cardio end sem

hypoxaemic resp failure

PaO2 < 60mmHg, PaCO2 - normal or low

hypoxaemic resp failure - S + Sx

dyspnoea, increased RR, agitation folloed by drowsiness, decreased mental acuity, organ failure (renal/brain)

hypercapnic resp failure

PaO2 - low, PaCO2 - > 50mmHg

hypercapnic resp failure - S + Sx

dyspnoea, increased RR, agitation, tremor, confusion → coma, increased ICP, H/A

intubation reasons

maintain pt airway, protect lower resp tract, allow vent support, facilitate a/w clearance

tracheostomy

artificial a/w surgically inserted into trachea, bypasses upper a/w, shorter than endotracheal tube

tracheostomy reasons

same as endotracheal tube but for longer period of ventilation, weaning from mechanical vent, tracheomalacia/tracheal stenosis

tracheostomy advantages

decrease dead space, easier to wean, decreased sedation (decreased gag stimulation, easier to communicate)

alveoli PO2 affected by:

decreased SA for gas exchange (interstitium changes → decreased diffusion → decreased blood PO2)

blood PO2 affected by:

decreased lung perfusion, Hb, decreased CO (tissue/cell affected by decreased O2 extraction and utilisation)

low flow O2 devices

device flow is less than pt’s own IFR → 100% O2 diluted by RA → decreased O2 concentration delivered to lungs

e.g. nasal prongs and face masks

high flow O2 devices

device can match pt’s IFR → less RA dilution → higher and more accurate FiO2

e.g. airvo

O2 therapy dangers - O2 toxicity

increased O2 concentration → acute tracheobronchitis, decreased cilial activity and diffuse alveolar damage

O2 therapy dangers - absorption atelectasis

high concentration of O2 washes N2 out (normally splints open alveoli)

O2 therapy danger - fire

O2 supports combustion

O2 induced hypercapnia

COPD → poorly ventilated alveoli → hypoxic pulmonary vasoconstriction, FiO2 increased → air into poorly ventilated alveoli → vasodilation → V/Q mismatch → increased PaCO2

increased FiO2 → increased PaO2 → increased O2 binding to Hb → structural Hb changes → removal of CO2 from Hb → increased PaCO2

chronically increased PaCO2 → decreased chemoreceptor sensitivity → hypoventilation

O2 induced hypercapnia S + Sx

confusion, drowsiness, SOB, twitching, H/A, decreased urge to breathe

CPAP

constant pressure delivered throughout inspiration and expiration (increases FRC, PaO2 and decreases WOB)

NIV mechanism

IPAP - assist ventilation by increasing VT, decreasing inspiratory mm load, WOB and CO2 levels, > EPAP
EPAP - provides end expiratory pressure to increase FRC

NIV uses

improve gas exchange, decrease WOB, increase PaO2, prevent acute resp acidosis, prevent intubation

NIV common pt groups

COPD exacerbations, NMD, obesity-related hypoventilation, chest wall deformity, post upper abdo/thoracic/cardiac surgery, weaning, COVID-19

NIV contraindications

facial issues - recent facial/upper a/w surgery, facial burns/trauma/deformities
GI issues - recent upper oesophageal/gastric surgery, bowel obstruction, vomiting
confusion/agitiation, low level of consciousness, inability to clear secretions, life threatening hypoxaemia, ICP >20mmHg, mutlisystem failure, undrained pneumothorax, frank haemoptysis

ECG

monitors heart rate, rhythm and regularity

arterial line

often in radial, femoral or dorsal pedis - monitors BP (systolic, diastolic, MAP), takes samples for ABGs

central line

placed in a central vein and ends in superior vena cava, right atrium or inferior vena cava - measures CVP, delivers fluids/drugs

pulmonary artery catheter

balloon tipped catheter that floats through R side of heart and sits in pulmonary artery - measures CVP, pulmonary capillary wedge pressure (PCWP), PAP

glasgow coma scale

measures level of consciousness - best eye response (/4), best vocal response (/5), best motor response (/6) = /15

