Cor Pulmonale & Respiratory Failure Dr M Prins With acknowledgement to: Dr S R Dawadi.
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Transcript of Cor Pulmonale & Respiratory Failure Dr M Prins With acknowledgement to: Dr S R Dawadi.
Cor Pulmonale
&
Respiratory Failure
Dr M Prins
With acknowledgement to: Dr S R Dawadi
Please note
These slides are complimentary to the
information in Davidson’s and does not
replace the textbook!
Cor pulmonale
= Pulmonary heart disease
= Right ventricular enlargement ( hypertrophy and / or dilatation) secondary to abnormality of Respiratory System.
Components of Respiratory system -
Gas exchanging organ - Lungs and its circulatory system
Pump that operates the ventilation of lungs- Thoracic cavity and related respiratory muscles
Controller- Areas in brain and related nerve tracts
& fibers
Causes leading to Cor pulmonale -
Gas exchanging organCOPDInterstitial lung diseasesThrombo-embolic diseases
PumpKyphoscoliosisGuillian-Barre syndromeMyasthenia gravis
ControllerSleep apnea syndromePrimary alveolar hypoventilationPost encephalitis
Sequence of events -
Acidemia Hypoxia
Pulmonary Vessels Viscous IdiopathicVasoconstriction Obliteration Blood PAH
Pulmonary Hypertension
RV Hypertrophy / Dilatation
Rt. Heart Failure
Classification -
Acute – massive pulmonary embolism
COPD – acute decompensation after resp. infection
* acute dilatation without prior hypertrophy
Chronic – COPD, ILD
recurrent PE
* slow development of hypertrophy and
dilatation
Symptoms & signs -
Loud P2, Parasternal heave
3/6 pan systolic murmur over LSB increasing with inspiration
Raised JVP, Pedal edema,
Tender, smooth, pulsating hepatomegaly
+ Ascitis
Respiratory Failure
= Condition in which Respiratory System fails in
one or both of its gas exchanging functions
Oxygenation of - mixed
CO2 elimination from - venous blood
Development
- Acutely = rapid and life threatening
- Chronically = slow and may be unapparent
Components of Respiratory system -
Gas exchanging organ - Lungs and its circulatory system
Pump that operates the ventilation of lungs- Thoracic cavity and related respiratory
muscles
Controller- Areas in brain and related nerve tracts & fibers
Types of Respiratory Failure -
Type I = Hypoxemic respiratory failure* PO2 < 60 mmHg* PCO2 Low or NormalVentilation perfusion mismatch / shunts
Type II= Hypercapnic respiratory failure * PO2 < 60 mmHg * PCO2 > 45 mmHg Hypoventilation
Clinical features
Hypoxia :
Dyspnoea
Central cyanosis
Agitation
Restlessness
Confusion
Hypercapnia :
Headache
Peripheral Vasodilatation
Tremor / flap
Bounding pulse
Drowsiness
Coma
Classification -
Respiratory Failure
Acute Chronic
Type I Type II Type I Type II
Po2 -
Pco2 -
pH -
HCO3 -
Acute Respiratory Failure -
Type I Type IICauses Pneumonia Acute asthma
Pulmonary embolus Acute foreign body Pulmonary edema Narcotic drugs Pneumothorax Muscle paralysis
ARDS Brain stem lesion
Therapy Maintain Airway Maintain airway Treat the disease Treat the cause High-concentration O2 Mechanical
ventilation Mechanical ventilation or tracheostomy
Chronic Respiratory Failure -
Type I Type IICauses Emphysema COPD
Lung fibrosis Primary alveolar hypovent.
Right –to-Left shunt Kyphoscoliosis
Anemia Ankylosing spondylitis
Therapy -Treat the disease - Treat the disease
- Controlled long-term - Controlled long-term
oxygen oxygen
- Ventilatory support if
necessary
Acute on Chronic Type II respiratory failure
Further insult on stable chronic condition
Acidemia, worsening hypercapnea, drowsiness and coma.
