Ventilation Perfusion Mismatch

Alveolar gas exchange depends not only on ventilation of the alveoli but also on circulation of blood through the alveolar capillaries. This makes sense. You need both oxygen in the alveoli, and adequate blood flow past alveoli to pick up oxygen, other wise oxygen cannot be delivered.

When the proper balance is lost between ventilated alveoli and good blood flow through the lungs, ventilation/perfusion mismatch is said to exist. The ventilation/perfusion ratio is often abbreviated V/Q. V/Q mismatch is common and often effects our patient’s ventilation and oxygenation. There are 2 types of mismatch: dead space and shunt.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

What Is The Importance Of Dead Space?

Dead space is the portion of the respiratory system where tidal volume doesn’t participate in gas exchange: it is ventilated but not perfused. There are three types of dead space: anatomic, physiologic, and that dead space belonging to any airway equipment being used to assist ventilation. They all impact how well a patient ventilates.

Anatomic Dead Space

Anatomic deadspace consists of the parts of the respiratory tract that are ventilated but not perfused. It consists of conducting airways such as the trachea, bronchi, and bronchioles —structures that don’t have alveoli. It’s called anatomic because it’s fixed by anatomy and doesn’t change.

About a third of each normal breath we take is anatomic dead space, which means that a third of each breath is essentially wasted. Dead space is age dependent. It’s highest in the infant at 3 ml/kg ideal body weight and is about 2 ml/kg in older children and adults. An adequate tidal volume must include enough volume to also fill the deadspace, otherwise not enough air enters the alveoli and the patient hypoventilates.

A healthy teenage boy weighing 60 kg (132 lb) will have about 360 ml of alveolar ventilation . A healthy infant weighs about 2.7 kg (6 lb) will have about 22 ml alveolar ventilation. In terms of liquid volume, that’s a can of soda vs. about a tablespoon — an impressive difference. Let’s look at an example of how anatomic deadspace impacts adequacy of breathing.

Anatomic dead space is an important concept in determining if tidal volume is adequate.

Anatomic dead space is an important concept in determining if tidal volume is adequate. It’s important to realize that for a particular patient, barring trauma or surgical alteration, anatomic dead space is fixed.

Our teenager will have an anatomic dead space of 120ml (2 ml/kg X 60 kg), which means that of his 480 ml breath, roughly 360 reaches the alveoli and 120 doesn’t participate in exchange gas at all. For our baby, the anatomic dead space is 8 (3 X 2.7). So again that’s 14 ml of air reaching the alveoli and 8 ml being effectively wasted.

Let’s say our baby is sick with nausea, vomiting, and a fever of 101F (38C) . She starts to hypoventilate and is now breathing tidal volumes of 10 ml. She’s still moving 10 ml of gas in and out of her mouth and you can feel her breathing and see her chest move, even though it looks shallow. Her dead space is still 8 so now the amount of gas reaching her alveoli is 2 ml (10 ml – 8 ml). That’s not enough.

Remember, oxygenation and ventilation are different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. If you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

Oxygenation mostly changes PaO2. Ventilation mostly changes PaCO2.

If you’re providing our baby with extra oxygen, she may not become hypoxic right away because enough oxygen will still reach her alveoli to maintain her oxygen saturation for a while. However, she is barely moving her dead space gas back and forth so her ventilation is poor. As a result, her carbon dioxide starts to rise. Hypoventilation leads to increased PaCO2.

Acute values above 50 mmHg are significant and require treatment, values above 70 mmHg can be life-threatening because of respiratory acidosis among other things. Each 10 mmHg change in PCO2 roughly changes your pH by 0.1. So all other things being equal,  a PCO2 of 70 is associated with a pH of 7.1. If carbon dioxide rises into the 70–80mmHg range it will also profoundly sedate the patient. This worsens hypoventilation, and increases carbon dioxide even more. Respiratory rate eventually slows and the patient can stop breathing.

