Presentation is loading. Please wait.

Presentation is loading. Please wait.

Cyanosis Pathophysiology rounds

Similar presentations

Presentation on theme: "Cyanosis Pathophysiology rounds"— Presentation transcript:

1 Cyanosis Pathophysiology rounds
Gideon Daniel, DVM Internal medicine resident 8/22/13

2 Objectives O2 transport Selected disease processes Shock
Methemoglobinemia Smoke inhalation Cyanide Carbon monoxide

3 Cyanosis Result of desaturation of Hgb
Central (abnormal pulmonary function) Peripheral Takes about 5 g/dL of unoxygenated hgb to manifest cyanosis “should invoke a feeling of panic and institution of aggressive oxygen, ventilation or fluid therapy” Central hypoxemia of d/t abnormal pulmonary fnc Peripheral- disease process where O2 is not utlized proprerly by the tissue Imp concept as think about the anemic patients who may suffer from hypoxemia without manifesting cyanosis.


5 O2 transport Ventilation Pulmonary gas exchange
O2 interaction with hemoglobin (hgb) O2 delivery to tissue Extraction of O2 at the tissue (Inspired O2 in the atm is transported to the pulmonary avveoli by process of alveoalr ventilation to determine the alevolar O2 tension (PAO2). O2 then is transferred from pulmonary alveoli to the pulmonary cap blood (gas exchange) to determine the arterial O2 tension. The A-a tension quantifies the efficiency of gas exhange. The Pa02 is the principle of determiantion of hb satuation (sa02) in relationship descirbed by O2hb saturation curve. Arterial O2 (Cao2) is the principally fnc of the Hgb conc of blood and Sao2. O2 delivery (Do2) to tissues is a fnc of CaO2 and CO).

6 Ventilation Mechanical process that causes gas to flow into and out of the lungs VT = VA + VD VT : total ventilation VA : alveolar ventilation VD : dead space ventilation PCO2 (arterial CO2 tension): primary driving force for ventilation PCO2 = VCO2/ VA x K VCO2 – total volume of CO2 produced by metabolism VT is propritoned into alevolar ventilation (where gas exchange occurs ) and dead space ventilation. VD- gas to anatomic areas that are not normally invovled in gas exchange (anatomic) as well as flow to alveoli that are venitlated but not perfused (physiologic) PCO2- tries to keep 40mmHg, regardless of total CO2 produced by metabolism of the patient. So be definition, hypoventilation > 40mmHg PaCO2 hyperventilation < 40mmHg PaCo2

7 Diffusion D: Diffusion rate ΔP: partial pressure difference
A: cross-sectional area of the pathway S: solubility of the gas D: distance of diffusion MW: molecular weight of the gas Take home message: rate of transfer proportional to tissue area and partial pressure of difference and inversely related to thickness Ex: CO2 diffuses 20x more rapidly than O2 Rate of transfer is propritonal to tissue area and partial pressure differences; but inversely related to thickness Why Co diffuses 20x more rapidly than O2 - b/c it has increased solubliity even though similar MW

8 Inspired Gas Warmed and saturated with water vapor (in trachea)
PH20 : 47mmHg at normal body temp (37 C) PIO2 (partial pressure of inspired oxygen) PIO2 = (PB – PH20) x FIO2 = (760-47) x 0.21 = 150mmHg Barmoetric pressure of atm

9 Alveolar Gas concentration
Less than inspired air in trachea Due to addition of CO2 from pulmonary capillary blood Estimated form alveolar gas equation PAO2 = PIO2 – PaCo2/ R R= Respiratory quotient = 0.8 Normal: 150 – (40/0.8) = 100mmHg PA02 calculated from subtracting alveolar Paco2 from the Pi02. PACO2 could be measured (end tidal CO2), but since alevolar-arteiral PCO2 gradient is normally very small, typically esitmated. R accts for difference b/w CO2 production and O2 consumption at steady state. Most use 0.8, some use 0.9.

