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)
Detrimental effects of increased filling pressures (4)
- A dilated heart is less efficient at contracting (Law of Laplace)
- Widening of the atrioventricular valve orifices leads
to regurgitation of blood through the valves - Increased filling pressure of the left ventricle leads
to pulmonary oedema and breathlessness - Increased filling pressure of right ventricle leads to
peripheral pitting oedema
Increased sympathetic tone: friend or foe?
- Probably beneficial in mild failure but in more severe cases the effects can be detrimental
Increased sympathetic tone: detrimental effects (3)
- Venoconstriction raises the filling pressure
- Vasoconstriction leads to increase in afterload and
hence myocardial oxygen consumption - Uncoupling and down regulation of beta 1
receptors reduces the positive inotropic effects of
sympathetic stimulation
Signalling molecules increased in plasma in HF: (3)
- ADH: Promotes water retention by kidney.
- Endothelin: Potent vasoconstrictor (future therapeutic target?)
- BNP: B-type natriuretic peptide
produced by failing myocardium
Plasma levels correlate with degree
of severity, used as a biomarker
Ventricular hypertrophy and remodelling: (2)
- Chronic elevations in wall stress and neuro-humoral factors lead to remodelling
- The associated decrease in compliance leads to increased diastolic filling pressures
How does cardiac failure produce oedema?: (3)
- Increased venous filling pressure increases capillary pressure
- Salt & water retention reduces conc. of proteins in plasma and decreases colloid osmotic pressure in plasma
- This increases production of tissue fluid by capillaries by ultrafiltration