Transcript Cor Pulmonale and Resp Failure Voordrag en Handout

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 organ
COPD
Interstitial lung diseases
Thrombo-embolic diseases
Pump
Kyphoscoliosis
Guillian-Barre syndrome
Myasthenia gravis
Controller
Sleep apnea syndrome
Primary alveolar hypoventilation
Post encephalitis
Sequence of events Acidemia
Hypoxia
Pulmonary
Vasoconstriction
Vessels
Obliteration
Viscous
Blood
Pulmonary Hypertension
RV Hypertrophy / Dilatation
Rt. Heart Failure
Idiopathic
PAH
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 -
CO2 elimination from -
mixed
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 Normal
Ventilation perfusion mismatch / shunts
Type II
= Hypercapnic respiratory failure
* PO2 < 60 mmHg
* PCO2 > 45 mmHg
Hypoventilation
Clinical features
Hypoxia :
Hypercapnia :
Dyspnoea
Headache
Central cyanosis
Agitation
Restlessness
Confusion
Peripheral Vasodilatation
Tremor / flap
Bounding pulse
Drowsiness
Coma
Classification Respiratory Failure
Acute
Type I
Po2 Pco2 pH HCO3 -
Type II
Chronic
Type I
Type II
Acute Respiratory Failure Type I
Type II
Causes
Pneumonia
Pulmonary embolus
Pulmonary edema
Pneumothorax
ARDS
Acute asthma
Acute foreign body
Narcotic drugs
Muscle paralysis
Brain stem lesion
Therapy
Maintain Airway
Treat the disease
High-concentration O2
Mechanical ventilation
Maintain airway
Treat the cause
Mechanical ventilation
or tracheostomy
Chronic Respiratory Failure Type I
Type II
Causes
Emphysema
Lung fibrosis
Right –to-Left shunt
Anemia
COPD
Primary alveolar hypovent.
Kyphoscoliosis
Ankylosing spondylitis
Therapy
-Treat the disease
- Controlled long-term
oxygen
- Treat the disease
- Controlled long-term
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
Pulmonary embolus
Retention of secretions
Sedative drugs
Cardiac failure
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
Po2
Hco3
O2Sats
52 mmHg ( )
54 mmHg ( )
32 mmol / l ( )
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
Conclusion
Development 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 Therapy
Dr M Prins
Div Pulmonology
Dept of Internal Medicine
Clinical Significance of PaO2 and SaO2 values
PaO2
mmHg
SaO2 (%) Clinical significance
150
99
Inspired at sea level
97
97
Normal young man
80
95
70
93
Normal young man
asleep, old man awake,
Inspired at 5700 m
Lower limit of normal
60
90
Respiratory failure, mild
Shoulder of dissociation
curve
TE Oh. Intensive Care Manual
PaO2
mmHg
SaO2 (%) Clinical significance
50
85
Resp failure: admit to
hosp
40
75
30
60
26
20
50
36
Venous blood, normal
Arterial, severe resp
failure
Acclimatized at rest at
2700 m
Unconscious if not
acclimatized
P50 or 50% saturation
TE Oh. Intensive Care Manual
Acclimatized at 5700 m
Hypoxic death
Oxygen Cascade
Inspired air
150 mmHg
Alveolar
103
Arterial
100
Capillary
51
Tissue
20
Mitochondrial
1-20
Ganong WF. Review of Medical Physiology
MRC 1981
87 patients
3 years
No oxygen
2 L/min: 15 hours/day
45 patients
42 patients
19 died
30 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
Oxygen delivery systems:
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
Picture: Afrox
Oxygen Concentrator
Afrox
Oxygen Concentrators
A
ADVANTAGES
DISADVANTAGES
Safe, no fire hazard
Dangerous with power failure
Easy to operate
When travelling a small cylinder
No inconvenience to replenish
or other equipment needed
as with cylinders
Electricity needs to be paid
Easy to move around in home
Electricity is essential
with extended supply line
Easy to transport
Cost effective
National Guideline on LTOT: Dept Health
Not unsightly
Medical Oxygen
Cylinders
Afrox
Oxygen Cylinders
Advantages
Disadvantages
Needs no electricity
•Costly
Small cylinder is easy
•Dangerous fire hazard
to handle when
•Not easy to open flow meter
travelling
•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
Cylinders: Advantage of Oxymatic Device
Oxygen without device
With oxygen device
2 litres /min = 29 hours
3 litres/min = 19 hours
4 litres/min = 14 hours
201,3 hours
134,2 hours
100,6 hours
National Guideline on LTOT: Dept Health