In part 1 I described the PH balance associated with the rapid breather. In part 2 we reviewed hyperventilation syndrome. In part 3 I gave a brief description of a chronic lunger, and how to treat them. In part 4 I am going to go over congestive heart failure(CHF). This happens to be one of my favorite topics.

Ok, in part 1 I explained the many causes of rapid breathing, and in part 2 we went over one of them, hyperventilation syndrome. In part 3 I am going to briefly go over some other causes of rapid breathing.

I plan on using quite a few images and videos in my blog to assist the visual learner. I hope this helps.

Most COPD patients have chronic bronchitis so lets start by explaining chronic bronchitis. As Dr. Fink stated, this condition occurs when the bronchial tubes become inflamed, hints the term bronchitis. This is different from the common respiratory infection, also termed bronchitis, that may accompany cold symptoms. This condition is more associated with smokers. Check out this video for a pretty cool look at the effect of smoking on the alveoli.

To the left here you can see a barrel chest. This condition is also present in some patients with asthma, dysplasia, cockayne syndrome, and silicosis. Emphysema patients, pink puffers, are the more commonly known barrel chested patients.

• Emphysema leads to weight loss, Chronic bronchitis leads to weight gain
• Edema is usually absent with emphysema and present with chronic bronchitis
• Central cyanosis is particular to advanced chronic bronchitis
• Emphysema patients are usually thin waisted.
• Hyperresonance is more commonly percussed on emphysema patients
• JVD may be more present in chronic bronchitis patients(sign of pulmonary HTN)
• Right axis deviation, RVH, and atrial arrhythmias are more associated with chronic bronchitis.

Above, to the left is a “pink puffer” and to the right is a “blue bloater”. Both images courtesy of bronchitis.com

The next type of patient I am going to describe is the asthma patient. Then, since asthma and COPD patients require similar treatment, I will go over treatment strategies.

Asthma is defined by the National Heart, Lung, and Blood institute as a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness(bronchospasm), and an underlying inflammation. While COPD usually effects people over the age of 40, asthma can be present in all age groups.

In terms of symptoms, asthma is defined by paroxysms of diffuse wheezing, dyspnea, and cough, resulting from spasmodic contractions of the bronchi. Airway obstruction is reversible(but not completely in some patients). The increased responsiveness is due to a variety of stimuli. Here is another video

The biggest indicator that you are dealing with an asthma or COPD patient will be a medical history. These patients will usually know that they have one of these conditions. Usually when these patients are having an exacerbation of symptoms they won’t even need us.

This is a significant thing to remember, because if they called us it could be bad.

Status asthmaticus is an acute exacerbation of symptoms that does not respond

bronchodilation or other primary treatments. These patients may be in tripod position, using accessory muscles, they may have chest tightness, and a dry cough. Extreme wheezing and labored breathing will be present. These patients are at high risk for hypoxic induced cardiac arrest. The picture to the right is of tripod position.

Treatment:

Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. delbridget@msx.upmc.edu

The treatment of acute asthma exacerbation consumes a significant portion of emergency medical services (EMS) system resources. Because few studies have addressed EMS treatment of asthma, most EMS providers model their approach to treatment on strategies thought to be effective in the emergency department. During the treatment of asthma, a patient’s history and current airway and respiratory status are important components of the initial assessment. Although the general evaluation may address a patient’s appearance, vital signs, mental status, level of fatigue, and ability to speak normally, the initial assessment of an asthmatic patient must focus specifically on his or her respiratory effort and quality and on objective measurement of the patient’s blood oxygenation. Inhaled beta-agonist therapy is the widely recommended first choice of treatment, but anticholinergic agents and steroids may also have roles. Although not routine treatments, parenteral magnesium and epinephrine may also be beneficial for certain patients. Endotracheal intubation is a procedure of last resort and should be reserved for patients at immediate risk of respiratory arrest. Finally, EMS providers must be alert to the danger of using a “treat and release” approach, as recommended by some protocols, in the treatment of acute asthma. The quick results and benefit that short-acting treatments provide can easily and erroneously lead a provider to believe that an attack has been adequately controlled when, in fact, a more serious exacerbation may be imminent. Treatment protocols, therefore, should discourage EMS personnel from this practice and advise them to always transport asthmatic patients they have treated to the hospital to undergo more extended care and monitoring.

Your treatment should be based on the severity of your patient’s condition. The following are treatments for COPD and asthma.

Mild respiratory distress with mild hypoxia – Use a calm and reassuring voice, provide increased supplemental O2. Nebulized Albuterol, if refractory. Remember, these patients may have chronic mild hypoxia.

Moderate respiratory distress and hypoxia – Albuterol(proventil) updraft, add ipratropium(atrovent) if the patient has been using their inhaler or nebulizer. Consider corticosteroids (Solumedrol). If refractory, consider magnesium sulfate or epinephrine.