It’s important to realize that by providing extra oxygen, a good practice, you delay the onset of hypoxia, but you may also delay the diagnosis of dangerous hypoventilation if you’re not looking for it. For another clinical explanation of how hypoventilation causes hypoxia and the difference between oxygenation and ventilation  click here.

Physiologic Dead Space

A second type of dead space, physiologic dead space, consists of alveoli that are ventilated but lack capillary blood flow to pick up oxygen and drop off carbon dioxide. In other words, they are not perfused.

In physiologic dead space, alveoli are ventilated but not perfused. Physiologic dead space can change as lung perfusion changes.

In physiologic dead space, alveoli are ventilated but not perfused. Physiologic dead space can change as lung perfusion changes.

However, unlike anatomic dead space, which is fixed, physiologic dead space can change from minute to minute with alterations in cardiac output and pulmonary blood flow. Many things can impair alveolar perfusion and increase physiologic dead space such as:

  • cardiovascular shock (blood flow to the lungs is decreased),
  • emphysema (lots of enlarged alveoli with less surface area and fewer alveolar capillaries)
  • pulmonary embolus (flow is blocked by clot).

Let’s go back to the baby in our clinical scenario. Perhaps the baby is hypoventilating because she is in shock from diarrhea. Now she has two reasons for respiratory failure:

She’s hypoventilating, and barely exceeding her anatomic dead space.

She’s in cardiovascular shock. Hypovolemia and acidosis is decreasing her cardiac output and lung perfusion. Her physiologic dead space has increased and she is not perfusing all of the alveoli that are still getting ventilated. Remember, hypovolemia and shock increases physiologic dead space. And this brings us to the concept of shunt.

What Is Pulmonary Shunt?

The second type of V/Q mismatch is shunt. Shunt is the opposite of dead space and consists of alveoli that are perfused, but not ventilated.

In pulmonary shunt, alveoli are perfused but not ventilated.

In pulmonary shunt, alveoli are perfused but not ventilated.

Blood flowing past poorly ventilated alveoli doesn’t pick up additional oxygen. This poorly oxygenated blood returns to the heart and mixes with oxygenated blood coming from other areas of the lungs that are ventilated. The mixture lowers the total oxygen content of the arterial blood, producing hypoxemia. The larger the shunt, the lower the oxygen content.

Giving a patient with an intrapulmonary shunt 100% oxygen to breathe won’t increase the PaO2 much, if at all, depending on the size of the shunt because the alveoli that are being ventilated are already filled with oxygen and the blood from the non-ventilated alveoli won’t pick up any more.

Common causes of shunt occur in lung tissue disease and include:

  • pneumonia and pulmonary edema: some alveoli filled with fluid
  • tissue trauma: alveolar wall swelling
  • atelectasis: collapse of alveoli from failure to expand, or absorbsion of the air out of the alveoli without replacing it
  • mucous plugging: air can’t get into the alveoli
  • pulmonary arteriovenous fistulas

You can also have certain defects in the heart that cause abnormal mixing of oxygenated and un-oxygenated blood, like a right to left shunt, but that’s a different mechanism from pulmonary shunt.

Many types of shunt can be improved with treatment. The most common example of shunt is atelectasis, which is collapse of alveoli. For example, taking deep breaths or sighs easily treats atelectasis, one of the most common day-to-day causes of shunt. We do this naturally several times an hour, often without even being aware of it. In contrast, patients who take very shallow breaths without sighing often develop atelectasis. Factors that can cause atelectasis to develop are:

  • painful breathing from surgery or trauma
  • depressed levels of consciousness such as from drug,  injury, or illness
  • the disease process itself

Ventilation Perfusion Mismatch

As you can see it’s possible, and quite common, for both deadspace and shunt to be present in the same patient. Looking back at our baby one more time her potential causes of hypoxemia/hypoxia include:

  • Hypoventilation: tidal volumes close to her anatomic dead space volume producing inadequate alveolar ventilation. If you think about it, this is producing poorly ventilated alveoli which are still being perfused- that’s shunt
  • Shock: increasing her physiologic dead space.
  • Fever of 101 which will increase her metabolic rate and cause her to need even more oxygen than normal

V/Q mismatch can lead easily lead to hypoxemia and hypercarbia.