ICP monitor

probe drilled through skull into brain ventricle - measures ICP (7-15mmHg), cerebral perfusion pressure (CPP)

hypoxameic resp failure vent support

hyperbaric O2 therapy/chamber - used in decompression illness, non-healing wounds, ulcers/serious soft tissue infection
nitric oxide - selective vasodilator (does to area of lung being ventilated, increases blood flow to alveoli → increased PaO2, decreased PAP and PVR)
extracorporeal membrane oxygenation (ECMO) - cardiopulmonary support outside body (allows for oxygenation and CO2 removal)

hypercapnic resp failure vent support - ventilator modes

controlled ventilation - set RR and VT, a/w pressure always positive, requires sedation, limited/no resp mm activity
assist/control ventilation - set RR and VT, mechanical breaths triggered by pt or ventilator, a/w pressure always positive, limited resp mm activity
SIMV, PSV, NIV

SIMV - synchronised intermittent mandatory ventilation

RR set between 2-14, triggered by machine or pt effort, either volume or pressure controlled

triggered by pt effort of machine, delivers positive pressure during inspiration up to specified volume or pressure, allows passive recoil for expiration down to specified PEEP

PSV - pressure support ventilation

pressure support ranges from 5-30mmHg, most common 10mmHg

triggered by pt effort, delivers positive pressure during inspiration and allows passive recoil for expiration down to specified PEEP

mechanical vent advantages

decreased disuse atrophy, need for sedatives as spontaneous breaths assisted and more comfortable

IPPB - intermittent positive pressure breathing

used with pts who are not dependent on mechanical ventilation, pt initiates inspiration and controls rate, physio sets positive pressure

intubation effects

increased a/w resistance - reflex bronchospasm, ET tube length and radius

decreased secretion mvmt/clearance - foreign body → increased mucus production, bypasses URT → decreased humidification → secretion drying and decreased sol layer, decreased cilial action, squamous cell metaplasia, impaired cough (glottis held open)

increased risk of a/w trauma - direct trauma on insertion, tracheal wall compression from balloon, goes through vocal cords

increased risk of infection - URT bypassed, decreased cough → microaspiration, vent associated pneumonia

increased dead space

PPV impact

resp - decreased FRC and lung compliance, altered ventilation distribution, risk of baro/volutrauma, O2 toxicity, resp mm deconditioning

CV - decreased venous return and BP, decreased alveolar perfusion

metabolic - increased excretion of Na, K, Ca, Mg, P, kidney stones

skin - pressure areas

GI - parenteral feeding, increased risk of stress ulceration

psych - difficulty communicating, sleep disturbed, noisy environment, painful/unpleasent interventions

manual hyperinflation

includes slow deep breath to decrease Raw and increase alveolar stretch, inspiratory hold to move air in behind secretions via collateral ventilation, and rapid release to create shearing force behind secretions to move to central airways

manual hyperinflation - detrimental effects

increased intrathoracic pressure - decreased VR and venous drainage from head, risk of baro/volutrauma

disconnection from vent - collapse due to loss of PEEP

anaesthetic circuits (mapleson A-E)

can do IH, deliver large volume, allow quick release to simulate cough → increased PEFR

ventilator hyperinflation

includes slow deep breath to decrease Raw and increase alveolar stretch, inspiratory hold to increase SA for gas exchange via alveolar interdependence and collateral ventilation, but no rapid release

recruitment manoeuvers

progressive incremental PEEP increased to a max peak pressure of 40-60cmH2O for 30-40 secs - increases alveolar pressure above normal tidal ventilation and sustains beyond normal time

suctioning

mechanical aspiration of secretions with or without artificial a/w

suctioning indications

artificial airway, secretion retention, unable to cough/ineffective cough, vomiting or recently vomited

suctioning detrimental effects

hypoxaemia, arrythmias, bradycardia, hypotension, mucosal trauma, atelectasis, bronchospasm, increased ICP

suctioning precautions

profound/severe hypoxaemia, compromised/unstable CV system, coagulopathies, frank haemoptysis, tracheal/oesophageal conditions (lung resection, trache trauma, head/neck/oesophageal surgery etc.)

factors influencing weaning

energy supply - O2 and nutritional state

energy demands - increased Raw, decreased Cl/Ccw and pump efficiency

NM competence - decreased resp drive, NM transmission, mm strength

cognitive/psychological - decrease opioids/sedatives, optimise sleep/wake cycle, delerium Mx, anxiety/depression

