Cardiology Flashcards
Name 5 causes of HF
Ischaemic Heart Disease Hypertension Dilated Cardiomyopathy Valvular Heart Disease RHF (Cor Pulmonale, RV infarct, PHTN, PE, COPD) Congenital Heart Disease Alcohol Pericarditis
What 4 things occur pathophysiologically in HF?
Activation of SNS - Raised HR and Contractility, Vasoconstriction resulting in increased preload to try and improve contractility, but this also increased afterload
Renin-Angiotensin System - reduced CO results in reduced renal perfusion, resulting in renin release. This raises water and Na retention, increasing venous return, to help maintain SV. As retention increases, can get P oedema and causes dyspnoea.
ANP and BNP released
Ventricular Dilatation and remodelling - when compensatory mechanisms become limited.
What x-ray findings are there in HF?
Cardiomegaly Kerley 'B' lines - interstitial oedema Peri-hilar shadowing (Bat's wing) - alveolar oedema Pleural Effusion Dilated vessels in upper lobe
What is the normal level of BNP?
< 100pg/ml
What investigations would you order for initial suspicion of HF? If any are abnormal what would you do next?
CXR, Bloods (BNP), ECG (if normal, unlikely HF)
Echo -TTE (if normal, unlikely HF)
How do you treat HF?
Vasodilator Therapy : Ace-Inhibitors* (ARAs if intolerable), Isosorbide Mononitrate (reduces preload) with Hydralazine (reduces afterload)
Ivabradine (alternative to ISMN)
Beta-Blockers* - helps block chronically activated SNS
Diuretics - used in pts with fluid overload
Loop (Furosemide, Bumetanide 20-40mg daily)
Thiazide (Bendroflumethiazide 2.5mg daily)
Aldosterone antagonists (Spironolactone)
How do ACE-i work?
Inhibit Angiontensin II (which usually causes vasoconstriction)
Increase levels of bradykinin, which causes vasodilation
Enhance salt and water excretion
Summarise the management of HF. (General, Pharmacological, Non-Pharmacological)
General: Educate, light exercise, diet, vaccine against influenza and pneumococcal, social changes
Pharmacological: ACE-i, BB, Diuretics, Digoxin, Inotropes
Non-pharmacological: CABG/PCI, cardiac resynchronisation therapy, implantable defibrillator, repair underlying cardiac problems (valve, congenital), cardiac transplant
What is the emergency management of Acute HF (caused by hypertensive HF/acute pulmonary oedema/cardiogenic shock/RHF)?
Same investigations as chronic HF
High flow oxygen, sometimes CPAP
Diuretic - Furosemide iv 50mg
Measure SBP
Give vasodilator if <100
Give vasodilator and/or inotrope if 85-100
Give inotrope and/or dopamine and/or noradrenaline if <85
If no response, try mechanical assist devices
Give some examples of Vasodilators
GTN
Isosorbide Mononitrate
Nitroprusside
ACE-i
What does an artheroma consist of?
Fatty streak, macrophages, lipids, smooth muscle cells (usually in the intima of the artery)
Name 6 RFs for IHD
Reversible: High cholesterol, high fat diet, Sedentary lifestyle, smoking, HTN,
Irreversible: Age, Gender, FH
What assessment tool do NICE recommend for estimated CVD risk?
QRISK2 - gives the 10-year risk of CVD
Use in high-risk people
Takes into account DM, BP, lipid profile, age, gender, fH
What is prinzmetal’s / variant angina?
Coronary artery spasm
What is decubitus angina?
Angina on lying down
What is cardiac syndrome X?
Pt has symptoms of angina, a positive exercise test, but on investigation has normal coronary arteries
What investigations would you perform in suspected angina?
Usually diagnosis is clinical
Resting ECG - normal between attacks, ST depression or T-wave flattening during attack
Exercise ECG - Positive in most people with CAD, ST depression at a low workload or a paradoxical fall in BP with exercise indicate CAD
Angiography - Only really used if intervention is planned, so exact coronary pathology can be found out
What is the long term management of angina?
Modify lifestyle factors
Aspirin - 75mg daily - inhibits COX2 and thus thromboxane A2
Clopidogrel - 75mg daily - if aspirin intolerable
Statin - aim for cholesterol <5.0 mmol/L
If persistent despite oral treatment, consider revascularisation therapy:
PCI - Try if 2 anti-anginals and still not improving, preferred in pts with isolated disease, complications are death, acute MI, need for restenosis, give aspirin and clopidogrel for 6-12 months after
CABG - use mammary artery to bypass stenosis, recommended in pts with triple artery disease, impaired LVF
What is the symptomatic treatment of angina?
GTN - tablet or spray
Encourage to use before exertion rather than waiting for pain to develop
S/E is severe headache
What prophylaxis is given to angina patients?
Nitrates - reduce the pressures in the heart by dilating coronary arteries (ISM,ISD)
BBs - reduce HR and contractility thus reducing myocardial oxygen demand
Ca+ Antagonists - Relax the coronary arteries and reduce contractility thereby reducing oxygen demand
What is most common cause of an ACS?
