Elderly patient with persistent hypoxia

We present an unusual case of hypoxemia that was difficult to diagnose. The clinical scenario contained several small clues which when added up could perhaps, in retrospect at least, have led to timely diagnosis if they had been identified earlier. As this is a condition often discrete yet important for the physician to recognize we have presented the case for others to learn from. It contains interesting learning points on how to approach the hypoxic patient. We have used the opportunity to review basic lung physiology relevant to the clinician.

A 75 year old female, smoker, presented to the emergency department in an ambulance after being found on the floor of her apartment. She was fully conscious but had left-side hemiparesis and dysarthria. She was dyspneic and complained about bilateral pain low in the chest, radiating to the back.

Previous history was of hypertension and “some kind of arrhythmia” and she was currently taking antihypertensive tablets, ASA and zopiclone. There was no history of lung disease.

Examination and labs

General: Patient is awake,> Vitals on arrival:
• BP 162/102, pulse 112/min
• temp 37°C
• RR 28/min, sat 84% with 6L O2 on a simple face-mask
• Cardiac auscultation: normal
• Pulmonary auscultation: prolonged expiration, bronchial sounds with fine crackles at the base.
• Chest: A fresh bruise at approximately 6-7th rib on the left side, laterally to midclavicular line.
• Neurological examination: dysarthria, flaccid hemiparesis of left side.
• Labs:
• WBC 8.6, CRP 29
• Hemoglobin 170, platelets 115
• Na 142 K 3.6 creatinine 73
• D-dimer 8.47 (<0.25), CK 2.933
• ECG: atrial fibrillation 108/min, otherwise normal
• CT head: Old infarcts at basal ganglia bilaterally, old infarct in left temporal lobe. No fresh infarcts, no intracranial bleeding.

tPA was judged as not appropriate as time from onset of stroke was far too long. Admission to neurology was prepared but patient was stuck in ED as there were no beds available in hospital.

It was noted that she was persistently hypoxic and not responding to O2 despite general maneuvers (increased FiO2, sitting patient up).

Why is the patient be better oxygenated by sitting up?

V/Q and shunting physiology is complicated but it is quite clear that body position affects both ventilation and perfusion (eg. use of prone position for patients with ARDS in ICU). All in all, supine position tends to decrease patient's own breathing and collapse alveoli in posterior (dependent) part of the lung - this leads to increased 'physiological (right to left) shunting' which is otherwise discrete and nonsignificant in the healthy subject. Patient sitting up or with head elevated (20-30') will do more efficient breathing (ventilation) and open more alveoli and decrease V/Q mismatch.
[Phys. Ther. 1985] Effect of Body Position on Pulmonary Function

An ABG was drawn (with 10L of O2):

• pH = 7.46
• pO2 = 52mmHg (80-100)
• pCO2 = 31mmHg (34-46)
• HCO3 = 24 (22-26)
• (calculated) SaO2 = 87%

How do you interpret the ABG?

Uncompensated, mild respiratory alkalosis and hypoxia. Patient is hyperventilating to compensate for hypoxic state. Notice that pCO2 is not elevated, an important clue in the underlying condition.

Does the patient need to be intubated?

This patient does not have an immediate need of endotracheal intubation but certainly has a risk of decompensating fast due to exhaustion from hyperventilating, further decreasing SaO2 and starting a downward spiral of rising pCO2 and acidosis. We should keep in mind that having a SaO2 of 86%, this patient is at the rim of the steep slope of the oxygen–haemoglobin dissociation curve and there is no room for further desaturation.

Hypoxia management - ABC first!

Endotracheal ntubation is not risk free and there are still other options to help this patient. Emergency physicians are trained to always have a plan B and C, being mentally prepared for intubation is wise in this scenario and the patient should absolutely be placed in the critical care bay where the airway wagon is near.

• A - Airway: patient is awake and protects her airway, excluding need of nasopharyngeal (Guedel) airway
• B - Breathing: patient breathes spontaneously and does not need BVM assisted ventilation. FiO2 is 100% but flow can be increased so we change from simple mask to 15L O2 on reservoir mask which theoretically can supply lungs with approximately 80% oxygen.
• C - Circulation: is not a problem here, she has minor tachycardia but not so that it reduces carriage of O2 to tissues.

This is a good time to review possible routes of oxygenation, although FiO2 from wall is 100% it can be difficult to provide the patient with air 100% saturated with O2 molecules.Oxygen therapy devices

Plan B - high flow O2 in nasal cannula!

Using the nasopharyngeal route for oxygenation has until recently been thought to provide only limited O2 to the lungs but airway guru Richard Levitan has proven otherwise and his work has led to game changers in approaching the desaturated patient. These two articles introduced the main publication in layman language; [EpMonthly] The neglected orifice [EpMonthly] No desat!

In our case we’d throw on 15L of 100% FiO2 with a nasal cannula and ensure patient is sitting upright - this simple maneuver would most likely be enough to prevent an unnecessary RSI. BIPAP is not recommended if patient is tired or drowsy but a CPAP trial could easily be done.

