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Congestive Heart Failure


vcfd35s

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Hey guys,

This might not be a BLS question.....but here it goes.

When dealing with CHF we know that one thing to look for is fluid in the lungs. That fluid is edema(sp)......however it could also be pnumonia. But my question is this.....what causes the "edema" or the fluid in the lungs?

Any help would be great.....thanks... :lol:

Jonathan

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CHF is when the heart is not effective as a pump. One side of the heart may still be effective putting more blood back into the other side of the heart than the heart can effictively put out. This inability to pump is what causes the back up. For an example, think of a funnel. Only so much fluid can pass thru the small opening (the damaged side of the heart). So if you put more in, it eventually backs up and overflows the system. When the vasculature becomes overloaded, it will "third space" into the lungs (or systemic depending on the side of the heart). Left sided heart failure will commonly cause the pulmonary edema where right sided heart failure will commonly cause the systemic edema (pedal, etc).

So in simple terms, CHF is the inability of heart to pump the vascular volume effectively. Sorry if it's not the clearest picture I'm just really tired at this point.

Shane

NREMT-P

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Simple path of blood through the heart.

1venous return through the vena cava into the right atrium.

2. Right atrium into right ventrical

3 right ventrical pumps into pulmonary arteries through the lungs and oxygenated blood returns to the left atrium through pulmonary veins.

4.blood goes from left atrium to left ventricle

5. pumped from left ventrical to systemic circulation.

The cause of fluid in the lungs occurs in between the left ventrical and the right ventrical. One normally works with the other. Lets say that you suffer an MI damaging the left ventricle. Now the right ventrical is pumping harder than the left. Pressure builds up in the pulmonary circulation and the only place for the fluid to go is into the lungs.

Simplistic, hope its what you are looking for.

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Simple path of blood through the heart.

1venous return through the vena cava into the right atrium.

2. Right atrium into right ventrical

3 right ventrical pumps into pulmonary arteries through the lungs and oxygenated blood returns to the left atrium through pulmonary veins.

4.blood goes from left atrium to left ventricle

5. pumped from left ventrical to systemic circulation.

The cause of fluid in the lungs occurs in between the left ventrical and the right ventrical. One normally works with the other. Lets say that you suffer an MI damaging the left ventricle. Now the right ventrical is pumping harder than the left. Pressure builds up in the pulmonary circulation and the only place for the fluid to go is into the lungs.

Simplistic, hope its what you are looking for.

Good job. Better way of putting it into words than I accomplished tonight.

Shane

NREMT-P

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  • 3 weeks later...

Acute Pulmonary Edema is due to an imbalance of the Starling Forces; it is the 'central' point to fluid accumulation in the interstitium and alveolus.

Regards

Sorry for the delay

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  • 3 months later...

Here's a link to a related teaching post here:::

http://www.emtcity.com/phpBB2/viewtopic.php?t=2496

(Prehospital Emergency Care

Publisher: Taylor & Francis Health Sciences @ part of the Taylor & Francis Group

Issue: Volume 10, Number 1 / January-March 2006

Pages: 41 - 45

URL: Linking Options

DOI: 10.1080/10903120500366938

Do Medications Affect Vital Signs in the Prehospital Treatment of Acute Decompensated Heart Failure?

Karl A. Sporer A1, A2, Jeff A. Tabas A1, A2, Roland K. Tam A4, Karen L. Sellers A1, A2, Jon Rosenson A1, Chris W. Barton A1, A2, Mark J. Pletcher A1, A3

A1 Department of Medicine, University of California, San Francisco, San Francisco, California

A2 Department of Emergency Services, San Francisco General Hospital, San Francisco, California

A3 Department of Epidemiology and Biostatistics, Albert Einstein School of Medicine, New York, New York

A4 Albert Einstein School of Medicine, New York, New York)

Abstract:

Introduction. Prehospital treatment of patients with acute decompensated heart failure (ADHF) has been shown to decrease mortality and morbidity. Vital sign changes have been proposed as clinical endpoints in the evaluation of prehospital treatment for this condition. Objective. To examine the effect of prehospital treatments on vital signs among patients with ADHF. Methods. Records of an urban emergency medical services system from September 1, 2002, through September 1, 2003, were queried for patients who had a paramedic impression of shortness of breath or respiratory distress and had received nitroglycerin and/or furosemide. Demographics, initial and repeat vital signs (blood pressure, heart rate, respiratory rate, and oxygen saturation), and medications and doses were collected. Results. Three hundred nineteen patients were included; the average age was 77 (±12) years and 47% were male. Treatments administered to these patients included nitroglycerin, 296 (93%); furosemide, 194 (61%); albuterol, 189 (59%); aspirin, 57 (18%); morphine, 20 (6%); and prehospital intubation, 15 (5%). Patients were initially hypertensive [mean ± standard deviation of systolic blood pressure (SBP) was 167 ±37 mm Hg], tachycardic (heart rate 106 ± 24 beats/min), tachypneic (respiratory rate 33 ± 7 breaths/min), and hypoxic (pulse oximetry 88% ± 9.5%). After treatment, mean changes included decreases (95% confidence interval) in (SBP), -10.6 mm Hg (-14.1 to -7.1), heart rate, -2.3 beats/min (-4.0 to -0.7), and respiratory rate, -3.0 (-3.6 to -2.3), and an increase in oxygen saturation, +8.2 (7.1 to 9.3). Changes in blood pressure and oxygen saturation after treatment correlated with initial values. There was no independent association of either nitroglycerin, furosemide, albuterol, or morphine with improvement in vital signs. Conclusion. Prehospital patients with ADHF are a heterogeneous group of patients with significant variability in vital signs. The change in systolic blood pressure or oxygen saturation after treatment depends greatly on the patient's starting point. There was no association of either nitroglycerin or other medications with the improvement in vital signs.

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