Severe respiratory distress – Consider immediate endotracheal intubation and/or epinephrine if the patient is pre-arrest. If possible, administer nebulized Albuterol/Atrovent, and magnesium sulfate before resulting to intubation.

*If you have a CPAP with adjustable PEEP, it may be possible to improve the outcome of your patient using a low PEEP setting. Higher PEEP settings run a high risk of causing a pneumothorax due to the increased intrathoracic pressure.

New Castle County EMS, DE, USA. R.Sullivan@co.newcastle.de.us

When used correctly, CPAP has been shown to alleviate symptoms and decrease the need for intubation for patients with CHF, COPD and asthma. It is safe, portable and easy to apply. CPAP does not replace intubation, but rather is a less-invasive means of providing respiratory support while medications work to correct the underlying cause of distress.

Intensive Care Unit, State University of Campinas, Brazil.

BACKGROUND AND OBJECTIVE: Hyperinflation with a decrease in inspiratory capacity (IC) is a common presentation for both unstable and stable COPD patients. As CPAP can reduce inspiratory load, possibly secondary to a reduction in hyperinflation, this study examined whether CPAP would increase IC in stable COPD patients. METHODS: Twenty-one stable COPD patients (nine emphysema, 12 chronic bronchitis) received a trial of CPAP for 5 min at 4, 7 and 11 cmH(2)O. Fast and slow VC (SVC) were measured before and after each CPAP trial. In patients in whom all three CPAP levels resulted in a decreased IC, an additional trial of CPAP at 2 cmH(2)O was conducted. For each patient, a ‘best CPAP’ level was defined as the one associated with the greatest IC. This pressure was then applied for an additional 10 min followed by spirometry. RESULTS: Following application of the ‘best CPAP’, the IC and SVC increased in 15 patients (nine emphysema, six chronic bronchitis). The mean change in IC was 159 mL (95% CI: 80-237 mL) and the mean change in SVC was 240 mL (95% CI: 97-386 mL). Among these patients, those with emphysema demonstrated a mean increase in IC of 216 mL (95% CI: 94-337 mL). Six patients (all with chronic bronchitis) did not demonstrate any improvement in IC. CONCLUSIONS: The best individualized CPAP can increase inspiratory capacity in patients with stable COPD, especially in those with emphysema.

I don’t really need to explain these treatments. If you have been a paramedic for any period of time, you have probably created your own treatment routine for these patients. That’s fine, this blog isn’t trying to change that. I’m just giving you some tools to better understand each patient’s physiological situation. This may assist you in making a better clinical decision in the future.

One thing I haven’t mentioned yet is hypoxic drive. I will leave it to this great link, “The death of the hypoxic drive theory“.

Ok, so that’s all I have to say about the chronic lungers. In part 4 I am going to go over the main cardiac cause of rapid respirations, congestive heart failure.

Developing a differential diagnosis for these patients is important. This isn’t very hard to do but it may be something that was never taught to you in paramedic school. It is important because treating a patient with hypoxia as if they had hyperventilation syndrome could absolutely be causing more harm than good. Don’t go into these calls just guessing as so many do.

So what is hyperventilation syndrome?

As classically defined, hyperventilation syndrome is a condition in which minute ventilation exceeds metabolic demands, resulting in hemodynamic and chemical changes that produce characteristic dysphoric symptoms. Inducing a drop in arterial pCO₂ through voluntary hyperventilation reproduces these symptoms. Recently, however, this model has been challenged with the observation that many patients with hyperventilation syndrome do not manifest low arterial pCO₂ levels during attacks. In some cases, patients with this syndrome have demonstrated altered respiratory physiology that is manifest as a slower return to baseline of the pCO₂ after voluntary hyperventilation to a defined level of pCO₂.
- eMedicine

Wow, okay now that we got through that I am going to explain what I am talking about a little better(well maybe not better, but definitely easier to understand).

Hyperventilation syndrome is a stress induced form of tachypnea. The rapid respirations are generally brought on by a stressful event or chronic stress that has just become too much. These rapid respirations cause the body to blow off too much CO2, and don’t allow for adequate cellular respiration. This situation may be termed a “panic attack”, and is most common, as you may have guessed, in people with a history of anxiety.

These patients tend to breath using their upper thorax and subsequently have hyperinflated lungs. This interferes with their tidal volume increasing dyspnea.

Here’s the problem:

Although these rapid breathers will feel like they can’t get enough air, the opposite is true. These patients will be retaining too much O2, and will have too little CO2 in their blood. This leads to respiratory alkalosis.