May The /Force Be With You

Christine Whitten MD, Author Anyone Can Intubate 5th Edition

all illustrations copyright Christine Whitten MD

 


Filed under: Anesthesia, Patient Safety, Respiratory physiology Tagged: anatomic dead space, dead space, hypoxia, physiologic dead space, pulmonary shunt, V/Q mismatch, ventilation perfusion mismatch

PHARM Podcast 158 My Divorce from SMACC


Hi folks

on todays episode I discuss my divorce from SMACC.

Show notes:

Thoughts on the Newman Crimes

David Newman betrayed patients and emergency medicine

Podcast ( available here and on iTunes)

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Filed under: FOAMEd, prehospital and retrieval medicine podcast, safety Tagged: 2017, itunes, SMACC

EM-CCM Conference: IT’S NOT A TOOMAH

Case:

A 77 year-old male h/o asthma, HTN, HLD, recently diagnosed CML p/w pain to recent bone marrow biopsy site and right lower extremity pain such that he cannot walk since last night. He also c/o nausea with few episodes of NBNB vomiting. He was prescribed imatinib but has not started it yet. He is having normal stools and passing flatus. He was admitted to the hospital last week for a malignancy workup after presenting to the ED with malaise and fever with a WBC of 68. An inpatient bone marrow biopsy was performed that confirmed CML with philadelphia chromosome. 

 

ROS: +subjective fevers; otherwise negative

 

PSH: denies

Meds: amlodipine, statin

NKDA

SH: Emigrated from middle east, no toxic habits

FH: Denies

PE:

VS: HR 94  RR 20  BP 117/65   T 97.5F  SaO2 97%   FSG 231

Gen: Ill-appearing man in distress secondary to pain

HEENT: Intact, atraumatic, MMM, PERRLA, no scleral icterus, oropharynx wnl

Neck: No LAD, no thyromegaly or nodules, supple

CV: RRR, no M/R/G

Resp: CTA b/l

Abd: Distended, diffuse mild tenderness, BS present, no CVA tenderness, no spinal tenderness or abnormalities, biopsy site with some induration but no fluctuance or erythema

Skin: Warm, dry, no rash

Extremities: No edema, cyanosis, or clubbing

Neuro: RLE weakness due to pain

 

EKG: Sinus tachycardia @108/min with normal axis, normal intervals; no ST elevations. Isolated T inversion with ST depression in lead III.

 

Labs

VBG: 7.36/44.6/21.2/26.2

iCal 4.46, creatinine 1.57, K+ 5.1, Na 131, Cl 102, Glucose 242, Lactate 1.7

UA: trace ketones, negative nitrite/LE/hemoglobin, 0-5 RBCs, 5-10 WBCs, 20-50 epithelial cells

 

 

Radiology

CXR

CT Abdomen/Pelvis

ED Course Symptoms and elevated potassium and creatinine were concerning for tumor lysis syndrome, so crystalloid bolus was given. Morphine was given for pain. FAST revealed gas in bowel but no free intraperitoneal fluid. Patient had persistent pain and had an episode of coffee ground emesis, after which he became tachycardic with notable increase in abdominal distension. He was given pantoprazole, and ondansetron. A nasogastric tube was placed to intermittent suction. Uric acid and lactate dehydrogenase levels were added, both of which were significantly elevated. Hemoglobin was noted to be 1-2 g/dl lower than his previous level just a day prior so 2 units of pRBC’s were ordered. CT abdomen/pelvis with IV contrast demonstrated retroperitoneal hematoma with possible active bleeding. Gastrointestinal, Hematology, Surgery, Critical Care Medicine and Interventional Radiology (IR) services were consulted. As per consultant recommendations, allopurinol was given, and the patient was sent to the IR suite for angioembolization. No bleeding vessel was found and he was admitted to the MICU for further management of tumor lysis syndrome and retroperitoneal hematoma.

