Cardio-Respiratory Failure

1. Cardio-Respiratory Failure Introduction Cardiovascular disease account for 40% of all death <75 years in Europe Cardiorespiratory failure may occur because of airway, breathing or cardiovascular problem Cardiovascular & respiratory systems often interact Ex. Hypoxaemia impair myocardial function Severe illness ↑ O2 consumption & ↑ respiration work Cardiac failure secondary to respiratory failure Respiratory failure follow from cardiac failure

2. Respiratory Failure 3 Reasons why one’s respiratory apparatus would fail: • Failure to protect one’s airway (i.e. airway obstruction), • Failure to ventilate, characterized by a high arterial CO2 level, • Failure to oxygenate, characterized by a low arterial PO2 level.

3. Failure to Protect the Airway • Foreign body, blood, vomitus • Trauma • CNS depression • Pharyngeal swelling (infection, oedema) • Laryngospasm • Bronchospasm • Bronchial secretions

4. Failure to Ventilate • Patients fail to ventilate due to loss of sensitivity of the brain to the main stimulus to ventilation, Co2. • It may also occur due to neurological, neuromuscular junction or muscular problems. • In addition, injuries to the chest wall, diaphragm or pleura will prevent chest expansion and ventilation.

5. Failure to Oxygenate • Failure to oxygenate occurs when there is an obstruction of gas exchange between the alveoli and capillaries • This may be due to an interstitial process (pulmonary oedema) – a diffusion defect • Or due a mismatch of ventilation and perfusion. • In many lung injuries, there are a mixture of problems, alveolar dead space, shunt and diffusion defects.

6. Acute Lung Injury[ALI] • ALI is a term used to describe a pulmonary syndrome, characterized by non cardiogenic pulmonary oedema, caused by a number of insults. • Most common cause of acute lung injury is systemic inflammation, • The injury to the alveolar-capillary interface is similar to that in sepsis: • There is a widespread  increase in capillary permeability, with resultant exudation of protein rich fluid into the interstitium and alveoli. • In addition, there is a deficiency of surfactant, and the wet soggy lungs become less compliant and have a tendency to collapse

7. Target: return the PaO2 to what is normal for this patient? • Be it 90mmHg in most of us, or 50mmHg in a patient with severe COPD). • The treatment for all lung injuries is, initially, oxygen therapy. • If the patient is requiring more than 60% oxygen, they usually have a significant diffusion defect or ventilation perfusion mismatch. • The treatment is to apply a positive pressure to the airway, increasing the pressure gradient to the alveoli, increasing mean interthoracic pressure, and reducing the work of breathing. • We call this CPAP (continuous positive airway pressure). • Due to the fact that the greatest effect of CPAP is to prevent airway collapse at the end of expiration, this is often called PEEP (positive end expiratory pressure), but actually exists during both phases of ventilation • Consider use of non-invasive ventilation

8. REVIEW Clinical Scenario 1An 18 year old male is brought to the recovery room following an appendectomy. He has just been extubated. He is awake and breathing normally, but his SpO2 is 88%. You administer 60% oxygen, and after a few moments his SpO2 increases to 99%. • What has just happened?

9. Cardiac Failure Definition • ‘Failure of the heart to maintain a cardiac output sufficient to meet the metabolic demands of the body’ • If cardiac failure is not detected earlier and managed properly it can lead to • CARDIAC ARREST [basic and advanced life support will be discussed during clinical skill session

10. CAUSES OF CARDIAC FAILURE Primary cause • Ischaemia • Myocardial infarction • Cardiac tamponade • Hypertensive heart disease • Valve disease • Drugs (antiarrhythmic, tricyclic antidepressant, digoxin) • Acidosis • Abnormal electrolytes (K+; Mg2+; Ca2+) • Hypothermia • Electrocution

11. Secondary cause Heart affected by pathology occurring elsewhere • Asphyxia • Airway obstruction • Apnoea • Tension pneumothorax • Severe blood loss • Hypoxaemia • Septic shock

12. Identifying patient at risk 80% cases  deterioration in clinical signs few hours beforearrest • Breathing problems & ↑ respiration rate • ↑ heart rate • Hypotension • Confusion • Restlessness • Lethargy or ↓ level of consciousness • Metabolic abnormalities [acidosis] Hence identify patients at risk by: • History taking • Continuous monitoring of haemodynamic status • Investigations

13. P A T H O P H Y S I O L O G Y

15. New York Heart Association classification of heart failure symptoms • Class I No limitations. Ordinary physical activity does not cause undue fatigue, dyspnoea or palpitation (asymptomatic left ventricular dysfunction). • Class II Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea or angina pectoris (symptomatically mild heart failure). • Class III Marked limitation of physical activity. Although patients are comfortable at rest, less than ordinary physical activity will lead to symptoms (symptomatically moderate heart failure). • Class IV Inability to carry on any physical activity without discomfort. Symptoms of congestive cardiac failure are present even at rest. With any physical activity increased discomfort is experienced (symptomatically severe heart failure).

16. Pharmacological interventions • Diuretics –frusemide, spirinolactone • ACE Inhibitors- enalapril, captopril • Beta blockers  Carvedilol, Bisoprolol • Digoxin • Inotropes [beware no I.V drug administration by students] • Warfarin/Aspirin  • Nitrates  Remember: Pharmacology exam