Cardiovascular and respiratory diseases Flashcards
main causes of death in England
dementia and Alzheimer diseases 12.8%
Leading cause of death by gender:
male: ischaemic heart disease 13.2%
Female: dementia and Alzheimer disease 16.7%
Main cardiovascular diseases
- coronary heart disease and failure
- hypertension, vascular disease and atherosclerosis
- thrombosis
main causes of CVD
genetics age lifestyle diet obesity smoking inactivity air pollution
main respiratory diseases
- lung cancer
- astham
- chronic obstructive pulmonary disease (COPD)
- infections
main causes of respiratory disease
genetics age allergy infectin smoking air pollutionn
no.1 world wide disease
cardiovascular disease
socioeconomic impacts of CVD and CR disease
- cardiovascular disease costs the UK £19 billion p.a
- Respiratory disease costs the UK £11 billion p.a
- NHS costs, days off work, premature death, disability and informal care costs etc
dyspnoea
breathlessness
causes of dyspnoea
multiple causes that are cardiac : - heart failure - angina with atypical features or respiratory causes: - COPD -asthma - pneumnia -plenary embolism - lung malignancy
other systems that effect oxygen delivery will also cause dyspnoea such as anaemia
Heart failure
when the heart is not pumping blood around the body as well as it should, most commonly when the heart muscle has been damaged e.g post heart attack
typical symptoms of heat attack
breathlessness
ankle swelling
fatigue
possible accompanying signs of heart failure
- elevated jugular venous pressure
- pulmoary crackles
- peripheral oedema
Physiological definition of heat failure
inability to provide adequate cardiac output to support the needs of the tissues; or can do so but only at the expense of a raised filling pressure
survival of heart failure
It is progressive syndrome with a less than 5 year survival
what determines Cardiac output
- heart rate and stroke volue
- preload, contractility and after load
enhanced heart function
increase contractility
increase HR
decreased after load
depressed heat function
decreased contractility
decreased HR
increased after load
systolic heart failure
impaired contractility
heart can’t pump or squeeze enough blood out to rest of body
- then weak heart muscle
diastolic heart failure
impaired filling/relaxation so heart can’t fill without enough blood
- stiff thick heart muscle
stiff thick heat muscle is associated with
diastolic heart failure
impaired filling/relaxation so heart can’t fill without enough blood
thin weak heart muscle is associated with
systolic heart failure
impaired contractility
heart can’t pump or squeeze enough blood out to rest of body
left heart failure
not pumping enough blood out of left ventricle
- commonly caused by coronary artery disease
- also caused by mitral/aortic valve disease or viral cardiomyopathies
right heart failure
not pumping enough blood out of right ventricle caused by: -COPD pulmonary hypotension -pulmonary embolism - valve disease
congestive heart failure
when left heart failure leads to right heart failure
most common cause of heart attack is
coronary artery thromboembolism
myocardial infarction
heart attack
coronary artery thromboembolism
blood clot
thrombosis
inappropriate formation fo blood clots, thrombi
types of thrombosis
coronary deep vein (DVT)
what does thrombosis cause
danger of embolisms
- venous, DVT or right atrial thrombosis leads to pulmonary emboli
- left arial thrombosis leads to cerebrovascular ischaemic stroke
primary cause of DVT
immobility
DVT
deep vein thrombosis
primary cause of atrial thrombosis
status and turbulence due to atrial fibrillation
treatment of thrombis
prophylaxis
arterial: anti-platelet e.g aspirin, clopidogrel
venous: anticoagulant e.g heparin, warfarin, DOAC
examples of anticoagulants
heparin, warfarin, DOAC
used to prevent venous thrombisis
examples of anti platelet drugs
aspirin, clopidogrel
used to prevent arterial thrombosis
Pathophysiology of heat failure
fall in BP is detected but normal mechanisms don’t work
- increased HR results in more work and more heart damage
- vasoconstriction doesn’t work before of muscle damage
- reabsorption of salt and water by kidneys to increase blood volume causes increased pressure and work causing more heat damage
eabsorption of salt and water by kidneys to increase blood volume causes breathlessness and oedema
fluid accumulation in tissue
peripheral oedema = right hart failure
fluid accumulation in lungs
breathlessness = left heart failure
why is heart failure progressive
largely caused by compensation mechanisms of the body adapting to:
