Renal Failure/CHF/Pulmonary Edema/Cardiogenic shock

Let's talk about the pathophysiology of this patient's treatment for a minute...

I understand how CPAP works in terms of adding PEEP, increasing inspiratory volumes which decreases work of breathing, stenting open alveoli that are under pressure from fluid which helps improve gas exchange, etc, but how does it work on a cardiovascular level? Also, NTG and morphine are indicated as vasodilators and to reduce preload which will reduce the amount of fluid being pumped through the pulmonary vein correct? Lastly, would pressors be a better choice if this patient became hyoptensive since they are in cardiogenic shock (and we wouldn't want to exacerbate the problem by giving more fluids) or is this going to be counterproductive to giving morphine and NTG?

Also, why is CPAP generaly not indicated in COPD and asthma? It seems like bronchospasm could be treated in the same way as pulmonary edema.
 
It's my understanding that CPAP does not "increase inspiratory volume". CPAP is about airway pressure, and not volume. For example, the device we use for CPAP is called the Oxy-PEEP which on inspiration it provides no pressure increase on the inspiratory phase... it is the same as a NRB during the inspiratory phase... its magic occurs during expiration where it forces a positive pressure in the chest which prevents alveolar collapse and increases the surface area available for diffusion. If I am wrong in my understanding someone please correct me.

CPAP works on the cardiovascular level by means of the positive pressure. The positive pressure created in the chest causes a pinching down of the vena cava which reduces preload. As you know (and in case others dont), when you decrease preload (blood return to the heart) you decrease the overall workload and myocardial oxygen demand of the heart. I remember it this way... think of hypoventilation induced hypotension and why that is detrimental during a cardiac arrest. The frequent ventilations (hyperventilation) keeps a positive pressure in the chest and does not allow for the negative pressure to come into play which is where blood return to the heart comes from.

So not only does the decreased preload help to take workload off the heart, it also helps to reduce pulmonary pressures which helps keep the fluid from crossing cell membranes and entering the alveoli.

In Maryland protocol, CPAP is indicated for Asthma and COPD... it has been found to work and be very effective in these conditions as well.

Since were talking a bit about CHF.... I haven't heard anyone mention using ACE inhibitors. Does ne one use SL captopril in the field for afterload reduction?
 
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but how does it work on a cardiovascular level?
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CPAP reduces the left ventricular preload and afterload by increasing intrathoracic pressure and lowering left ventricular transmural pressure.


Also, why is CPAP generaly not indicated in COPD and asthma? It seems like bronchospasm could be treated in the same way as pulmonary edema.
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Bronchospasm is often causes by an inflammation. Sometimes you can splint the airways and sometimes you will just cause more air trapping. The same for certain types of COPD as there are more than emphysema which also comes with various phases and etiologies. The FRC may be extended to where it becomes most of the TLC which makes each VT ineffective. Also, if their muscles are fatiqued, without access to bilevel ventilation, you may increase the work of breathing. Secretions might also be an issue where you would not want to utilize CPAP unless you could clear the airway appropriately. In the hospital and for some CCT, we do use CPAP and Bilevel (BiPAP, BIPAP) to rescue some patients with asthma and COPD. But, we vary the pressures and flows by CXR and hemodynamic monitoring as well as having the ability to support BP if needed.

Mechanical Ventilation of Patients with COPD and Asthma (this includes NIPPV)

http://www.slideshare.net/scribeofegypt/copd-asthma
 
ResTech said:
CPAP works on the cardiovascular level by means of the positive pressure. The positive pressure created in the chest causes a pinching down of the vena cava which reduces preload.
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No, it does not "pinch" the vena cava.

Also:
CPAP doesn't push the lung water and lidocaine does not numb the heart.
 
ResTech said:
For example, the device we use for CPAP is called the Oxy-PEEP which on inspiration it provides no pressure increase on the inspiratory phase...
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I think you're describing PEEPing instead of a CPAP device.

PEEP-- Positive End Expiratory pressure, keeps all the air from being exhaled thereby keeping the pressure up in the lungs, while CPAP, Continuous Positive Air Pressure, continually forces air into the lungs at a certain pressure, during inhalation and exhalation.

BiPAP is where it switches between 2 pressures for inhalation and exhalation.
 
VentMedic said:
Also:
CPAP doesn't push the lung water
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Now this is where I am of no clue.

Yes, I know it reduces preload.


But I have had a physician, and NOT my paramedic instructor like some people think, tell me that an increase in lung pressure will keep more fluid out of the interstitial space, to which the fluid goes to because of the increased pressure in the vessels and decreased pressure in the lungs.
 
Linuss said:
I think you're describing PEEPing instead of a CPAP device.