 

Inpatient Course:

Creatinine continued to rise until HD2 before it began to improve and return to baseline levels. Rasburicase was initially recommended by hematology but was never given as the G6PD level took days to return, and the patient’s kidney function had already begun to recover. During his workup, it was noted he had hepatitis B and thus was not started on imatinib. On HD3, he developed right hip pain and a lower extremity ultrasound showed no DVT or pseudoaneurysm. He returned to the IR suite and a bleeding right iliopsoas artery was embolized. He received an additional 2 units of pRBCs. On HD6 he was downgraded to the medical floors and days later signed out against medical advice.

 

 

Retroperitoneal Hematoma

Retroperitoneal hematoma (RPH) is a hemorrhage contained within the retroperitoneum. It can be life threatening and difficult to diagnose due to its nonspecific presentation. Symptoms can include abdominal pain, back pain, leg or hip pain, neurological deficits, hematuria, or vomiting. Patients may also present with hypovolemic shock depending on the amount of hemorrhage that has occurred. Risk factors for the development of RPH include anticoagulation, exercise, coughing, invasive procedures involving the abdomen or flanks, trauma, and coagulopathies (1,2). They can also occur spontaneously, usually associated with antiplatelet or anticoagulant use, advanced age, or impaired renal function (2,3). The retroperitoneum is divided into three anatomical zones that can affect management. Zone I (central RP) includes the area medial to the renal hila encompassing the abdominal aorta, inferior vena cava, proximal renal vasculature, pancreas, and part of the duodenum. Zone II (lateral RP) contains the adrenals, kidneys, and proximal genitourinary tract. Zone III (pelvic RP) contains the rectum, iliac vessels, and their branches (1).

Zones of retroperitoneum (1)

In our case, the patient’s RPH arose from a zone III bleed that was likely secondary to his bone marrow biopsy. Bone marrow biopsy is a relatively safe procedure, with the majority of complications involving pain at the site. Rare, but more serious complications include infections, neuropathy, fractures, needle breaks, retropneumoperitoneum, and RPH (4,5). A 2002 survey, conducted in the UK after a BM biopsy related death, found an adverse event rate of 0.12%. The most common serious adverse event was hemorrhage, which led to three deaths. A follow up survey in 2004 found similar results and revealed that a diagnosis of myeloproliferative neoplasm was an independent risk factor for serious bleeding after BM biopsy (4).

 

Diagnosis:

RPH is difficult to diagnose clinically. CT is the ideal diagnostic modality as it is noninvasive, highly sensitive, and can also demonstrate active extravasation (if contrast-enhanced) to help localize source of bleeding (2,5,6). CT scan also has the benefit of being able to diagnose other etiologies of the patient’s symptoms. In a small study of ED patients with non-traumatic, non-iatrogenic, non-aortic cases of RPH, there was 100% sensitivity of CTA for detecting RPH and in 63% of patients demonstrated active contrast extravasation. CT was also able to identify the exact source of bleed in 40% of cases (6). In an observational cohort study by Sunga et al, ultrasound was able to diagnose spontaneous RPH in 12 of 19 cases in which ultrasound was utilized. In my literature search, I was unable to find any studies that evaluated the use of ultrasound specifically for the diagnosis of RPH (2). Theoretically, this diagnosis could readily be made with ultrasound if due to a ruptured abdominal aortic aneurysm. However, other etiologies of RPH may be much more difficult to diagnose, and ultrasound would be unable to localize the source of the bleed. CT is the preferred diagnostic tool.