The articles mentioned above have been widely accepted by front-line emergency physicians as breakthrough publications for airway management and considered a must-read for every physician practising airway management especially RSI. The authors, Richard Levitan and Scott Weingart, are both highly respected teachers of airway and high-intensive care management and one of todays most wanted speakers in emergency medicine conferences. Luckily they are also advocators of FOAM and thus provide most of their material on the world wide web, free of charge!

Hypoxia workup

We now had time to focus on the cause of hypoxia. The patient had no fever thus pneumonia was considered unlikely. With the bruised left chest wall, pneumothorax was considered and bedside ultrasound done. The ultrasound found absence of lung sliding (not normal!) on left side so a chest x-ray was ordered to evaluate for suspected pneumothorax. Noticeably, there were no signs of pleural fluid and absence of B-lines, ruling out hemothorax and pulmonary edema.

What is the DDX for lack of lung sliding on ultrasound

• pneumothorax
• pleural effusion
• massive consolidation/atelactasis
• pulmonary contusion
• advanced COPD
• pleural adhesion/pleurodesis
• severe fibrosis
• if intubated
• mainstem intubation
• poor ventilation
[Sonosite] Lung sliding explained

Bedside CXR showed no signs of pneumothorax but elevated left diaphragm and mediastinal shift to left side, indicating decreased left lung volume.

Formal radiologist review: “Decreased volume of left lung with shift of mediastinum and trachea to the left side. No evident infiltrates but suspected smaller peribronchial consolidations behind cardiac contour. No pulmonary stasis. “

Pneumonia could not be excluded even with lack of fever (remember elderly patients commonly have inappropriate vital signs) but ARDS was ruled out.

The meaning of mediastinal shift was not clear at this moment and the grossly elevated D-dimer value could not be explained so the next logical step was to have order a CT angiography of the lungs. Avid readers should by now be able to make a definite diagnosis as enough clues have stacked up!

What is the DDX for mediastinal shift?

• 1. Pulled (loss of lung volume)
• atelectasis
• fibrosis
• agenesis
• surgical resection
• pleural fibrosis
• 2. Pushed (space occupying lesions)
• pleural effusion
• pneumothorax
• large mass lesions
• 3. Mediastinal masses and thyroid tumors
• 4. Kypho-scoliosis

Radiologist's answer: "No sign of pulmonary embolism. Small consolidations posterobasally left side. No pathological lymph nodes. No pneumothorax."

Progress

IV antibiotics were initiated and we decided to consult the pulmonologist who then asked the radiologist to review the CT which on more thorough examination revealed a bronchial mucous plug (marked by red arrow at 0:28 in video). The patient went for bronchoscopy where the plug was drawn out and SaO2 rose.

Final diagnosis: obstruction atelectasis secondary to mucous plug. Not surprising for a patient - a smoker - who has been lying immobilised for a longer time with pain in thorax, restricting air movement and dehydration contributing to the mucus buildup. Not unlikely she also has an undiagnosed, underlying COPD.

Finally - why was the D-dimer increased in this patient?

D-dimer is probably the single most incorrectly used lab test in the ED, commonly leading to unnecessary CTs. Remember, d-dimer was designed to RULE-OUT thrombosis in low-risk settings - the way we're using it today is no how it was supposed to be!
A study made 2007 demonstrated that immobility can elevate D-dimer titers by 50-60%. Other conditions and habits of the patient are also known to elevate D-dimer titres. Of the non-pathologic reasons include cigarette smoking and old age and pathological conditions including atrial fibrillation, stroke and infection. [LITFL] Dealing with d-dimer debacles

Atelectasis

Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology and leads to a deflated lung segment or even whole lung collapse causing hypoxia. There are several different types of atelectasis, depending on the cause, as exlained below.

The video above shows how recruitment (=PEEP + ventilation) re-expands a deflated lung and helps us understand the importance of atelectasis. Lung collapse is atelectasis of the whole lung.

Atelectasis is primarily obstructive or non-obstructive, seperated mainly by their pathophysiology. Common causes of obstruction are foreign bodies, tumors and mucus plugs and the size of atelectasis mostly depends on where the obstruction is located (main-, lobal- or segmental bronchi). Obstructive atelectasis (the more common type) is also called resorptive atelectasis, refering to gas absorption distal to the obstruction. In a few hours this leads to retraction of the affected lung and ventilation-perfusion (V/Q) mismatch and shunting as circulating blood is not oxygenated. Secondary infection may occur. If the area is large there will be significant volume loss of the affected lung and secondary hyperinflation of the healthy lung leading to the distinct x-ray features of elevated diaphragm and mediastinal shift towards affected area.

Chronic atelectasis will eventually lead to fibrosis and widening of the bronchi, better known as bronchiectasis.

Non-obstructive atelectasis is caused by loss of contact between parietal- and visceral pleura and shares the same final outcome or total lung collapse. There are different types of non-obstructive atelectasis as well. Relaxation/passive atelectasis is caused by pneumothorax or pleural effusion, compression atelectasis caused by any-space occupying lesion within the chest and adhesive atelectasis by any disruption in surfactant, classically ARDS.