PEEP-- Positive End Expiratory pressure, keeps all the air from being exhaled thereby keeping the pressure up in the lungs, while CPAP, Continuous Positive Air Pressure, continually forces air into the lungs at a certain pressure, during inhalation and exhalation.
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It depends on how the PEEP is delivered. The Oxy-PEEP is a mask with a resistive valve. CPAP that is generated continuously is generally more effective and less likely to fatique the patient.

If you go into CCT and use various ventilators you will notice the difference. Vents with an external resistive valve for PEEP are not as effective as those with internal continuous flow for CPAP/PEEP.


Linuss said:
BiPAP is where it switches between 2 pressures for inhalation and exhalation.
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The baseline or EPAP flow may be continuous and the 2nd level can augment inspiratory effort. However, the differences comes again with how the CPAP/PEEP is delivered as to if the inspiratory effort is from EPAP baseline or Zero.
 
Linuss said:
But I have had a physician, and NOT my paramedic instructor like some people think, tell me that an increase in lung pressure will keep more fluid out of the interstitial space, to which the fluid goes to because of the increased pressure in the vessels and decreased pressure in the lungs.
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Yes it will move the fluid by making the lymphatic system more effective with the pressure changes.
 
ResTech said:
The Oxy-Peep CPAP and PEEP are really one in the same in terms of desired effect.
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Again that will depend on how each is delivered as the names state:

CPAP: Continuous Positive Airway Pressure

PEEP: Positive End Expiratory Pressure

Some believe all technology is the same and fail to understand how each device works to appreciate the differences. Thus, we hear various comments about the effectiveness without actually analyzing "why".

The Ford Escort and the Ferrari are both cars but are not the same.
 
ResTech said:
I remember it this way... think of hypoventilation induced hypotension and why that is detrimental during a cardiac arrest. The frequent ventilations (hyperventilation) keeps a positive pressure in the chest and does not allow for the negative pressure to come into play which is where blood return to the heart comes from.
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Hyperventilation is a reduction of PaCO2. If the patient is tachyneic (high respiratory rate) allowing little time for expiration or there is air trapping caused by the tachypnea the patient may present with Auto-PEEP and hyperINFLATION which will cause hypotension. As well, when the FRC is extended, the PaCO2 may increase.
 
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I noticed a typo in my post... I meant HYPERventilation induced, not hypo.

I might be lost... I always thought hyperventilation meant as the name implies... a faster than normal rate of breathing (or over breathing) and not the level of PaCO2. Hyperventilation is a cause of low PaCO2... where a low PaCO2 is known as hypocapnia and not termed hyperventilation since you can have brief hyperventilation without hypocapnia or respiratory alkalosis.
 
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ResTech said:
I noticed a typo in my post... I meant HYPERventilation induced, not hypo.

I might be lost... I always thought hyperventilation meant as the name implies... a faster than normal rate of breathing (or over breathing) and not the level of PaCO2. Hyperventilation is a cause of low PaCO2... where a low PaCO2 is known as hypocapnia and not termed hyperventilation since you can have brief hyperventilation without hypocapnia or respiratory alkalosis.
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Fast breathing is tachypnea.

Hyperventilation is ONLY confirmed by the presence of a low PaCO2.

Babies, as are adults, with impending respiratory failure are tachypneic as the PaCO2 rises. They are NOT hyperventilating.

Hypocapnia is a term used for many states in which the PaCO2 is reduced either pharmacologically, mechanically or in the face of various disease processses. For TBIs, in some cases we will use the term "hyperventilate" ONLY if we have actually lowered the PaCO2 as confirmed by analysis of blood.

Hypoventilation can refer to various syndromes including those that are congenital which may being on a chronic increase in PaCO2 unless mechanically or pharmacologically controlled. If you get into analyzing respiratory patterns you will learn more about hyponea.
 
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medic417 said:
So everyone is talking about Lasix are you intending to give it to the OP's patient? If so explain your reasoning.
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Anyone? Anyone?
 
I was going to say "Yes" just to elicit the correct answer from you, but I already know why it's a no.




Renal failure = lasix is pretty useless.
 
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Darn you and your non-answering ways!


I'm going to go out on a limb and say it has to do with getting rid of excess potassium, and since potassium follows sodium, using a loop diuretic to get rid of the sodium should also get rid of the excess potassium.
 
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ResTech said:
Smash... why the Epi infusion over Dopamine or Dobutamine for cardiogenic shock?
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Well, there are a number of reasons, but the most simple is 'because it's there'.

There is scant (or no) evidence that inotropes in cardiogenic shock improve outcomes. In fact the opposite is true. Inotropes are merely a temporizing measure until interventional cardiologists can get their hands on the patient.

There is also little to suggest that any particular flavor of inotrope is better than any other. Given this it was decided that epi has at least one advantage over dobutamine/dopamine in that it has been used for decades so medics are familiar with it and it is cheap.

Ms Hochman has written a large number of papers on cardiogenic shock of various etiologies and is well worth a read regarding inotropes.
 
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