Blood Gases

1.    Anion Gap
    (Na + K) - (Cl + HCO)     Normal = 10 - 16mmol
    >20    Primary metabolic acidosis regardless of pH or serum bicarbonate concentration

Low anion gap: dilution, low albumin, increased unmeasured cation (calcium, magnesium, lithium)
Non anion gap acidosis: HARD UPS
  Hyperalimentation, acetazolamide, renal tubular acidosis, diarrhoea, uretero-pelvic shunt, post-hypocapnia,  spironolactone
Raised Anion Gap: MUD PILES
Methanol, uraemia, DKA, paraldehyde, iron/ isoniazid, lactic acidosis, ethanol, ethylene glycol, salicylates

2.  Excess Anion Gap = total anion gap - 12 + measured bicarb        If >30    Metabolic alkalosis
        If <23 Non gap metabolic acidosis
 
3. Delta Gap = Anion Gap - 12 (normal anion gap) < 0.4     Hyperchloraemic normal anion gap acidosis
 < 1        High AG & normal AG acidosis
 1 to 2    Pure Anion Gap Acidosis
                 Lactic acidosis: average value 1.6
                 DKA more likely to have a ratio closer to 1 due to urine ketone loss
 > 2        High AG acidosis and a concurrent metabolic alkalosis or a pre-existing compensated respiratory acidosis





4. Osmolality -  2 (Na + K) + Glu + Urea
 - Calculated vs measured should be 15- 20mmol / kg H20
 - Elevation suggests the presence of exogenous osmotically active particles and includes 4 main groups:
    Alcohols - Ethylene Glycol, methanol, ethanol, acetone, isopropyl alcohol
    Sugars - Mannitol, Sorbitol
    Lipids - e.g. hypertryglyceridaemia
    Proteins - Hypergammaglobulinaemia

5. Expected CO2
The CO2 is a very swift compensatory change. The bicarb takes a while to change. This means you can use the bicarb to calculate what you would expect the CO2 to be. You can predict what you expect the CO2 to be. If it's not what you expect it to be, then there's a hidden acidosis or alkalosis.

Acute Respiratory Acidosis 1:10- The [HCO3] will increase by 1 mmol/l for every 10 mmHg elevation in pCO2 above 40 mmHg.
Expected [HCO3] = 24 + { (Actual pCO2 - 40) / 10 }

Chronic Respiratory Acidosis 4:10- The [HCO3] will increase by 4 mmol/l for every 10 mmHg elevation in pCO2 above 40mmHg.
Expected [HCO3] = 24 + 4 {(Actual pCO2 - 40) / 10}

Acute Respiratory Alkalosis  2:10
- The [HCO3] will decrease by 2 mmol/l for every 10 mmHg decrease in pCO2 below 40 mmHg.
Expected [HCO3] = 24 - 2 { ( 40 - Actual pCO2) / 10 }

Chronic Respiratory Alkalosis 5:10

Metabolic Acidosis 1 1/2 + 8
Expected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2)

Metabolic Alkalosis 0.7 + 20 Expected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5)

6. Alveolar Gas Equation
Alveolar pO2 = inspired pO2 - arterial pCO2 x 1.2.

7. CausesRespiratory Alkalosis
Anxiety, pregnancy,  hypoxia, sepsis, lung disease, hepatic encephalopathy, CNS disease, drugs

Respiratory Acidosis Acute airway obstruction, pulmonary embolism etc.

Metabolic AlkalosisVomiting, NG suction, diuretic use, post hyper-capnia
Excess mineralocorticoid activity, diuretics, excess alkali administration

Lactic Acidosis
- Ethylene glycol has a metabolite called glycolate, which is similar in structure to lactate. This can be wrongly interpreted by blood gas machines as an abnormally elevated lactate
- Sodium Bicarbonate is not routinely recommended. It can cause fluid overload, post recovery metabolic alkalosis, hypernatraemia. Often get rebound raise in CO2. 


Venoarterial ParadoxDuring resuscitation and manual resuscitation, VBG and ABGs may be completely different. On the venous side of the circulation, the lungs are poorly perfused and there is a build up of CO2.

CO2 Units
from kPa to mmHg you multiply by 7.5
from mmHg to kPa you divide by 7.5

Pathophysiology Reminder

Chemoreceptors in the medulla and the carotid and aortic bodies sense changes in pCO2 and H+. This is then used to regulate alveolar ventilation. When ventilation rises, pCO2 falls. This occurs because ventilation lowers the alveolar pCO2 below that of mixed venous blood. CO2 molecules then diffuse into the alveolar gas, thus lowering the CO2 concentration in pulmonary capillary blood.