T-piece weaning

pt removed from vent circuit and connected to humidified O2 circuit (via T-piece), increase T-piece use during day then progress to night

decannulation criteria

no resp distress on minimal O2 for ≥ 24hrs, stable clinical condition, no a/w obstruction, adequate swallowing and vocal cord function, effective cough, alert

weaning process

increase time spontaneously breathing humidified O2 via T-piece/trache mask → cuff deflation trials → decannulation → NIV (if needed)

ICU acquired weakness causes

prolonged bed-rest, critical illness, long duration of mechanical vent, hyperglycaemia, corticosteroids, NM blocking agents

most commonly associated with systemic inflammation, multiple organ failure, ARDS, sepsis

ICU acquired weakness consequences

prolonged mechanical vent, longer ICU/hospital stay, increased mortality, decreased physical function, decreased HRQoL

ICU acquired weakness outcome measures

MRC sum score, physical function in ICU test (PFIT), handheld dynamometry, ICU mobility scale

direct chest trauma - aspiration

gastric contents → aspiration pneumonitis and/or aspiration pneumonia

inert fluid (e.g. blood and water), particulate matter (e.g. food → atelectasis/collapse)

direct chest trauma - aspiration pneumonitis

chemical lung injury from inhalation of sterile gastric contents → destruction on bronchial and alevolar cells, disrupts alveolar capillary membrane

direct chest trauma - non-fatal drowning

fluid dilutes and/or denatures surfactant → decreased Cl, also disrupts and increases permeability of alveolar capillary membrane → water in blood stream → breaks down RBCs OR fluid in alveoli → pulmonary oedema, reflex laryngo/bronchospasm → atelectasis and obstruction → hypoxaemia

direct chest trauma - inhalation injury

thermal injury - in upper a/w → oedema → UA obstruction

chemical injury - inhalation of toxic gas → inflammatory response in LRT → mucosal damage, oedema amd surfactant de-activation

asphyxiation - fire uses up O2 → inhales CO and cyanide

blunt chest wall trauma - rib #/flail segment

acutely results in pain and decreased/paradoxical rib mvmt → decreased O2 mvmt (general and local), CO2 mvmt (increased load and/or decreased ability to cope with load, efficiency of CW mvmt, secretion mvmt

4/12 post-rib injury → decreased lung volumes (FRC, VC), PEFR and chest wall deformity

blunt chest wall trauma - sternal #

most common MOI - MVA, impact sports, vehicle/pedestrian accidents, falls, assaults

blunt chest wall trauma - lung contusion

bruising of lung with alveolar haemorrhage and oedema, activation of coagulation cascade → clots, platelet aggregation, fibrin formation, inflammation/oedema → decreased local Cl, consolidated/collapsed alveoli → decreased gas exchange → decreased PaO2

blunt chest wall trauma - lung contusion S + Sx

dyspnoea, hypoxaemia, haemoptysis, tachycardia, wheezing, chest pain

blunt chest wall trauma - lung contusion long term

fibrous changes in lungs → decreased lung volumes (FRC, VC), PEFR, PaO2, disabling dysponea

blunt chest wall trauma - pleural space disorders

pneumothorax, haemothorax, subcutaneous emphysema

ARDS

acute inflammatory lung injury → increased pulmonary vascular permeability, lung weight, loss of aerated tissue with hypoxaemia and bilateral radiographic opacities

ARDS Dx

acute onset, bilateral infiltrates on CXR consistent with pulmonary oedema, PF ratio > 300mmHg with minimal PEEP (<5), no HF, fluid overload or CLD evidence

ARDS severity

mild = 200-300mmHg PF ratio, mod = 100-200mmHg, severe = <100mmHg

ARDS common causes

direct lung injury - non-fatal drowning, inhalation injury, aspiration pneumonia, lung contusion

other major body insult - sepsis, multi-trauma, major blood loss/transfusion, acute pancreatitis, severe burns, head injury

