Cardio Flashcards
Stroke volume eqn
EDV- ESV
CO eqn
HR xSV
BP eqn
CO x TPR
PP eqn
SP - DP
MAP eqn
DP + 1/3PP
Ejection fraction eqn
SV/EDV
Ohm’s Law
F = Pressure difference/R
Poiseuille law
Q = Pi(Pressure difference) r^4 /8nl
Preload
Volume of blood in ventricles before they contract
Afterload
Force against which the ventricles must contract to expel blood out of ventricles
Contractility
Inherent strength and vigor of the heart’s contraction during systole
Elasticity
Ability of heart to return to its normal shape after stretching by recoiling once the force is removed
Compliance
How easily the heart will stretch when filled with a volume of blood
Resistance
Force that must be overcome to push blood through the circulatory system
Atherosclerosis
Deposition of fatty deposits in the artery walls and hardening/stiffening of blood vessel walls
Where does atherosclerosis affect
Medium and large arteries
,mainly affecting Cx, LAD, RCA
Structure of atherosclerotic plaque
Lipid
Necrotic Core
Connective tissue
Fibrous Cap
Atherosclerosis formation
- Endothelial dysfunction
- High levels of LDL in blood
- Inflammation
- Macrophages take up oxidised LDLs, to form foam cells
- Foam cells promote migration of SMC from tunica media to intima. When they die, lipid content released causing plaque growth
- Formation of fatty streak in intimal layer
- Activated macrophages release cytokines and growth factors
- Smooth muscle proliferation around lipid core, leading to formation of fibrous cap
Three main things atherosclerosis causes
Stiffening -> HTN
Stenosis -> Ischaemia -> angina
Plaque rupture -> thrombus -> ischaemia -> ACS
Hypertrophic Cardiomyopathy?
Marked ventricular hypertrophy in the absence of abnormal loading conditions such as hypertension and valvular disease
Hypertrophic Cardiomyopathy
Second most common cardiomyopathy after dilated
Most common cause of sudden cardiac death in young
Inheritance pattern Hypertrophic Cardiomyopathy
Autosomal dominant
Pathophysiology hypertrophic cardiomyopathy
Caused by sarcomeric gene mutations
They hypertrophic, non compliant ventricles impair diastolic filling causing reduced SV and CO
Disarray of cardiomyocytes so conduction is affected
Hypertrophic Cardiomyopathy presentation
Asymptomatic
SOB, Angina, Syncope
Hypertrophic Cardiomyopathy investigation
ECG (LVH hypertrophy- Progressive T wave inversion and deep Q waves)
ECHO and MRI show ventricular hypertrophy, MRI shows fibrosis
Genetic Analysis
Hypertrophic Cardiomyopathy management
Amiodarone (risk of arrhythmia)
B blockers, verapamil (Chestpain dyspnoea)
Hypertrophic Cardiomyopathy complications
Sudden death, cardiac arrhythmias, thromboembolisms, infective endocarditis, heart failure
Dilated Cardiomyopathy
Dilated left ventricle that contracts poorly
Dilated Cardiomyopathy epidemiology
Most common cardiomyopathy
Inheritance pattern dilated cardiomyopathy
Autosomal dominant
Dilated Cardiomyopathy causes
Genetic
Alcohol
Ischaemia
Thyroid Disorder
Dilated Cardiomyopathy pathophysiology
Cytoskeleton gene mutations
Poorly generated contractile force leads to progressive dilation of heart with some diffuse interstitial fibrosis
Dilated Cardiomyopathy presentation
SOB
Fatigue
Heart Failure
Embolism from mural thrombus
Dilated Cardiomyopathy investigations
CXR - Cardiac enlargement
ECG - Arrhythmia, t wave flattening
Echo - Dilated ventricles
Dilated Cardiomyopathy management
HF and AF treated in conventional way
Restricted Cardiomyopathy
condition where the chambers of the heart become stiff over time.