Fortunately, this problem usually doesn’t kill people. In fact, I have never heard of a case where a patient died as a result of a panic attack. I guess they could be driving and end up in a deadly traumatic event, but you know what I mean. The reason they don’t die is that they will usually end up passing out before their condition becomes deadly.

*The image above was borrowed from a stress treatment website.

I remember a call that I ran involving a more severe case of hyperventilation syndrome. The patient was a 19 year old female with a history of panic attacks. She was breathing about 40-50 times per minute upon arrival. I attempted to talk her down, which usually works for me, but to no avail. She ended up passing out. I figured this would be a good thing and she had just fixed herself. While she was unconscious her respirations returned to normal but the second she awoke, her rate was sky high once again. Her mother was contacted and she told us that the patient usually receives Ativan at the ER. I administered 5mg of Versed intranasal which helped us get her to the ambulance, and I received orders for 1mg of Ativan during transport.


So how did I know that she was having a hyperventilation crisis?

First, obtain a SAMPLE history(Hx):
S (signs/symptoms) – This will obviously include rapid respirations and possibly any of the following: Dizziness, parasthesia (tingling in hands and mouth), stiffness in fingers and hands, cold hands/feet, palpitations, or anxiety.

A(allergies) – Not relevant for inclusion criteria, but a good way to rule out anaphylaxis.
M (medications) – anxiety meds (ex. Xanax) will help for inclusion criteria, and lack of repiratory meds would help to rule out a chronic lunger(COPD/asthma patient).
P (past medical Hx) – Obviously anxiety or agorophobia would be inclusive, and the lack of chronic respiratory problems, recent surgeries, smoking, etc. would help rule out other issues.
L (last oral intake) – Another way to rule out possible allergic reaction and/or dehydration.
E (events leading up to) – Any stress induced event would be inclusive, usually emotional stress but physical stressors are a possibility.

Next, conduct an assessment:

Skin – pink, warm, & dry skin indicates hyperventilation syndrome. Cyanosis would indicate a more severe hypoxic situation.
Vitals – HR usually increased with hyperventilation syndrome. Initially increased with hypoxia then it may rapidly decrease. *SPO2 should be about 100%.

*The SPO2 finding is pretty important when differentiating hypoxia-induced tachypnea from hyperventilation syndrome. Because we are retaining too much O2 and not enough CO2, our O2 saturation should be 100% while our ETCO2 will decrease. This may be your most conclusive finding.

Above is an image from capnography.com which shows how hyperventilation will appear on wave form capnography. As respirations increase, CO2 output decreases. This results in smaller wave forms. Your readings will drop well below 35 mmHg.

So obviously it is not necessary to do all this just to decide if your patient is just hyperventilating. These are just some tools to assist you if you are having one of those tough cases. If your patient has a history of anxiety, 100% SaO2, and has clear breath sounds, they are probably just hyperventilating. Time to treat them, and this is another way to help you make your differential diagnosis. If they are refractory to your treatment, they may be having another issue. If they respond, abracadabra!

Treatment:
The best way to treat the majority of these patients will be firm instruction. I say firm, but that doesn’t mean to be hostile. Be calm and explain the situation. It helps to have the patient rub their tingling/stiff hands on their legs while you instruct their breathing. Have them take a deep breath and hold it. Then have them exhale on your command and breath when you tell them to. It is also helpful if you tell them to breath from the belly. This may help them use their diaphragm more effectively. Stay away from deflated non-rebreathers and paper bags. We don’t do that!

If the patient is in hyperventilation syndrome and does not respond to the above treatment, pharmaceutical therapy may be indicated. My protocol allows me to administer Versed for these patients. Any prehospital benzodiazepine would probably do pretty well.

More from eMedicine:

Because respiratory distress or chest pain has many potentially serious causes, this diagnosis should never be made in the field. Even when a patient carries a prior diagnosis of hyperventilation syndrome (HVS), it is still necessary to transport patients with these complaints to a hospital for a more complete evaluation. Rebreathing into a paper bag is not recommended in the field. Deaths have occurred in patients with acute myocardial infarction (MI), pneumothorax, and pulmonary embolism who were initially misdiagnosed with HVS and treated with paper bag rebreathing.

Okay, the talk down method and benzodiazepines will probably not harm these patients. I think eMedicine is stretching with the first statement. Putting them in the ambulance and driving is not a solution. We are clinicians and we have the ability to help these people. Treating paramedics like cab drivers is a result from the few bad apples in our field. We need to raise the bar for ourselves if we want the respect we deserve. I’m starting to rant here, so I am going to stop myself before I get too far off topic. Anyhow, treat these patients, please.

So that is hyperventilation syndrome. In part 3 I will explain other causes of rapid respirations.

Check out this video for simple treatment methods of hyperventilation.

Some other sources:

• eMedicine
• Archives of Internal Medicine
• JNNP(need subscription)