In 1970, the Centers for Disease Control and Prevention (CDC) began to record the statistics regarding ectopic pregnancy, reporting 17,800 cases. By 1992, the number of ectopic pregnancies had increased to 108,800. Concurrently, however, the case-fatality rate decreased from 35.5 deaths per 10,000 cases in 1970 to 2.6 per 10,000 cases in 1992. Problem: Ectopic pregnancy is derived from the Greek word ektopos, meaning out of place, and it refers to the implantation of a fertilized egg in a location outside of the uterine cavity, including the fallopian tubes, cervix, ovary, cornual region of the uterus, and the abdominal cavity. This abnormally implanted gestation grows and draws its blood supply from the site of abnormal implantation. As the gestation enlarges, it creates the potential for organ rupture because only the uterine cavity is designed to expand and accommodate fetal development. Ectopic pregnancy can lead to massive hemorrhage, infertility, or death. Frequency: Since 1970, the frequency of ectopic pregnancy has increased 6-fold, and it now occurs in 2% of all pregnancies. An estimated 108,800 ectopic pregnancies in 1992 resulted in 58,200 hospitalizations with an estimated cost of $1.1 billion. Etiology: Multiple factors contribute to the relative risk of ectopic pregnancy. In theory, anything that hampers the migration of the embryo to the endometrial cavity could predispose women to ectopic gestation. The most logical explanation for the increasing frequency of ectopic pregnancy is previous pelvic infection; however, most patients presenting with an ectopic pregnancy have no identifiable risk factor. The following risk factors have been linked with ectopic pregnancy: Pelvic inflammatory disease The most common cause is antecedent infection caused by Chlamydia trachomatis. Patients with chlamydial infection have a range of clinical presentations, from asymptomatic cervicitis to salpingitis and florid pelvic inflammatory disease (PID). More than 50% of women who have been infected are unaware of the exposure. Other organisms causing PID, such as Neisseria gonorrhoeae, increase the risk of ectopic pregnancy. A history of salpingitis increases the risk of ectopic pregnancy 4-fold. The incidence of tubal damage increases after successive episodes of PID (ie, 13% after 1 episode, 35% after 2 episodes, 75% after 3 episodes). History of prior ectopic pregnancy After one ectopic pregnancy, a patient incurs a 7- to 13-fold increase in the likelihood of another ectopic pregnancy. Overall, a patient with prior ectopic pregnancy has a 50-80% chance of having a subsequent intrauterine gestation, and a 10-25% chance of a future tubal pregnancy. History of tubal surgery and conception after tubal ligation Prior tubal surgery has been demonstrated to increase the risk of developing ectopic pregnancy. The increase depends on the degree of damage and the extent of anatomic alteration. Surgeries carrying higher risk of subsequent ectopic pregnancy include salpingostomy, neosalpingostomy, fimbrioplasty, tubal reanastomosis, and lysis of peritubal or periovarian adhesions. Conception after previous tubal ligation increases a women's risk of developing ectopic pregnancies. Thirty-five to 50% of patients who conceive after a tubal ligation are reported to experience an ectopic pregnancy. Failure after bipolar tubal cautery is more likely to result in ectopic pregnancy than occlusion using suture, rings, or clips. Failure is attributed to fistula formation that allows sperm passage. Ectopic pregnancies following tubal sterilizations usually occur 2 or more years after sterilization, rather than immediately after. In the first year, only about 6% of sterilization failures result in ectopic pregnancy. Use of fertility drugs or assisted reproductive technology Ovulation induction with clomiphene citrate or injectable gonadotropin therapy has been linked with a 4-fold increase in the risk of ectopic pregnancy in a case-control study. This finding suggests that multiple eggs and high hormone levels may be significant factors. One study has demonstrated that infertility patients with luteal phase defects have a statistically higher ectopic pregnancy rate than patients whose infertility is caused by anovulation. The risk of ectopic pregnancy and heterotopic pregnancy (ie, pregnancies occurring simultaneously in different body sites) dramatically increases when a patient has used assisted reproductive techniques to conceive, such as in vitro fertilization (IVF) or gamete intrafallopian transfer (GIFT). In a study of 3000 clinical pregnancies achieved through in vitro fertilization, the ectopic pregnancy rate was 4.5%, which is more than double the background incidence. Furthermore, studies have demonstrated that up to 1% of pregnancies achieved through IVF or GIFT can result in a heterotopic gestation, compared to an incidence of 1 in 30,000 pregnancies for spontaneous conceptions. Use of an intrauterine device The presence of an inert copper-containing or progesterone intrauterine device (IUD) traditionally has been thought to be a risk factor for ectopic pregnancy. However, only the progesterone IUD has a rate of ectopic pregnancy higher than that for women not using any form of contraception. The modern copper IUD does not increase the risk of ectopic pregnancy. Nevertheless, if a woman ultimately conceives with an IUD in place, it is more likely to be an ectopic pregnancy. The actual incidence of ectopic pregnancies with IUD use is 3-4%. Increasing age The highest rate of ectopic pregnancy occurs in women aged 35-44 years. A 3- to 4-fold increase in the risk for developing an ectopic pregnancy exists compared to women aged 15-24 years. One proposed explanation involves the myoelectrical activity in the fallopian tube, which is responsible for tubal motility. Aging may result in a progressive loss of myoelectrical activity along the fallopian tube. Smoking Cigarette smoking has been shown to be a risk factor for developing an ectopic pregnancy. Studies have demonstrated elevated risk ranging from 1.6-3.5 times that of nonsmokers. A dose-response effect also has been suggested. Based on laboratory studies in humans and animals, researchers have postulated several mechanisms by which cigarette smoking might play a role in ectopic pregnancies. These mechanisms include one or more of the following: delayed ovulation, altered tubal and uterine motility, or altered immunity. To date, no study has supported a specific mechanism by which cigarette smoking affects the occurrence of ectopic pregnancy. Salpingitis isthmica nodosum Salpingitis isthmica nodosum is defined as the microscopic presence of tubal epithelium in the myosalpinx or beneath the tubal serosa. These pockets of epithelium protrude through the tube, similar to small diverticula. Studies of serial histopathological sections of the fallopian tube have revealed that approximately 50% of patients treated with salpingectomy for ectopic pregnancy have evidence of salpingitis isthmica nodosum. The etiology of salpingitis isthmica nodosum is unclear, but proposed mechanisms include postinflammatory and congenital as well as acquired tubal changes such as observed with endometriosis. Other Other risk factors associated with increased incidence of ectopic pregnancy include previous diethylstilbestrol (DES) exposure, a T-shaped uterus, prior abdominal surgery, failure with progestin-only contraception, and ruptured appendix. Pathophysiology: Most ectopic pregnancies are located in the fallopian tube (see Image 1). The most common site is the ampullary portion of the tube, where over 80% occur. The next most common sites are the isthmic segment of the tube (12%), the fimbria (5%), and the cornual and interstitial region of the tube (2%). Nontubal sites of ectopic pregnancy are a rare occurrence, with abdominal pregnancies accounting for 1.4% of ectopic pregnancies and ovarian and cervical sites accounting for 0.2% each. Clinical: The classic clinical triad of ectopic pregnancy is pain, amenorrhea, and vaginal bleeding. Unfortunately, only 50% of patients present typically. Patients may present with other symptoms common to early pregnancy, including nausea, breast fullness, fatigue, low abdominal pain, heavy cramping, shoulder pain, and recent dyspareunia. Astute clinicians should have a high index of suspicion for ectopic pregnancy in any woman who presents with these symptoms and who presents with physical findings of pelvic tenderness, enlarged uterus, adnexal mass, or tenderness. Remember, however, that only 40-50% of patients with an ectopic pregnancy present with vaginal bleeding, 50% have a palpable adnexal mass, and 75% may have abdominal tenderness. Approximately 20% of patients with ectopic pregnancies are hemodynamically compromised at initial presentation, which is highly suggestive of rupture. Fortunately, using modern diagnostic techniques, most ectopic pregnancies may be diagnosed prior to rupturing. Numerous conditions may have a presentation similar to an extrauterine pregnancy. The most common of these are appendicitis, salpingitis, ruptured corpus luteum cyst or ovarian follicle, spontaneous abortion or threatened abortion, ovarian torsion, and urinary tract disease. Intrauterine pregnancies with other abdominal or pelvic problems such as degenerating fibroids must also be included in the differential diagnosis. Medical therapy Medical therapy involving methotrexate may be indicated in certain patients. A number of factors must be considered. The patient must be hemodynamically stable, with no signs or symptoms of active bleeding or hemoperitoneum. Furthermore, she must be reliable, compliant, and able to return for follow-up. Another factor is size of the gestation, which should not exceed 3.5 cm at its greatest dimension on ultrasound (US) measurement. She should not have any contraindications to the use of methotrexate. Surgical therapy Within the last 2 decades, a more conservative surgical approach to unruptured ectopic pregnancy using minimally invasive surgery has been advocated to preserve tubal function (see Surgical therapy). Laparoscopy has become the recommended approach in most cases. Laparotomy is usually reserved for patients who are hemodynamically unstable or patients with cornual ectopic pregnancies. It also is a preferred method for surgeons inexperienced in laparoscopy and in patients where laparoscopic approach is difficult (eg, secondary to the presence of multiple dense adhesions, obesity or massive hemoperitoneum). In a patient who has completed childbearing and no longer desires fertility, in a patient with a history of an ectopic pregnancy in the same tube, or in a patient with severely damaged tubes, total salpingectomy is the procedure of choice. Expectant management Candidates for successful expectant management are asymptomatic and have no evidence of rupture or hemodynamic instability. Furthermore, they should portray objective evidence of resolution, such as declining bhCG levels. They must be fully compliant and must be willing to accept the potential risks of tubal rupture. Now let's have someone find some information on RHABDOMYOLYSIS!!! And some extra credit for disseminated intravascular coagulation. Had to mention that one before I forgot about it. Shane NREMT-P

