chbare

Sounds good. A review of cardiac A&P along with the cardiac cycle is also recommended. Check out this link for a basic review. The tutorial is pretty neat and you not only have sounds, but a real time diagram and text that explains the sounds. http://www.blaufuss.org/ Take care, chbare.

I am glad the scenario was well received. Actually, the pre-hospital course is very similar to the "standard" interventions we typically associate with acute cardiogenic pulmonary edema. Some experts suggest using nipride because it specifically targets afterload, even if the blood pressure is normal. In addition, beta blockers should not be considered because they can blunt the compensatory tachycardia associated with this problem. One of my points is also based around the physical exam. While we may not have picked up on this in the field, it is important to make note of our assessment findings. While we may not have initially put the puzzle together, having the history and assessment to include heart sounds could actually benefit the patient during their course within the hospital. Advising the receiving facility of your findings very well could hasten diagnosis and definitive care for this patient. The consideration of past step infection would also have been valid. Somebody in a prior post had considered this problem. Rheumatic heart disease as a result of a strep infection is in fact a leading cause of mitral valve problems. This is especially true in younger patients with mitral valve disorders. Many people will not develop the sudden severe signs and symptoms of our patient and you may actually see more chronic problems develop. Chronic signs and symptoms of heart failure can occur. Atrial fibrillation is also commonly seen in patients with mitral valve problems. Take care, chbare.

Nailed it. Acute mitral regurgitation with pulmonary edema. So, the story was most likely: Pt had an MI in the past few months, atypical signs and symptoms most likely a result of his diabetes, mitral valve papillary muscle dysfunction ensued, and sudden rupture of the papillary muscles occurred following the MI. Treatment in the pre-hospital setting will be similar to most types of cardiac pulmonary edema. The aim is to reduce afterload. The tachycardia is a good thing and to a point may actually prevent some of the mitral backfill. Even with normal blood pressures, nitrates should be considered to assist with afterload reduction. I hope everybody enjoyed this scenario. I thought something a little different from the typical massive MI leading to LV dysfunction and L sided failure would make for a great learning experience. Take care, chbare.

Bell's palsy may be something to consider with isolated signs and symptoms only. Take care, chbare.

-Ah..heart sounds! You appreciate the following: a high pitched systolic murmur is noted and you also note radiation of this sound into the axilla. For the sake of the scenario, you can assume this is a new development for this patient. -From what you gather, he had some tightness suddenly develop and dyspnea within several minutes of the chest tightness. No chest pain in the prior weeks, just the comment about slowing down in the past few months. -No surgery, trauma, immobilization, or chemical exposure. -Plateau pressures with a 20% inspiratory hold are running in the 30-34 range. -Temp is 98.9 F via rectal probe. -The intubation was performed without incident. Suctioning of airway secretions was required; however, no problems were encountered. Take care, chbare.

- JVD is noted, no distal edema is noted, skin is pale and diaphoretic, no N/V. -The activity did not seem to be strenuous and no additional stressors are noted. -Hard to assess for weakness. The onset was quite sudden. You gather from you primary assessment that he has felt "like he has slowed down a bit" over the pat few months. Take care, chbare.

-Bilat pressures are within a few mm/hg. -Vital Signs B/P- 118/88, P-133, R-14 on a ventilator, Pulse oximetry-94% with Fio2 of 1, ETCO2-26, 12 lead is unchanged. -The patient does not take any known cardiovascular medications. -The patients peak pressures spike up to 38 and he requires frequent ETT suctioning. PIP's following suctioning range from 30-32. -A specific assessment technique may provide you with a clue that when combined with all of the other information will help solve this puzzle. Unfortunately, I suspect it is a technique that is often not covered in any depth. Take care, chbare.

-The leads are placed properly. -Think about conditions that cause acute pulmonary edema. The guy had pretty sudden onset pulmonary edema, so you may consider that perhaps he developed an acute problem. -Would you assess anything else? Think about things you want to assess in a CARDIAC patient. Take care, chbare.

Did you check her BGL? A quick, easy, and often overlooked assessment. Take care, chbare.

-There is a twist. Everything points to your run of the mill massive MI left sided failure type patient. However, the 12 lead indicates that the patient may not actually be actively infarcting. What if the MI may only be part or a contributing factor to the problem at hand? Are we able to gather any more information on this patient? -You did not notice any chemicals at the scene otrhan dish soap. -His blood pressure is still 120/72. You are able to RSI and intubate without difficulty. You still have about 15 minutes to the hospital. Take care, chbare.

V4R is negative for any acute changes. So, we can tell that this patient has had an MI at some point. How long ago? Hard to tell based on the information we have. However, if the pulmonary edema developed as a direct complication from the MI, would we not have seen it occur during the acute phase of the MI? So, the question still remains. What is going on with this guy? It looks like we may need to RSI. If he is not awake and alert, BIPAP will most likely not be an option. NTG is not a bad idea. We are looking to reduce both preload and afterload with NTG? Lasix may be an option, perhaps we could discuss the rationale for using it with this patient? Any other meds to consider? Is there something that may help us figure out what is going on with this patient? The BGL is 175 mg/dl. The frothy sputum is white in color.