 

Treatment:

The tenets of RPH management include addressing inciting factors such as anticoagulation use and reversal as indicated, transfusion of blood products, and supportive care (2,3,7). Patients with RPH should be monitored in an intensive care setting as they are at high risk of decompensation. For active bleeds, angioembolization via interventional radiology is likely the preferred treatment strategy; however, there remains a small role for surgical decompression (2,5,8). If the patient fails embolization or there are significant neurological symptoms, abdominal compartment syndrome, or has other concomitant surgical issues, laparotomy may be indicated (2,8). Surgical decompression also carries a risk of worsening hemorrhage since doing so may in fact remove the tamponade effect on the bleeding artery (8). All RPH’s due to penetrating trauma and all zone I injuries should be considered for surgical exploration due to risk of injury to vital vascular structures. Zone II and III should only be explored after blunt injury if there is pulsatile or expanding RPH (1).

 

Tumor Lysis Syndrome (TLS)

Tumor lysis syndrome (TLS) is an uncommon complication of malignancies that can be life-threatening. It often occurs early in the diagnosis and treatment of highly proliferative malignancies and is defined by specific lab abnormalities that result from the destruction of malignant cells. It can occur spontaneously but is most often precipitated by induction of chemotherapy, radiation, or high dose steroid therapy (9,10).

 

As cancer cells are lysed, intracellular contents are released, such as potassium, phosphorus, proteins, and nucleic acids. Hyperkalemia is the most concerning electrolyte abnormality of TLS as it can lead to neuromuscular weakness, GI distress, cardiac arrhythmia, and death. As the body catabolizes the released purine nucleic acids via xanthine oxidase, serum uric acid levels are increased. Calcium levels are decreased through increased phosphate binding. Uric acid is renally eliminated, but the high uric acid loads can overwhelm the kidney’s clearance rate, resulting in crystal formation, deposition, and renal failure. The risk of developing TLS is further stratified based upon the specific malignancy involved, the choice of chemotherapeutic agents, comorbid medical conditions, and baseline serum uric acid (9,10). The following table groups malignancies by risk for developing TLS.

Risk Criteria for TLS (10)

It is important to distinguish between patients who present with the lab abnormalities of TLS and patients with clinical manifestations of TLS. The Cairo-Bishop definition of laboratory tumor lysis syndrome is defined as at least two of the following alterations of metabolites three days before through seven days after starting anticancer treatment. Lactate dehydrogenase levels will be elevated due to cell lysis, but this is not a diagnostic criteria for TLS. Clinical TLS is defined as laboratory TLS AND either renal failure, cardiac arrhythmias, or seizures (10).

Cairo-Bishop definition of laboratory TLS (10)

The most important intervention for the management of TLS is prevention with close electrolyte monitoring, hydration, and allopurinol. However, when these patients present to the ED, the cornerstone of management will be aggressive fluid hydration with a goal urine output of 80-100 mL per square meter body surface area per hour. This translates to roughly 150-200 mL/hr of urine output for your standard 70 kg patient with normal BMI. Hyperkalemia will be treated as it would normally be treated from other etiologies, except with cautious calcium administration. The hypocalcemia of TLS generally resolves without repletion, especially if the hyperphosphatemia is treated. Phosphate binders can be given, in addition to fluid hydration or hemodialysis, to decrease phosphate levels. Asymptomatic hypocalcemia should not be treated with calcium repletion as the risk of metatstatic calcification from elevated phosphate levels is high. For this reason, caution is advised when administering calcium for hyperkalemia. However, if the patient is peri-arrest or has ECG changes associated with hyperkalemia, calcium must be given and hemodialysis should be considered if other treatments fail. Urine alkalinization is not routinely recommended, as it can precipitate calcium-phosphorus or xanthine crystals, further exacerbating electrolyte abnormalities and increasing risk for clinical TLS (9,10).

 

For the acute treatment of hyperuricemia, allopurinol is not recommended as it decreases the production of uric acid, but not decrease the already elevated uric acid levels. Furthermore, allopurinol must be renally dosed, may produce xanthine nephropathy and calclui, increases risk for Stevens-Johnson Syndrome, and has a slow onset of action of 24-72 hours. Rasburicase is a recombinant urate-oxidase, produced by Aspergillus flavus, that humans are unable to synthesize. Urate-oxidase converts uric acid to allantoin, which is soluble in urine and allows it to be renally eliminated. Its use is contraindicated in G6PD-deficiency since hydrogen peroxide is a byproduct of the urate-oxidase reaction. Rasburicase is well tolerated and can be given in a single dose of 3 mg or 6 mg, with the latter providing larger decreases in serum uric acid but without clear improvement in patient oriented outcomes (10). Administration of rasburicase in the ED should be highly considered based on patient presentation and in consultation with hematology/oncology.

