Respiratory Flashcards

Question

What is the alveolar ventilation equation?

Answer 1

0.2 - 0.35

Answer 2

Physiological dead space will be bigger than the anatomic dead space

Answer 3

0.75 seconds

Answer 4

Diffusion limited - The gas that enter the capillary can be rapidly picked up/bind to the red blood cells due to high affinity → minimal change in partial pressure → minimal back pressure to slow it down → the rate of diffusion depends on the property of the blood gas barrier - Example: CO Perfusion limited - The gas that enter the capillary is barely bound to RBCs due to very low affinity → partial pressure rapidly increase → the faster the blood flow is, the more gas that can enter the capillary - Example: N2O

Answer 5

A combination of both Under normal resting condition, O2 is already partially saturated in the blood due to mixed venous blood. O2 usually reach fully saturated state when the RBC is at 1/3 way of the capillary → perfusion limited * If the patient's blood gas barrier is abnormal and the oxygen cannot reach fully saturated state when the RBC is at the end of the capillary → perfusion limited + diffusion limited

Answer 6

Carbon monoxide Because the gas is purely diffusion limited

Answer 7

Surfactant → alveolar epithelium → alveolar epithelium basement membrane → interstitial space → capillary basement membrane → capillary endothelium → plasma → red blood cell

Answer 8

Pulmonary artery: 25/8 (15) mmHg Aorta: 120/80 (100) mmHg

Answer 9

1) Distension - Predominant when pulmonary pressure is already high 2) Recruitment - Main mechanism for pulmonary artery - Open up more closed capillaries

Answer 10

When the lung volume is very small - Extra-alveolar vessels become narrow/collapse (pull from the parenchyma <<< vascular smooth muscle tone) → increased resistance - Pulmonary capillary remains open When the lung volume is very big - Extra-alveolar vessels are pulled open by the lung parenchyma → decreased resistance - Pulmonary capillary are collapsed because alveolar pressure >>> capillary pressure * There is a sweet spot when the total resistance is the lowest

Answer 11

True * It can happen when patient's hypotensive or alveolar pressure increased significantly

Answer 12

When the interstitial pressure is higher than alveolar pressure and pulmonary venous pressure (but no pulmonary arterial pressure) Pa > Pinterstitial > Pv > PA Pulmonary edema at the base of the lung

Answer 13

Zone 2: gradient between alveolar and pulmonary arterial pressure Zone 3: gradient between pulmonary arterial and pulmonary venous pressure

Answer 14

Zone 2: gradient between alveolar and pulmonary arterial pressure Zone 3: gradient between pulmonary arterial and pulmonary venous pressure

Answer 15

False Alveolar hypoxia (not blood!) cause vessel wall hypoxia → vasoconstriction

Answer 16

Alveolar PO2 < 70 mmHg

Answer 17

Inhibition of voltage-gated K+ channel → Decrease the efficiency of Na/K-ATPase → increase intracellular Na → more Na to exchange for Ca (Na/Ca channel) → Increase Ca inflow → vasoconstriction

Answer 18

Angiotensin I Bradykinin

Answer 19

Bradykinin Serotonin Norepinephrine Leukotriene Prostaglandin E2 and F2𝜶

Answer 20

A-a gradient = PAO2 - PaO2 = [FiO2x(Patm-PH2O) - PaCO2/0.8] - PaO2 Normal: < 10 * Normal PH2O = 47 mmHg

Answer 21

This formula should only be used at 100% O2 to eliminate hypoventilation, low FiO2 and low V/Q mismatch as causes of hypoxaemia and leaving only physiologic or anatomic shunts as differentials

Answer 22

Higher at the top of the lung

Answer 23

The sigmoid shape (specifically, the plateau) of the oxygen-haemoglobin dissociation curve gives rise to a phenomenon whereby it is impossible to compensate for low V/Q areas. As blood travelling through well-ventilated regions of the lung (high V/Q) is already maximally oxygenated (i.e. lays along on the plateau), there is no way you can get any better oxygenation by increasing ventilation. In contrast, because the CO2 dissociation relationship is more linear, increasing ventilation of the already well-ventilated regions will still continue to improve the CO2 clearance from those regions.

Answer 24

The amount of gas dissolved in the liquid/blood is proportional to its partial pressure

Answer 25

Left (increased O2 and hemoglobin binding)

Answer 26

Bohr effect: at the peripheral tissue, the increased partial pressure of CO2 and H+ decrease the affinity of hemoglobin affinity to O2 → facilitates unloading of O2 Haldane effect: at the lung, the increased partial pressure of O2 decrease the affinity of hemoglobin affinity to CO2 → facilitates unloading of CO2 * Deoxygenated hemoglobins have higher affinity to CO2

Answer 27

T-state * It becomes more relaxed as more and more oxygen binds to the hemoglobin

Answer 28

Shift to the right (higher O2 → decrease hemoglobin affinity to CO2)

Answer 29

1) Hypoxic hypoxia 2) Anemic hypoxia 3) Circulatory hypoxia 4) Histotoxic hypoxia

Answer 30

Hysteresis pressure required for inspiration is greater than the pressure required for expiration because of the surface tension and surfactant, as well as the alveolar recruitment and elastic property of the lung.

Answer 31

The volume change per unit pressure change

Answer 32

1) elasticity of the lungs 2) elasticity of the chest wall 3) surfactant

Answer 33

Elasticity= ΔP/ΔV Compliance= ΔV/ΔP

Answer 34

Decreased compliance: lung fibrosis, pulmonary edema, atelectasis Increased compliance: pulmonary emphysema, normal aging lung

Answer 35

Specific compliance = Cstat/FRC FRC=functional residual capacity It is a way to normalise compliance to lung volume (or patient size)

Answer 36

1) Reduce **surface tension** of the alveoli 2) Decrease **work of breathing** 3) Keep the **lung dry** 4) Promote **stability of alveoli**

Answer 37

Base of the lungs Because the resting volume is smaller and the change of volume during inspiration is bigger (expanding pressure is smaller at the base due to smaller transmural pressure due to the weight of the lung)

Answer 38

False -5 cmH2O (because of elastic recoil of the lung)

Answer 39

Medium-sized bronchi

Answer 40

0ABCD represents work of breathing ABCE represents the work to overcome the airway and tissue resistance 0AECD represents the work to overcome the elastic force

Answer 41

WOB = pressure x volume

Answer 42

Brainstem (pons, medulla)

Answer 43

Medullary respiratory center, Pre-Botzinger complex

Answer 44

Apneustic center: excite the inspiratory center Pneumotaxic center: inhibit inspiratory

Answer 45

Inspiration: Dorsal respiratory center Expiration: Ventral respiratory center

Answer 46

By changing the pH of CSF Blood Pco2 rises ➜ CO2 diffuses into the CSF from the cerebral blood vessels ➜ liberates H+ ions that stimulate the chemoreceptors ➜ hyperventilation ➜ blood Pco2 reduces and therefore in the CSF

