Ventilation / perfusion / P.HTN Flashcards
Mechanical ventilation
Indications for mechanical ventilation:
(1) Hypercapnic respiratory failure / type 2
- due to reduced respiration drive, chest wall abnormalities, respiratory muscles fatigue
(2) Hypoxic respiratory failure / type 1
- due to intrapulmonary shut, ventilation-perfusion mismatch, decreased FRC
Goals of mechanical ventilation:
(1) Relieve respiratory distress
(2) Decrease work of breathing by:
- reducing ventilatory demand by limiting CO2 production, reducing dead space, decreasing respiratory drive
- improve respiratory impedance by decreasing airflow resistance, increasing thoracic compliance, meeting patient’s ventilatory demands
- improve breathing efficiency by use of auto-PEEP and appropriate positioning
(3) Improve pulmonary gas exchange
(4) Reverse respiratory muscle fatigue
(5) Permit lung healing
(6) Avoid complications
Ventilator modes:
(1) Controlled mechanical ventilation
- paralysed patients
- ‘ventilator does everything’
- delivers preset # of breaths / min, preset volume
(2) Assist control ventilation (assisted breaths)
- delivers a preset volume when patient triggers a breath by generating change in pressure or flow in the ETT.
- Automatically triggers breath after certain time if patient fails to.
- preset Vt (tidal volume), back up and flow rate
(3) Intermittent mandatory ventilation / SIMV + PS (synchronised mandatory ventilation + pressure support).
- RR, Vt, FiO2, PEEP are all pre-set.- Delivers a preset volume at a preset rate
- permits spontaneous breathing (unlike AC), but delivers mandatory RR if pt does not trigger, and supported breath with pressure support.
(4) Pressure support ventilation
- delivers fixed (preset) amount of pressure that supports each breath. Patient controls RR, inspiratory time, inspiratory flow rate
- Supported breaths: ventilator provides support to complete the full breath
- Pressure breaths: delivers pre-set pressure once the ventilator is triggered (reaches set pressure very quickly and remains there for a set inspiratory time)
Ventilator adjusted settings:
(1) Ventilator mode (as above)
(2) Oxygen concentration (FiO2)
- initially set it high. Obtain ABG after 20mins and titrate to lowest, to achieve paO2 60-70 or spO2 92%
- Oxygenation depends on the paO2 and ventilation-perfusion matching. paO2 depends on FiO2, alveolar pressure, and ventilation. VQ matching depends on PEEP (PEEP reduces intrapulmonary shunting).
- How to improve oxygenation:
- increase FiO2
- increase alveolar pressure (by increasing PEEP and I:E ratio). I:E ratio is normally set to 1:2 (mimicks normal breathing). This allows for lower FiO2 to be used.
(3) Tidal volume
- normal Vt = 5ml/kg.
- Preferred Vt during mechanical ventilation = 7-8ml/kg
(4) Ventilator rate
- when attempting to wean off set ventilatory rate, should use AC (back up rate)
(5) Inspiratory flow rate
- optimal IFR = 60L/min
- 100L/min in pts with COPD
(6) Inspiration:expiration ratio
- usually 1:2
(7) PEEP
- refer below
PEEP:
- goal is to improve oxygenation and minimize risk of oxygen toxicity.
- increases functional residual capacity (FRC i.e. volume remaining at end of expiration) by:
- Increasing alveolar recruitment (recruits collapsed alveoli)
- Increasing lung compliance
- Decreasing the work of breathing (done against compliance)
- this increases alveolar recruitment which improves V/Q mismatch, decreases shunting, increases total gas exchange surface. PEEP may also redistribute lung water out of the lung interstitium
- should increase PEEP by 3-5cm increments, may allow for FiO2 to be lowered. When weaning PEEP, obtain ABG, and if paO2 falls by <20%, safe to reduce PEEP
- Excessive positive pressure can lead to: (1) Overdistension and lung injury, (2) Worsening V/Q matching, (3) “Biotrauma”, i.e. cytokine leak and extrapulmonary organ dysfunction.
Carbon dioxide elimination:
- depends on alveolar ventilation
- Alveolar ventilation = RR x (TV - dead space)
- increase elimination by increasing RR and TV
- Capnography can be used to assess end-tidal carbon dioxide (EtCO2) concentration (estimates paCO2). Normal EtCO2 is 35-37mmHg.