Atelectasis has many faces and the key to understanding its presentation, diagnosis and treatment is to know basic lung anatomy and the pathophysiologic mechanism. A detailed description of these can be found in the following excellent articles from eMedicine;AtelectasisPulmonary Atelectasis (pediatrics)

Atelectasis is a common concern in the ICU and post-operative ward. Decreased respiratory movements (eg. pain, diaphragma irritation), dehydration, O2 therapy and prolonged bed rest all contribute to atelectasis. The main methods to "recruit" alveoli are active adjustment of ventilator PEEP settings and the work of respiratory therapists encouraging patients to sit up and breathe properly with PEEP valves.

Symptoms and signs

They symptoms of atelectasis are subtle and non-specific; hacking, dry cough and sometimes mild fever. As atelectasis grows larger symptoms of hypoxia will dominate - cyanosis, dyspnea, tachycardia etc. On physical examination, dimishing breathing sounds may be the only clue.

Radiology

Plain chest X-ray (PA) is usually enough to diagnose the presence of an atelectasis but does neither define the type nor the exact cause.

• Direct signs:
  • displacement of interlobar fissueres (most reliable)
  • crowding of broncho-vascular markings
  • increased lung opacity (non specific)
• Indirect signs:
  • hilar displacement
  • mediastinal shift
  • diaphragmatic elevation
  • Compensatory hyperinflation (if chronic)

In case of obstruction atelectasis air bronchograms are typically not present unlike the non obstructive types. The exact CXR signs to look for differ depending on which segment is involved. The signs are somewhat complicated, however, this short illustrated video gives an excellent explanation

A bedside chest X-ray (AP), as in our case has lower accuracy and will only reveal gross atelectasis and volume reduction of affected side. If there is a concurrent pleural effusion or large mass it can be difficult to define the cause of the atelectasis on CXR alone and CT is needed. CT scan will show the exact size, shape and location of the atelectasis. It can help in differentiating the obstructive type from the non-obstructive type, and serves as a guide for subsequent bronchoscopy. Although the obstructing lesion can be seen it may be difficult to define the exact cause, e.g. whether it is due to a tumor or a mucous plug. Such distinction will often require bronchoscopy and sampling of bronchial material by suction, endobronchial biopsy or transbronchial biopsy.[Radiopedia] Lung atelectasis

Systematic approach to hypoxia

The patient´s data included the following important clues in the systematic approach to hypoxia:

• pCO2 was not increased and hypoxia therefore not caused by hypoventilation
• A-a gradient was very high or 622mmHg (expected 21.5) excluding the cause to be low inspired O2 (see http://www.mdcalc.com/a-a-o2-gradient)
• pO2 was not correctable by giving O2, suggesting shunt rather than V/Q mismatch and shunt is commonly caused by atelectasis, oedema, pneumonia or vascular shunt

Now wait a minute - what is the difference then between shunt and vascular shunt? Why doesn't pO2 increase with O2 when there's a shunt? It's time for a pulmonologist to explain some basic physiology! TIP: use Youtube's play faster feature for 1-2x playback speed (lower right corner)

Recommended reading on hypoxia: [The Medical Media Review] Hypoxia: Critical but Often Poorly Understood Concepts [Sashidhar Reddy] Hypoxia

Further reading

Life in the Fast Lane is one of the giants in the emergency medicine blogosphere and contains vast amounts of free teaching material for emergency physicians. It is one of our favorite websites. The LITFL guys have summarised all kinds of vital information for both new and experienced EPs;

• Airway management from A to Z, text and videos, the best out there!
  Own the airway
• A case of atelectasis with even more learning points. Also reviews possible treatment options which we have not done here.
  Lung collapse, recruitment and bronchoscopy

Pulmonologist's comment

Great case with many aspects and learning opportunities! In brief, if I had seen the patient I would have been immediately worried about the severe hypoxemia with respiratory alkalosis, commonly seen in pulmonary embolism. Therefore a lung CT angiogram would probably have been my first radiology test (I certainly hope so, but these things are so much easier in retrospect), after seeing the blood gas result. No CXR needed and I agree, definitely NO D-dimer! But the CT is difficult to read.
The case reminds us how easy it is to miss the unexpected on imaging studies, and that we should remember to thank our good colleagues in that field on a daily basis.
To view another aspect, this is a smoker with a mediastinal shift on CXR. This combination should make us think about lung cancer with endobronchial involvement. This was appropriately ruled out by bronchoscopy. Mucus plugs are common, especially in chronically ventilated patients, in those with asthma and in those with hypoventilation in general. Conservative treatment with mucolytics and respiratory therapy is often sufficient, however bronchoscopic suction with the help of saline may be required to remove plugs. In severe cases, mostly encountered in the ICU, different types of bronchoscopic instruments may be needed to pull out large, dry, and amazingly hard plugs, such as the one depicted above. Large or small, it is important to follow up on the removal of plugs with mucolytics, bronchodilators and physical therapy for several days to prevent the common problem of recurrence. /Ólafur Baldursson

Summary

So it turns out that the patient had a mucus plug leading to a large atelectasis resulting in hypoxia. The underlying mechanism is shunting where a large obstruction hinders blood flow from pulmonary arteries and redirects it to other areas already well oxygenated. Thus no increase in SaO2 is seen despite high flow FiO2 on a rebreather mask. As described, normal pCO2 is also typical for this type of hypoxia as ventilation itself is mostly unaffected.