Answer 47

Ventral surface of the medulla

Answer 48

Change in PO2, pH and PCO2

Answer 49

**Hering-Breuer reflex** Vagus efferent --> inhibition of DRG and VRG --> stop inflation of the lung (protective mechanism)

Answer 50

Pulmonary stretch receptors: within airway smooth muscles Irritant receptors: between airway epithelial cells

Answer 51

In the **alveolar walls (close to the capillary)** When the pulmonary capillaries are enlarged or there is increased **interstitial fluid** in the alveolar wall → J receptors are stimulated → signals are transmitted through **non-myelinated C fibers **→ increased respiratory rate

Answer 52

False Only peripheral chemoreceptors

Answer 53

Renal compensation → the change in pH is abolished * In this case, hypoxemia becomes the main stimulus to ventilate

Answer 54

Peripheral chemoreceptors

Answer 55

Pressure for suction: 10-20 cmH2O

Answer 56

From the nose to the mandibular ramus

Answer 57

From the nose to the lateral canthus

Answer 58

24-72 hours

Answer 59

False When the PaO2 is below 100 mmHg, the statement is true, but when the PaO2 is above 100 mmHg, the SaO2 will always show as 100% no matter how high PaO2 is.

Answer 60

Low inspired oxygen Global hypoventilation Venous admixture - Low V/Q regions - Diffusion impairment - Atelectasis - Right-to-left shunt Very low venous oxygen content

Answer 61

ETCO2 is about 5mmHg lower than PaCO2

Answer 62

CVCO2 is about 5mmHg higher than PaCO2

Answer 63

N2 560 mmHg O2 105 mmHg CO2 40 mmHg H2O 50 mmHg (47 mmHg)

Answer 64

pO2 in the atmosphere: FiO2xPatm = 760x0.21 = 160 mmHg However 47mmHg is due to pH2) FiO2 x (760-47) = 150mmHg (pO2 inspired) By the time O2 reaches alveoli there's dilution with other gases (i.e. CO2) = 100mmHg

Answer 65

120 PaO2 = 80 mmHg PaCO2 = 40 mmHg * If the added value is not 120 → presence of venous admixture

Answer 66

The P/F ratio can be very misleading when used at 21% inspired oxygen concentrations if PaCO2 values are elevated. PaCO2 values have been ignored in this calculation, but when breathing room air, changes in PaCO2 can have a significant impact on PaO2.

Answer 67

less invasive and good correlation found in dogs undergoing surgery and GA, however consider limitation in pulseox measurements. S/F < 315 = P/F <300 S/F < 235 = P/F <200

Answer 68

Anatomic: upper airway, trachea Alveolar Physiologic: anatomic + alveolar dead space Apparatus: dead space resulting from devices placed between the ET tube and the Y-piece of the breathing circuit (e.g. the ET tube that is too long)

Answer 69

PvCO2 is about 3-6 mmHg higher than PaCO2

Answer 70

The nerve fibers mediating inspiration converge on the phrenic motor neurons in the ventral horns from C3 to C5.

Answer 71

When the alveolar is inflated, the pulmonary stretch receptors will be stimulated and send signals through vagus nerve to the apneustic center in lower pons → slowing of respiratory frequency by increasing expiratory time

Answer 72

True A large decrease in arterial blood pressure causes hyperventilation, whereas a large increase in arterial blood pressure causes respiratory depression.

Answer 73

1) Hypoventilation 2) Increased inspired CO2 3) Increased CO2 production with a fixed minute ventilation 4) Increased dead space ventilation

Answer 74

1) respiratory acidosis leading to decreased myocardial contractility and decreased vascular tone 2) tachyarrhythmias 3) pulmonary vasoconstriction 4) increased ICP 5) AKI due to afferent arteriole vasoconstriction 6) right shift of Hb curve

Answer 75

Increased Decrease tissue perfusion → increased tissue CO2 production due to increased H+ production secondary to lactate formation and hydrolysis of ATP

Answer 76

Dead space ventilation Increased gradient means increased physiological dead space (alveolar dead space?) either increased V/Q or decreased V/Q

Answer 77

1) depress the hypoxemic-driven peripheral chemoreceptor stimulation → depress respiratory drive → worsening of hypoventilation 2) reverse the hypoxemic-induced pulmonary vasoconstriction → worsening the V/Q ratio (increased perfusion without concomitant increased ventilation → worsening of hypercapnea 3) When the hypoxemia is corrected, the increased partial pressure of O2 will decrease the affinity of Hb to CO2 → release more CO2 from the Hb → worsening of hypercapnea

Answer 78

1. oxygen toxicity 2. absorbtion atelectasis (nitrogen washout) 3. decreased respiratory drive 4. vasoconstriction

Answer 79

Mainstream - Pros: near real-time waveform - Cons: device is bulky, increase apparatus dead space Sidestream - Pros: less bulky, less dead space, more comfortable - Cons: delayed waveform, dilutional effect from other gas

Answer 80

1) Doxapram 2) Caffeine 3) Progesterone 4) Aminophylline/theophylline

Answer 81

1. non-selective PDEi 2. Adenosine antagonist 3. interferes with Ca++ mobilisation Less potent as a bronchodilator than beta2 agonists, but it has shown to have effects on **strengthening the respiratory muscles** --> important in MV patients Theophylline can only be given orally but aminophylline can ge given IV.

Answer 82

Blocks serotonin and cats' airways are particularly sensitive to serotonin

Answer 83

flaccidity of dorsal trachealis muscle + **chondromalacia** of tracheal rings (decrease synthesis of glycosaminoglycan, chondroitin and Ca++) --> collapse during respiration --> repeated mucosal contact --> severe inflammation --> failure of muco-ciliary escalator + metaplasia --> coughing as only mechanism for airway clearance

Answer 84

Grade IV might have a different patophysiology with congenital malformation being most likely vs chondromalacia

Answer 85

Trachea rostral to the thoracic inlet

Answer 86

Up to 70% dogs can be managed medically with rest and steroids for up to 12 months Extraluminal rings (75% success rate, risk of nerve and vascular damage with subsequent necrosis) Tracheal stenting (chose diameter +10-20% of current one, need fluoroscopy + endoscopy, risk of granuloma, fracture and migration)

Answer 87

Inward movement of the arytenoids during inspiration.