It's the helicopter. If I jump out of an A-Star with blades turning and a cool flight suit on my body, I must know everything...right? And by the way, we are the best of the best. See the above comment. Take care, chbare.

You may be onto something with the torsion. Syphilis, possibly. PID, unlikely in this guy, but not unheard of I suppose. :shock: About 20 minutes into your 45 minute transport you have the following V/S: P-130, R-36, B/P-120/84, Pulse oximetry-86%. He is developing a noticeable amount of lethargy and appear to be very "tired of breathing." Do we continue onto BIPAP therapy at this point? What is going on with this patient? Take care, chbare.

-12 lead ECG: Sinus tachycardia without ectopy. LBBB noted with Q waves in V1, V2, V3, and V4 along with poor R wave progression. No ST elevation, depression, or acute T wave changes noted in any leads. -You administer NTG 0.4 mg SL and ASA 160 mg chewed. In between doses of NTG you begin to set up your BIPAP machine. Take care, chbare.

-IV life line is established. Lung sounds: crackles throughout all lobes anterior and posterior aspects. Or any other type of nomenclature you use to describe wet lung sounds. Take care, chbare.

-Your partner attempts to assist his respiration; however, he becomes agitated and pulls away from attempts at BVM assisted ventilation. He continues to tolerate the NRB however. He currently has a GCS of 15. -Rhythm strip in lead II: Sinus tachycardia without ectopy. Intervals appear within acceptable limits. -No history of CHF or COPD is noted. Take care, chbare.

Not a problem, glad to contribute something. -NRB is placed. You gather that he may be experiencing a little chest pressure, but he continues to state with strained effort, "I cannot breath." -He has strong movement of all extremities and you do not appreciate any facial droop. his is sitting up in a tripod like stance in a chair. -Vital signs: R-32, P-128, B/P- 128/94, Pulse Oximetry-88% -His past history is significant for NIDDM and he takes metformin 500 mg PO BID. -He was washing dishes when his signs and symptoms began suddenly. -He is awake, alert, oriented to person, place, time, situation, and appears to be answering questions appropriately and to the best of his ability. Take care, chbare.

-He is awake and responsive; however, his ability to speak and articulate in sentences greater than a few words long is quite limited. He does respond appropriately to questions to the best of his abilities given his respiratory status. -He is sitting in a chair and appears acutely ill. He is pale, diaphoretic, and appears to be having allot of difficulty breathing. -His respiratory rate is around 32 and shallow, he is working hard to breath, and spitting up frothy sputum. -His chief complaint is actually difficulty breathing. Take care, chbare.

You are called to the residence of a 56 year old male complaining of chest pain. Take it from here. Take care, chbare.

Agreed, thank you ERDoc. Take care, chbare.

I would KVO her IV's for the moment and let the ER staff deal with calculating the fluid type and rate in 10 minutes. I would not push bicarb with this patient. While it may be tempting to reverse her acidosis with bicarb, we would have to deal with the consequences of such an action. (Hypokalemia, increased Co2, etc.) With a 10 minute time to the ER, I would hesitate to RSI. If we can control her airway adequately with BLS maneuvers, I will let the ER deal with it. Sounds like a cop out dump job, shameless. I know. Take care, chbare.

This is also why I will never advocate for insulin use pre-hospital. We can appreciate the nightmare if we had followed the "insulin protocol" and started running regular insulin at 0.1U/KG/hr on top of our fluid therapy. All DKA patients are critical in my book. I remember a pediatrician tell a new onset DKA kid's mom and dad, "he may not look that bad on the outside, but he is very sick on the inside." Take care, chbare.

This is where the signs and symptoms point. At this point we may be forced to perform ET intubation. We will need to hyperventilate this patient, not only because of increased ICP, but because we will most likely need to keep her C02 lower than normal related to her underlying metabolic acidoses. Many DKA patients will have a compensatory respiratory alkalosis and if we ventilate with "normal" setings we could really screw this one up. In addition, we may need to consider Mannitol in the range of about 0.3-1 g/kg IV gtt. Take care, chbare.

We can still consider giving a little dextrose IV and see if this helps. Take care, chbare.

Looks like I missed the above post. I would hesitate to give bicarb to this patient. Remember she is most likely in a state of relative hyperkalemia, but in fact will require potassium supplementation. Without labs and serial potassium levels, we could cause a catastrophic drop in the patients potassium level if we administer bicarb. In the early stages of DKA without labs, fluids are actually the primary treatment. In some cases of DKA, fluids alone will nearly correct the acidosis. Remember, this patient is severely dehydrated. Take care, chbare.