Causes (precipitating events) –
Airway infections Bronchospasm
Pneumothorax Sedative drugs
Pulmonary embolus Cardiac failure
Retention of secretions Trauma ( head injury, rib
fracture )
Case study
Patient’s History
76 year old male patient
40 pack year smoking history
Diagnosed 4 years ago with COPD
Now complaining of – worsening SOB
- increased sputum
- swollen legs
- RUQ pain
No orthopnoea or PND
Physical Examination
Plethoric, Central cyanosis, resp. distress
Raised JVP, Bilateral pedal edema,
Hyper inflated chest, Reduced breath sounds, Diffuse end expiratory wheezes
Parasternal heave, Loud P2, 3/6 pan systolic murmur over LSB increasing with inspiration
Tender, smooth, pulsating 6 cm hepatomegaly
No spleen palpable, No ascitis
Investigations
FBC – Hb 20,2; Hct 0,614;
WCC 8,3; Plt 215
Arterial blood gas –
pH 7,34 (N)
Pco2 52 mmHg ( )
Po2 54 mmHg ( )
Hco3 32 mmol / l ( )
O2Sats 86% ( )
Symptoms & signs -
Hyper inflated chest, Reduced breath sounds, Diffuse end expiratory wheezes
Plethoric, Central cyanosis, resp. distress
Parasternal heave, Loud P2, 3/6 pan systolic murmur over LSB increasing with inspiration
Raised JVP, Pedal edema,
Tender, smooth, pulsating 6cm hepatomegaly
No spleen palpable, No ascitis
Clinical problem -
COPD ( etiology – smoking)
- Cor pulmonale, features of right heart failure
- Secondary polycythaemia
- Chronic Type II respiratory failure
Therapy -
Before RHF ensues
- Decrease RV workload ( reduce PHT)
- treatment of underlying cause
- prompt achievement of arterial oxygenation
After RHF has developed
- Cardio tonic measures – rest; diuretics
- Oxygen
Long Term Oxygen Therapy
Continuous: = For > 16 hours / day
- resting PO2 < 55 mmHg or O2 saturation < 88%
- resting PO2 55 – 59 mmHg or O2 SATS. < 89%
but with - pulmonary hypertension
- Cor pulmonale
- polycythaemia (Hct > 56%)
Non-continuous:
- during exercise PO2 < 55mmHg or O2 SATS< 88%
- during sleep if - hypoxia
or- pulm hpt, daytime somnolence
cardiac arrhythmia
Long-term O2 therapy
Benefits :
- improves survival
- symptomatic improvement in effort tolerance
- reduces polycythaemia
- prevents progression of pulm. hypertension
Aim :
- PO2 > 60mmHg without worsening PCO2
- O2 saturation > 90%
Diuretics therapy
Decrease RV filling volume Reduction of peripheral edema Improve function of both RV and LV Great caution required
Volume depletion with reduced cardiac output
Hypokalemic metabolic alkalosis ( reduce ventilatory drive)
Cardiac arrhythmia ( electrolytes and acid base imbalance)
Loop diuretic + spironolactone
Venesection
Indication Polycythemia
Aim Hkt 55
ConclusionDevelopment of Cor pulmonale indicates poor prognosis
Left heart diseases must be excluded prior to diagnosis
Varieties of diseases of respiratory system should be considered
Co-existence of multiple diseases possible
Oxygen and diuretics are mainstay of therapy
Oxygen TherapyDr M Prins
Div PulmonologyDept of Internal Medicine
PaO2 mmHg
SaO2 (%) Clinical significance
150 99 Inspired at sea level
97 97 Normal young man
80 95 Normal young man asleep, old man awake, Inspired at 5700 m
70 93 Lower limit of normal
60 90 Respiratory failure, mildShoulder of dissociation curveTE Oh. Intensive Care Manual
Clinical Significance of PaO2 and SaO2 values
PaO2 mmHg
SaO2 (%)
Clinical significance
50 85 Resp failure: admit to hosp