Answer 88

Elongated soft palates, stenotic nares, tracheal hypoplasia Everted laryngeal saccules, tonsillar eversion, laryngeal collapse, chronic GI signs

Answer 89

Ventral bulla osteotomy (VBO) Horner's syndrome (57%, can last for 4 weeks) Other approach is traction-avulsion but higher rate of recurrence

Answer 90

20 - 30 cmH2O

Answer 91

Increased (due to air-trapping)

Answer 92

Toxocara canis

Answer 93

High-pressure edema Increased-permeability edema

Answer 94

Normally ongoing fluid reabsorbition due to: - Na/K ATPase creates gradient for Na reabsorbtion by ENaC channel on alveolar side - Cl- follows due to electroneutrality via Cl- channels - K brought in by Na/K expelled on alveolar side by ROMK During inflammatory states ROS can damage ion channels and alter fluid balance --> non-cardiogenic pulmonary oedema Beta agonist by increasing CAMP and Na/K activity --> increased ENac intake of Na and quicker oedema reabsorbtion

Answer 95

The result of two mechanisms: **high hydrostatic pressure** + pulmonary **endothelial injury** due to **sympathetic surge** After a massive, neuronal event, the sympathetic nerve system is activated and it can cause high-pressure edema due to increased capillary hydrostatic pressure. The high hydrostatic pressure & sympathetic nerve system activation also cause the barotrauma to the capillary endothelium, which leads to the formation of increased-permeability edema.

Answer 96

1) Decreased **surfactant** production 2) **Mechanical force** leading to pulmonary parenchyma injury 3) **Reperfusion injury**

Answer 97

False Cats rarely cough, the most common clinical signs is dyspnea

Answer 98

breakdown of the disulfide bonds

Answer 99

**Phase I - airway response** 1-2 hours after aspiration Initial insult is caused by direct chemical irritation → damage of bronchial epithelium and alveolar endothelium → the acid aspirate also stimulates tracheobronchial substance P–immunoreactive neurons → induces tachykinin neuropeptide release → **neurogenic inflammation, bronchoconstriction, vasodilation, increased vascular permeability** **Phase II - lung inflammation** 4-6 hours after aspiration Inflammatory mediator cascades producing **neutrophil** chemotaxis (IL-8, TNF-α,17 and macrophage inflammatory proteins), sequestration, and subsequent increased permeability **edema**, **hypoxic vasoconstriction** (pulmonary hypertension)

Answer 100

It cause inotropic and vasodilation → potentially increase V/Q mismatch

Answer 101

True Also CRP showed normalization much earlier than changes on XRAYs Dogs can safely have ab treatment discontinued after normalisation of CRp (70% less than 1 week total duration) POCUS and CXRs are useful for diagnosis but not follow up as after 1 week lesion persisted in 88% of CXR and 71% of POCUS despite CRP normalisation

Answer 102

No difference in outcome --> 4 weeks likely unnecessary Clinical resolution occurs much earlier than radiographic resolution --> no longer recommended to base the length of treatment on serial CXR

Answer 103

Decreased compliance **Hallmark of ARDS**

Answer 104

1. implosion 2. spalding 3. inertia 1.hemorrhage 2.inflammation 3.alveolar flooding 4.proliferation 5. resolution

Answer 105

1% pre-emptive antibiotic use not justified

Answer 106

High V/Q mismatch

Answer 107

1) Right sided pressure overload 2) Hypoxemia (due to dead space ventilation) 3) pulmonary hypertension 4) Decreased cardiac output 5) Hypotension

Answer 108

Massive PTE = low BP and CV instability

Answer 109

Injury to 3 or more sequential ribs in which both proximal and distal end are fractured. Paradoxycal movement of the segment ensues.

Answer 110

The side with the flail chest down

Answer 111

No fractured ribs, but severe muscle injury of the chest wall resulting in mild paradoxycal pattern

Answer 112

**Immune-mediated demyelination** and degeneration of axons of the **ventral roots** and spinal nerves * Decreased segmental reflexes, normal sensation, hyperesthesia * Treatment: supportive care (**steroid doesn't seem to help**) * usually take 3+ weeks to recover

Answer 113

Racoon saliva or Campylobacter infection Hunting dogs are most at risk

Answer 114

Type C toxin

Answer 115

Botulinum toxin blocks release of ACh at the pre-synaptic terminal of skeletal muscle and cholinergic autonomic synapsis * The toxin cause irreversible enzymatic cleavage of Soluble N-ethylmaleimide-sensitive factor activating protein receptor (SNARE) proteins. SNARE proteins are essential for “docking” synaptic ACh vesicles to pre-synaptic membranes, allowing release of ACh into the synaptic cleft.

Answer 116

Aminoglycoside, because it can prolong or lead to complete NM blockage MOA: interfere with Ca movements through the Ca channels of the membrane of the nerve-endings → inhibits acetylcholine release at the synaptic cleft

Answer 117

1) * Some 4) are post-synaptic too

Answer 118

Air leaks into the thoracic cavity but cannot exit fully (one way valve at the leakage site)

Answer 119

When PaO2 < 50 mmHg

Answer 120

It is a reflex mediated by **trigeminal nerve**. When the animal's face touch cold water, the trigeminal nerve will send signal to the CNS and cause **bradycardia**, hypertension, and preferential **shunting of blood** to the cerebral and coronary circulations → protect the brain and heart from hypoxia-induced injury The cold temperature also decreased the **metabolic rate**.

Answer 121

Hydrogen cyanide (HCN)

Answer 122

1) thermal injury causing laryngeal edema 2) bronchoconstriction from irritant gases and Particulate Matter 3) Increased bronchial secretion and edema fluid

Answer 123

Room air: 250 min 100% Oxygen: 26-148 min

Answer 124

Hydroxocobalamin *Bind to cyanide to form cyanocobalamin (vitamin B12)

Answer 125

A: Respiratory baseline B: Expiratory upstroke C: Alveolar plateau D: EtCO2 E: Inspiratory downstroke

Answer 126

The aerodynamic equivalent diameter (AED) should be < 5 𝜇m

Answer 127

levalbuterol The main components is **R-albuterol**, which is an effective bronchodialtor. Racemic mixture has both R-albuterol and S-albuterol. The S-albuterol is proinflammatory and can cause bronchoconstriction.

Answer 128

Gram negative, obligate aerobic coccobacillus

Answer 129

Bronchoconstriction/Asthma

Answer 130

Rebreathing

Answer 131

Patient is breathing spontaneously

Answer 132

Cardiac oscillation

Answer 133

True It can provide some degree of PEEP and increase FRC → improve compliance, decrease V/Q mismatch

Answer 134

calculate patient's minute ventilation (estimated tidal volume = 10-15 ml/kg)

Answer 135

1. delivery of high FiO2 2. provision of continuous positive airway pressure 3. CO2 washout (elimination of rebreathing of air in the upperwairways) 4. reduction of upper airways resistance 5. potential to reduce need for intubation and invasive MV

Answer 136

ROX is RR-Oxygenation index used to predict need to escalate to MV in patients receiving HFNO (in humans SF ratio/RR >4.8 = successful weaning from HFNO) ROX-HR (ROX/HR x100) improves predictive ability of ROX alone (in humans >6.8 at 10h = significantly lower risk of failure)

Answer 137

ROX<3.68 and SF<143 (sens 75% spec 90%)