• A chest X ray can be used to diagnose atelectasis but CT and/or bronchoscopy may be required to find the cause
• A-a gradient, pCO2 and pO2 response to oxygen are important to find the underlying cause of hypoxia
• Elevated D-dimer is specific for thrombosis but there are many other causes that need to be considered as well

Authors: Bergþóra Þorgeirsdóttir / David Thorisson

Young female with retrosternal pain and fever

Following is a case of a disease not so commonly encountered but worth knowing because of a concerning presentation - chest pain.

A female presents to the emergency department with a two day history of epigastrial pain. The pain is located right under the xiphoid process, and described as a sharp pain radiating through her chest and to the back. The pain is constant and worsens while lying on her back, on deep inhalation and when she eats or drinks. Lying on her left side alleviates the pain somewhat.

Her previous medical history includes Darier's disease (time to freshen up on your dermatology) and gastritis. Medications include Hydroxyzine (Atarax), oral contraceptive pill and isotretinoin (Accutane).

On examination there are no major clues as to her condition. Normal examination of lung­ and heart. Abdomen is non­distended, soft without guarding but diffuse tenderness mostly in the upper region. Bedside ultrasound shows no pericardial effusion, contraction is seen as normal and no signs of hypo- or akinesia. Gallbladder is not distended and no calculi are found. ECG is evaluated as normal with sinus rhythm, minimal inferolateral ST depressions and T ­inversions - concluded as nonspecific in the current clinical scenario. In the tachycardic patient with dyspnea pulmonary embolism could have been suspected.

Blood tests reveal slightly elevated CRP at 54 but other tests normal, Troponin T and d-dimer included. Chest x-ray is normal.

The morning after she develops fever 39°C. A trial of Gaviscon and Xylocain is unsuccessful. Augmentin 1,2g IV is administered empirically. On day three a gastroscopy is performed revealing multiple small, white, indented lesions in the esophagus. Candida infection is suspected and samples taken for PAD. CLO test is negative. She is suspected to have candida infection and admitted for treatment. The fever spikes occasionally up to 39.0°C but spontaneously resolves.

What do you think is causing retrosternal pain and fever in this young female?

Results come back from PAD and virology, surprisingly revealing an active infection with Herpes Simplex 1 (PCR positive). Other common causes of infectious esophagitis are candida and cytomegalovirus (CMV) and their presentation is similiar, requiring endoscopy for definite diagnosis.

A rare presentation for the above condition has been described where patient presented with intractable hiccups.

How are persistent hiccups defined and what are other important ddx to consider?

Hiccups for >48h are true 'persistent hiccups'. Many etiologies have been described but scaring ED physicians the most is the patient with ACS presenting as hiccups, it's been documented with several cases - enough for the lawyers to recognize it and the media to write about it. [Huffington Post 2012] Hiccups Were Patient's Only Heart Attack Symptom [Am J Emerg Med 2012] Hiccups as the only symptom of non-ST-segment elevation myocardial infarction

There are many treatment options and surely you should try rectal massage before pushing in that chlorpromazine!

Further reading

eMedicine has an extensive and excellent review as always [eMedicine] Esophagitis Amal Mattu as ever brilliant in his weekly ECG episodes, this time reviewing ECG findings in pulmonary embolism, do not start seeing patients in the ED until you have seen this! [Amal Mattu] ECG findings in pulmonary embolism

Authors: JMÆ/DBT

A shocking blood gas!

A healthy young man comes to the ED after having been chased by the police. They say he ran for his life at least 1km after which they found him lying down, presumably unconscious. With all systems intact and stable vitals he's presumed to be faking (pseudocoma).

A quick glance in the ED reveals nothing new to refuse this theory - the patient has closed eyes and is totally resistant to pain stimulation but has all reflexes intact (eg. gag, cornea-) and with eyes forced open he's looking straight forwards (to contrast with eg. roving eye movements if true coma). ECG comes in normal.

The police officers are informed that patient can return to police station as soon as blood results have been seen. And here they come...

With a hefty metabolic acidosis and lactate of 12,9 there's a minute of silence and doctors start thinking if there's a red herring in the room...

Could the patient be intoxicated after all?

Alcohols maybe?

He doesn't smell - but do all alcohols smell?

That's an anion gap of 18 - is it all explained by lactate?




With a presumed intoxicated patient fluids are ordered and patient is prepared for admission. Just that 45mins later the policemen come to let know that the patient is now awake and feeling well and ready to leave the ED with the officers. So a new blood gas (venous of course, who's sticking arteries these days anyways!) is drawn and voila;

All results normal... So the lactate acidosis turns out to be caused by strenuous physical exercise. Now howzaaat!



Learning points

• Lactate can be very high after exercise! I remember a study where alpine ski-ers had 6-7 after coming down a slope and I've heard experienced clinicians state it may temporarily reach 20 after seizure). But you can even get disturbing pH levels from it!
• Ethylene-glycol and methanol are odorless!