10 Pulmonary gas exchange
Impaired when PaO2 < PAo2 Degree can be quantified by calculating alveolar-arterial O2 (PAO2 – PaO2 or A-a) gradient Normal < 10mmhg (room air) Short formula: 150-PaCo2 x 1.25 (if using R= 0.8) PaO2/Fio2 Ratio Normal > 500 mmHg The “120” Rule Since alveolar O2 and CO2 should ~ 150mmHg “Up/Down Offset” Method Using reciprocal relationship b/w PaO2 and PaCo2 Assuming PaCo2 40mmHg and PaO2 100mmHg So if getting a number < 120- indicates reduced lung oxygenation efficiency So should get a proportional increase or decrease- if the discrepnscy is higher than calculated (i.e > 20)- then venous admixture is present A-a for breathing room air P/F ratios mild oxygenation insuff, moderate, < 200- severe


12 Causes of hypoxemia low PIO2 Hypoventilation R-to-L Shunts**
Diffusion barrier VQ mismatch Most texts break them down into these 5 categories RL shunts have a star as this is the only one that doesn’t improve with oxygen

13 Low PI02 Relatively uncommon
Decrease in barometric pressure (high altitudes) Improper inhalant anesthetic technique

14 Hypoventilation If alveolar ventilation is abnormally low, then PO2 falls and PCO2 rises CNS depression (disease or drugs- opioids, barbiturates) Damage to chest wall High resistance to breathing Obstructive airway disorders Restrictive lung dz Results in increased arterial and alveolar CO2

15 Diffusion impairment When there is inadequate equilibration of O2 tension across the alveoli and capillaries Relatively infrequent Due to thickening of alveolar- capillary membrane Diffuse pulmonary interstitial dz Loss of alveolar or capillary surface area (vasculitis) Physiology (high cardiac output during exercise) i.E IS edema, fibrosis, emphyseam

16 Right-to-left shunt Blood enters arterial system without passing ventilated areas of lungs Cardiac disease PDA, VSD, ASD, tetralogy of Fallot Have a decreased PaO2 with a normal or decreased PaCO2 and widened (A-a) O2 gradient FAILS TO IMPROVE WITH O2 PCO2 can be normal d/t hypoxemia increasing respiratory drive Can be calculated: Qs/Qt = (SC02 – Sao2) / (SC02- SvO2) > 10% abnormal Sm amt (2-3%) of shunting is present in normal animals throught the bronchial and thesbian circulations (veins in myocardium). b/c venous adminsteure has does not have a opportunity for gas exchange, hypoxemia arising from shunt is unreponsive ot O2. Doesn’t Affect PaCO2 until its severe. Formula calculates the % of CO that would have to flow through the lung as anatomical shunt, assuming that the remaining BF is optimally arterialized, in order to acct for the observed difference b/w measured venous and arterial oxygen. (Calculates % of CO that would have to flow thru the lung as anatomic shunt, assuing that the remaining BF is optimally arterialized, in order to acct for the observed difference b/w the measuresd venous and artieral oxygen. Req venous blood sample (preferble form the PA, but can use RA and anterial VC). SCO2- not measured but assumed to be 100% during pure O2 SVO2- from central venous cath- ideally from pul artery)

17 VQ mismatch B) Low VQ- decreased ventilation, results in decrease functional lung units (increaed dead space ventilation); blood flow is normal to the those areas of lung (hypoxic blood is returnned to pulmonary aa) High VQ: decreased perfusion, results in increased dead space ventilation; generally results in compensation by other functional lungs Generally b/c the efficiency of CO2 is 20x that of O2- increased minute ventiilation hypocapenia. Increase in A-A gradient b/c more blood is passing lungs w/o oxygenation Ex (high): PTE

18 Clinical approach Supplying 28% of FI02 can be achieved using a single nasal cannula and an o2 flow rate of 50ml/kg/min


20 O2 content in blood CaO2 = (1.34 x Hgb x SaO2) + (0.003 x PaO2)
1.34: the amt of oxygen (mL) that each gr of hgb can hold If it is 100% saturation SaO2- measured or calculated % hgb saturation with oxygen 0.003 is the solubility of oxygen in plasma Normal in dogs ~20 mL o2/dL SaO2 (%) 0.97 x 15 x 97 x 0.003 =

21 Hemoglobin Hgb consists of two alpha and two beta polypeptide chains, each bound to a heme grp. Each heme grp contains a porphyrin ring and a ferrous atom capable of reversibly binding one oxygen molecule.