exercise intolerance, weakness, breathlessness, pleural congestion, pulmonary oedema, dilated heart, peripheral oedema, pitting oedema & hepatomegaly
but, attempts at controlling cardiac output slowly cause weakness, oedema and increased work
how to treat heat failure
reduce symptoms to improve QoL and prolong survival but doesn’t cure
- beta blockers
- diuretics
- ACE inhibitor
COPD
Chronic obstructive pulmonary disease
what is COPD
Chronic obstructive pulmonary disease
a common preventable and treatable disease
characterised by:
– persistant respiratory symptoms and air flow limitation
due to:
- airway or alveolar abnormalities
common cause of COPD
significant exposure to noxious particles or gases:
- tobacco smoking, active and passive
- biomass fuel exposure from poorly ventilated dwellings
- occupational exposure e.g dust, chemical agents, fumes
- rare inherited alpha anti-trypsin deficiency
common symptoms of COPD
Dyspnea
coughing
sputum production
clinical feats of COPD
- Barrel chested
- difficult to locate cardiac apex beat
- reduced chest wall expansion on inspiration
pathophysiology of airways in COPD
- hypertrophy and hyperplasia of bronchial submucuocal glands
- increased no. goblet cells = hyper secretion of mucus
- destruction of cillia
- narrowing of airways from remodelling
- increased airway resistance
pathophysiology of parenchyma in COPD
- proteolytic enzymes destroy alveolar tissue
- elastin an collage are destroyed =reduced elasticity and structural integrity of lungs
- reduced surface area for gas exchange
COPD pathophysiology
- impaired gas exchange causes hyperaemia
- airways poorly supported & collapsible
- reduced driving pressure for expiratory flow
what drives movement of air through airways
pressure gradient between mouth and alveoli
what is turbulence
when laminar flow is disrupted. causes by high velocity, sharp edges and branching points in airways
what is the effect of turbulence
significant increase in resistance and causes vibrations = wheezing noice as air tries to move through narrowed airways at high velocity
why is a silent chest ominous for an asthmatic
wheezing only occurs if air flow is present, If obstruction worsens such that there is no airflow then there will be no wheezing
resistance is inversely proportionate to
r^4
R = 1/r^4
if radius is hated, resistance increases 16 fold with same pressure gradient so flow is reduced to 1/16th
two main factors causing variations in airway resistance
factors within the airways
pressure across airway wall
RAW
airway resistance
factors within the airways
- bronchial smooth muscle tone
- inflammation of epithelium
- hypertrophy of glands and secretion like mucus
what affects airway smooth muscle tone
- prostaglandins
- arenaline
- co2
- sympathetic stimulation
- parasympathetic stimulation
negative intrapleural pressure in normal breathing =
airways held open
positive intrapleural pressure in normal breathing =
collapsing force on airways
which airways are most likely to collapse
- bronchi around generation 3 or 4 which is site of maximum resistance
this is because here the pressure within the airways falls below Ppl during forced expression
why is expiratory airflow limited for everyone
because of dynamic compression of airways.
At low lung volume, expiratory airflow will not increase no matter how hard you try
It is effort independent
difference in airflow in normal and COPD
high airway resistant increases the limitation of airflow. Slow expiration = - slow expiratory flow rate - air trapping - expiratory wheezes
summary of COPD
- Air flow obstruction
- loss of lung elasticity
- loss of alveoli
- # airway inflammation
- expiratory flow limitation
- reduced elastic recoil of lungs
- reduced gas exchange
- hyperinflation
- sputum production
- chest infections
Diagnosing COPD
use of to measure how fast and how much air you breath out.
use FEV1 and FVC to distinguish between Obstructive disease and Restrictive lung disease
FEV1
forced expiratory volume in 1 second
FVC
forced vital capacity
normally FEV1/FVC >
75%
COPD
significantly reduced FEV1
reduced or normal FVC
Reduced FEV1/FVC
Restrictive disease
- reduced FEV1
- reduced FVC
- normal FEV1/Fvc
spiral of disability of cardiorespiratory disease
reduced breathlessness leads to inactivity leads to muscle deconditioning which leads to excess lactate and co2 production which leads to breathless ness :(
muscle deconditioning also adds to leg fatigue and weakness which increases inactivity
importance of exercise training pulmonary rehab