And my question to the audience: can I somehow calculate presumed anion gap from lactate levels, so that I can exclude other agents?

Acute dyspnea and bedside ultrasound

Elderly gentleman seeks the emergency department because of sudden dyspnea. He has no previous diagnosis of relevance such as COPD or heart failure. EMS notices crepitations on lung auscultation and treats patient with diuretics and CPAP with some relief. In the ED patient is still dyspneic and using accessory muscles for breathing but no clear crepitations are to be heard on auscultation and patient is not obviously obstructive. Stable vital signs, systolic blood pressure of 160mmHg.
Bedside chest x-ray is ordered but image result is not expected for a while. The ultrasound machine is turned on and the cardiac probe put on patient's thorax, revealing...

1. Heart, subxiphoid view

# Left > right ventricle => right strain and pulmonary embolism very unlikekly
# No pericardial effusion anteriorly, 2-3mm black line seen and assumed to be physiologically normal fluid
# Visually, decreased contractibility of left ventricle

2. Right pleura

Pleural effusion and several B-lines are clearly seen as the base of the lung reaches down, indicating right sided pulmonary edema

3. Left pleura

Great amounts of pleural effusion. No clots seen and thus no suspicion of blood. Multiple B-lines indicating left sided lung edema.

4. Right lung, apex

'Lung sliding' exludes pneumothorax. Multiple B-lines => edema reaches apex, suggesting massive pulmonary edema.

5. Left lung, apex

Same as right side; thus patient has massive, bilateral pulmonary edema.

The investigation was done in about 2 minutes.

The X-ray image arrives 45mins later

It shows enlarged heart with widened pulmonary veins and interstitial fluid bilaterally. Bilateral pleural effusion, more on left side. ProBNP arrives at 2500 with minimal Troponin elevation. Patient is treated as acute left sided heart failure and treated with CPAP and nitro infusion (SCAPE).

Discussion
Previously, ultrasound has been said to be impossible to use for evaluating lungs, after all "air is ultrasound's greatest enemy". Experimenting with this has shown that indirect signs can be seen such as A- and B- lines and as air is replaced with consolidations and edema, ultrasound will immediately pick this up. For pneumothorax and pleural effusion, pulmonary edema and consolidations (pneumonia or ARDS), ultrasound is becoming a first choice for quick bedside evaluation. Increasing amount of data is supporting this and in some emergency departments, bedside chest x-ray has been replaced by ultrasound as only CT has better sensitivity for most conditions of relevance in the ED.

Pneumothorax:
Acad Emerg Med. 2005 Sep;12(9):844-9
“The sensitivity for chest radiography was 75.5% (95% CI = 61.7% to 86.2%) and the specificity was 100% (95% CI = 97.1% to 100%). The sensitivity for US was 98.1% (95% CI = 89.9% to 99.9%) and the specificity was 99.2% (95% CI = 95.6% to 99.9%)”

Pleural effusion, pulmonary edema, consolidation:
Anesthesiology. 2004 Jan;100(1):9-15
“Auscultation had a diagnostic accuracy of 61% for pleural effusion, 36% for alveolar consolidation, and 55% for alveolar-interstitial syndrome. Bedside chest radiography had a diagnostic accuracy of 47% for pleural effusion, 75% for alveolar consolidation, and 72% for alveolar-interstitial syndrome. Lung ultrasonography had a diagnostic accuracy of 93% for pleural effusion, 97% for alveolar consolidation, and 95% for alveolar-interstitial syndrome. “

Let's summarize the data above:

	Auscultation	Chest X-ray	Ultrasound
Pleural effusion	61%	47%	93%
Consolidation	36%	75%	97%
Pulmonary edema	55%	72%	95%

Pulmonary embolism
The story of ultrasound becomes only better and better. Here, ultrasound is compared with CT for diagnosis of pulmonary embolism - the condition every physician fears to miss.
Chest. 2001 Dec;120(6):1977-83:
“The sensitivity of TS [transthoracic sonography] for detecting PEs was 80% (sensitivity of CT scanning, 82%), and the specificity of TS for detecting pulmonary lesions was 92%”


Volume status and heart - ultrasound for evaluation for shock
With ultrasound, a rough estimate of cardiac function and volume status (~vena cava status) can be done in instant. Together with above mentioned evaluation of thorax, ultrasound can in only 2-3 minutes give the physician a reliable diagnosis of acute dyspnea or shock. Add to this testing for free abdominal fluid, evaluating aorta and DVT diagnosis of lower extremities and then we have a full RUSH protocol (also known as FATE):
 RUSH: Rapid ultrasound for Shock and Hypotension

Yes folks, the ultrasound is certainly here to stay!

Iceland to the foreigner

Iceland is a country of 320.000 inhabitants known for welcoming visitors wholeheartedly. The landscape is rough yet soothing and has fostered inspiring artists such as Björk and Sigurrós and lately been attracting Hollywood’s film-makers. The wild highlands, mountains and clean water provide the world’s best raw-materials such as salmon and lamb-meat and Reykjavik is renowned for it’s high quality restaurants. The atmosphere in Iceland is unique and if you at anytime need peace from all the ongoing events you never far a way from a natural hot spring to soak in. Iceland is definitely the place to visit for the adventurer seeking something different!