Quick simple terms, heorrhagic shock would be the inability to maintain adequate perfusion secondary to a fluid volume loss where cadiogenic shock would be the inability to provide perfusion due to a lack of an effective heart (or pump). While the two conditions may sometimes present similar, the history of the event is usually helpful in distinguishing the two and requires two different treatment modalities. Hemorrhagic Shock...from emedicine.com once again. Background: Shock is a state in which adequate perfusion to sustain the physiologic needs of organ tissues is not present. Many conditions, including sepsis, blood loss, impaired autoregulation, and loss of autonomic tone, may produce shock or shocklike states. Pathophysiology: In hemorrhagic shock, blood loss exceeds the body's ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes. Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic conditions with subacute blood loss. Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen delivery (ie, DO2), and increased oxygen consumption (ie, VO2) by tissues. Lactate levels, the acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and comorbid factors all may affect a patient's response to hemorrhagic shock. Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure. Frequency: * In the US: Accidental injuries are the leading cause of death in individuals aged 1-44 years. History: History taking should address the following: * Specific details of the mechanism of trauma or other cause of hemorrhage are essential. * Inquire about a history of bleeding disorders and surgery. * Prehospital interventions, especially the administration of fluids administered, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information. Physical: Findings at physical examination may include the following: * Head, ears, eyes, nose, and throat o Sources of hemorrhage usually are apparent. o The blood supply of the scalp is rich and can produce significant hemorrhage. o Intracranial hemorrhage usually is insufficient to produce shock, except possibly in very young individuals. * Chest o Hemorrhage into the thoracic cavities (pleural, mediastinal, pericardial) may be discerned at physical examination. Ancillary studies often are required for confirmation. o Signs of hemothorax may include respiratory distress, decreased breath sounds, and dullness to percussion. o Tension hemothorax, or hemothorax with cardiac and contralateral lung compression, produces jugular venous distention and hemodynamic and respiratory decompensation. o With pericardial tamponade, the classic triad of muffled heart sounds, jugular venous distention, and hypotension often is present, but these signs may be difficult to appreciate in the setting of an acute resuscitation. * Abdomen o Injuries to the liver or spleen are common causes of hemorrhagic shock. o Blood irritates to the peritoneal cavity; diffuse tenderness and peritonitis are common when blood is present. However, the patient with altered mental status or multiple concomitant injuries may not have the classic signs and symptoms at physical examination. o Progressive abdominal distention in hemorrhagic shock is highly suggestive of intraabdominal hemorrhage. * Pelvis o Fractures can produce massive bleeding. Retroperitoneal bleeding must be suspected. o Flank ecchymosis may indicate retroperitoneal hemorrhage. * Extremities o Hemorrhage from extremity injuries may be apparent, or tissues may obscure significant bleeding. o Femoral fractures may produce significant blood loss. * Nervous system o Agitation and combativeness may be seen in the initial stages of hemorrhagic shock. o These signs are followed by a progressive decline in level of consciousness due to cerebral hypoperfusion or concomitant head injury. Lab Studies: * Laboratory studies are essential in management of many forms of hemorrhagic shock. Baseline levels are determined frequently, but these infrequently change the initial management after trauma. Serial evaluations of the following can help guide ongoing therapy. o CBC o Prothrombin time and/or activated partial thromboplastin time o Urine o ABGs (Levels reflect acid-base and perfusion status.) * Lactate and base deficit are used in some centers. * Typed and crossmatch packed red blood cells should be obtained immediately. * Fresh frozen plasma and platelets also may be required to correct coagulopathies that develop in severe hemorrhagic shock. Imaging Studies: * Standard radiography o Cervical spine, chest, and pelvis radiographs are the standard screening images for severe trauma. o Other radiographs may be indicated for orthopedic injuries. * Computed tomography o Image the appropriate for region of suspected injury. o CT scanning frequently is the method of choice for evaluating possible intra-abdominal and/or retroperitoneal sources of hemorrhage in stable patients. o Oral contrast material may not increase the diagnostic yield of abdominal CT scanning in blunt trauma. Scanning should not be delayed to administer oral contrast material. * Ultrasonography o Bedside abdominal ultrasonography can be useful for the rapid detection of free intra-abdominal fluid and, sometimes, specific parenchymal injury. o Thoracic ultrasonographic findings can immediately confirm hemothorax or pericardial tamponade. * Directed angiography may be diagnostic and therapeutic. Interventional radiologists have had good success achieving hemostasis in hemorrhage caused by a variety of vessels and organs. Other Tests: * An ECG can be useful for detecting dysrhythmias and cardiac sequelae of shock. Procedures: * Tube thoracostomy is necessary in hemothorax and hemothorax with or without pneumothorax. * Central venous access facilitates fluid resuscitation and monitoring of central venous pressure and is necessary if peripheral intravenous access is inadequate or impossible to obtain. * Diagnostic peritoneal lavage is used to detect intra-abdominal blood, fluid, and intestinal contents. It is sensitive but not specific for abdominal injury. It is not used to evaluate the retroperitoneum, which can hold significant hemorrhage, and does not identify the source of hemorrhage. Prehospital Care: * The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care. * Intravenous access and fluid resuscitation are standard. However, this practice has become controversial. o For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question. o Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled. o These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet. Emergency Department Care: * Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs. * Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock. * Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access) should be initiated. o Intravascular volume and oxygen-carrying capacity should be optimized. o In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock. o Blood products may be required. * Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care. * Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions. Consultations: Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, radiologist, and others as required Cardiogenic Shock taken from emedicine as well for continuity. Background: Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI). Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [bP] less than 90 mm Hg lasting more than 30 min) with evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure (Hochman, 1999). Tissue hypoperfusion was defined as cold peripheries (extremities colder than core), oliguria (<30 mL/h), or both. Pathophysiology: The most common initiating event in cardiogenic shock is AMI. Dead myocardium does not contract, and classical teaching has been that when more than 40% of the myocardium is irreversibly damaged (particularly, the anterior cardiac wall), cardiogenic shock may result. On a mechanical level, a marked decrease in contractility reduces the ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilatation, and ultimately univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. The SHOCK trial, however, demonstrated that left ventricular ejection fraction is not always depressed in the setting of cardiogenic shock. Additional surprising findings included nonelevated systemic vascular resistance on vasopressors and that most survivors have only New York Heart Association (NYHA) class I congestive heart failure. A systemic inflammatory response syndrome–type mechanism has been implicated in the pathophysiology of cardiogenic shock. Elevated levels of white blood cells, body temperature, complement, interleukins, and C-reactive protein are often seen in large myocardial infarctions. Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during myocardial stress. iNOS induces nitric oxide production, which may uncouple calcium metabolism in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the expression of interleukins, which may themselves cause hypotension. Myocardial ischemia causes a decrease in contractile function, which leads to left ventricular dysfunction and decreased arterial pressure; these, in turn, exacerbate the myocardial ischemia. The end result is a vicious cycle that leads to severe cardiovascular decompensation. Other pathophysiological mechanisms responsible for cardiogenic shock include papillary muscle rupture leading to acute mitral regurgitation (4.4%); decreased forward flow, ejection fraction, and ventricular septal defect (1.5%); and free wall rupture (4.1%) as a consequence of AMI. Right ventricular (RV) infarct, by itself, may lead to hypotension and shock because of reduced preload to the left ventricle. The management of RV infarcts is discussed elsewhere but should be considered in the setting of inferior wall MI. Cardiac tamponade may result as a consequence of pericarditis, uremic pericardial effusion, or in rare cases systemic lupus erythematosus. Whenever patients who present in shock have been exposed to medications that may cause hypotension, these drugs should be considered as possible culprits in the disease. Calcium channel blockers may cause profound hypotension with a normal or elevated heart rate. Beta-blocking agents may also cause hypotension. Hypotension can be seen with or without bradycardia, or AV node block can be seen with either of these types of medications. If these medications are the culprits, therapy directed at these toxicities is beneficial. Nitroglycerin, angiotensin-converting enzyme inhibitors, opiate, and barbiturates can all cause a shock state and may be difficult to distinguish from cardiogenic shock. Initiating events other than AMI and ischemia include infection, drug toxicity, and pulmonary embolus. Frequency: * In the US: Cardiogenic shock occurs in 8.6% of patients with ST-segment elevation MI with 29% of those presenting to the hospital already in shock. It occurs only in 2% of non–ST-segment elevation MI. Mortality/Morbidity: Cardiogenic shock is the leading cause of death in AMI. * The overall in-hospital mortality rate is 57%. For persons older than 75 years, the mortality rate is 64.1%. For those younger than 75 years, the mortality rate is 39.5%. * Outcomes significantly improve only when rapid revascularization can be achieved. The recent SHOCK trial demonstrated that overall mortality when revascularization occurs is 38%. When rapid revascularization is not attempted, mortality rates approach 70%. * Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement, thrombolytic therapy), but they have been reported to be as low as 30-50%. Race: * Race-stratified mortality rates are as follows: Hispanics, 74%; African Americans, 65%; whites, 56%; and Asians/others, 41%. * Race-based differences in mortality disappear with revascularization. Sex: Women comprise 42% of all cardiogenic shock patients. History: Most patients with cardiogenic shock have an AMI and, therefore, present with the constellation of symptoms of acute cardiac ischemia (eg, chest pain, shortness of breath, diaphoresis, nausea, vomiting). Patients experiencing cardiogenic shock also may present with pulmonary edema, acute circulatory collapse, and presyncopal or syncopal symptoms. Physical: The physical examination findings are consistent with shock. Patients are in frank distress, are profoundly diaphoretic with mottled extremities, and are usually visibly dyspneic. Clinical assessment begins with attention to the ABCs and vital signs. * Although the patient may eventually require endotracheal intubation, the airway usually is patent initially. * Breathing may be labored, with audible coarse crackles or wheezing. * As in any shocklike state, circulation is markedly impaired. Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings. * Other signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present. * Initial vital sign assessment should include BP measurements in both arms to evaluate possible thoracic aortic aneurysm or dissection. Vital signs should be regularly updated with continuous noninvasive physiologic monitoring. * Neck examination may reveal jugular venous distention, which may be prominent. This finding is evidence of RV failure. * LV dysfunction, characterized by florid pulmonary edema, can be auscultated as crackles with or without wheezing. * Careful cardiac examination may reveal mechanical causes of cardiogenic shock. o Loud murmurs may indicate a valvular dysfunction, whereas muffled heart tones with jugular venous distention and pulsus paradoxus may suggest tamponade (Beck triad). o A gallop may also be heard. The presence of an S3 heart sound is pathognomonic of congestive heart failure. The presence of pulmonary edema increases the likelihood of cardiogenic shock in the setting of hypotension. Causes: The vast majority of cases of cardiogenic shock are due to acute myocardial ischemia. * Mechanisms not related to acute infarction include the following: o Systolic - Beta-blocker overdose, calcium channel blocker overdose, myocardial contusion, respiratory acidosis, hypocalcemia, hypophosphatemia, and cardiotoxic drugs (eg, doxorubicin [Adriamycin]) o Diastolic - Ventricular hypertrophy and restrictive cardiomyopathies o After load - Aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow obstruction, aortic coarctation, and malignant hypertension o Valvular/structural - Mitral stenosis, endocarditis, mitral or aortic regurgitation, atrial myxoma or thrombus, and tamponade * Risk factors for the development of cardiogenic shock include preexisting myocardial damage or disease (eg, diabetes, advanced age, previous AMI), AMI (eg, Q-wave, large or anterior wall AMIs), and dysrhythmia. Lab Studies: * No one test is completely sensitive or specific for cardiogenic shock. Laboratory studies are directed at the potential underlying cause. * In most cases, the usual workup includes tests of all of the following, which usually are assessed in cases of suspected cardiac ischemia: o Cardiac enzymes (eg, creatine kinase, troponin, myoglobin) o CBC o Electrolytes o Coagulation profile (eg, prothrombin time, activated partial thromboplastin time) o An ABG may be useful to evaluate acid-base balance because acidosis can have a particularly deleterious effect on myocardial function. Elevated serum lactate level is an indicator of shock. o Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure and as an independent prognostic indicator of survival. A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension; however, an elevated BNP level does not rule in the disease. Imaging Studies: * A portable chest radiograph is helpful because it gives an overall impression of the cardiac size, pulmonary vascularity, and coexistent pulmonary pathology, and it provides a rough estimate of mediastinal and aortic sizes in the event that an aortic etiology is being considered. Other Tests: * An ECG is helpful if it reveals an acute injury pattern consistent with an AMI. A normal ECG, however, does not rule out the possibility. ECGs are often most helpful when they can be compared with previous tracings. * An echocardiogram obtained in the ED can be extremely useful. o It may be diagnostic and reveal akinetic or dyskinetic areas of ventricular wall motion. o It may reveal surgically correctable causes, such as valvular dysfunction and tamponade. Procedures: * Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure and pulmonary capillary wedge pressure. Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which LV preload is difficult to determine. Central venous pressure may also be used to guide fluid resuscitation. Cardiogenic shock may be indicated by a cardiac index of less than 1.8 L/min/m2 with a pulmonary capillary wedge pressure greater than 18 mm Hg. * An intra-aortic balloon pump may be placed in the ED as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) to decrease myocardial workload and to improve end-organ perfusion. Prehospital Care: Prehospital care is aimed at minimizing any further ischemia and shock. * All patients require intravenous access, high-flow oxygen administered by mask, and cardiac monitoring. * Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may be useful in decreasing door to PCI times and/or thrombolytics because acute ST-segment elevation myocardial infarctions can be identified earlier. The ED physician, can thus be alerted, and may mobilize the appropriate resources. * Inotropic medications should be considered in systems with appropriately trained paramedical personnel. Emergency Department Care: ED care is aimed at making the diagnosis, preventing further ischemia, and treating the underlying cause. Treatment of the underlying cause is directed in the case of acute myocardial infarction (AMI) at coronary artery reperfusion. This is best accomplished with rapid transfer of the patient to a cardiac catheterization laboratory. The ED physician should be alert to the fact that the SHOCK trial demonstrated that PCI or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best. Treatment begins with assessment and management of the ABCs. * The airway should be assessed for patency and breathing evaluated for effectiveness and increased work of breathing. Endotracheal intubation and mechanical ventilation should be considered for patients with excessive work of breathing. Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. * Other interventions are directed at supporting myocardial perfusion and maximizing cardiac output. Intravenous fluids should be provided to maintain adequate preload. The administration of such fluids should be guided by central venous pressure or pulmonary capillary wedge pressure monitoring. * Intravenous vasopressors provide inotropic support increasing perfusion of the ischemic myocardium and all body tissues. However, extreme heart rates should be avoided because they may increase myocardial oxygen consumption, increase infarct size, and further impair the pumping ability of the heart. o Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption. o Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and afterload. o Natrecor (nesiritide) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for acute congestive heart failure and currently retains Food and Drug Administration (FDA) approval. It should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension. o Nitrates and/or morphine are advised for the management of pain; however, they must be used with caution because these patients are in shock, and excessive use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock. * The use of an intra-aortic balloon pump (IABP) is recommended for cardiogenic shock not quickly reversed with pharmacologic therapy. It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available. Counterpulsation of the IABP reduces LV afterload and improves coronary artery blood flow. Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended. Although complications may occur in up to 30% of patients, extensive retrospective data support its use. Consultations: Consult a cardiologist at the earliest opportunity because his or her insight and expertise may be invaluable for facilitating echocardiographic support, placement of an IABP, and transfer to more definitive care (eg, cardiac catheterization suite, intensive care unit, operating room). ***And now onto the next topics, how about a triad of triads? Cushings triad? Beck's triad? And the classical triad as it applies to OB calls?*** Shane NREMT-P