Lung compliance:
- compliance = volume / pressure
- lower in ARDS / stiff lung (higher pressures required to deliver set TV), but higher in emphysema (lower pressure required to deliver TV)
Positive pressure ventilation (IPPV):
- produces lung inflation by generating and applying positive pressure to the airways.
- Pressure-cycled ventilators (preset pressure limit) vs volume-cycled ventilators (preset volume limit)
- PPV increases the gradient for gas transfer, but not by much
PIP:
- peak inspiratory pressure
- maximum pressure required to deliver a breath during active inspiration. The sum of the resistive pressure and the elastic pressure
Negative pressure ventilation:
- iron lung
- chest cuirasse
Complications of mechanical ventilation:
- VAP / nosocomial pneumonia
- barotrauma
- gas trapping
Invasive ventilation:
- invasive ventilation decreases anatomical dead space
Oxygenation
Limitations of pulse oximetry:
- time lag (it may take 30 seconds or more for the pulse oximeter to reflect conditions of life-threatening hypoxia)
- Hypovolemia, vasoconstriction, peripheral vascular disease or nail polish may cause false readings.
VAP
Reported incidence, 9-10% (usually, 30%)
Mortality, 50-80% (vs 30% is comparable patients without pneumonia)
Risk factors
- Underlying disease
- Impaired host defenses
- Depressed mucociliary transport
- Endotracheal/tracheostomy tube
- Aspiration
- Nebulizers
Clinical diagnosis is very unreliable
Pulmonary hypertension overview + PAH (group 1 PH)
Overview of P HTN:
- Group 1: PAH; group 2: PH due to left heart disease; group 3: PH due to lung diseases and/or hypoxia; group 4: PH due to pulmonary artery obstructions; group 5: PH with unclear and/or multifactorial mechanisms.
- PH can also be classified as pre- capillary PH (ie, that involving the pulmonary arterial system) or post-capillary PH (ie, that confined to the pulmonary venous system)
- When all five groups are discussed collectively, the term PH is used.
- Clinical features: typically present with exertional dyspnea, lethargy, fatigue that progresses over time until severe PH with overt R) ventricular failure develops (exertional CP, exertional syncope esp w L)H failure, oedema, ascites/anorexia)
- associated illness: LH failure, CTD, chronic lung dx, VTE, OSA, CKD, thyroid disorder, metabolic disorders. Risk fx inc obesity, age, dyslipidemia, HTN, DM, AF, structural heart disease
- examination: loud P2 / splitting of S2, elevated JVP, prominant v wave (signifies TR), 3rd or 4th heart sound (atrial gallop), parasternal heave, pansystolic murmur (TR), signs of RH failure (oedema, ascites, effusion, splenomegaly (in schistosomiasis)
- ECG: RAD, RV strain (R wave/S wave ratio greater than one in lead V1 with deep T-wave inversion in V1 through V5), p pulmonale (peaked; RA enlargement).
- labs: elevated BNP
- TTE: TRV (tricuspid regurgitant jet velocity) >3.4 (and >2.9 in the presence of other features) suggests PH. ePASP >50mmHg means PH is likely. IV septal hypertrophy. Evaluation for left heart disease (diastolic/systolic dysfunction, LA dilatation, contributing to PH)
- Right heart catheter:
for pts with high suspicion PH (and TTE is non diagnostic), unclear cause (after extensive workup), group 1 (PAH) is suspected, cause is mixed (group 2 and 3). Can also perform vasoreactive testing
mean PAP >20mmHg is diagnostic for PH (mPAP 8-20 is normal).
PH can also be classified as pre- or post-capillary PH.
- Pre-capillary PH (inc group 1 PAH, 3 hypoxia/CLD, 4 CTEPH, 5 multifx) is due to a primary elevation of pressure in the pulmonary arterial system alone (eg, PAH). meanPAP >20mmHg; PVR (pulm vasc resistance) >or=3 WU (wood units); PAWP (PA/capillary wedge pressure indicative of LHD)
- post-capillary PH (inc group 2 LHD and 5 multifx) is that due to elevations of pressure in the pulmonary venous and pulmonary capillary systems (pulmonary venous hypertension; eg, group 2 LHD). mPAP >20 mmHg; PAWP >15 mmHg; PVR <3 WU
- In practice, some patients have mixed pre-and post-capillary features (inc grp 2 LHD and 5 multifx. mPAP >20 mmHg; PAWP >15 mmHg; PVR ≥3 WU
- PFTs, HRCT, 6MWT, sleep study, VQ scan (chronic PEs) — assess for group 3 CLD/hypoxia. PFTs must be more than mildly abnormal to contribute to P HTN.
