Cardio (NEW) Flashcards
1
Q
Overview aortic stenosis
A
Epidemiology
- increases in prevalence with age
- > approx 10% over 80yr olds
Aetiology
- Calcific disease of trileaflet
- > most common in developed world
- Rheumatic valve disease
- > most common in developing world
- Congenital bicuspid valve
- > most common in children
Pathophys
- complications
- > HFrEF
- > pulmonary HTH
- > IE
- > acquired vWD (turbulent flow disrupts multimers)
- > AF
Hx
- > dyspnoea on exertion (HFrEF)
- > syncope/presyncope
- > stable angina (hypertrophy/high end diastolic pressure)
2
Q
Overview pulmonary stenosis
A
Epidemiology
-more common in children
Aetiology
- congenital (most common)
- > TOF
- > congenital rubella syndrome
- > Noonans
- acquired (rare)
- > carcinoid heart disease
Pathophys
- complications
- > IE
- > arrhythmia
Hx
- > exertional dyspnoea (right sided HF)
- > exertional fatigue/syncope/presyncope
- > exertional chest pain
- > cyanosis in severe cases
3
Q
Mitral regurgitation
A
Epidemiology
- myxomatous degeneration most common
- common post MI
Aetiology
- myxomatous degeneration
- > primary prolapse
- > secondary prolapse (marfans/ehlers danlos)
- secondary
- > IE
- > MI and papillary muscle rupture
- > trauma and rupture of chordae/papillary muscle
- > ARF
- > cardiomyopathy (dilated/hypertrophic)
- congenital
- > epsteins anomaly
Pathophys
- myxomatous degeneration
- > thickened and redundant leaflet tissue
- > fibroelastic deficiency
- > mucopolysaccharide and water accumulation
Hx
- fatigue/weakness/reduced exercise tolerance (HFpEF)
- tachypnea and dyspnoea (pulmonary HTN and oedema)
- palpitations (AF)
4
Q
tricuspid regurgitation overview
A
Epidemiology
- common
- usually found in association with pulmonary HTN
Aetiology
- 90% secondary (RV/LA dilatation)
- > pulmonary HTN/PE
- > post MI
- > cardiomyopathy
- > right HF/cor pulmonale
- > ASD/VSD/total anomalous venous return
- primary (rare)
Pathophys
- high RA pressures
- > symptoms of right HF
- volume/pressure overload
- > reduced systolic function
- > reduced CO
Hx
- pulmonary HTN and low CO
- > weakness
- > fatigue
- > SOB/reduced exercise tolerance
- high RA and venous pressures
- > pulsating sensation in neck
- > oedema
5
Q
Aortic regurgitation overview
A
Epidemiology
-increasing prevalence with age
Aetiology
- most commonly rheumatic heart disease
- aortic root dilatation
- > HTN
- calcific degenerative valve disease
- other
- > connective tissue disease
- > IE
- > dissection
- > rheumatological diseases
Pathophys
- regurgitation
- > increased end diastolic volume
- eccentric LV hypertrophy
- > chamber enlargement
- increased SV
- > distension of peripheral arteries and high SBP
- regurgitation
- > rapid collapse of arteries and low DBP
Hx
- signs of HFrEF
- > exertional dyspnoea
- > orthopnea
- > PND
- > stable angina
6
Q
mitral stenosis overview
A
Epidemiology
-appears approx 2 decades after ARF
Aetiology
- nearly all is rheumatic heart disease
- other
- > congenital
- > atrial myxoma
Pathophys
- follows ARF
- > repetitive scaring
- initially incompetent
- becomes thickened, calcified and fused
- > stenosis
Hx
- past ARF
- classic
- > exertional dyspnoea (pulmonary HTN)
- less common
- > fatigue (low CO)
- > haemoptysis (pulmonary HTN)
- > palpitations (AF)
- > thromboembolism and stroke (AF)
- > hoarseness (recurrent laryngeal nerve large LA)
- > right HF (cor pulmonate and tricuspid regurgitation)
7
Q
background left HF
A
Epidemiology
- incidence increases steeply with age
- HFpEF
- > accounts for approx. 30% of the incidence
- > mortality rate approx. 30% lower
Aetiology
- MI
- HTN
- Valvular disease
- Diabetes
- Obesity
- Smoking
Pathophys HFrEF (LVEF <40%)
- systolic dysfunction
- > down and right shift of frank starling curve
- > lower SV for a given preload
- neurohumoral response
- > increased sympathetic activity = inotropy + chronotropy
- > RAA = volume expansion/increased preload and SV
- eccentric remodelling
- > sarcomeres laid down in series
- > increased cavity volume
- > normal or reduced wall thickness
- adaptations eventually become pathological
- reduced systolic reserve/flattened frank starling curve
- > afterload dependence
- > small changes in BP = large changes in SV
- volume/pressure loops right shifted
- > dilation = higher LV volumes
- > decreased contractility = reduced SV
- > hypertrophy/decreased compliance = high end diastolic
- outcome
- > reduced CO sensitive to increased BP
- > high end diastolic pressures and volumes
Pathophys HFpEF (LVEF >50%)
- pressure overload
- > associated with inflammatory milieu
- > endothelial dysfunction drive hypertrophy
- concentric remodelling
- > sarcomeres laid in parallel
- > increased wall thickness = decreased afterload