22 The HemoCue for point-of care hemoglobin measurement and packed cell volume estimation in cats. Posner et al JVECC 2005 Hgb measured in clinical pathology laboratory or is estimated from pack cell volume HemoCue used only 10 uL of blood and is portable and quick PCV can be estimated by multiplying HgHQ by 3.1

23 Oxygen binding to hemoglobin
The globin units of deoxyhemolgobin are tightly held by electrostatic bonds in T conformation w/ a reltivley low affinity for O2. Binding of O2 imposes chemical and mechancial strsses that break these electrostatic bonds, leading to a relaxed ® conformation, Conformational chagnes lead to cooperativiey among binding sites, so that binding of one oxygen molecule to doexoyhgb increase the oxygen affinity of the remaining binding sites on the same hgb molecule. Why the binding curve has a sigmoid shape. The major effectors of hgb are hydrogen Ion, CO2 and 2,3 DPG (or Cl in cats)

24 Oxyhemoglobin dissociation curve
SpO2 PaO2 95-99% Normal 90-94% Moderate Hypoxia <90% Severe Hypoxia Plateau phase- hgb remains saturated over a wide range of O2 tension. I.e if hgb is saturated already around ~97%- cannot be increased substantially by higher Pao2 Steep phase- allows for efficient O2 release in peripheral tissue where O2 tension normally is decreased P50: PO2 at which the Hb is 50% satured and is a commonly used value to define whether the curve is shifted. So lower than normal P50- left shift and represents increase Hb affinity for oxygen. A higher than normal P50 is termed a right shift and represents a decrease in Hb affinity for oxygen.

25 Factors affecting the curve

26 Summary Shift to the right (tissue) Shift to the left (lungs) Effects
Decreases affinity for O2 Increases affinity for O2 P50 Increase Decrease CO H+ Temp 2,3 DPG Borh- ie shift to the right w/ increases in CO2 and H+ Haldane- so can carry CO2 (will decrease affinity for O2) in deoxygenated blood Bohr effect: hgb’s oxygen binding affinity is inversely related to acidity and Co2 Haldane effect: deoxygenating blood assists in carrying CO2

27 Carbon dioxide transport
Carried in 3 forms: Dissolved Bicarbonate CO2 + H20 ⇋ H2Co2 ⇋ H+ ⇋ HCO3- Carboxyhemoglobin More linear than O2 dissociation curve Small differences between arterial and venous CO2 (5mmhg) Dissolved 20x more soluable than oxygen; 10% of exhaled in the lungs is in the dissolved form Hco3 diffuses out of cells, H cannot; Cl moves out of cell to remain electroneutral (chloride shift), some of the H+ ions bound to reduced hemoblobin Presence of reduced Hb in peripheral blood helps w/ loading of CO2 at tissue and oxygenated hgb in the lungs helps w/ offloading CO2- haldene effect- deoxygenation of blood assiss in carrying CO2 Compared to O2- where the difference is large (60mmHg)


29 DO2 and VO2 Oxygen delivery (DO2): mL of o2 delivered to peripheral tissue each min DO2 = CaO2 x CO = [(1.34 x Hgb x SaO2) + (0.003 x PaO2)] x (HR x SV) Oxygen consumption (VO2): mL of O2 consumed by the tissue each min Vo2 = (CaO2 – CvO2) x Q The value calculated using the reverse Fick method is slightly lower than the value determined from expired gas analysis because it does not take into account oxygen consumption from the alveolar compartment.

30 Oxygen extraction ratio (OER)
OER: O2 consumed (VO2)/(DO2) OER = [(SaO2- SvO2)/SaO2] x 100 Normal ~ Lowered OER represents improved relations of DO2 to VO2

31 The “critical” DO2 B: Point at which compensatory mech fail to meet tissue requirements Below critical point- oxygen extraction falls in proportion to decrease in oxygen delivery and products of anaerobic metabolism start to accumulate in blood Oxygen extraction normally stays constant over a wide variety of DO2 values and is then termed supply independent. This reflects the physiologic reserves in the patient and does not cause anaerobic metabolism. In the area below the critical value of DO2 the oxygen extraction falls in proportion to the decrease in oxygen delivery, and products of anaerobic metabolism start to accumulate in blood.