Shift to the right:
Alkalosis, raised pCO2, raised temperature, raised concentration of 2, 3-DPG

A shift to the left may be seen in:
Alkalosis, reduced pCO2, reduced temperature, reduced concentration of 2, 3-DPG

Henderson Hasselbach Equation : CO2 + H2O ? H2CO3 ? H+ + HCO3-



References
http://www.enlightenme.org/learning-zone/blood-gas-brain-freeze
http://www.enlightenme.org/the-curriculum-zone/diagnostics/blood-test-interpretation/arterial-blood-gas-analysis/learning-objectives
http://www.enlightenme.org/learning-zone/its-been-gas
http://www.enlightenme.org/learning-zone/alkalosis-has-gas-machine-broken-again
http://www.enlightenme.org/node/990/take
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1604
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1512
http://lifeinthefastlane.com/ccc/arterial-blood-gas-in-hypothermia/
http://lifeinthefastlane.com/ccc/arterial-blood-gas-abg/
http://lifeinthefastlane.com/a-most-discombobulating-gas/http://learning.bmj.com/learning/modules/flow/JIT.html?execution=e1s1&locale=en_GB&action=start&sessionTimeoutInMin=90&moduleId=5004327&status=LIVE&_flowId=JIT

Pulmonary Embolism

PEs are the big diagnosis that we never want to miss, but we haven't yet decided the significance of all these tiny PEs we're picking up.


Statistics
PEs are very common: 60 to 70 per 100 000 population. They have an untreated mortality of about 30%, cause 15% of all postoperative deaths and are the most common cause of maternal death in the UK. 35 - 45% of thrombi are DVTs and up to 50% embolise.  65% of below knee DVTs are asymptomatic.

Pathogenesis:
Virchow's Triad:

    Stasis:    Immobility, surgery, casts
    Vessel wall injury: trauma, sepsis, IVDA
    Hyper-coaguable state: Primary    Antithrombin and heparin cofactor II deficiencies
                        Protein C and S deficiencies
                        Factor V Leiden   
                        Disorders of the fibrinolytic system
                        Lupus
                        Anticardiolipin antibodies
                        Prothrombin gene variant
                Secondary    Dehydration
                        Pregnancy
                        OCP
                        Malignancy
                        HONK

Risk Factors
*    Major risk factors (relative risk increased 5-20-fold) include:
-    Surgery - major and/or abdominal surgery
-    Lower limb orthopaedic surgery, fracture or varicose veins.
-    Obstetrics - late pregnancy (higher incidence with multiple births), caesarian section, pre-eclampsia
-    Malignancy - pelvic, abdominal, metastatic (occult in 7 - 12% of patients)
-    Previous proved VTE
-    Reduced mobility - any major illness with prolonged bed rest.

*    Minor risk factors (relative risk increased 2-4-fold) include:
-    Cardiovascular - congenital heart disease, congestive cardiac failure, hypertension, central venous access
-    Oestrogens - OCP (especially "third generation" pills), HRT (risk greatest in first year)
-    Miscellaneous - occult malignancy, neurological disability, obesity, thrombotic and myeloproliferative disorders, nephrotic syndrome, inflammatory bowel disease.

*    Inherited thrombophilias -  need to interact with an additional risk factor to cause venous thromboembolism.

Clinical Signs & Symptoms

-     Circulatory collapse in a previously well patient - happens in 5%.
    Massive PE causes RHF.

Tachycardia in 30%.
-     Pulmonary infarction syndrome (60%) -
    pleuritic pain, with or without haemoptysis. Pleural rub.
-     Isolated dyspnoea (25% - 73%) - sudden onset SOB
-     Collapse, poor reserve (10%) -
    In elderly patient with limited cardiorespiratory reserve. Small PE can be catastrophic.

-    New onset AF and chest wall pain
-    Prominent JVP “a” waves
-    Right heart failure
-    Pulmonary area murmur
    May be completely normal, but tachycardia (classically with a loud P2 and splitting of the second heart sound) with tachypnoea are common
-    Signs of a deep vein thrombosis are present in about 25%

Pregnancy
The diagnosis can be difficult to make in women who are pregnant. The standard pre-test clinical probability score should be used, recognising that pregnancy is a major risk factor for venous thromboembolism. The D-dimer test is of no use in this situation because it is raised (in the absence of PE) from about six weeks' gestation, until about three months post-partum.
The risk of pulmonary embolism increases throughout pregnancy, with more pulmonary emboli occurring after delivery than before. The risk of pulmonary embolism in pregnancy increases with maternal age and multiple births.
Pregnancy women normally have a mild compensated respiratory alkalosis.
Penicillins and cefalosporins safe in pregnancy. Avoid co-amox.

