2.01 - Heart Flashcards
What is the difference between STEMI, NSTEMI, and UA
STEMI -
ST elevation
New onset LBBB
Raised troponin
NSTEMI -
No ST elevation or LBBB
Raised troponin
UA -
No ST elevation or LBBB, normal troponin
What is the most common cause of ACS
Artery narrowing or blockage secondary to IHD or atherosclerosis
What are the causes of coronary artery occlusion
Vasculits (Kawasaki disease)
Coronary vasospasm (cocaine)
Coronary dissection
What are some causes of changes of oxygen demand leading to ACS
Anaemia
Hyperthyroidism
Severe sepsis
What are the modifiable risk factors for ACS
High cholesterol
HTN
Smoking
Diabetes
Obesity
What are the non-modifiable risk factors for ACS
Agę
Family history
Male sex
Premature menopause
what is the frank starling law
the ability of the heart to respond to increased venous return by increasing stroke volume
how does the frank starling law work normally
increased venous pressure ->
raised EDV ->
increased preload (due to stretch) ->
more forceful contraction ->
increase in stroke volume
how does heart failure break down the frank starling law
over stretching of cardiomyocytes -> impaired contractlity -> stroke volume cannot increase to match EDV
-> oedema in lungs and ankles
what are the vascular causes of heart failure
ischaemic heart disease
hypertension
what are the muscular causes of heart failure (3)
dilated cardiomyopathy
hypertrophic cardiomyopathy
congenital heart disease
what are the valvular causes of heart failure (2)
stenosic valves
regurgitant valves
what is an electrical cause of heart failure
arrhythmia
what are the causes of high output heart failure (SALT)
Septicaemia
Anaemia
Liver failure
Thyrotoxicosis
what compensatory mechanisms are involved in the pathophysiology of heart failure (4)
increasing preload
increasing heart rate
RAAS activation
SNS activation
how does increasing preload contribute to heart failure
increase EDV to compensate for reduced ejection fraction -> maintain cardiac output
large increase in EDV can lead to pulmonary oedema, ascites, peripheral oedema
how does increasing heart rate contribute to pathogenesis of heart failure
cardiac output = stroke vol * heart rate
unable to increase stroke vol so increase heart rate instead
sustained tachycardia leads to cardiomyocyte death and remodelling -> cardiomegaly
how does RAAS activation contribute to pathogenesis of heart failure
renal hypoperfusion due to reduced CO -> RAAS
-> vasoconstriction and water retention
-> increased mean arterial pressure (BP)
-> oedema
How does SNS activation contribute to pathogenesis of heart failure
increases myocardial contractility and heart rate
can trigger cardiomyocyte death when chronicall activated
causes a positive feedback loop and increases RAAS activation
what are the clinical features of left sided heart failure (7)
paroxysmal nocturnal dyspnoea
orthopnoea
cyanosis
fatigue
SOB on exertion
tachycardia
Sx of pulmonary congestion
what are the clinical features of right sided heart failure (7)
raised JVP
fatigue
peripheral oedema
ascites
anorexia, nausea, vomiting
weight gain
Hx of chronic pulmonary problems
What are the diagnostic investigations for heart failure
B Natiuretic Peptide (BNP)
Transthoracic Echocardiography (TTE)
what (other than heart failure) can cause a raised BNP
sepsis
diabetes
old age
hypoxia
CKD
liver cirrhosis
what are the three positive (yes heart failure) results of a TTE
HFrEF - LVEF <40%
HFmrEF - LVEF 40-49%
HFpEF - LVEF >50%
what are the requirements for each class of heart failure (new york classification)
1) no limitation to activity, no symptoms
2) slight limitation, symptomatic on exertion
3) marked limitation, symptomatic on light activity
4) physical activity impossible without discomfort, symptomatic at rest
what further blood tests (other than BNP) are done when investigating heart failure
FBC - anaemia, infection
U&E - renal failure as cause of oedema
LFT - liver failure as cause of oedema
Cholesterol and HbA1c - risk stratification
TFT - exclude thyroid disease
what imaging (other than TTE) is done to investigate heart failure
chest x ray
cardiac mri
what can be seen on a chest x ray of a heart failure patient (5)
cardiomegaly
alveolar oedema
kerley B lines
pleural effusion
upper love diversion
what is cardiac mri used for when investigating heart failure
follow up if TTE was non diagnostic
determine aetiology of heart failure
what is the conservative management of heart failure
lifestyle modification
patient education
annual flu vax
smoking cessation
alcohol support
travel and driving advice
what is the medical management in HFrEF and HFmrEF
ACE inhibitors
Beta blockers
Mineralocorticoid Receptor Antagonists (MRAs)
Loop diuretic
What is the medical management in HFpEF
loop diuretic (furosemide) if symptomatic of fluid overload
specialist referral
comorbidity management