Answer 138

- nasal irritation - mild increase in PaCO2 (due to increased resistance to expiration - important to choose prongs that won't occlude more than 50% diameter of nostrils) - aerophagia - pneumothorax

Answer 139

- hypoxemic respiratory failure (pneumonia, pulmonary oedema, asthma) - post-GA recovery for BOAS - CO toxicity (reduced half-life as much as with MV)

Answer 140

100% FiO2 minute ventilation as flow rate temperature close to patient's body temperature

Answer 141

1) Congenital (degeneration neurons in nucleus ambiguous) 2) GOLPP (geriatric acquired form) 3) Neoplasia 4) Trauma 5) Toxin (e.g. organophosphate, lead) 6) Hypothyroidism 7) Iatrogenic (e.g. previous surgery, ventral slot) 8) Immune-mediated 9) Infectious disease 10) SLE

Answer 142

33% proprioceptive deficits 69% oesophageal dysfunction

Answer 143

Damage to recurrent laryngeal nerve innervating the dorsal cricoarytenoideus muscle that abducts arytenoids

Answer 144

unilateral arytenoid lateralization

Answer 145

Achieves wider rima glottis however not associated with difference in long term survival (possible that wider rima glottis = increased risk of aspiration pneumonia)

Answer 146

Yes, but much higher risk of aspiration pneumonia and shorter survival time

Answer 147

Aspiration pneumonia (up to 1/3 of patients) in dogs In cats laryngeal paralysis is rare and post-op Horner's syndrome is the most common complication

Answer 148

From the nose to the 5th intercostal space * This length should place the tube’s tip just cranial to the tracheal bifurcation.

Answer 149

False It should be 1/2-1/3 of the tracheal diameter to minimize iatrogenic tracheal trauma and decrease the incidence of post-intubation stenosis.

Answer 150

6-7 tracheal rings down from the insertion site

Answer 151

1. Collect necessary supplies. 2. Anesthetize and orotracheally intubate the patient with a cuffed ET tube. 3. Position the animal in dorsal recumbence with a towel rolled under the neck. Clip and aseptically prepare a large surgical field on the ventral cervical surface. 4. Perform hand hygiene, and don cap, mask, and sterile gloves. 5. Isolate the prepared surgical site with a barrier drape. 6. Make a ventral midline cervical skin incision just **caudal to the cricoid cartilage** for a distance of approximately 3 to 4cm. 7. Apply a self-retaining retractor (e.g. Gelpi) to hold open the skin edges and clear just enough subcutaneous tissue to identify the midline division of the sternohyoideus muscles. 8. Using Metzenbaum scissors, bluntly separate the sternohyoideus muscles on the midline, taking care to avoid the **thyroidea caudalis** vein on the midline between these two muscles. Retract the thyroidea caudalis vein to one side along with one of the **sternohyoideus muscle**. 9. Reposition the self-retaining retractors on the sternohyoideus muscles to expose the trachea and clear the loose fascia away at the proposed tracheotomy site. Application of a second self-retaining retractor at a right angle to the original retractor to retract the skin in a craniocaudal direction enhances exposure. 10. Using a scalpel blade, incise the interannular ligament between the **2nd and 3rd tracheal rings**. Do not incise the interannular ligament beyond **50% of the tracheal circumference**. 11. Place stay sutures around the second and third tracheal rings, knot the sutures to create large suture loops, and tag the suture strands with mosquito hemostatic forceps. 12. Use the stay sutures to manipulate the interannular opening while the orotracheal tube is removed. Insert the tracheostomy tube with the obturator in place, and then quickly remove the obturator and replace it with an inner cannula. 13. Leave the stay sutures in place for postoperative nursing care manipulations. 14. Secure the tracheostomy tube by attaching umbilical tape to the flange eyelets and tying the tapes behind the neck. 15. Do not suture the tracheostomy wound unless the incision was made too large. In that case, place a few interrupted sutures in the subcutaneous tissue and/or skin to decrease the size of the wound, taking care not to make the wound too small. 16. Once the surgical procedure is completed, the area is gently cleaned and left uncovered for easy observation.

Answer 152

Exudative Proliferative Fibrotic

Answer 153

Direct lung injury --> epitelial damage first Indirect lung injury --> endothelial damage first

Answer 154

- extrapulmonary vs pulmonary causes: extrapulmonary homogeneously diffused damage, so more likely to respond to recruitment strategies - hyperinflammatory vs hypoinflammatory: hyperinflammatory more likely to have extra-pulmonary causes and benefit from high PEEP and immunomodulatory drugs - radiological phenotypes: focal vs diffuse

Answer 155

1) Onset: Within 7 days of the known insult or new or worsening of respiratory signs 2) Chest images: Bilateral opacities (no fully explained by nodules, effusion or lobar collapse) 3) Origin of edema: rule out cardiac failure or fluid overload (by echo) 4) Oxygenation - Mild: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg with PEEP or CPAP ≥ 5 cmH2O - Moderate: 100 mmHg < PaO2/FiO2 ≤ 200 mmHg with PEEP or CPAP ≥ 5 cmH2O - Severe: PaO2/FiO2 ≤ 100 mmHg with PEEP or CPAP ≥ 5 cmH2O

Answer 156

- introduction of S/F ratio instead of P/F - POCUS instead of CXR - introduce HFNO settings as well as MV However application of Kigali showed higher false positives vs traditional Berlin definition

Answer 157

**Protein-rich edema** and eosinophilic **hyaline membrane** in the alveolar wall

Answer 158

1) Sepsis 2) Inflammation 3) Infection 4) SIRS 5) Major trauma - Long bone fractures - Head injury - Pulmonary contusion 6) Multiple transfusion 7) Smoke inhalation 8) Near drowning 9) Aspiration of stomach content * Neoplasia is not one of them

Answer 159

- baby lung - open lung - protective lung ventilation - proning - avoiding hyperoxia - conservative IVFT - other (currently under investigation): pressure release ventilation, recuiting manourver, reduction of driving pressure, reduction of mechanical power, NMB and corticosteroids

Answer 160

Current Recommendations: Early Administration: Corticosteroids may be considered in moderate-to-severe ARDS within the first 7-14 days, particularly in patients not improving with conventional treatment. Dexamethasone is commonly used in such cases. Late-Phase ARDS: Corticosteroids might be used in the fibroproliferative phase, but this should be done cautiously, weighing the potential benefits against the risks of prolonged corticosteroid therapy.

Answer 161

Low tidal volume: 4-8 ml/kg High PEEP Keep the target plateau pressure < 30 cmH2O *Permissive hypercapnea

Answer 162

The baby lung concept focuses on protecting the small remaining functional lung from overdistension. The open lung concept focuses on recruiting collapsed lung units to enhance ventilation and oxygenation and reduce ventilator-induced lung injury (VILI) from alveolar collapse and re-opening.