 

Summary

Certain factors put the patient in our case at an increased risk for RPH due to a post-procedure complication. He was on daily aspirin and enoxaparin for DVT prophylaxis prior to the bone marrow biopsy, in addition to having philadelphia chromosome-positive CML. CML put our patient at lower risk for TLS, however, he was not started on allopurinol and the RPH may have reduced renal perfusion and contributed to the development of TLS.

 

TLS

  • ↑ Postassium ↑ Phosphate ↑ Uric Acid ↓Calcium
  • Clinical manifestations: Renal failure, seizures, cardiac arrest
  • “B” malignancies at high risk – B-ALL and Burkitt’s lymphoma
  • IV hydration, phosphate binders, insulin/D50, rasburicase

RPH

  • CTA abdomen/pelvis or CT abdomen/pelvis with IV contrast (contrast is not required to diagnose RPH)
  • Consider in patients on anticoagulant/antiplatelet agents, patients s/p invasive abdominal/pelvic procedures, trauma, coagulopathies
  • IR consult

 

References

  1. Kasotakis G. Retroperitoneal and rectus sheath hematomas. Surg CLin N Am (2014);94:71-76
  2. Sunga KL, Bellolio MF, Gilmore RM, Cabrera D. Spontaneous retroperitoneal hematoma: etiology, characteristics, management, and outcome. The Journal of Emergency Medicine (2012);43(2):157-161
  3. Salemis NS, Oikonomakis I, Lagoudianakis E, et al. Enoxaparin-induced spontaneous massive retroperitoneal hematoma with fatal outcome. Am J Emerg Med. 2014;32(12):1559e1–1559e3
  4. Wan Jamaludin W.F. et al. Retroperitoneal hemorrhage associated with bone marrow trephine biopsy. American Journal of Case Reports (2013);14:489-493
  5. Al Zahrani Y, Peck D. Median sacral artery injury following a bone marrow biopsy successfully treated with selective trans-arterial embolization: a case report. Journal of Medical Case Reports (2016);10(42):1-4
  6. Caleo, O., Bocchini, G., Paoletta, S. et al. Radiol med (2015) 120: 133. doi:10.1007/s11547-014-0482-0
  7. Neesse A, Kalinowski M, Walthers EM, Gorg C, Neubauer A. Clinical management of massive retroperitoneal hemorrhage after bone marrow biopsy. Leukemia & Lymphoma. March 2009;50(3):475-477
  8. Chan Y, Morales J, Reidy J, Taylor P. Management of spontaneous and iatrogenic retroperitoneal haemorrhage: conservative management, endovascular intervention or open surgery?. International Journal Of Clinical Practice [serial online]. October 2008;62(10):1604-1613.
  9. Pi J, Kang Y, Smith M, Earl M, Norigian Z, McBride A. A review in the treatment of oncologic emergencies. Journal of Oncology Pharmacy Practice. October 2016;22(4):625-638
  10. Criscuolo, L. Fianchi, G. Dragonetti & L. Pagano. Tumor lysis syndrome: review of pathogenesis, risk factors and management of a medical emergency. Expert Review of Hematology. 2016;9(2):197-208

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12. Bullying, Threats & Intimidation — patientsafe

If patient safety is to improve healthcare needs to change. The historical top down approach which has hindered improvement requires a transition into one where decisions are driven from the front line. Those corporations who’ve introduced front line driven frameworks (e.g. Toyota Production System – see here) provide the highest quality in the most efficient way to […]

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Filed under: human-condition, humanity Tagged: bullying