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
Heart failure signs: dysponea and orthopnoea
- Dysponea: Abnormal feeling of need to breath due to pulmonary venous congestion
- Othopnoea: Breathlessness upon laying flat due to redistribution of blood from lower limbs
Heart failure signs: PND and fatigue
- PND: Paroxysmal nocturnal dysponea, wakes patient from sleep. Gradual reabsorption of peripheral oedema fluid when laying flat
- Fatigue: reduced perfusion of skeletal muscle
Signs of acute LVF: (4)
- Tachypnoea: Due to stimulation of J receptors
- Cold hands: Due to increased sympathetic tone
- Tachycardia: Due to increased sympathetic tone
- Crackles or wheeze: Due to pulmonary oedema
Breathlessness investigations: Lungs
- Full Blood Count
Result
Possible diagnosis
- Raised WCC
- Possible infection
Breathlessness investigations: Lungs
- BNP
Result
Possible diagnosis
- > 400pg/mL
- Heart failure if over, if under then rule out
Breathlessness investigations: Lungs
- U & E
Result
Possible diagnosis
- Increased urea and creatinine
- Acute kidney injury which can cause breathlessness via several mechanisms
Breathlessness investigations: Lungs
- D-dimer
Result
Possible diagnosis
- Positive
- DVT/PE, if negative then rule out
Breathlessness investigations: Lungs
- ABG
Result
Possible diagnosis
- Respiratory acidosis/alkalosis
- Many, including COPD, severe asthma, panic attack
Breathlessness investigations: Lungs
- CRP
Result
Possible diagnosis
- Raised
- inflammation, non-specific infection, blood cultures needed
Breathlessness investigations: circulation
- FBC
Result
Possible diagnosis
- Decrease in Hb
- Anaemia, further tests needed to distinguish the type
Breathlessness investigations: circulation
- Troponin
Result
Possible diagnosis
- Positive
- Myocardial damage
Breathlessness investigations: circulation
- Carboxyhaemoglobin
Result
Possible diagnosis
- Raised
- CO poisoning
Breathlessness investigations: circulation
- Methaemoglobin
Result
Possible diagnosis
- Raised
- Congenital, drugs
Breathlessness investigations: circulation
- LFTs
Result
Possible diagnosis
- Deranged
- Several
Lung cancer causes: (3)
- Smoking 72%
- Workplace exposure 13%
- Air pollution 8%
Lung cancer subtypes:
1.
2. (3)
- Small cell (15-20%)
- Non-small cell (80-85%)
- Adenocarcinoma
- Squamous cell
- Large cell
Lung cancer: symptoms
- Usual
- Red flags (3)
- Usually no signs or symptoms in early stages
- Persistent cough/chest infection/breathlessness/tiredness
- Coughing up blood
- Loss of appetite/unexplained weight loss
Lung cancer: metastatic tumour effects (4)
- Cervical or supraclavicular lymphadenopathy
- Palpable liver edge
- Bone pain or pathological fracture
- Persistent vomiting, seizures, focal neurology, headaches, confusion
lung cancer screening: low dose CT scan
- Detection
- Shift?