Answer 163

Refractory hypoxemia

Answer 164

1. Onset: Acute onset (<72 hours) of respiratory distress at rest 2. Known risk factors 3. Evidences of pulmonary capillary leakage without increased capillary hydrostatic pressure (no evidence of cardiogenic edema) - bilateral pulmonary infiltrates on TXR - bilateral dependent density gradient on CT - proteinaceous fluid within the conducting airway - increased extravascular lung water 4. Inefficient gas exchange - PaO2/FiO2 ratio WITHOUT PEEP or CPAP ≤ 300 mmHg (VetALI) ≤ 200 mmHg (VetARDS) - Increased A-a gradient - Increased dead space ventilation 5. Evidence of diffuse pulmonary inflammation (optional) - TTW/BAL samples show neutrophilia - TTW/BAL samples biomarkers show inflammation - Molecular imaging (PET)

Answer 165

1. Spontaneous 2. Assisted 3. Controlled

Answer 166

Volume: usually benefit from lower volume Pressure: usually need higher airway pressure (to be able to reach the tidal volume needed)

Answer 167

Flow rate (ml/min) = Tv / I time 10ml/kg/min / 1sec = 0.6ml/kg/min

Answer 168

flow change of 1-2 L/min Airway pressure dropped 1-2 cmH2O

Answer 169

150-250 ml/kg

Answer 170

1. Severe hypoxemia despite oxygen therapy (PaO2 < 60 mmHg) 2. Severe hypoventilation (PaCO2 > 60 mmHg) 3. Respiratory fatigue 4. Severe hemodynamic compromise that is refractory to therapy → goal is to decrease oxygen consumption

Answer 171

- oxygenation goals with paO2 55-80mmHg with SpO2 88-95%. Achieved by a combination of high PEEP/low FiO2 or low PEEP/high FiO2 (no evidence one approach superior to the other) - Pplat <30cmH20. Check Pplat with inspiratory hold of 0.5 sec every 4h and at each change of settings. If Pplat>30cmH20 try to decrease Vt. If breath stacking increase Vt to meet patient's demand. - normal pH. If pH <7.3 increase RR, if no changes increase Vt. If alkalotic reduce RR. - keep I:E with I

Answer 172

It is used to describe the force that drive ventilation Pmuscle + Pvent = (Tidal volume/compliance) + (resistance x flow) Pmuscle: pressure generated by the muscle Pvent: pressure generated by the ventilator Tidal volume/compliance: elastic load Resistance x flow: resistant load

Answer 173

A: Pressure-control B: Volume-control * Pressure-controlled → pressure is the same * Volume-controlled → shark fin volume time scalar → flow stops once volume is reached

Answer 174

CPAP (Continuous positive airway pressure) PSV (Pressure support ventilation)

Answer 175

Assisted breath: patient initiates the breath; machine provide entire inspiratory flow and terminates the cycle Supported breath: patient initiates the breath and finishes the whole cycle; the machine support the patient with the inspiratory flow

Answer 176

1) Auto-PEEP (air stacking) 2) Hypotension (decreased venous return)

Answer 177

1) Barotrauma 2) Decreased cardiac output due to decreased venous return 3) Compression of some alveolar capillaries → increased alveolar dead space 4) Increased pulmonary vascular resistance 5) Decreased LV compliance

Answer 178

Low Airway Pressure Alarm - 5-10 cmH2O lower than peak airway pressure - Circuit leak High Airway Pressure Alarm - 10 cmH2O higher than peak airway pressure - Pneumothorax, ET tube kink or obstruction, patient-ventilator asynchrony

Answer 179

Low Tidal Volume Alarm - 15% lower than the patient's tidal volume - leak, disconnection of the circuit, drop in compliance High Tidal Volume Alarm - 20% higher than the patient's tidal volume - Increased in compliance

Answer 180

* **Stepwise approach** Increase PEEP by 2cm H2O every 3-5 minutes. At each increment monitor P/F, PaO2, Cstat and driving pressure (Pplat-PEEP). Keep going until no more improvement in Cstat (driving pressure starts increasing) * **Sustained inflation** Put patient on CPAP mode (no mandatory breaths) with a pressure of 30-45cmH20 for 30-40sec Kepp patients in A/C mode increase PEEP 20cmH2O and step down by 2cmH2O every 2 min

Answer 181

Patient-related - Hypoxemia - Hypercapnea - Hyperthermia - Drug-induced panting - Inadequate anesthesia depth Equipment-related - Circuit/Equipment leak - Inappropriate trigger setting - ET tube/circuit kink/obstructed - Insufficient tidal volume - Inspiratory time too long/short

Answer 182

Airway resistance

Answer 183

Key of Jet ventilation: tiny Tv and very high RR - When mechanical ventilation is needed but traditional positive pressure ventilation cannot be delivered (e.g. tracheal/laryngeal surgery, bronchoscopy, bronchial resection, laryngoscopy) - If ventilation is required in patients with a tracheal lesion secondary to tracheostomy or prolonged intubation *Jet ventilation still requires intubation, but often with **smaller or more specialized tubes **that are designed to allow for both ventilation and access to the airway.

Answer 184

More homogeneous diffusion of gas in diseased lungs due to: 1. turbulence in large airways = mixing gas 2. direct ventilation of proxymal alveoli 3. radial mixing in medium size bronchi 4. pendelluft 5. laminar flow in small airways 6. asymmetric inspiratory vs expiratory flow (outflow of gas spiralling out vs parabolic flow in) 7. use of pores between alveoli (collateral ventilation)

Answer 185

1: pressure used to overcome the circuit and airway 2: pressure used to expand the lung/alveoli 3: pressure throughout the expiratory phase 4: PEEP a: peak inspiratory pressure (PIP) c: plateau pressure

Answer 186

Dynamic compliance = tidal volume/(PIP-PEEP) Static compliance = tidal volume/(Pplateau - PEEP) Dynamic compliance < static compliance Because dynamic compliance includes the pressure needed to overcome the airway and circuit

Answer 187

A: increased airway resistance B: decreased compliance

Answer 188

Whether or not there is intrinsic PEEP (auto-PEEP).