- > decreased cavity volume
- diastolic dysfunction
- > slow, delayed, incomplete relaxation
- > smaller volumes
- > filling occurs later in diastole/dependent on atrial kick
- pressure/volume loops left shifted
- > lower end diastolic volumes
- > higher end diastolic pressures
- consequences
- > inability to augment CO with exercise
- > high LA pressures = pulmonary HTN
- > pulmonary HTN = RV dysfunction
- > susceptible to atrial arrhythmias
8
Q
Clinical manifestations heart failure
A
Hx
- assess
- > risk factors
- > current medications
- > lifestyle factors
- low CO
- > dyspnoea
- > fatigue
- > reduced exercise tolerance
- > functional impairment
- > exertional chest pain in right HF
- fluid retention
- > peripheral oedema
- > ascites
- > orthopnoea/PND
- > anorexia/unintentional weight loss
- right sided
- > RUQ pain
Exam
- appearance
- > cachexia
- hands
- > delayed cap refill
- > vasomotor = cool, pale/cyanotic
- > sympathetic = diaphoretic/clammy
- pulse
- > irregularly irregular (AF) or tachycardia (low CO)
- > pulsus alternans (high specificity)
- BP
- > narrow pulse pressure (<25mmHg)
- > pulsus alternans
- JVP
- > elevated
- > +ive hepatojugular reflex
- > +ive kussmauls signs in right sided
- praecordium
- > lateral and inferior displacement apex beat
- > forceful and sustained apex beat
- > parasternal heave
- auscultation
- > S3 gallop
- > tricuspid regurgitation in right sided
- additional
- > signs of pulmonary HTN
- > crackles (more so in acute)
- > ascites
- > peripheral oedema
- > hepato/splenomegaly
9
Q
Investigations chronic HF
A
ECG -strong negative predictive value -may indicate aetiology ->past MI -LV hypertrophy -arrhythmias Glucose -diabetes
FBC -anaemia Iron studies -iron deficiency common EUCs -hyponatraemia -high creatinine LFTS -raised GGT -transaminitis BNP or NT proBNP -low values have negative predictive value Albumin -hypoalbuminaemia common in advanced Lipids -cardiovascular risk TSH -hyper/hypo thyroidism as cause
CXR
- cardiomegaly
- cephalic vascular markings (stags signs)
- > pulmonary venous HTN
- kurley B lines
- > congested interlobular septa
- batwing opacifications
- > cardiogenic pulmonary oedema
- pleural effusions
Doppler echo
- ejection fraction
- > HFrEF <40%
- > HFpEF >50%
- E:A (normal 1-1.5)
- > abnormal in HFpEF
- size/pressure of ventricles and atria
- estimate pulmonary capillary wedge pressure
- aetiology and ddx
- > abnormal wall motion
- > valvular disease
- > pericardial disease
10
Q
right HF background
A
Epidemiology
- approximately half of HFrEF
- approximately half as common in HFpEF
Aetiology
- acute
- > PE
- > right sided MI
- > myocarditis
- > tamponade
- chronic
- > pulmonary HTN due to any cause
- > congenital heart disease
- > right sided valvular disease
- > cardiomyopathies
Acute pathophys
- pulmonary circulation is low pressure/high compliance
- > LV usually generates low pressures
- LV is afterload sensitive
Chronic pathophys
- remodelling in response to high afterload
- increase in RV volumes
- > dilated tricuspid apparatus = regurgitation
- > regurgitation = large LA and AF
- constrained by pericardium
- > bulging of inter ventricular septum
- > reduced LV filling
- reduced forward CO due to
- > TR
- > RV systolic dysfunction
- > reduced LV filling
- neurohumeral adaptation and volume expansion
- > pulmonary oedema
- > systemic venous hypertension
11
Q
Causes of HTN
A
Primary
- > age
- > family hx
- > african heritage
- > obesity
- > physical inactivity
- > excess salt
- > excess alcohol
Secondary (DR PEACOCK)
- drugs
- > OCP
- > steroids
- > anti depressants
- renal artery stenosis
- pheochromocytoma
- endocrine disorders (cushings/thyroid)
- aldosteronism (pituitary adenoma or idiopathic)
- cocaine
- obstructive sleep apnea
- coarctation of the aorta
- kidney disease
12
Q
complications HTN
A
- HF
- LV hypertrophy
- IHD
- CVD
- intracranial haemorrhage
- hypertensive retinopathy and blindness
- chronic kidney disease
13
Q
rheumatic heart disease and ARF natural history
A
Epidemiology
- RHD is most common cause of acquired heart disease for children in developing world
- almost 3/4 with ARF will develop RHD eventually
Presentation
- by age
- > most commonly present aged 20-50
- > MR most common in 20’s
- > MS most common in 30’s
- > multivalvular most common thereafter
- by valve
- > mitral involved in nearly all cases
- > aortic valve regurg in approx 20%
- > tricuspid valve may be involved
Disease course
- MR
- > HF/LV dilatation
- MS
- > RHD is chief cause
- > associated with high mortality
- > pulmonary HTN
- > AF and systemic embolism
- AR
- > often compensated for many years
- mixed MR/MS
- > grossly deformed valve
- > late development