ARDS common S + Sx

Sx - SOB, fatigue, cough and/or secretions

obs - increased RR< accessory mm use, cyanosis

ABGs - hypoxaemia and/or hypercapnia

CXR - diffuse, bilateral patchy infiltrates

ausc - decreased BS, wheeze and crackles

cough - moist and/or white or pink, frothy sputum

Cl - decreased shown by increased a/w pressure

ARDS pathogenesis

exudative stage (up to 5 days) - insult → activation of inflammatory cells and mediators → damage to alveolar-capillary membrane → increased permeability → alveolar flooding with protein rich fluid and inflammatory cells, surfactant dysfunction

proliferative stage (up to 14 days) - repair process begins (e.g. macrophages help alveolar clean up), cells regenerate, surfactant produced

fibrotic phase (> 2wks) - not always reached

ventilator induced lung injury

barotrauma - pressure induced damage

volutrauma - alveolar overdistension

biotrauma - ventilator induced inflammation

atelectrauma - repeated alveolar recruitment and collapse → pneumothorax, pneumomediastinum, subcutaneous emphysema

primary brain injury

extradural haematoma (pooling between inner skull surface and outer dura layer

subdural haematoma

subarachnoid haemorrhage

intraventricular haemorrhage - bleeding into ventricle post trauma often in conjunction with other bleeds

brain contusion

diffuse axonal injury

secondary brain injury - ICP

normal - 7-15mmHg, elevated - >15mmHg, critical - >25mmHg, herniation - >40mmHg

cause - increased blood volume in skull, diffuse cerebral oedema, increased CSF volume, increased cerebral blood flow

secondary brain injury - CCP

pressure gradient driving cerebral blood flow, normal 70-90mmHg, must be maintained within narrow limits - too little pressure → ischaemia, too much → increased ICP, CPP = MAP - ICP

secondary brain injury - cerebral blood flow (CBF)

driven by CPP and CVR, rate of delivery of arterial blood to capillaries in brain, CBF = CPP/CVR

Exercise GCS < 5

passive, in bed/fully supported - PROM, supported sitting, functional ES, in bed cycle ergometry, tilt table

Exercise GCS ≥ 6

volitional/out of bed activities - AROM, bed mobility, balance, transfers, mobilisation ± gait aid, resisted strengthening

mm of resp innervation

inspiratory - diaphragm (C3-5), ext intercostals (T1-T11), SCM (C1-2, accessory nerve XI), upper traps (accessory nerve XI), scalenes (C3-C8)

expiratory - abdominals (T5-T12), int intercostals (T1-T11), pec major clavicular head (C5-6)

breathing mechanics post Cx/Thx SCI

flaccid paralysis of chest wall mm and abdominals, fast RR, shallow breathing, paradoxical POB (epigastric rise, intercostal recession), resp mm fatigue

physio post-SCI

techniques to increase inspiratory lung volumes - NIV/IPPB, abdo binder, inspiratory mm training

technqiues to improve cough effectiveness - manual assisted cough, cough assist devices (insufflation/exsufflation device)

prevent resp mm fatigue - supine, abdo binder when sitting upright, may need overnight rest on NIV, IMT

early mobilisation - gentle and progressive upright positioning with abdo binder, individualised seating prescription, preserve shoulder function and Thx mobility, prevent pressure areas

physio in NMD

techniques to increase inspiratory volumes - NIV, IPPB, lung volume recruitment, MSK Rx

techniques to augment cough - manual assisted cough, MI-E

mucociliary clearance techniques - percs/vibes/shaking, chest wall oscillation therapies (IPV)

peak cough flow in NMD

baseline to maintain cough effectiveness = >270-300L/min, ineffective cough = <160L/min, normal adults = 360-840L/min

cough augmentation techqniues - lung volume recruitment

breath stacking/glossopharyngeal breathing - maintains inspiratory lung volume, chest wall and lung compliance, increase inspiration to assist cough effectiveness

cough augmentation techqniues - manually assisted cough

adding compression to chest wall to increase EFR, aim for PCF >270L/min

cough augmentation techqniues - mechanically assisted cough

MI-E applies positive pressure on inspiration followed by rapid change to negative pressure on expiration, PEF > PIF to aid secretion mvmt from large a/w (EF bias)

measurements of overall ex capacity

VO2 max - O2 uptake increases quickly when dynamic ex begun or increased (normal = 84% of predicted)