I can't imagine a medic saying that they would coerce someone into going. There are many laws regarding that matter. The fact that a patient can refuse medical treatment is their right. There's nothing that says that we have to take someone just because someone tells us to. There are times when it's appropriate, and times that it's not. If someone is alert and able to make their own decisions while understanding the risks involved, they can sign the refusal. One thing that I hate more than anything is when someone says "you have to make them go." That's not my job. I will do what's appropriate and within the law. The other question I hate is "do you think they have to go?" I'm not going to be the one to say "no, they will be fine" in this litigation motivated society. As far as the scenario of the original poster, you could have called back medical control and explained that there are no family or friends that are able to stay with the patient and request permission to obtain a refusal. At least that way you're attempted to share the responsibility. If you take a refusal (witnessed or not) and it's proven that the patient wasn't able to understand the consequences, the refusal is no good and you may be held liable. Documentation is key, as is asking a higher medical authority then yourself in this case if you truely felt the patient should go to the hospital. You should also document the PD's response to your request for help in this scenario...or lack of response as the case is. Shane NREMT-P

+1. I don't care if you can recite the book to me word for word. If you can't assess your patient you can't perform an intervention. Your knowledge of anatomy and physiology is what should help to guide you through your assessment and determine where it should go next. If you've made it all the way though paramedic school and are still unable to perform a competent assessment on a live patient, I might suggest that you spend some time working somewhere as a basic until you get the lay of the land. Only when you're 100% confident as a basic provider (including assessment) should you consider providing a higher level of care. With no offense intended, it doesn't sound like you're to that level yet. It would be in your best interests, and more importantly your patients interests to be sure you can perform the proper assessment in order to perform the proper intervention. Shane NREMT-P