More about Iceland

The 5 best hot springs in Iceland

A few selected videos from Iceland...

Chest pain with subtle yet serious ECG changes

Following is a classic case underlining the importance of "STEMI equivalents" or ECG patterns requiring prompt attendance and cath lab activation as if it were a true STEMI.

A 74 year-old previously healthy woman presented to the emergency department by ambulance with chest tightness and left arm numbness following exercise. She was stable on arrival, BP was 140/65 and pulse regular 65/min and pain free after receiving nitroglycerin.

Describe the T waves shown on the ECG

This ECG mainly shows prominent inverted T waves in V2-5.

What are they indicative of?

Biphasic or inverted T waves in precordial leads strongly suggest critical left anterior descending coronary artery stenosis. This pattern is referred to as Wellens syndrome or "LAD coronary T-wave syndrome". Generally, there is a history of angina and troponin levels are either normal or mildly elevated. ST elevations are rarely present. The majority of patients with this ECG pattern will develop extensive anterior myocardial infarction within weeks if no intervention is taken. Therefore, recognizing this pattern is of critical importance and cardiac catheterization should be performed promptly, despite a pain free patient.

Which test could be lethal for this patient?

This patient is likely to have very limited circulation to the anterior myocardium. A stress test could easily induce arrhythmias or in worst case cardiac arrest.

What are STEMI equivalents?

Patients with STEMI equivalents have acute coronary artery occlusion without the classic ST elevation patterns we have all been taught not to miss.

A paper by Rokos et al published in the American Heart Journal in 2010* reviewed STEMI equivalents requiring cath lab activation:
1) Posterior (V1-3) ST depressions
2) ST elevation >1mm in aVR along with depression of anterior leads
3) de Winter ST/T wave complexes anteriorly

This article is free to view in link below but our great colleague and emergency physician Andy Neill in Ireland has reviewed the article nicely on his blog.

Wellens syndrome is a chronic coronary artery occlusion and therefore not a STEMI equivalent. It is nonetheless a serious and unstable condition that requires prompt intervention and every physician should be able to recognize it.

Our patient was admitted to the cardilogy ward and was scheduled for cardiac catheterization the following day. She was stable and pain free on admission. A few hours later she developed a circulatory collapse and underwent acute catheterization which revealed critical stenosis of the left main coronary artery, LAD, circumflex artery and right coronary artery.

* IC Rokos, WJ French, A Mattu, G Nichol, ME Farkouh, J Reiffel, GW Stone. Appropriate Cardiac Cath Lab activation: Optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J, 160 (2010), pp. 995–1003.

Read more about Wellens at LITFL What is Wellens syndrome?

Maria Reynisdottir (stud. med.)

A case of extreme heart failure

This is a case of a complex heart failure patient I encountered in my residency. It contained many learning points which I'd now like to share, especially relating to clinical examination and approach to the patient with dyspnea and heart failure.

60 y/o female comes with an ambulance to the ED because of increasing dyspnea for the last week. No chestpain, no fever, no coughing. She had initially sought her GP who noted low systolic blood pressure of 80mmHg and called an ambulance to send her directly to the hospital. Because of hypotension, paramedics decided not to give diuretics.

In the emergency department, the patient is awake but tired and has resting dyspnea. Cheyne-Stokes breathing pattern is noted (frequency of 30 respirations/minute with few seconds of apnea intermittently). She has central and peripheral cyanosis and is peripherally cold, her skin is not marmorized or clammy. Vital signs show varying blood pressure, initial measurement 128/70, pulse 90/min. Intermittently her systolic pressure is as low as 75mmHg. Pulsoximeter shows show saturation of 74% with 3L O2, it has been placed on both hands and even earlobes and always has same values. She is afebrile.

Patient has a previous history of 3-vessel coronary disease and end-stage heart failure, EF has previously been evaluated as 15-20%.

What is Cheyne-Stokes breathing and what does it imply in this case?

It is the pattern of alternating periods of hyperventilation and apnea and is often frightening to those who see it for the first time. CS is generally coupled to neurological diseases and palliative care but has a strong correlation (30-50%) with congestive heart failure. The pathophysiology is not fully understood but is thought to derive from an imbalance between central respiratory drive and pCO2 in blood. [Clinics (Sao Paulo). 2005] Cheyne-Stokes respiration in patients with congestive heart failure: causes and consequences

What is the difference between central and peripheral cyanosis?

Central cyanosis is a sign of desaturated blood because of poor ventilation or low cardiac output while peripheral cyanosis is because of poor perfusion. Not so important to distinguish clinically but central cyanosis is generally more serious.

Is the saturation of 74% in this case a reliable value?