- Mortality
- Increases lung cancer detection
- With stage shift towards treatable disease
- Reduction in lung cancer mortality
Upper respiratory tract infections:
- Symptoms (4)
- Complications
- Signs (3)
- Pain, fever, headache, stridor
- Quinsy (peri-tonsillar abscess)
- Raised temperature, erythema, exudate
Lower respiratory tract:
- Symptoms (5)
- Complications (2)
- Signs (5)
- Cough, wheeze, sputum, production, pleuritic chest pain
- Empyema, pulmonary cavity
- Raised RR and intercostal , muscle movement, wheeze, dull percussion, bronchial breathing
Pneumonia and LRTI:
- Detection
- Difference
- Pneumonia = consolidative change on radiology
- LRTI = no consolidative change on CXR
- Any pathogen can cause either, all about radiological change
- LRTI and pneumonia are a spectrum of disease
Streptococcus pneumoniae (pneumococcus):
- Prevalence
- Structure/variation
- 50-60% community-acquired pneumonia
- Gram positive coccus, surrounded by polysaccharide capsule, over 90 serotypes
Streptococcus pneumoniae (pneumococcus)
- Variation
- Infections (7)
- Over 90 serotypes,
- Can cause multitude of infections (LRTI/pneumonia, empyema, meningitis, infective endocarditis, abscesses, otis media and externa)
Legionella pneumophila:
- Description
- Incubation
- Transmission (4)
- Atypical pneumonia
- 2-10 days
- Spread by breathing contaminated aerosolised water or soil: AC units, hotels/conferences, care homes, water sprinklers
Legionella pneumophila:
- Outbreak definition
- Symptoms
- 2+ cases where onset is closely linked in time and in space
- Hyponatraemia and liver dysfunction
Pneymocytsis pneumonia (PCP):
- Cause
- Effects
- Diagnosis
- Caused by fungus
- Associated with immunosuppression, high risk of pneumothorax
- Diagnosis by PCR on sputum (beta glucan usually posistive)
Tuberculosis (TB):
- Transmission
- Culture
- Relevance
- Transmission by droplets
- Very difficult to culture in the lab
- Notifiable disease of public health importance
TB: active infection risk factors (5)
- Young children
- Immunocompromised hosts
- Prison contact
- Recent contact with TB
- Country of high incidence
TB: latent infection risk factors (4)
- Exposure at some time
- Evidence of scars on CXR
- Immune response to TB (memory T-cell recognition of TB)
- Risk of reactivation in later life
TB signs and symptoms:
P
C
L
Chest
H
Pale
Cachexic
Lymphadenopathy
Chest: dullness to percussion, bronchial breathing, clear
- High temperature
Is TB vaccine-preventable:
- BCG recommended at birth in areas with high incidence
- Protects children from severe forms of TB (TB meningitis)
stenotic valve:
- Blood flows backwards through the valve (turbulent flow)
Bacteraemia: (3)
- Presence of bacteria in the blood
- Detected by blood cultures
- Assessment of significance
Infective Endocarditis (IE): definition
- definition
- Clinical presentation
- Diagnosis requirements
- Bacterial (or fungal) infection of a heart valve or area of endocardium
- Either acute or sub-acute
- Constellations of clinical signs and investigations required to make diagnosis
IE: Epidemiology
- Prevalence
- Mortality
- Infecting organisms / pre-disposing factors
- <10 per 100,000 population per year
- 20%
- Have changed over time, rheumatic fever was a risk factor pre-antibiotic era (75%)
IE: Rheumatic fever
- Group A Streptococcus
- Post-infectious, autoimmune, multi-system disease
IE: Epidemiology
Risk factors (4)
NVIE
PVIE
P-AE
NIE
A. Native valve infective endocarditis
B. Prosthetic valve infective endocarditis
C. PWID-associated endocarditis
D. Nosocomial infective endocarditis
A. Native Valve Endocarditis
- C
- PDH
- U
- BC
- Cardiac abnormalities
- Poor dental hygienes: viridans streptococci
- Urinary tract infection: Enterococcus
- Bowel cancer: S. gallolyticus
B. Prosthetic valve endocarditis:
- Cause
- Prevalence
- Pathogen
- Presentation
- Prosthetic valve or cardiac device related
- 1-5% of cases, within first 2 months of surgery
- Coagulase negative staphylococci
- Low virulence pathogens so often sub-acute
C. IVDU-associated endocarditis
- Age
- Features
- Pathogen
- Median age 30 (M>F)
- Right sided infection more common
tricuspid 50%; Aortic 25%; Mitral 20% - Staphylococcus aureus (including MRSA) predominates, can be other organisms
D. nosocomial infective endocarditis
- Incidence
- Age
- Causes
- Increasing (>10%)
- > 60 years
- Often underlying cardiac disease, IV lines, invasive procedures
IE pathogenesis:
- Immune system
- The immune system is unable to eradicate an organism once located on the endocardium
IE pathogenesis: transient bacterium
- Dental related
- Procedures in non-sterile sites e.g. urethral catheterisation
- Portals of entry for bacterium (wounds, lines)
- Source of bacterium often not found
IE clinical syndrome:
- Common (=/>70%)
M
P
Cm
H
- Malaise (95%)
- Pyrexia (90%)
- Cardiac murmurs (90%)
- Haematuria (70%)
IE clinical syndrome:
- Uncommon (<70%)
A
CF
ON
JL
SH
RS
S
CE
- Arthraglia (25%)
- Cardiac failures (5%)
- Oslers node’s (15%)
- janeway lesions (5%)
- Splinter haemorrhages (10%)
- Roth spots (5%)
- Splenomegaly (40%)
- cerebral emboli (20%)