Cor Pulmonale is also commonly referred to as pulmonary hypertension. One of the more common causes is left sided heart failure causing a fluid backup in the pulmonary vasculature. This can potentitally lead to pulmonary edema and can require emergent management, as well as being a contributing factor to congestive heart failure. That's the quick, simple off the top of my head at 0240 hrs version. Below is the version from emedicine.com that offers a rather interesting read on the condition. Background: Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur. Pathophysiology: Several different pathophysiologic mechanisms can lead to pulmonary hypertension and, subsequently, to cor pulmonale. These pathogenetic mechanisms include (1) pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia; (2) anatomic compromise of the pulmonary vascular bed secondary to lung disorders, eg, emphysema, pulmonary thromboembolism, interstitial lung disease; (3) increased blood viscosity secondary to blood disorders, eg, polycythemia vera, sickle cell disease, macroglobulinemia; and (4) idiopathic primary pulmonary hypertension. The result is increased pulmonary arterial pressure. The right ventricle (RV) is a thin-walled chamber that is more a volume pump than a pressure pump. It adapts better to changing preloads than afterloads. With an increase in afterload, the RV increases systolic pressure to keep the gradient. At a point, further increase in the degree of pulmonary arterial pressure brings significant RV dilation, an increase in RV end-diastolic pressure, and circulatory collapse. A decrease in RV output with a decrease in diastolic left ventricle (LV) volume results in decreased LV output. Since the right coronary artery, which supplies the RV free wall, originates from the aorta, decreased LV output diminishes blood pressure in the aorta and decreases right coronary blood flow. This is a vicious cycle between decreases in LV and RV output. Right ventricular overload is associated with septal displacement toward the left ventricle. Septal displacement, which is seen in echocardiography, can be another factor that decreases LV volume and output in the setting of cor pulmonale and right ventricular enlargement. Several pulmonary diseases cause cor pulmonale, which may involve interstitial and alveolar tissues with a secondary effect on pulmonary vasculature or may primarily involve pulmonary vasculature. Chronic obstructive pulmonary disease (COPD) is the most common cause of cor pulmonale in the United States. Cor pulmonale usually presents chronically, but 2 main conditions can cause acute cor pulmonale: massive pulmonary embolism (more common) and acute respiratory distress syndrome (ARDS). The underlying pathophysiology in massive pulmonary embolism causing cor pulmonale is the sudden increase in pulmonary resistance. In ARDS, 2 factors cause RV overload: the pathologic featuresof the syndrome itself and mechanical ventilation. Mechanical ventilation, especially higher tidal volume, requires a higher transpulmonary pressure. In chronic cor pulmonale, right ventricular hypertrophy (RVH) generally predominates. In acute cor pulmonale, right ventricular dilatation mainly occurs. History: Clinical manifestations of cor pulmonale generally are nonspecific. The symptoms may be subtle, especially in early stages of the disease, and mistakenly may be attributed to the underlying pulmonary pathology. * The patient may complain of fatigue, tachypnea, exertional dyspnea, and cough. * Anginal chest pain also can occur and may be due to right ventricular ischemia (it usually does not respond to nitrates) or pulmonary artery stretching. * Hemoptysis may occur because of rupture of a dilated or atherosclerotic pulmonary artery. Other conditions, such as tumors, bronchiectasis, and pulmonary infarction, should be excluded before attributing hemoptysis to pulmonary hypertension. Rarely, the patient may complain of hoarseness due to compression of the left recurrent laryngeal nerve by a dilated pulmonary artery. * Variety of neurologic symptoms may be seen due to decreased cardiac output and hypoxemia. * In advanced stages, passive hepatic congestion secondary to severe right ventricular failure may lead to anorexia, right upper quadrant abdominal discomfort, and jaundice. * Syncope with exertion, which may be seen in severe disease, reflects a relative inability to increase cardiac output during exercise with a subsequent drop in the systemic arterial pressure. * Elevated pulmonary artery pressure can lead to elevated right atrial pressure, peripheral venous pressure, and then capillary pressure and by increasing the hydrostatic gradient, it leads to transudation of fluid, which appears as peripheral edema. Although this is the simplest explanation for peripheral edema in cor pulmonale, other hypotheses explain this symptom, especially in a fraction of patients with COPD who do not show increase in right atrial pressure. A decrease in GFR and filtration of sodium and stimulation of arginine vasopressin (which decreases free water excretion) due to hypoxemia play important pathophysiologic roles in this setting and may even have a role for peripheral edema in patients with cor pulmonale who have elevated right atrial pressure. Physical: Physical findings may reflect the underlying lung disease or pulmonary hypertension, RVH, and RV failure. * On inspection, an increase in chest diameter, labored respiratory efforts with retractions of chest wall, distended neck veins with prominent a or v waves, and cyanosis may be seen. * On auscultation of the lungs, wheezes and crackles may be heard as signs of underlying lung disease. Turbulent flow through recanalized vessels in chronic thromboembolic pulmonary hypertension may be heard as systolic bruits in the lungs. Splitting of the second heart sound with accentuation of the pulmonic component can be heard in early stages. A systolic ejection murmur with sharp ejection click over the region of the pulmonary artery may be heard in advanced disease, along with a diastolic pulmonary regurgitation murmur. Other findings upon auscultation of the cardiovascular system may be third and fourth sounds of the heart and systolic murmur of tricuspid regurgitation. * RVH is characterized by a left parasternal or subxiphoid heave. Hepatojugular reflex and pulsatile liver are signs of RV failure with systemic venous congestion. * On percussion, hyperresonance of the lungs may be a sign of underlying COPD; ascites can be seen in severe disease. Medical Care: Medical therapy for chronic cor pulmonale is generally focused on treatment of the underlying pulmonary disease and improving oxygenation and RV function by increasing RV contractility and decreasing pulmonary vasoconstriction. However, the approach might be different to some degree in an acute setting with priority given to stabilizing the patient. Cardiopulmonary support for patients experiencing acute cor pulmonale with resultant acute RV failure includes fluid loading and vasoconstrictor (eg, epinephrin) administration to maintain adequate blood pressure. Of course, the primary problem should be corrected, if possible. For example, for massive pulmonary embolism, consider administration of anticoagulation, thrombolytic agents or surgical embolectomy, especially if circulatory collapse is impending, consider bronchodilation and infection treatment in patients with COPD and consider steroid and immunosuppressive agents in infiltrative and fibrotic lung diseases. Oxygen therapy, diuretics, vasodilators, digitalis, theophylline, and anticoagulation therapy are all different modalities used in the long-term management of chronic cor pulmonale. * Oxygen therapy is of