No. A standard ED pulsoximeter estimates O2 saturation by using infrared light to calculate the difference between bound and unbound hemoglobin. It therefor depends on several factors such as pulsation of blood and thus adequate circulation. Which is not true in this case (previously documented decreased EF and clinical signs such as cold, cyanotic hands). Other factors known to interrupt the pulsoximeter are carboxyhemoglobin and methemoglobin (false normal values). LITFL has more details on the clockwork of a pulsoximeter

How can we obtain a more correct value?

Obviously, whatever we do with this kind of pulsoximeter, we will always get a false saturation value. Some ICUs use a more advanced pulsoximeter e.g. Masimo which doesn’t rely on peripheral circulation. In the ED, we need an arterial blood gas. Masimo pulsoximeter

Patient was evaluated as critically ill but did not show clincal signs of immediate threatening circulation or organ failure; she was awake and alert so we decided we had some time to work her up and wanted to start with blood samples, first of all blood gas. The patient was cachetic and we had a hard time finding proper, pulsating arteries; the radial pulses could not be found and the inguinal ones were very vague.

Would it be safe to draw an ABG from the femoral artery?

The risks involved in punctuating an artery are infection, bleeding and hitting other structures such as the accompanying femoralis nerve.
Using sterile techniques the infection risk can be minimized and the fact that we are only punctuating, not inserting a catheter, makes the risk even lower. Bleeding risk with a small needle such as the one mounted to the blood gas syringe is minimal. The risk of hitting the femoral nerve is overestimated, especially if ultrasound is used where the needle can be seen to hit the artery and nothing else. Even in the case of touching or even penetrating the thick sheath of the femoralis nerve, the risk of permanent damage is astronomical with needle so small. This has been thoroughly documented in the literature from research of femoral nerve blocks where complications are extremely rare. Expect the femoral artery at 1,5cm depth in the normal-sized patient and expect problems in obese patients where it may lay as deep as 5-7cm, far beyond reach for the short ABG needle.
Despite very low risk of injury, punctuating the femoralis artery (or vein even) is in my opinion rarely seen unless in extremis such as cardiac arrest and should be considered as a valid option when other sites are not possible.

What other punctuation sites would be feasible for an ABG?

An alternative for those not so intrigued would be to find the brachialis artery which in most patients is easily palpated in the antecubital fossa, between the medial epicondyle and biceps brachii tendon.

The brachialis artery lies much deeper and will commonly move away from needle and thus harder to get to. It is though though commonly used in pediatrics where it is easier to maneuver.

We have been taught that volume status can be estimated from hemoglobin levels, what in the ABG tells us that Hb=153 is likely false?

Estimating volume status from Hb is known practice but should not be done from the sole value but rather the clinical picture. This patient is a heavy smoker and it shows in the CO-Hb value of 6.9% (normal: less than 1%). The patient has developed secondary polycythemia and the Hb values should be considered as falsely elevated.

A decent brachialis vein was seen and a venous blood gas (VBG) was drawn, revealing the following values:

• pH 7.280
• pCO2 6.42 kPa
• pO2 2.74 kPa
• Na 128
• K 4.8
• Crea 86 umol/L
• Ca 1.13 mmol/L
• Cl 95 mmol/L
• Glu 6.1 mmol/L
• Lactate 7.0
• Hb 153 g/L
• CO-Hb 6.9%
• MetHb 0.8%
• calcluated SatO2 27.6%
• HCO3 19.0mmol/L
• BE -3.8mmol/L

A lactate of 1.0 was found only a week ago. This VBG shows a state of mixed respiratory (uncompensated) and metabolic acidosis with normal anion gap (14) - most likely explained by lactic acidosis. As expected, the patient is sick! Increased lactate tells us that tissues are not being perfused adequately and most likely this is because of the heart failure and impending respiratory failure - the patient was getting tired of prolonged hyperventilation and needs help.

Lactate from VBG... that's not possible?!

So untrue, it's perfectly doable as long as it's correctly done; put on ice, take it to the analyzer within 10 mins! Scott Weingart's Lactate FAQ

A pO2 value of 2.74kPa is low, even for a VBG. Is the patient severely hypoxic?