Pulmonary oedema higher risk in pregnant women because they have a lower serum osmotic pressure, and increased vascular permeability. Causes include pre-eclampsia, beta adrenergic agonists used to postpone premature labour, cardiac disease, amniotic fluid embolism.

Amniotic fluid embolism is typically associated with rapid changes in coagulation and evidence of DIC. PE does not cause such changes.

Investigations
*    SI QIII TIII  pattern - deep S wave in lead I, Q wave in III, inverted T wave in III.
    20% of patients with PE.

*    Chest x-ray:    wedge shaped infarction or infection
            regional oligaemia (Westermark sign)
            pleural effusions
*    ABG: Hypoxia results from reduced cardiac output and a low mixed PaO2 with ventilation/perfusion mismatching. A normal PaO2 and alveolar arterial gradient is possible in a young, healthy person.
           
Definitions
Massive PE:    Acute PE with obstructive shock or SBP <90mmHg: at least 1 of the following:
    - Sustained hypotension from PE itself (SBP < 90 mmHg for = 15 min, or requiring inotropic support)
    -  Pulselessness
    - Persistent profound bradycardia (HR < 40 bpm with signs/symptoms of shock)

Submassive PE: Acute PE without systemic hypotension (SBP = 90 mmHg) but with either:
*    RV dysfunction (of at least 1 of the following):
        - RV dilation
        - BNP > 90 pg/mL
        - N-terminal pro-BNP > 500 pg/mL
        - ECG changes: New complete or incomplete right BBB, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion
•     Myocardial necrosis is defined as either of the following:
        - Troponin I > 0.4 ng/mL, or
        - Troponin T > 0.1 ng/mL

Low Risk PE: Acute PE and the absence of the clinical markers of adverse prognosis
that define massive or sub-massive PE.

Scoring Systems
The original ‘PERC’ study excluded patients:
*    patients in whom shortness of breath is not the most important, or equally most important, presenting complaint
*    cancer
*    thrombophilia or strong FHx
*    beta blockers that may mask tachycardia
*    transient tachycardia
*    patients with amputations
*    massively obese and in whom leg swelling cannot be reliably ascertained
*    baseline hypoxemia

PERC rule can’t be used on:    HAD CLOTS
Hormone, Age >50, DVT/PE history, Coughing blood, Leg swelling, O2 >95%, Tachycardia 100+, Surgery/trauma <28 d

Treatment
Massive PE - Alteplase 50mg ASAP.

Anticoagulation for three or six months for a first idiopathic pulmonary embolism. A British Thoracic Society trial comparing three and six months' treatment is ongoing. Some trusts use PESI  to work out whether outpatient anticoagulation is suitable.


Flight prophylaxis. Current British guidelines suggest considering aspirin or LMWH, or formal anticoagulation for those at high risk of pulmonary embolism. Limited evidence to support this. Compression stockings may be beneficial.

Differentials
Venous air emboli may cause:
    Raised venous pressure
    Cyanosis
    Hypotension
    Tachycardia
    Syncope.

Treatment is by lying the patient on their right side, with head down and feet up, to allow air to collect and stay at the cardiac apex. From here it can be aspirated. This may be done by ultrasound guided needle aspiration.

Fat embolism
This occurs in association with long bone fractures, with bone marrow fat droplets released into the venous circulation at fracture. It is more common in non-immobilised fractures.

It typically presents with:
    Hypoxia
    Coagulopathy
    Transient petechial rash on neck, axillae, and skin folds
    Neurological disturbance, such as confusion.
    Fat globules can be identified in the urine.
Treatment is supportive.

References
http://www.enlightenme.org/knowledge-bank/cempaedia/pulmonary-embolism
http://lifeinthefastlane.com/education/ccc/pulmonary-embolism/
http://lifeinthefastlane.com/ecg-library/pe/
http://lifeinthefastlane.com/cicm-saq-2012-2-q5/http://lifeinthefastlane.com/education/ccc/thrombolysis-submassive-pulmonary-embolus/
http://lifeinthefastlane.com/cardiovascular-curveball-011/
http://lifeinthefastlane.com/pulmonary-puzzle-016/
http://lifeinthefastlane.com/hematology-hoodwinker-001/
http://www.enlightenme.org/the-curriculum-zone/node/2091http://www.enlightenme.org/the-curriculum-zone/node/11779http://m.eurheartj.oxfordjournals.org/content/early/2014/09/17/eurheartj.ehu283

HAP6

Respiratory and Breathing problems basically covers:

Asthma
Pulmonary embolism - including echo
COPD and NIV
Aspiration
Pneumonia
Pulmonary Oedema
Pneumothorax
Dysproportionate hyperventilation
Pleural effusion
Inhalation
ABG interpretation
CXR interpretation