Answer 189

1) The PIP for constant flow pattern will be higher 2) The decelerating ramp flow allow fine-tuning of inspiratory time 3) decelerating ramp more comfortable as more physiological and less likely to cause barotrauma

Answer 190

b: the inspiratory time is too short → flow asynchrony c: optimal inspiratory time d: the inspiratory time is too prolonged → increase risk of patient-ventilator dyssynchrony

Answer 191

1) Expiratory hold 2) Check the flow scalar → if the expiratory flow does not return to baseline → Auto-PEEP

Answer 192

Number of dyssynchrony breaths/total breaths If >10% increased duration of ventilation and increased need for tracheostomy

Answer 193

Increased circuit/airway resistance slightly decrease dynamic compliance

Answer 194

A: decreased dynamic compliance B: increased dynamic compliance

Answer 195

LIP (lower inflection point): where the lung compliance suddenly increases due to opening of the collapsed conducting duct/alveoli UIP (higher inflection point): where the lung compliance significantly decreases due to overdistension of alveoli * PEEP should be set above LIP PIP lower than UIP

Answer 196

Increased airway resistance

Answer 197

Excessive airway secretion

Answer 198

Mismatch between the breaths delivered by the ventilator and the patient's needs. Gold standard to detect dyssynchrony would be phrenic neurogram and oesophageal baloon catheter for pressure measurement but in clinical practice relying on waveform analysis

Answer 199

1) Initiation/trigger phase 2) Flow delivery phase 3) Breath termination point (cycling) 4) Expiratory phase

Answer 200

1) Ineffective triggering 2) Auto-triggering - the ventilator "thinks" the patient is trying to initiate a breath when they are not, leading to unintended breaths 3) Double triggering - two breaths are delivered in quick succession, often because the patient’s effort or demand for air is not fully met by the first breath, leading them to trigger another breath immediately afterward.

Answer 201

1) Patient has higher ventilatory demand 2) Tidal volume is too small 3) Inspiratory time is too short or "flow-cycle threshold set too high" (the ventilator is ending the inspiratory phase too early. The ventilator switches to expiration before the patient has finished inhaling)

Answer 202

Premature cycling: the patient is continuing to make inspiratory efforts at the time the ventilator cycles off Delayed cycling: the patient initiates active expiratory efforts while the ventilator is continuing to deliver inspiratory flow

Answer 203

Flow starvation

Answer 204

Excessive inspiratory flow

Answer 205

Delayed cycling - the patient is trying to exhale while machine still delivery inspiratory breath

Answer 206

1) It inhibits the hypoxic induced vasoconstriction → make hypoxemia worse 2) irritating to lung parenchyma

Answer 207

No higher rates of gastric colonization and VAP

Answer 208

1) The primary disease has improved and stable 2) PaO2/FiO2 > 150-200 with FiO2 < 0.5 3) PEEP ≤ 5 cmH2O 4) Adequate respiratory drive 5) Hemodynamically stable 6) No evidence of organ failure

Answer 209

slow-deep breathing pattern

Answer 210

- unresolved primary cause - muscle weakness - inappropriate recovery from sedation/GA - increased WOB - CV instability Re-intubation increases odds of developing VAP by 7.6x

Answer 211

1) Tachypnea (RR > 50) 2) PaO2 < 60 mmHg or SpO2 < 90% 3) PaCO2 > 55 mmHg or PvCO2 > 60 mmHg or EtCO2 > 50 mmHg 4) Tidal volume < 7 ml/kg 5) Tachycardia 6) Hypertension 7) Hyperthermia or temp increase > 1C 8) Anxiety 9) Clinical judgement

Answer 212

Spontaneous breathing trial (with CPAP) PSV SIMV

Answer 213

30 cmH2O 40 ml/kg

Answer 214

Volutrauma Barotrauma Pneumothorax Oxygen toxicity Atelectrauma Biotrauma

Answer 215

Endotracheal intubation

Answer 216

Ventilator-associated pneumonia Pneumonia that arises more than 48 hours after endotracheal intubation that was not present at the time of intubation.

Answer 217

Biofilm formation within the endotracheal tube Microaspiration pass the endotracheal tube cuff Additional factors: - pulmonary and GI dysbiosis during critical illness - biotrauma with activation of resident macrophages + recruitment of neutrophils (upregulation of cytokines production) - impairment of muco-ciliary protection during mechanical ventilation

Answer 218

Early (48-96h post ET tube placement) vs late VAP * early VAP: antibiotic susceptible Staph and Streptococcus * late VAP: antibiotic-resistant Pseudomonas and Acinetobacter

Answer 219

1) Fever 2) Leukocytosis/leukopenia 3) Purulent airway secretions

Answer 220

**Clinical Criteria** 1) Presence of ET tube/tracheostomy at least 48 hours prior to the presence of clinical signs 2) Radiologic criteria: consolidation, cavitation, new or progressive and persistent pulmonary infiltrates 3) Systemic criteria: fever, leukocytosis/leukopenia 4) Pulmonary criteria (need 2): purulent airway discharge or increased secretion, worsening of gas exchange, new onset or worsening of coughing, dyspnea or tachypnea, crackles or bronchial breath sounds **Microbiological Evidence** 1) Positive Cultures: Sputum, tracheal aspirate, or bronchoalveolar lavage (BAL) samples showing growth of pathogenic organisms are a key microbiological criterion. Quantitative cultures: e.g., from BAL (>10⁴ CFU/mL) or tracheal aspirates (>10⁵ CFU/mL). 2) Positive blood cultures from a sterile site (when not attributed to another source) can also support the diagnosis. 3) histopathological evidence

Answer 221

1. early bronchiolitis 2. focal broncopneumonia 3. confluent bronchopneumonia 4. lung abscess These phases usually occur simultaneously in different areas of the lung

Answer 222

False Routine changing of the ventilator circuit should not occur unless contamination is noted.

Answer 223

hypercoagulable Chronic hypoxia → inflammatory state

Answer 224

1) Wedge nasoplasty (rhinoplasty/alarplasty) 2) Soft palate resection (staphylectomy) 3)Everted laryngeal saccules resection (ventriculectomy or sacculectomy) Turbinectomy if CT findings supportive and if patient not responding to traditional medical and surgical treatment. Surgical complications are reported to be uncommon with a success rate of up to 94%

Answer 225

Trigeminal ganglia

Answer 226

Stage 1: laryngeal saccule eversion Stage 2: loss of rigidity and collapse of the cuneiform processes of the arytenyoid cartilages Stage 3: complete laryngeal collapse characterized by midline collapse of the corniculate processes

Answer 227

Osteochondroma

Answer 228

Mechanical receptors (myelinated afferent nerves): larynx, trachea, large bronchi Chemoreceptors (C-fibers; unmyelinated axon): within all segments of the respiratory tree, including the larynx, carina, terminal bronchioles, and alveoli

Answer 229

Bacterial bronchopneumonia

Answer 230

gram - : Pasteurella, Bordetella. E.Coli gram +: Staph, Strep Mycoplasma Polymicrobial in 74% of dogs and 38% of cats

Answer 231

Hematogenous spread

Answer 232

Dogs: right bronchus Cats: trachea or carina

Answer 233

86% in dogs but only 40% in cats Consider Cuterebra spp. in cats as a differential

Answer 234

Cryptococcosis Histoplasmosis

Answer 235

Bronchoconstriction Epithelial toxicity

Answer 236

1) Patient needs to be > 15kg 2) Patient is restrained in sternal recumbency with nose tipped dorsally 3) The ventral cervical area is clipped and aseptically cleaned 4) Local anesthesia (2 to 5 mg/kg, 2% lidocaine) is instilled intradermally and SC at the intended needle insertion site 5) A stab incision is made through the skin using a #11 blade at that site to facilitate passage of a sterile 14-gauge needle through the **cricothyroid ligament**. 6) Measure the insertion site to **4th ribs** 7) Inserting a sterile 3.5-French red rubber or polypropylene catheter through the needle 8) Inject sterile saline **0.5 to 5 mL/kg per aliquot and aspirate when patient coughs** 9) After removal of the catheter and needle from the trachea, the area is covered with a sterile, nonadherent gauze sponge and lightly bandaged

Answer 237

Furosemide is secreted from the blood into the tubule lumen using an organic ion transporter located in the proximal convoluted tubule. The efficacy of this process is regulated by renal perfusion, competition by other organic anions, such as NSAIDs, and the degree to which furosemide is bound to albumin in the circulation.