great importance in patients with underlying COPD, particularly when administered on a continuous basis. With cor pulmonale, the partial pressure of oxygen (PO2) is likely to be below 55 mm Hg and decreases further with exercise and during sleep. Oxygen therapy relieves hypoxemic pulmonary vasoconstriction, which then improves cardiac output, lessens sympathetic vasoconstriction, alleviates tissue hypoxemia, and improves renal perfusion. The Nocturnal Oxygen Therapy Trial (NOTT), a multicenter randomized trial, showed that continuous low-flow oxygen therapy for patients with severe COPD resulted in significant reduction in the mortality rate. In general, in patients with COPD, long-term oxygen therapy is recommended when PaO2 is less than 55 mm Hg or O2 saturation is less than 88%. However, in the presence of cor pulmonale or impaired mental or cognitive function, long-term oxygen therapy can be considered even if PaO2 is greater than 55 mm Hgor O2 saturation is greater than 88%. Although it is not clear whether oxygen therapy has a mortality rate benefit in patients with cor pulmonale due to pulmonary disorders other than COPD, it may provide some degree of symptomatic relief and improvement in functional status. Therefore, oxygen therapy plays an important role in both the immediate setting and long-term management, especially in patients who are hypoxic and have COPD. * Diuretics are used in the management of chronic cor pulmonale, particularly when the right ventricular filling volume is markedly elevated and in the management of associated peripheral edema. Diuretics may result in improvement of the function of both the right and left ventricles; however, diuretics may produce hemodynamic adverse effects if they are not used cautiously. Excessive volume depletion can lead to a decline in cardiac output. Another potential complication of diuresis is the production of a hypokalemic metabolic alkalosis, which diminishes the effectiveness of carbon dioxide stimulation on the respiratory centers and lessens ventilatory drive. The adverse electrolyte and acid-base effect of diuretic use can also lead to cardiac arrhythmia, which can diminish cardiac output. Therefore, diuresis, while recommended in the management of chronic cor pulmonale, needs to be used with great caution. * Vasodilator drugs have been advocated in the long-term management of chronic cor pulmonale with modest results. Calcium channel blockers, particularly oral sustained-release nifedipine and diltiazem, can lower pulmonary pressures, although they appear more effective in primary rather than secondary pulmonary hypertension. Other classes of vasodilators, such as beta agonists, nitrates, and angiotensin-converting enzyme (ACE) inhibitors have been tried but, in general, vasodilators have failed to show sustained benefit in patients with COPD and they are not routinely used. A trial of vasodilator therapy may be considered only in patients with COPD with disproportionately high pulmonary blood pressure. Beta-selective agonists have an additional advantage of bronchodilator and mucociliary clearance effect. Right heart catheterization has been recommended during initial administration of vasodilators to objectively assess the efficacy and detect the possible adverse hemodynamic consequences of vasodilators. The Food and DrugAdministration (FDA) has approved epoprostenol, treprostinil, bosentan, and iloprost for treatment of primary pulmonary hypertension. Epoprostenol, treprostinil, and iloprost are prostacyclin PGI2 analogues and have potent vasodilatory properties. Epoprostenol and treprostinil are administered intravenously and iloprost is an inhaler. Bosentan is a mixed endothelin-A and endothelin-B receptor antagonist indicated for PAH, including PPH. In clinical trials, it improved exercise capacity, decreased rate of clinical deterioration, and improved hemodynamics. PDE5 inhibitor sildenafil has also been intensively studied and recently approved by the FDA for treatment of pulmonary hypertensionbased on a large randomized study. Sildenafil promotes selective smooth muscle relaxation in lung vasculature. Not enough data are available regarding the efficacy of these drugs in patients with secondary pulmonary hypertension such as in patients with COPD. * The use of cardiac glycosides, such as digitalis, in patients with cor pulmonale has been controversial, and the beneficial effect of these drugs is not as obvious as in the setting of left heart failure. Nevertheless, studies have confirmed a modest effect of digitalis on the failing right ventricle in patients with chronic cor pulmonale. It must be used cautiously, however, and should not be used during the acute phases of respiratory insufficiency when large fluctuations in levels of hypoxia and acidosis may occur. Patients with hypoxemia or acidosis are at increased risk of developing arrhythmias due to digitalis through different mechanisms including sympathoadrenal stimulation. * In addition to bronchodilatory effect, theophylline has been reported to reduce pulmonary vascular resistance and pulmonary arterial pressures acutely in patients with chronic cor pulmonale secondary to COPD. Theophylline has a weak inotropic effect and thus may improve right and left ventricular ejection. As a result, considering the use of theophylline as adjunctive therapy in the management of chronic or decompensated cor pulmonale is reasonable in patients with underlying COPD. * Anticoagulation with warfarin is recommended in patients at high risk for thromboembolism. The beneficial role of anticoagulation in improving the symptoms and mortality in patients with primary pulmonary arterial hypertension clearly was demonstrated in a variety of clinical trials. The evidence of benefit, however, has not been established in patients with secondary pulmonary arterial hypertension. Therefore, anticoagulation therapy may be used in patients with cor pulmonale secondary to thromboembolic phenomena and with underlying primary pulmonary arterial hypertension. Surgical Care: * Phlebotomy is indicated in patients with chronic cor pulmonale and chronic hypoxia causing severe polycythemia, defined as hematocrit of 65 or more. Phlebotomy results in a decrease in mean pulmonary artery pressure, a decrease in mean pulmonary vascular resistance, and an improvement in exercise performance in such patients. There is, however, no evidence of improvement in survival. Generally, phlebotomy should be reserved as an adjunctive therapy for patients with acute decompensation of cor pulmonale and patients who remain significantly polycythemic despite appropriate long-term oxygen therapy. Replacement of the acute volume loss with a saline infusion may be necessary to avoid important decreases in systemic blood pressure. * No surgical treatment exists for most diseases that cause chronic cor pulmonale. Pulmonary embolectomy is efficacious for unresolved pulmonary emboli, which contribute to pulmonary hypertension. Uvulopalatopharyngoplasty in selected patients with sleep apnea and hypoventilation may relieve cor pulmonale. Single-lung, double-lung, and heart-lung transplantation are all used to salvage the terminal phases of several diseases (eg, primary pulmonary hypertension, emphysema, idiopathic pulmonary fibrosis, cystic fibrosis) complicated by cor pulmonale. Apparently, lung transplantation will lead to a reversal of right ventricular dysfunction from the chronic stress of pulmonary hypertension. Strict selection criteria for lung transplant recipients must be met, however, because of the limited availability of organ donors. And now one that we should all be familiar with...Munchausen Syndrome and also Munchausen by proxy. Shane NREMT-P

