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