Pulmonary arterial hypertension (Group 1 PAH)
Causes of PAH:
- Idiopathic PAH
- Heritable PAH (BMPR2 mutation, 5HTT mutation, many others)
- Drug- and toxin-induced PAH
- PAH associated with:
- Connective tissue disease inc scleroderma, RA, SLE, raynauds, mixed CTD (tests to order inc: ANA, RF, anticentromere antibodies, anti-topoisomerase, anti-RNA polymerase III, anti-dsDNA, anti Ro, anti La, U1RNP antibodies); or vasculitis (ANCA)
- HIV infection
- Portal hypertension (mostly due to chronic liver dx)
- Congenital heart disease
- Schistosomiasis (check stool and urine parasites)
- PAH long-term responders to calcium channel blockers. Diagnosed by vasoreactivity testing and consistent response to ca-chann blockers for 1 year.
- PAH with overt features of venous/capillaries involvement (PVOD - pulm veno-occlusive diseasesa / PCH - pulmonary cap hemangiomatosis) - characterized by extensive diffuse occlusion of the pulmonary veins resulting in tortuous dilation of the pulmonary capillaries.
- Persistent PH of the newborn syndrome (PPHN) due to abnromal pulmonary vasculature
P HTN 2 (left heart dx)
PH due to left heart disease.
Description:
- Left-sided heart failure (left heart disease [LHD]) is the most common cause of pulmonary hypertension
- Patients with PH-LHD typically present with symptoms and signs related to HF such as dyspnea, fatigue, and signs of pulmonary and/or peripheral edema
- loud P2 or parasternal heave
Causes of T2 P HTN:
- PH due to heart failure with preserved LVEF (HFpEF)
- PH due to heart failure with reduced LVEF (HFrEF)
- Valvular heart disease (left disease valvular heart disease - mitral or aortic)
- Congenital/acquired cardiovascular conditions leading to post-capillary PH (eg, restrictive cardiomyopathy, constrictive pericarditis, left atrial myxoma, congenital or acquired inflow/outflow tract obstruction, and congenital cardiomyopathies).
Evaluation:
- TTE demonstrating systolic or diastolic dysfunction (more than mild)
- RH cath: mPAP ≥20 mmHg, pulmonary capillary wedge pressure (PCWP which estimates left atrial pressure) ≥15 mmHg, and a normal or reduced cardiac output
P HTN 3 (hypoxia, lung dx)
PH due to lung disease and/or hypoxia
Causes of T3 P HTN:
- Obstructive lung disease
- Restrictive lung disease
- Other lung disease with mixed restrictive/obstructive pattern
- Hypoxia without lung disease
- Developmental lung disorders
Evaluation:
- evidence of moderate to severe lung dysfunction and/or hypoxemia
- rule out other causes (inc PAH due to CTD, HIV, or liver disease; PH due to left heart disease, and PH due to pulmonary artery obstructions eg, thromboembolic disease).
P HTN 4 (CTEPH)
PH due to pulmonary artery obstructions
- *Causes of T4 P HTN**:
- Chronic thromboembolic PH (CTEPH)
- Other pulmonary artery obstructions (tumors, pulm artery stenosis, parasitic obstructions)
Evaluation:
- V/Q scan has sensitivity 96%, specificity 90-95% for CTEPH. CTPA is the gold standard.
- tests for cause of CTEPH: anticardiolipin antibodies, lupus anticoagulant, and anti-beta2-gylycoprotein antibodies.
P HTN 5 (unclear / multifactorial)
PH with unclear and/or multifactorial mechanisms
Causes of T5 P HTN:
- Hematologic disorders (Chronic hemolytic anemia, sickle cell disease, Myeloproliferative disorders)
- Systemic and metabolic disorders (Pulmonary Langerhans cell histiocytosis, Gaucher disease, Sarcoidosis)
- Others (CKD/CRF, Fibrosing mediastinitis)
- Complex congenital heart disease
CO poisoning