Just another point, her seizures weren't "obviously" fake if the ED staff felt the need to medicate her with another millgram of Ativan. As far as the motor activity being equal vs non equal, I'm not sure I buy into that comment. People have isolated focal seizure frequently. There's no rule (that I know of) that says that all seizure activity has to be equal. Using the doc's theory, I'd be curious to have him explain a focal motor seizure. Also a 45 minute seizue that really lasts the full 45 minutes would either leave the pt so hypoxic and/or exhausted that they would remain very lethargic. All in all, it sounds like an interesting call. Shane NRMET-P

Now that we've gotten some discussion going on about the topic. The large response is in a town that's rather well off financially. The police go to every medical call, the FD goes to chest pain, SOB, unresponsive. Bascially anything that might sound decent. The police officers are trained to the MRT level and are typically very helpful to us. When I'm working in the city, we're lucky to get a cop for anything that doesn't sound like it's a police matter and the fire department comes to just about every call. There are calls that we get sent to often just as the ambulance. It's not the best use of resources, but it's better than what the wealthier town does. Shane NREMT-P

This is something I had posted about in another thread a while back, but it got lost somewhere so I'll bring it up again. Do we do patients any good by having so many different providers on an emergency scene? Here's an example from the service I work in. It's not uncommon to have a BLS engine first respond, a transporting ambulance, at least one (usually two) police officers, and depending on the location of the call an intercept paramedic unit. So let's go on the short side and say it's a 3 person engine (usually 4-5 people though), one to two police officers, two members from the ambulance crew and one intercept paramedic (even if the transporting ambulance is an ALS unit). That's a minimum of 8 different people coming to someone's house for one medical call. Is this really the most effective use of resources? And does it really provide any level of benefit for the patient? Something to think about... Shane NREMT-P

Here is a blog about capnography written by one of the paramedics that I work with. It contains many great links to other studies as well as a fair amount of good information. Shane NREMT-P *EDIT* Would have been nice if I included the link... http://www.emscapnography.blogspot.com/

+1, the waveform doesn't look obstructed at all, so there isn't the "shark wave" look like you see with asthma of COPD. As the patient tires, they begin to hypoventilate or have insufficient respiration causing an increase in ETCO2. As the number rises, the likihood of having to assist w/ventilations increases significantly. As the patient has their O2/CO2 exchange impeded by edema within the lungs, the number will drop indicating a lack of or poor cellular exchange occuring. Shane NREMT-P

So I'm curious about one thing. If you were able to determine her to be suffering from heat exhaustion, as an off-duty EMT-B could you have done anything different from what the life guards were doing for the patient? My guess is that you couldn't, and in a case like that you don't have much to offer in the way of patient care other than an extra set of hands. If they didn't need your "hands," since it's their response zone I would assume that they could ask you to leave. There was nothing that you could do that would have changed the outcome of the call, and no negative effect was had from the interaction. You said that her partner asked you for help, but who was most senior of the on-duty personnel? Or more importantly, who had control of the scene? As a paramedic, if my partner asks someone to help, I have the ability to refuse the help if I don't feel it necessary. It doesn't matter that he/she asked for it, I'm the one running the call. You were off duty and it doesn't sound much like you had a duty to act in this case. As far as the ID's, anyone can produce a badge, t-shirt or photo ID. They aren't hard to make and there are plenty of Rescue Randy's out there. We hear cases of people impersonating personnel more frequently then we should. Shane NREMT-P

Sure there is. More and more services are going to non-latex gloves in order to prevent this from happening. Our service requires non-latex gloves, and many of the hospitals do the same. Shane NREMT-P

I'm surprised this hasn't turned into a discussion of weather basic level providers should be giving albuterol/atrovent and epi medications. For those that can give the albuterol and atrovent, do you know when to use one over the other? Just curious if this is taught in your in service sessions. Shane NREMT-P

I use the same format for just about every PCR that I write. By using a set system, I find that I don't leave things out and it can help with performing an assessment should you ever find yourself stuck. Example: Called priority _ to above location for pt 28 y/o male restrainted driver involved in two car, head on style MVC. Vehicle with heavy front end damage. + Airbag deployment, - Steering wheel/dash deformity, - windshield intact, ? Loss of conciousness. Upon arrival found pt sitting in drivers seat a/o x 3/4 (confusion of event), + ABC, GCS=14 (4/4/6), PERRLA, skin warm/dry, + Headache, + Dizziness, + laceration approx 1/2" long above left temple, + neck pain @ midline, - JVD, - Trach dev, + chest pain 5/10 that increases w/respiration and palpation, - SOB, - increased work of breathing, lung sounds clear and equal bilaterally, abd soft w/tenderness at RUQ, + nausea/-vomit, + R flank pain, + back pain, hips/pelvis stable, + PMS X 4, Neuro assessment w/o deficit, - extremity injury x 4. Pt placed in manual c-spine stabilization --> c-collar --> LSB --> CID. + PMS x 4 before and after immobilization. LSB --> Stretcher --> Ambulance. v/s as noted below. Pt on O2 @ 15 LPM NRB. IV established, 18 gage NSS @ KVO L AC. EKG = Sinus Tach w/o ectopy. During transport pt with short term memory loss and repetitive questioning of "what happened to me?" Pt transported priority one to ABC Medical Center without change or incident. Transfer care with report to RN and/or MD. *I think I got most everything. It's hard to write a narrative on a call you just made up.* Most of what I write is also checked off in the check boxes of our run forms. Our blood glucose gets written in a specific location, so I don't usually write it in the narrative, along with the vitals. By using the same format, you're less likely to forget something in your assessment or your report. Shane NREMT-P

If the employer sets forth a requirement that they have to turn in a criminal background investigation yearly, then by agreeing to employment you have agreed to the "rules" of the employment. You have no grounds to cry upon on invasion of privacy as it's something you agreed to by accepting the position with the service. If you've done nothing wrong, then it shouldn't be a big deal either way. I'm going through a criminal background check currently for a per diem position at another service. I don't care what they look for since they won't find anything that shouldn't be on there and that would prevent me from getting the position. If the service feels the need to perform yearly checks, that's their initative. If you don't like it or fear that you won't be compiant, find a service that's more relaxed. Kudos to the service for maintaining such high standards. Shane NREMT-P

Did I miss part of the question? Why would it be a problem? Regardless of occupation, if you have a medical condition, you should wear one. We advocate to our patients all the time that they should wear one, we're not any different. We have all the same medical conditions the general public has. Shane NREMT-P