Restricted Cardiomyopathy causes
Amyloidosis
Idiopathic
Sarcoidosis
End-myocardial fibrosis
Restricted Cardiomyopathy pathophysiology
Normal/decreased ventricular volume with bi-atrial enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filling
Restrictive physiology
Poor dilation of the heart restricts the ability of the heart to pump blood to the rest of the body
Restricted Cardiomyopathy presentation
SOB
Fatigue
Embolic symptoms
Restricted Cardiomyopathy investigations
CXR
Echo (abnormal but non-specific)
Cardiac Catheterisation
Restricted Cardiomyopathy management
None, poor prognosis
Arrhythmogenic right ventricular cardiomyopathy
progressive fatty and fibrous replacement of ventricular myocardium
Arrhythmogenic right ventricular cardiomyopathy inheritance pattern
Autosomal dominant with incomplete penetrance but can be recessive
Arrhythmogenic right ventricular cardiomyopathy presentations
Arrhythmia
Syncope
RHF
Arrhythmogenic right ventricular cardiomyopathy investigation
ECG (T wave inversion)
Echo (normal/right ventricular dilation)
Genetic testing
Arrhythmogenic right ventricular cardiomyopathy management
Beta blockers
Amiodarone
Cardiac transplant
Atherosclerosis Risk factors
Older age
FHx
Male
Smoking Alcohol poor diet (reduced veg, omega 3, high salt) Low exercise obesity Poor sleep Stress
Medical co-morbidities increasing risk of atherosclerosis
Diabetes HTN CKD Inflammatory conditions i.e. RA Atypical antipsychotics
End results of Atherosclerosis
Angina MI TIA Stroke PVD MI
Primary Prevention Cardiovascular disease
Do a Q risk score
If more than 10%, offer a statin, 20mg at night
All patients with CKD/T1DM for >10 years should be offered too
Secondary prevention Cardiovascular disease
Aspirin (and second antiplatelet (clopidogrel)
Atorvastatin (80mg)
Atenolol (100mg once daily) /other B-blockers (5-10mg once daily)
ACE inhibitor (Ramipril 1.25mg once daily)
Side effects of statin
myopathy
T2DM
Haemorrhagic strokes
Primary cause of IHD
atherosclerosis
IHD epidemiology
Largest cause of death in UK
IHD RF
Age, Gender, FHx
Smoking, HTN, Obesity, DM, Sedentary lifestyle, High Fat, low antioxidant, stress, alcohol, high coagulation factors
Angina presentation and classifications
- Constricting discomfort in chest, neck, shoulder, jaw
- Precipitated by exertion
- Relieved by rest/GTN
all 3= typical angina
2 = atypical angina
1/0 = non-anginal pain
IHD investigations
ECG (normal- Lipid profile (may be increased) FBC (exclude anaemia) HBA1C (exclude DM) CT coronary angiography (may show narrowed/blocked areas on vessel)
IHD treatment
Antiplatelet (aspirin/clopidogrel)
Statin
HTN control
Angina control
GTN spray
Beta blockers
Secondary Aspirin Atorvastatin ACEi PCI/CABG if extensive
Angina DDx
Pericarditis PE Chest Infection Dissection of aorta GORD
Angina features
Central, retrosternal pain Crushing Radiates to arms and neck Exacerbated by cold, exertion, large meal Relieved with rest
Causes of Prinzmetal’s angina
Coronary artery spasm
Cardiac syndrome X?
patients with symptoms of angina, positive exercise test but normal coronary arteries
Angina investigations
ECG (possible ST depression, T wave flattening/incersion) Exercise ECG positive FBC (exclude anaemia) U+E (prior to ACEi) LFT (prior to statin) Lipid profile TFT (check hypo/hyper) HBA1C (exclude diabetes) CT coronary angiography
Angina Management
RAMP
Refer to cardiology if unstable
Advise about diagnosis, management and when to call ambulance
Medical treatment
Procedural/surgical intervention