40 75 Venous blood, normalArterial, severe resp failureAcclimatized at rest at 2700 m
30 60 Unconscious if not acclimatized
26 50 P50 or 50% saturation
20 36 Acclimatized at 5700 mHypoxic death
TE Oh. Intensive Care Manual
Oxygen Cascade
Inspired air 150 mmHg
Alveolar 103
Arterial 100
Capillary 51
Tissue 20
Mitochondrial 1-20
Ganong WF. Review of Medical Physiology
MRC 198187 patients
3 years
No oxygen
45 patients
2 L/min: 15 hours/day
42 patients
30 died 19 died
Lancet 1981
NOTT (USA) 1980
203 patients
12 hours 19 hours continuous
• Follow-up for 19 months• Added one liter during sleep/exercise• Mortality
• 12 hours 21%• 19 hours / continuous 11%
Ann Intern Med 1982
Vital Air Home Heallthcare
Indications for Long Term Oxygen Therapy (1)
Chronic obstructive pulmonary disease: Non-smokers with stable, severe COPD
(FEV1<1,5l) PaO2 < 55 mmHg With or without hypercapnia
(PaCO2>45mmHg) Disease must be stable for 3 months
after exacerbation
Indications for Long Term Oxygen Therapy (2)
Other lung disorders with respiratory failure: Diffuse interstitial lung disease Cystic fibrosis Bronchiectasis Primary or metastatic lung tumors
Indications for Long Term Oxygen Therapy (3)
Hypoxia-related symptoms / conditions that may improve with oxygen therapy: Pulmonary hypertension Congestive heart failure due to Cor
pulmonale Erythrocytosis Impairment of the cognitive process
Guidelines for Long Term Oxygen Therapy
The aim of long term oxygen therapy is to maintain oxygen
saturation above 90%
Oxygen Delivery Methods
At least 15 hours per day Start at
24% 1-2 l/min Nasal cannulae Increase gradually to avoid CO2 buildup Aim: Saturation 90%
Dual-prong nasal Cannula
Standard in stable hypoxemic patient Low flow of pure oxygen Each litre per minute adds 3-4% to FIO2:
1 L/min increase FIO2 to 24% 2 L/min increase FIO2 to 28% 3 L/min increase FIO2 to 32%
Face Masks
Smith RA. Oxygen Therapy. Critical Care 3rd ed 1997
1. Oxygen Concentrators
Air 21% oxygen, 78% nitrogen, 0,9% argon, 0,1% other
Adsorbent material remove nitrogen from air
Deliver 95,5% oxygen into tank
Oxygen delivery systems:
Picture: Afrox
Afrox
Oxygen Concentrator
National Guideline on LTOT: Dept Health
Oxygen Concentrators
AADVANTAGES
Safe, no fire hazard
Easy to operate
No inconvenience to replenish
as with cylinders
Easy to move around in home
with extended supply line
Easy to transport
Cost effective
Not unsightly
DISADVANTAGES
Dangerous with power failure
When travelling a small cylinder
or other equipment needed
Electricity needs to be paid
Electricity is essential
Medical Oxygen Cylinders
Afrox
Oxygen Cylinders
Advantages
Needs no electricity
Small cylinder is
easy to handle when
travelling
Disadvantages
• Costly
• Dangerous fire hazard
• Not easy to open flow meter
• Can be damaged while transporting
• Older and sick patients cannot handle
the cylinders
• Large cylinders are heavy and can
cause damage or injury
• Unsightly, many cylinders have to be
accommodated
• Patients try to save on oxygen and
benefit is lost if used incorrectly
Medical Oxygen Cylinders
VitalAir
National Guideline on LTOT: Dept Health
Cylinders: Advantage of Oxymatic Device
Oxygen without device
2 litres /min = 29 hours3 litres/min = 19 hours4 litres/min = 14 hours
With oxygen device
201,3 hours134,2 hours100,6 hours