Breathlessness Flashcards
Hypoxaemia (hypoxic hypoxia):
- Abnormally low arterial partial pressure of oxygen (PaO2)
- Associated with clinical signs of central cyanosis
Hypoxia:
- Low tissue partial pressure of oxygen. Either due to a reduced O2 supply or inability to utilise it
- Hypoxaemia is one, but not the only, cause of hypoxia
Alveolar-arterial (Aa) difference:
Aa difference = PAO2 - PaO2
- PA02: calculated using the alveolar gas equation
- PaO2 is measured via blood gas analysis
How to find PAO2 and PaO2:
- PA02: calculated using the alveolar gas equation
- PaO2 is measured via blood gas analysis
Aa difference: healthy ranges
- Healthy subjects
- Elderly
- 2 KPa
- 5 KPa
Causes of tissue hypoxia: Hypoxaemia
- Hypoxaemia leads to a decrease in total oxygen content by lowering oxygen saturation (SaO2) and partial pressure of arterial oxygen (PaO2)
- Total content (C) = (O2 binding capacity X SaO2) + (PaO2X solubility)
- Rate of O2 delivery = Cardiac output (Q) X O2 content (C)
Causes of tissue hypoxia: stagnant hypoxia
- Cardiac output is insufficient due to cardiac failure at normal filling pressures
Causes of tissue hypoxia: Anaemic hypoxia (2)
- Rate of O2 delivery is reduced by a decrease in O2 content, this is due to a reduction in oxygen binding capacity
- This reduced O2 binding capacity is caused by a reduction in viable RBCs
Causes of tissue hypoxia: histotoxic hypoxia
- Explanation (2)
- Cause
- Rate of O2 delivery is normal but the tissues are unable to utilise the O2
- Causes elevated CvO2 and a low arteriovenous difference in blood O2 content
- Classic cause is cyanide poisoning (also smoke inhalation)
Alveolar ventilation equation:
- PACO2 = PaCO2 § Rate of CO2 production by metabolism / Rate of CO2 removal by AV
- PACO2 is directly proportionate to CO2 production rate and inversely proportionate to Rate of CO2 removal by AV
Type 2 respiratory failure:
- “Pump failure”: CO2 production rate remains constant, hypoventilation causes hypercapnia (+PaCO2)
Clinical features of type 2 respiratory failure: (4)
- vary according to underlying cause
- Headache (cerebral vasodilation)
- Flapping tremor of wrist
- Bounding pulse
Type 1 respiratory failure:
- When the respiratory system is unable to supply the body with an adequate amount of oxygen
(lower PaO2)
Heart failure definition: (2)
- An inability of the heart to maintain an adequate perfusion of the tissues (cardiac output) at a normal filling pressure
- It is not a diagnosis but a syndrome of signs and symptoms caused by a variety of pathological conditions
Pathophysiology of Chronic Left-sided Heart Failure:
- Systolic dysfunction (emptying): (2)
- Impaired emptying due to reduced contractility and/or increased afterload
- End-systolic volume is increased due to the reduction in stroke volume and ejection fraction
Impaired contractility causes: (3)
- MI or ischaemia
- Dilated cardiomyopathy
- Chronic “volume overload” e.g. mitral or aortic regurgitation
Excessive afterload cause: (3)
- Aortic stenosis: narrowing of the aortic valve outlet
- May result in a slow rising pulse and an ejection systolic murmur in aortic area
- Systemic hypertension (+TPR)
Physiology of chronic left-sided heart failure:
- Diastolic dysfunction:
- Increased stiffness of the ventricle impairs filling during diastole
- Fibrosis and hypertrophy of ventricular wall or pericardium constriction
Right-sided heart failure:
- Definition
- Causes
- Right ventricle fails if the afterload is too high
- Secondary to LVF (commonest), Cor pulmonale, Acute PE, pulmonary stenosis
Cor pulmonale:
- Definition
- Symptoms (6)
- RHF due to hypoxic lung disease (COPD)
- Central cyanosis, raised JVP, pitting oedema, hepatomegaly, Parasternal heave (RVH), tricuspid regurgitation
Compensatory mechanisms for CHF:
- Increased renal salt …..
- Increased renal salt and water retention leading to
increased filling pressures (↑JVP) and (hopefully!)
stroke volume by Frank-Starling mechanism
Compensatory mechanisms for CHF:
- Baroreceptor …..
- Baroreceptor reflex increases sympathetic tone
increasing heart rate and contractility and producing
increased peripheral vasoconstriction with a relative
diversion to the coronary and cerebral circulations
Compensatory mechanisms in CHF:
- Heart
- Ventricular hypertrophy (LVH) and remodelling
What causes the increase in filling pressure?: (3)
- Renin-angiotensin-aldosterone system
The release of renin is stimulated by
(1) Reduced renal artery pressure secondary to the fall in cardiac
output
(2) Increased renal sympathetic tone (due to baroreceptor reflex)