Answer 238

1) Hypoalbuminemia 2) Concurrent use of NSAIDs 3) Poor cardiac output

Answer 239

Kussmaul breathing can be seen with severe metabolic acidosis and is defined as an extremely deep, rapid breathing pattern associated with hypocapnia

Answer 240

5) * Cardiac output increases

Answer 241

Decreased → patient becomes polyuric

Answer 242

1) Hypoxemia 2) Aspiration pneumonitis 3) Arrhythmias 4) Metabolic acidosis 5) Neurological signs

Answer 243

Active rewarming should stop when core temperature reaches 37 °C (98.6 F) to prevent rebound pyrexia

Answer 244

PTE * Areas of relative oligemia (less blood) secondary to decreased caliber of regional pulmonary arteries

Answer 245

5-10 ml/kg

Answer 246

Dog: 30-60 ml/kg Cat: 20 ml/kg

Answer 247

1) Nebulization & airway humidification 10-15 min q4-6 hours - Postural drainage and coupage (percussion) after 2) Clean the skin around the tracheostomy site with diluted chx (0.05%) 3) Check the tube ties 4) Tracheostomy tube suctioning - Preoxygenation - The entire suctioning procedure should be completed in less than 15 seconds - No suction after eating 5) Tracheostomy tube cleaning - q4-6 hours - Replace the inner piece 6) Change the entire tracheostomy tube every 24 hours

Answer 248

it is a phenomenon describing the gas movement between **lung regions with different compliances and airway resistance**. Pendelluft is often seen when: Different lung regions have unequal time constants (the product of resistance and compliance). During the inspiratory phase, one lung region fills with air more quickly, while another fills more slowly due to higher resistance or lower compliance. Air then moves from the faster-filling region to the slower-filling region, even while the airway pressure is constant.

Answer 249

Driving pressure = Pplateau - PEEP

Answer 250

- venous catheterization above the level of the heart - laparoscopic procedure (use CO2 as more likley to be reabsorbed and at a pressure <15mmHg so no gradient to get into vessels) - HBO - lung biopsies -CBP procedures

Answer 251

0.003ml/dL/mmHg Part of the CaO2 equation (PaO2 x 0.003)

Answer 252

- transpulmonary pressure = pulmonary pressure - pleural pressure (positive and keeps lung open) - transthoracic pressure = intrapleural pressure - atmospheric pressure (negative and opposing elasticy of chest that wants to spring open) - transrespiratory pressure = pulmonary - atm pressure

Answer 253

sensory cells in aortic and carotid bodies - sense drop of pO2, actovate Kv channels, open Ca channels, depolarization, neural input or respiratory centers in medulla and pons

Answer 254

- muscolo-skeletal proprioceptors (tachypnoea during exercise before hypercapnoea) - aortic and carotid baroceptors (tachypnoea secondary to drop in BP) - pain receptors - thermoreceptors (tachypnoea secondary to hyperthermia)

Answer 255

- anaesthetics - opioids - benzodiazepines

Answer 256

Dyspnoea is a subjective unpleasant sensation of perceived inadequate ventilation

Answer 257

Although similar to pain in the subjective perception of real or perceived threat, dyspnoea doesn't have specific receptor. The sensation is created by several peripheral afferent pathways including upper airways, lower airways (main generators of dyspnoea sensation), chest wall and chemoreceptors. These will be matched with the output generated in the CNS. If there is a mismatch between afferent input and output generation --> NEUROVENTILATORY MISMATCH and dyspnoea perception

Answer 258

- air hunger (from stretch and chemoreceptors - i.e. J receptors and furosemide) - increased WOB (from mechanoreceptors) - asthmatic thightness (bronchoconstriction)

Answer 259

- furosemide (acts on slow adaptive receptors and J receptors) - opioids (opioid receptors present in bronchioli and parenchyma) - steroids (? possibly helping with reducing inflammatory mediators) - chest wall vibration (reduce mechanoreceptor firing - less perception of WOB)

Answer 260

70% HCO3- 20% HHb 10% CO2 disolved in plasma

Answer 261

- restrictive ("small lungs") - obstructive ("big lungs")

Answer 262

FEV1: forced expiratory volume (how much air can be expelled from the lungs in 1s) FVC: forced vital capacity - total amount of air that a patient can forcibly exhale from their lungs after taking the deepest breath possible.

Answer 263

FEV/FVC decreased in obstructive disease (improves with administration of bronchodilators) FEV/FVC decreased in restrictive disease

Answer 264

Left is obstructive patter (increased total lung volume) and right is restrictive lung pattern (decreased total lung volume)

Answer 265

time constant = compliance x resistance After 1 time constant, about 63% of lung volume has been inhaled or exhaled. After 2 time constants, about 86% of lung volume has been inhaled or exhaled. After 3 time constants, about 95% of lung volume has been inhaled or exhaled. After 4 time constants, about 98% of lung volume has been inhaled or exhaled.

Answer 266

Usually ratio I:E is 1:2 so expiration usually calculated as 4xtime constant to ensure complete exhalation

Answer 267

1. thiopental has the least impact on laryngeal function 2. dexmedetomidine alone or in combination with opioids > titration of propofol 2. ACP+butorphanol an anticholinergic can be added to reduce secretions Doxapram test - normal dogs have their larynx "pin open"

Answer 268

PAP≧25mmHg and PAWP ≧ 15mmHg

Answer 269

Back pressure into pulmonary capillaries causes endothelial damage and vascular remodelling inducing pre-capillary PH

Answer 270

PAP-PAWP gradient >7mmHg as PAP↑↑↑

Answer 271

TV is closed in systole --> PAPs PA closed in diastole --> PAPm/d

Answer 272

1. Ventricles (flattening IV septum, underfilling LV, RV enlargement and wall thickening) 2. PA/Ao>1.4 and distensibility <30% 3. RA and vena cava enlargement

Answer 273

1. tachypnoea/dyspnoea at rest 2. syncope 3. split S2 4. RH failure 5. exercise intolerance