There are two important learning points here and we should spend some time discussing this. The pO2 is very low and reflected in the SatO2 of 28% which is *calculated* from PO2. But that's where the fallacy begins.
A VBG has been show to correlate very well with ABG except for very high pCO2 states, uncommonly encountered and mostly irrelevant (have you heard of the patient who was incredibly hypercapnic? Would you run faster than if he was "just" hypercapnic?). For obvious reasons, VBG cannot measure PO2 since it is always presumed to be arterial and more commonly denoted as PaO2 (note that extra "a") to indicate it's arterial origin. Thus the calculated SaO2 value will always be wrong from a VBG - something I learned by error in this case!
But more important is the distinction between PaO2 and SaO2, mistakenly believed to correlate pretty well. After all they both measure the amount of oxygen in the blood. But PaO2 does not measure effective oxygen, ready for use by the tissues. It's just free O2 molecules and they need to be bound to hemoglobin to be of any use peripherally in tissues. Indeed, too high PaO2 (eg FiO2 100% for longer periods) sets ground for harmful free radicals - Amal Mattu recently had a great post on this on EmRap, reminding us to use O2 sparingly in the post-resuscitative phase after cardiac arrest.
Nontheless - PaO2 clearly indicates how much O2 the patient is taking in through the alveoli and low values suggest you should increase FiO2 and/or assist ventilation and even intubate if everything else fails. What PaO2 does not indicate is if the tissues are *receiving* O2 - the intubated patient on 100% FiO2 can die from hypoxia if hemoglobin is not working (eg. CO poisoning, severe anemia) or perfusion decreased (heart failure, severe bleeding). Indeed, that's the definition of shock, whatever it's cause.
The "perfusing O2" in blood is called 'oxygen content', CaO2 and it's value is calculated by the following formula:
CaO2 = SaO2 * 1.34 * Hb + 0.003 * PaO2
Which underscores the above; perfusing oxygen is literally independent on PaO2. To actually measure tissue perfusion (or hyperperfusion to be accurate), we need... lactate (there are more advanced tools in the ICU eg. Picco)! It's not the most important clinical knowledge but one of the cornerstones of understanding O2 in clinical medicine and reminder to the physician to not only look at the PaO2 value but the whole clinical picture. Excellent in-depth explanation of difference between pO2 and SatO2 Amal Mattu on EmRap: Post Cardiac Arrest Syndrome

Because of hypotension the nurse was getting impatient and wanted to start fluids. A more thorough examination is done:

• Skin: no turgor but general, diffuse pitting edema of whole body, hands, feet, sacrum and even up to flanks.
• Cardiac: distant heart sounds, possibly S3 and a pansystolic murmur. Neck vein distension.
• Lungs: normal respiratory sounds, no crackles, no wheezing heard.
• Bedside ultrasound: a large liver but IVC was hard to visualize properly (this was in my first months of doing ultrasound, no pleural windows were done!). A rough "ECHO" shows all four chambers diffusely dilated and severe global hypokinesia of left ventricle, EF estimated 5-10%.

A chest x-ray is done revealing considerable amounts of pleural fluid on right side, none on left. Slightly dilated central veins, no edema, no infiltrates.

Should this patient have fluids or diuretics?

This is a topic of great debate and a very interesting one as myths have been debunked and treatment protocols changed in only recent years (eg. Morphine is now out of AHF treatment unless palliative). All in all - recent studies have taught us that we have been doing it wrong for a long time and there is no single approach to the acute heart failure patient. The Forrester classification is an excellent categorization into four general categories of warm/cold (degree of perfusion where cold is hypoperfused as in this case) and wet/dry (with regard to pulmonary edema - our patient is dry). The different types of AHF need different treatment modalities and the patient above is a cold/dry one (with regards to pulmonary edema - chronic heart failure has collected edema peripherally with pitting edema, neck vein- and liver stasis).
Diuretics may be causing more harm than good as admitted patients get electrolyte imbalances and kidney failure. Their immediate circulatory effects are minimal and very short living and thus doubtful if they fit in AHF treatment at all. Inotropic medicines such as dopamine or simdax are much more relevant in this scenario, even vasopressors to induce better perfusion to tissues.
As Amal Mattu has so excellently pointed out, what seems “most correct” is to use diuretics to treat volume overload, not AHF by itself. If the lungs are full of edema because the whole body is and that fluid puts even more strain on the decompensated heart - whole body fluid needs to be removed. But these patients most commonly will present with acute onset of symptoms and with high blood pressure and need nitro and CPAP, not diuretics. These are the SCAPE patients, standing for “Sympathetic Crashing Acute Pulmonary Edema”. Scott Weingart’s podcast about SCAPE is a must listen as you will encounter these patients often in the ED and with no time to prepare yourself. They will be terrified when you see them because their adrenaline levels are sky high - thus the hypertension. European Heart 2005 guidelines on acute heart failure

What is the medical jargon for massive pitting edema?

Anasarca.

Could unilateral, right sided pleural fluid originate from heart failure?

The most common cause of pleural effusion is heart failure. Frequently the effusions are bilateral (approximately 75%) but may occur alone on either side with the right side being more common.

Cardiology was consulted and was a little puzzled on the diuretics question but decided it was worth trying small dose lasix on the assumption that some inotropy (contractility) might be gained by shifting the Frank-Sterling curve. Patient was not obviously dehydrated and hypotension is most likely because of low cardiac output. In the cardiology unit Simdax and vasopressors (noradrenaline) were infused to treat a previous diagnosed 'dilated cardiomyopathy' on ischemic basis. The patient had previously stated she didn't want to be operated and only wanted medicines for symptomatic relief.

Major learning points from case

• Standard pulsoximeters in the ED cannot be relied on for SaO2 in heart failure or any form of decreased circulation.
• VBG can be drawn from femoral vein, as long as sterile technique is used and navigated by ultrasound.
• VBG correlates excellently with ABG values except for PO2, in low perfusion states an ABG must be used since the pulsoximeter gives false values.
• Hypotension does not equal hypovolemia!
• Diuretics should not be pushed thoughtlessly in acute heart failure and are seldomly first line treatment anymore - not even in acute, pulmonary edema or congestive heart failure!

David

/David