32 Shock Definition: inadequate cellular energy production
Secondary to poor tissue perfusion  decrease in DO2 in relation to VO2 Decreased DO2 d/t Loss of intravascular volume (hypovolemic) Maldistribution of vascular volume (distributive) Cardiac pump failure Hypoxemia (severe anemia, pulmonary dysfunction, methemoglobinemia) Other= hypoglycemia, cytopathic

33 Monitoring oxygen delivery
Indirect indicators pH, HCO3, BE, CO2 gradient, lactate, HR, BP, CVP, crt, extremity temp, UOP SvO2 (venous oxygen saturation) Assesses whole body Vo2/Do2 relationship Reflects changes in Cao2, CO, local blood flow, local VO2, affinity of Hb for O2 Normal: 65-80%

34 Assessment of Svo2 SvO2- mixed venous O2 saturation
Assessed from pulmonary artery ScvO2- central venous O2 saturation Cr vena caval/RA via central line < 70% indicates tissue hypoxia Can be a surrogate for SvO2 Desaturation indicates tissue hypoxia


36 Methemoglobinemia Hgb with oxidized Fe 3+ Incapable of carrying O2
Increases the affinity for oxygen in the remaining ferrous Hgb Shifts the curve to the left High levels (> 20%) can cause cellular hypoxia and shock May see concurrent heniz bodies Gives blood a darker brown color and results in dusky cyanotic or chocolate- colored mm MetHg is Hgb in which the ferrous (Fe2+) molecule is oxidized to Ferrice Fe3+ form. MetHb is incapable of carrying oxygen and high levels (> 20%) can cause Approx 0.5-3% of hgb is oxidized to methgb q24 nromally. Numerous mech to prevent oxidative injury in rbcs- superoxide dismutase, catalase, glutthione peroxidase, glutathione, methb reductase. Rbcs are esp vulnerable b/c they carry oxygen, are exposed to various chemicals and have no nucleus or mitochondira. Hbs are aggregates of denatured precipitated hgb w/in rbcs that have undergone oxidative damage- oxidation of the SH grp of hgb causes confromation changes in the globin chain that results in the precipation of the denatured globin. Feline ghb are more susceptible ot oxidative damage b/c it has 8 SH grps in the globin part instead of 4 like in dogs. Gives blood a darker brown color and reulsts in dusky cyantoic or chocolate-colored mm. Methgb increase the affinity for oxygen in the remaing ferrous moieties of the hgb molcule, decreasing release of oxygen to the tissues and shifting the oxyhgb dissociation curve to the left.

37 Etiologies Acetominophen Topical benzocaine Phenazopyridine
Nitrates/nitrites Skunk musk Acetaminophen- metabolized in the liver via- conjugated to sulfate compound or glucruonide compound. Trnasformed and oxidized by the cyto-chrome p450 system which converts it to the reactive intemediate NAPQI (n-acetyl-p-benzoquinone-imine). The toxicity is d/t NAPQI. The glucuronide and sulfare conjugations are nontoxic and are excreted in the bile and urine in most spp. Rem that can have limited degree of glucuronide conjugation – NAPQI causes intracelluar oxidative damage, converting hgb to methgb and oxidizing SH grp on hgb. Benzocine in dogs and cats; skun musk in dogs. Nitrates and nitrties do not cause HBs. I.e from NG or nitroprusside. NO may reduced methb reductase activity, also inteacts w/ oxygen to form NO2 which dissovles in solution to yield nitrite and nitrate. Nitrite can convert oxyhemologin to methgb. After exposure to oxygen in the air, blood w/ more than 10% met hgb will remain dark w/ brown disocoloation. Can measured via co-oximeter

38 Case reports Methemoglobinemia caused by hydroxycarbamide (hydroxyura) ingestion in a dog – Wray, JSAP 2008 Treated with methylene blue, oxygen, prbc transfusion, NAC and fluids Methgb resolved within 16hrs Cyanosis and congenital methemoglobinemia in a puppy – Fine JAAHA 1999 Due to deficiency of methemoglobin reductase enzyme Causes mild signs Consider preemptive measures before surgical procedures 13 yo FS greyhound brought in for collapse and dyspneia. Was tachycardic and cyantoic at presentation.