Answer 274

≧ 47mmHg 10% 0.98

Answer 275

Respiratory epithelium has PRRs for DAMPs and PAMPs --> nfKB and cytokine production + activation alveolar macrophages --> recruitment of neutrophils and platelet activation Also concurrent anti-inflammatory response with secretion of IL-10 and phenotype M2

Answer 276

1. congestion 2. red hepatization 3. grey hepatization 4. resolution (if type I shift to type II + scarring if basal membrane severely damaged)

Answer 277

Main barrier is the broncho-alveolar-blood barrier Best drugs should be lipophylic and small molecular weight. Index of bronchial [drug]/plasma[drug] TMPS 100% Fluoroquinolones 70% vs penicillin 9% (but with inflammation can still penetrate) aminoglycosides (38% but used effectivey against Bordetella when nebulised)

Answer 278

Elapids (coral snake). Two main toxins: 1. phospholypidase: binds and hydrolyses phospholipids of nerve terminals 2. 𝛼-neurotoxin: binds post-synaptic ACh receptors at the NMJ Clinical signs consistent with progressive LMN defects and ultimately flaccid respiratory paralysis

Answer 279

Anti-venom (IgG against venom --> immunocomplexes easily phagocytized) - polyvalent best one as no need for specific snake identification Nerve regeneration after phospholipidase (PLA2) occurs over 3-4 days --> prolonged MV need 72% survival with aggressive treatment (MV + antivenom)

Answer 280

Australia: Ixodex USA: Dermatocentor Pre-synaptic inhibition of Ach in the NMJ Also toxin can cause ALI/ARDS, myocardial failure

Answer 281

**Antiserum + MV** (average duration 4 days - weaning best with pressure support vs SIVM) Consider **tracheostomy** due to high incidence of upper airway obstruction (flaccid paralysis upper airways)

Answer 282

Gait and respiratory scores High scores significantly associated with poorer prognosis 75% survival overall (much better if MV started due to hypoventilation rather than hypoxemia)

Answer 283

- VAC 24%: hypothermia, hypotension, arrhythmia, positive fluid balance, oral and corneal lesions - VAP 14%

Answer 284

66% cardiac patients vs 35% non-cardiac development of azotemia in CHF anaemia in non-cardiac group

Answer 285

PaO2<60mmHg despite FiO2 0.8-1, PEEP 10-30 cmH20, Pplat >30cmH20

Answer 286

Very controversial, no clear definition. Low vs high responders Also anatomic recruitment (assessed by CT) ≠ functional recruitment (assessed by improved oxygenation)

Answer 287

False over 50% of cats with pyothorax present with hypothermia

Answer 288

False CT is the most sensitive method to detect both pneumothorax and pleural effusion. In humans features of pleural effusion are predictive of type but not in dogs.

Answer 289

Triglycerides 3:1 vs serum (or>100mg/dL) Cholesterol < than in serum Small lymphocytes cellularity

Answer 290

- CHF - obstruction of thoracic duct - idiopathic - lung lobe torsion - CVC thrombosis

Answer 291

9 cmH2O --> constant flow into pleura to lubricate

Answer 292

Mainly surgical with pericardiectomy and thoracic duct ligation Medical management can be attempted with low fat diet and rutin (increase lymphatic fluid uptake)

Answer 293

neutrophilia in 93% of dogs and 73% of cats

Answer 294

Less than 20%

Answer 295

Dogs are much more likely to require surgical exploration (sternotomy preferred) as dogs not undergoing surgery were 5.4x more likely to fail to resolve pyothorax. Cats undergoing surgery also more likely to survive, but significantly longer hospitalisation time.

Answer 296

14% Actinomyces, Nocardia and migrating FBs

Answer 297

47% of dogs involved in RTA and 20% of cats post high-rise fall

Answer 298

A/C the patient can trigger a breath but all breath delivered are mandatory

Answer 299

SIMV - patient can trigger breaths and they can be spontaneous or assisted if the fall within the pre-set cycle

Answer 300

- patient: resistance and compliance - ventilator: pressure, volume and flow

Answer 301

- what triggers the delivery of a breath (time, pressure or flow) - what determines the change from inspiration to expiration (time, I:E, RR) - parameter that can't be exceeded during the inspiration phase (it limits but doesn't terminate the breath≠from cycling variable)

Answer 302

Volume controlled pressure limited

Answer 303

Functional Hb saturation obtained with pulseox and is the ratio between HbO2 and the sum of HbO2 and HHb. It reflects the pulmonary function best. Fractional Hb saturation is obtained via co-oxymetry and it it the ration of HbO2 and the sum of all Hb (HHb, MetHb, SulfHb, CoHb and HbO2)

Answer 304

Yes, two studies confirmed good correlation in both healthy and critically ill dogs with and without oxygen supplementation

Answer 305

In medium to large dogs 2x25ml saline vs small dogs and cats 2x10ml. First sample more representative of airways vs second sample more representative of alveoli. Sample with foam = presence of surfactant Cytologically should see large amount of alveolar macrophages.

Answer 306

Airways are not sterile so significant only when CFU>10 (5) If on abx CFU>10 (3)

Answer 307

Include: - breed - emergency presentation - BCS - hyperthermia/hypothermia - procedures planner - surgical history Predictor of negative surgical outcomes: BRISK>4 high risk BRISK>3 mediumm to high risk

Answer 308

Muscular part > central tendon or crural portion Right side also most commonly affected

Answer 309

False Only 25%, so don't discard possibility of hernia despite no other findings on clinical exam Also 25% completely asymptomatic

Answer 310

Right middle and Left cranial

Answer 311

vescicular emphysema

Answer 312

Pugs and large breeds

Answer 313

1. pleural disease 2. aspiration pneumonia 3. previous surgical manipulation

Answer 314

Yes, due to possible damage of thoracic duct and lymphatics system Often requires revision surgery

Answer 315

True Aspiration and SIRS were the most common In cats are equally distributed

Answer 316

Dogs 84% and cats 100%

Answer 317

C2-C5 ventral slot 4.9% of cervical lesion required MV 80% survival with appropriate interventions

Answer 318

No difference has been found in multiple trials, cochrane review and meta-analysis

Answer 319

VetBLUE and CalgaryPlus * Asterix = **VetBlue** + subxiphoid view * **CalgaryPlus** with S-pattern + subxiphoid view + turn probe parallel to ribs ventrally to look for small pockets of fluid An additional protocol is the **Vezzosi protocol** which is performed by scanning dorsally to ventrally within each intercostal space from caudally to cranially

Answer 320

Vertical hyperechoic line, originating from the visceral pleura, synchronised with breathing and extending to the far fiels of the image while obliterating A-lines

Answer 321

Sharp vertical line identified at the caudal border of the thorax where air-filled lung overlies the soft tissue of the abdomen. It moves synchronous to the breathing in a motion similar to a curtain being open and closed.

Answer 322

True If there are no associated clinical signs

Answer 323

2.5 4 Pericardial effusion is also strongly associated with CHF in cats