work/work rate

RPE

ex capacity - CV/cardiac measurements

HR - increase to >90% of age predicted max

rhythm - shouldn’t change

BP - normal max = < 200/90, SBP increases, DBP stays the same/decreases

no chest pain

CAD - impaired endothelial function → decreased vasodilatory response → angina

ex capacity - resp measurements

increased VT and RR, VT/MVV <70-80%, SpO2 shouldn’t change, borg scale - relatively mild/not severe, shouldn’t be reason ex stopped, decreased EELV, may use acc and exp mm at max ex and during recovery

ex capacity - peripheral measurements

complaint of mm tiredness (usually cause of stopping), no claudication, respiratory exchange ration (R/RER) > 1.1 means peak VO2 reached, during submax should be 0.7-1

atherosclerosis → decreased lood flow to mm → decreased capillarisation, mitochondria enzymes, mm fibre number and size, impaired vasodilation responses

pulmonary rehab - goals

functional - decrease Sx, improve QoL, optimise functional status, improve activity participation

informational - increase knowledge of lung condition, promote self-Mx

economical - decrease health care costs

pulmonary rehab - inpatient phase

starts during exacerbation to increase ex capacity (e.g. bed exs, floor bike pedals, STS, mobilisation), pt and carer education

strategies to assist ex ability - decrease dyspnoea via positioning and breathing strategies, supplemental O2, forearm/elbow support frame, NIV, a/w clearance

pulmonary rehab - outpatient phase

6-12wks, 2-3x/wk, includes pt Ax, intervention (ex program, education sessions and re-Ax)

inclusion criteria - any pt with reps disease who is limited by dyspnoea on physical activity (COPD, asthma, bronchiectasis, CF, ILD, pre-surgery, willing to participate)

exclusion criteria - severe cognitive impairment, infectious disease, MSK/neuro disorders preventing gentle ex, unstable CV disease, known metastatic cancer

common co-morbidities - HTN, DM, dyslipidaemia, heart disease, OP, anxiety/depression, OA, hearing/visual impairments

pulmonary rehab - community programs

ex maintenance - HEP and maintenance class (local gym, specific programs - breathe easy, heart moves, lungs in action, local walking program)

COPD ex limitations

ventilatory constraints - EF limitation, dynamic hyperinflation, inspiratory mm function, gas exchange abnormalities

CV - hypoxic vasoconstriction → increased PVR → increased strain on R heart → RHF or hyperinflation → increased ITP → decreased VR → decreased LV SV

peripheral - decreased mm endurance, type 1 fibre proportion/type 2 atrophy, strength

nutrition - underweight/low BMI → increased mortality, increased BMR from increased WOB → depletion of fat free mass, loss of appetite/SOB while eating

pulmonary rehab - pre-test CIs

SpO2 < 85% RA, HR ≥120 or <50, SBP > 200mmHg and/or DBP > 100mmHg, mBORG ≥4, unstable angina/MI in previous month

pulmonary rehab - test termination criteria

onset of angina/angina like Sx, signs of poor perfusion, pt requests, severe fatigue, abnormal gait pattern, tachycardia, SpO2 < 85%, abnormal HR response

pulmonary rehab - lab tests

incremental cycle ergometry, constant wok rate cycle endurance tests - provide physiologic measurements to assess cause of ex limitation and prescribe ex

pulmonary rehab - field tests - 6MWT

need to do twice at least 30mins apart, record distance walked, HR, SpO2, mBORG, BP

advantages - easy to administer, better tolerated, more reflective of ADLs, self-paced, standardised instruction, minimal equipment needed, rests allowed

pulmonary rehab - field tests - ISWT

externally paced max ex test where walking speed increases with each level, continued until pt misses target 2x in a row, 12 speeds @ 1 min each

more useful for milder disease, harder to administer, less reflective of ADLs

pulmonary rehab - UL tests

university of california san diego SOB questionnaire (UCSD SOBQ), arm ergometry, incremental unsupported UL ex test (UULEX)

pulmonary rehab - QoL Ax

chronic respiratory disease questionnaire (CRDQ) - measures dyspnoea, fatigue, emotional function and mastery of disease

st george resp questionnaire (SGRQ) - measures Sx, activity, impact on social activity, psychological

medical outcomes study short form 36 (MO SF 36) - meaures functioal health and well-being

pulmonary rehab - aerobic FITT

F - 3x/wk (2 supervised, 1 HEP), I - 60-80% 6MWD, T - 30 mins (can start with intervals 3×10min), T - walking, cycling