40 Smoke inhalation Death due to hypoxia from carbon monoxide toxicity
Other complications seen Direct thermal or irritant gas injury- URT, LRT Dermal burn injury ARDS Bacterial pneumonia Neurologic signs Hypoxia from CO tox is presumed to the be themost common cause of acute death. Other complications include direct thermal injury to the URT, LRT injury from irritant gases, ARDS, bacterial pneumonia, dermal burn injury Thermal injury, irritant gases/superheated particulate matter, reduced lung complaince (from atelectasis and edema), airway obstruction, bacterial pneumonia, dermal burn injury. Rem that O2 saturation via pulse ox may be nromal b/c cannot differtiate b/w Cohgb and Oxyhgb. Co-ox allows direct measurement. From one study- the PaO2-FiO2 ratio had a nadir at 32hrs postadmision Prognosis- MR in ppl < 10% w/o dermal injury and 25-65% w/ dermal injury. Of 27dogs in one retrospective study, 4 died and 4 were euthanized. In uncomplicated cases, dogs recovery from the initial CO tox had a favorable prognosis, w/ iprovemnts in resp signs over 24hrs. However, dogs that were clinically worse the following day were more likely to die, euthanized or req prolonged hosp.

41 Cyanide toxicity Incidence and significance remains undefined
May contribute in smoke inhalation Found in very low concentrations in foods in the form of amygladalin Iatrogenic sources (nitroglycerin, nitroprusside) Several intrinsic biochemical pathway for CN detox exists Formation of thiocynate Hallmark- histotoxic hypoxia Cyanohemoglobin further contributes to hypoxia HCN is most prevlent in fires involving wools, silks and synthetic nitrogen containg polymer. It is a nonirritant gas that interfers w/ the utilatzation of O2 by cellular cytochrome oxidase, thereby cuasing histotoxic hypoxia (inability of cells to take up or utilize oxygen from the bloodstream, despite physiologically normal delivery of oxygen to such cells and tissues) The incidence and sig of HCN remains undefined. Found in very low conc in foods in the for of amygladalin (sugar compound w/ cynaide attached)- met to HCN in the GIT. The most well known source in food is the seeds nad pits from Prunus spp (apples, bitter almonds, apricots, some in lima beans and cassava). Exposure in enclosed space fires. Combustion of many substances (nylon, plastic, wool and silk may reelase HCN). Iatrogenic sources- Na nitroprousside can release up to 5 CN grp during its metabolism and toxicity may dev as CN accmulates. Despite widespread sources, no known reports of CN tox from naturally occuring sources- but may contribute in smoke inhalation. Hallmark- histotoxic hypoxia due to inhibition of aerobic metabolism. This can lead to “brick red” mm color indicative of poor tissue oxygen extraction that has been clasically assoicated w/ CN toxicity. B/ c of disrutpion of cellular respiration, a switch to anaerobic met occurs nad results in a sig metabolic acidosis w/ dramatically elevated lactate. Death from CN can happen quickly, however antidotes are availbe and typically are effect if admin in time.

42 Carbon monoxide toxicity
Nonirritant gas, colorless, odorless CO binding to hgb is > 200x the affinity than of O2 to hemoglobin Also shifts O2-hemoglobin curve to the left Produced by incomplete combustion of hydrocarbons in fire, car exhaust, charcoal grills, generators CO is a nonirritatant gas that competitively and reversibly binds to hgb at the same sites as O2, w/ an affinity that is 230 to 270x greater and results in marked anemic hypoxia. It is produced by IC combustion of carbon-containg material and is therefore most sig in enclosed fires as there is increasingly less O2 avliable. Cohb also shifts the O2-hgb dissoicaiton curve to the left, resuling in less offloading at the tissue level. 3 outocmes in pure, uncomplicated CO tox- 1) complete recovery w poss treansient hearing loss but no perm effects 2) recvery w/ perm CNS abnormalities or death. Death is due to cerbral and myocardial hypoxia. Is a colorless, odorless, nonirritating gas that is produced by IC combustino of hydrocarbons in fires, car exaust, charcoal grills, and gasoline powered generators, broilers and heating systems. In fires it can be produced by the IC combustion of common substances like wood, cotton, paper, polyvinyl chloride, polystyrene. CO is produced endogenously as an end product of rbc and heme catbolism and the CNS as a neurotransmitter. It is ubiqutious in the enviro but typically in concentrations of < 0.001%. As a result of endogenous production of CO, and its presence in air, normal individuals have Cohgb levels of 1-3%.

43 Carbon monoxide pathophysiology
Two main mechanisms Hypoxic injury Cellular toxicity May explain acute and delayed effects Cellulary theroies- binding of CO to mitochondrian cytochromes. CO activates PMN leukocytes, which diapedese and cause brain lipid peroxidation, affects plt scavenging of NO which will interfere w/ PMN binding to endothelial cells- so diapedesis will be delayed until after the CO is withdrawn. Lipid peroxidation in the brain tissue can lead to reperfusion injury. CO may be an endogenous neurotransmitter.

44 Clinical signs Initial clinical signs reflects the gas’s effect on the CNS Cardiopulmonary signs (tachycardia, tachypnea, arrhythmia) Delayed neurologic signs Classic cherry red mucous membranes Initial CS- reflects the gas’s effect on the CNS- lethargy, depression, confusion, syncope, sz, uncons and death. Concurrent signs reported include tachypneai, tachycardia, vomiting, arrhythimas. Classic cherry red mm- reported to be rare in humasn, but happened in 7/24 dogs and 2/17 cats in a retrospective smoke inhalation paper. Severity os signs ranges from mild to severe and does not correlate consistently w/ Cohb levels. Genrally, Cohb levels > 15% result in overt signs of tox such as tachypnea and headache, over 30% in neuro dysfnc. Levels of 50% or more typically result in LOC that can progress to apnea and death. Delayed neuropsychiatric syndrome (DNS) in humasn. CS dev 3-240d following the toxic episode and include cognitive and persontality change, incontinace, dementia, parkisonism, gait distubance, hearing loss and pyschosis. Incidence varies but is ~10-30%, increass to 25-50% who suffered LOC or w/ Cohb levels > 25%. ~50-75% of humans who suffer form DNS recover w/ 1yr. Risk factors include age (older), duration of unrespo, history of illnesss. Hypoxia alone is consider unliely to cause these changes. Precise mch unclar- compromise of autoregulation of BF resulting in hypoxia, followed by oxidative damage and lipid peroxidation. Have been reported in animals following smoke inhalaiton and CO tox. Rnage from an ataxic gait to inability to ambulate, depressed to stupor emtation and deafness. One reto paper of 11 dogs w/ neuro signs associated w/ smoke inhalation noted a 46% occurrence of initial improvement in CS followed by acute recurrance of neuro dysnf 2-6d after the insult. Eliminatin of CO depends on minute ventilation, duration of oxposure and the fraction of inspired oxygen. O2 tx is the mainstray of tx for CO tox, b/c increasing the amt of Ox in the blood decreases the ½ life of CO as dissovled O2 competes w/ CO for hgb bindin sites. CO is displaced form hgb and exhaled through the lungs. In humas, the ½ life of CO is 4-6hrs in room air and min w/ 100% O2. Therotetically animals will have comorbid pulmonary dz and have longer CO ½ life. In ppl at elast this didn’t matter (looked at CO alone and CO w/ smoke). HBO in severe human cases- ½ life decrease to 15-30min. Data on the benefits are conflicting though- as some suggest no benefits. In vet patients- 100% o2 until Cohb is < 3%. It has been recommended to maintain a PaO2 of at least 300mmHg to theroretically inhibit diapedesis of PMLs and brain lipid peroxidation (rodent studies). Prognosis-

45 CO toxicity literature review
Carbon monoxide toxicity: a case series – Berent 2005 JVECC 4 dogs and 2 cats from the same household 5/6 survived (one euthanized for abdominal mass) 4/5 were thought to be temp deaf during recovery Treated with supportive care, o2, oxyglobin Full recovery following delayed neurologic signs after smoke inhalation in a dog- Mariani JVECC 2003. DNS (delayed neuropsychiatric syndrome) Mech not completely understood Berent JVECC case series of 4dogs and 2 cats. 6 animals from the same fm were brought to UMN- with the complain of recumbency, stiffness and dyspnea of unknown duration (6-8hrs). Dogs were left free in a large warehouse overnight, in which an RV was parked w/ a generator running. The 2 cats were in an office w/in the warefhouse. 5/6 survived (one was euthanized d/t abdominal mass). 4/5 animals were temp deaf (although was never rechecked) and made a full recovery. Treated w/ O2 and oxyglobin. Full recovery following delayed neurologic signs after smoke inhalation in a dog- Mariani JVECC yo Aussie presented for dementaia and tetraparesis. Been in a house fire 5d prior and was found unconsicous on an upper floor. Was given o2 for 15min. Was ataxic at the rDVM- treated w/ supporive care and sent home w/ ab’s and pred. Neuro signs were worsening (mentally inappro, decrease in CN) progressive ataxia- eventually made full recovery w/ supporitve care for pneumonia. HBO- controversy- appears to accelerate the resolution of acute symptoms, there are conflicting reports of its efficacy in preventin glate sequale. Antioxidants were given but efficacy unk. Previous repots of DNS 3/5 dogs died or euthized, the other 2 made full recovries. Clinical and neuro findings of acute CO toxicity in chiahuahuas following smoke inhalation- 3 adult chiahuahuas were present UGA for smoke inhalation after 12hrs during a house fire. Removed after 30m in a smoke-fillled room. All 3 were depressed w/ cyanosis, 2/3 were lat recumbent. Alll 3 received supporitve care and O2. After initial improvement the dogs dev sz- which were non responsive. Ashbaugh et al- goal was to char the Cohb concentration in a group of dogs that were exposed to a structural fire and to relate the conc of Cohgb w/ clinical parameters, to describe the use of O2 and document the duration of hosp in these dogs. Also had a control group. Clinical parameters, 2 samples (24hrs apart) were taken. Suspected exposure for 30-60min, 3 were dead at the scence. Included 21 dogs. Only 1/21 dogs died during hosp, duration of hosp ranged from 2-28d. There is debatel about whether there is a true relationship b/w temp and Cohb levels in human patients, a a rapid return to euthermia improves survivaling following acute signs- dogs w/ a temp < 100 had sig higher Cohgb concn. RR not correlated, but increased RE and abnormal auscultation had a greater Cohb. Dogs w/ altered mental status had a sign increased presenting COhgb as did length of hosp stay. O2 therapy resuled in a more rapid decline in Cohb but 5 dogs still had a mildly increased level. Guillaumin- 1st descriptino of extensive management of a patient suffering both neuro and resp complication d/t smoke inhalation with a successful outcome.

46 Newer literature The association of physical exam abnormalities and carboxyhemoglobin concentrations in 21 dogs trapped in a kennel fire - Ashbaugh JVECC 2012 Recorded clinical parameters, samples were taken on admission and 24hrs later Clinical parameters associated with high levels of carboxyhemoglobin RE/abnormal auscultation, lower temp Altered mental status and longer hospital stay O2 therapy resulted in faster decline in carboxyhemoglobin Successful outcome in a dog with neurologic and respiratory signs following smoke inhalation- Guillaumin JVECC 2013

47 Pulse oximetry Pulse Ox
Estimate of Sao2 Based on the measurement of the ratio of light absorbed by tissue (660nm) to that at an infrared wavelength (940nm) Absorption ratio reflects arterial oxygen saturation Does not account for various hemoglobin species (carboxy, methgb) Co-oximetry Pulse ox gap: difference between the % saturation measured and PaO2 Co-oximetry- direct measurement of carboxyhemoglobin, and methemoglobin. Pulse ox gap seems to correlate well in people


49 References Full recovery following delayed neurologic signs after smoke inhalation in a dog. Mariani JVECC Clinical and neuropathologic findings of acute carbon monoxide toxicity in Chihuahuas following smoke inhalation. Kent, et al JAAHA 2010. Methemoglobinemia caused by hydroxycarbamide ingestion in a dog. Wray 2008. Successful outcome in a dog with neurologic and respiratory signs following smoke inhalation. Guillaurmin, et al JVECC 2013 The association of physical examination abnormalities and carboxyhemoglobin concentrations in 21 dogs trapped in a kennel fire. JVECC 2012. Carbon monoxide toxicity: a case series. JVECC 2005. Small animal critical care medicine. Silverstein, Hopper, 1st edition. Chapters 28, 86, 87, 9 Cyanosis and congenital methemoglobinemia in a puppy. Fine, et al JAAHA 1999. The hemoCue for point of care hemoglobin measurement and packed cell volume estimation in cats. Posner JVECC 2005.

50 Determination of p50 for feline hemoglobin. Herrmann JVECC 2005.
Guyton Textbook of medical physiology 11th edition. Chapter 39 and 40 Fluid, electrolyte and acid-base disorder in small animal practice 4th edition. DiBartola Pages Textbook of respiratory disease in dogs and cats. King Pages Respiratory physiology 8th edition. West Ch 3-6. Respiratory function of hemoblobin. Hsia NEJM 2007. Hypoexima: A quick reference. Bach Vet Clincs of NA 2008. The veterinary ICU book. Wingfield, Raffe. Ch 2 and 21.

51 Questions?

Download ppt "Cyanosis Pathophysiology rounds"

Similar presentations

Ads by Google