Rupture of a fibrous cap of a coronary plaque
How is Unstable Angina different to NSTEMI?
In an NSTEMI, the occluding thrombus is large enough to cause myocardial damage, and thus a rise in troponin and creatine kinase.
What are the similarities of NSTEMI and UA?
ECG may be normal / show ischemia with T-Wave inversion and ST depression
Troponin may be 0 on arrival to hospital (measure 12h later, if still normal it suggests UA)
Both can be complicated by a STEMI if not treated
Name some risk stratification scoring systems for MI
TIMI, GRACE
Looks at age, cardiac markers, ECG results to see if there is a risk of a STEMI/death in patients with either NSTEMI or UA
What is the immediate management of an ACS?
IV access
Investigations - Bloods (Troponin, CKMB), ECG
Treatment (mona)- Morphine 5mg IV, Metaclopromide, Oxygen, GTN, Aspirin 300mg/Clopidogrel/Ticagrelor
What is the management of STEMI?
MONA
Pts presenting within 90minutes of onset = primary angioplasty with dual anti-platelet therapy
Between 90mins and 12h = thrombolysis (tenecteplase)
Metaprolol if HR > 100, Insulin if BM > 11 mmol/L
What ECG changes are there in a STEMI?
Minutes - Tall T waves and ST elevation
Hours - Inverted T waves, pathological Q waves (broad + deep)
Days - Normal ST segment
Weeks - T wave returns upright, Q wave persists
Which leads ‘face’ which aspect of the heart?
Leads II, III, aVF = Inferior
I, aVL and V5-6 = Lateral
V2 - 4 = Anterior
What is the post-acute management of a STEMI?
Re-measure cardiac markers, electrolytes and repeat ECG at 24 and 48h
Initiate secondary prevention
Exercise tolerance ECG test before discharge
Refer to cardiac rehab programme
No driving for 1 month, no work for 2 months
What is secondary prevention of STEMI?
ACE-i - start day 1 after attack
Continue DAPT (Aspirin + Clopidogrel/Ticagrelor)
Continue Statin, BB
What are the complications of an MI?
HF, Arrhythmias, Pericarditis, Mitral Regurgitation, Heart block
Dressler’s Syndrome - weeks or months after, give NSAIDs/steroids (fever/pericardial effusion and pericarditis)
Which bacteria causes Rheumatic Fever?
Group A Streptococcus (Strep Pyogenes)
What is the modified Duckett Jones criteria for RF?
Requires 2 major or 1 major + 2 minor present with streptococcal infection (antistreptolysin O)
Major Criteria:
Polyarthritis - large joints
Carditis - which can cause murmurs
Subcutaneous nodules - non-tender and over the joint ususally
Erythema Marginatum - pink rings on the trunk
Sydenham’s Chorea - fidgety movements
Minor Criteria:
Fever, Arthralgia, raised ESR/CRP, Leukocytosis, previous episode of RF, ECG showing heart block
How do you treat RF?
Bed rest and high-dose aspirin
Penicillin to treat the infection, given long-term for those who get cardiac damage
What type of pt gets RF?
Kids, 5 - 15 year olds
But, over 50% of those who have carditis, will present again 10-20 years later with chronic rheumatic valvular disease (mainly aortic and mitral)
What is the pathophysiology of Mitral Stenosis?
Thickening and immobility of the leaflets leads to stenosis between the LA and LV.
Therefore the pressure increases in the LA, leading to PHTN and right-heart dysfunction.
AF is common (increased likely hood of embolism too) due to the increased pressure in LA.
Chronically elevated pressure in LA leads to Pulmonary Oedema.
Eventually leads to RVH and RHF.
What are the signs/symptoms of Mitral Stenosis?
Malar flush (cyanotic/pink discolouration of cheeks),
Low-volume pulse (irregular if AF)
Tapping apex beat
Mid-Diastolic murmur
Signs of PHTN (Raised JVP, parasternal heave, ascites, peripheral oedema)
Progressive exertional dyspnoea, coughing of blood, AF, Fatigue, Oedema
Give 5 causes of Mitral Regurgitation.
Prolapse (most common cause) RF Infective endocarditis Rupture of the chordea tendinae or papillary muscle Ehlers-Danlos syndrome
What is the pathophysiology of Mitral Regurgitation?
Long-standing regurgitation does not produce a significant increase in pressure in the LA as it is accomodated by an enlarged LA.
LV dilation and hypertrophy follow, late on in the disease process.
What are the symptoms and signs of Mitral Regurgitation?
Exertional dyspnoea, fatigue, lethargy, symptoms of RHF eventually
Displaced apex beat
Pan-systolic murmur
What investigations are used in diagnosing valvular disease?
Echo + Doppler Echo to see severity is key
CXR and ECG can also be helpful
How do you treat Mitral Stenosis?
Mild = no treatment, just treat complications (BB for AF, anti-coagulate)
Severe = Percutaenous Balloon Valvotomy (cardiac catheterisation) or Valvotomy
How do you treat Mitral Regurgitation?
Serial Echo’s every 1-5 years if mild
Medical = diuretics and ACE-i
Surgical if severe (depends on symptoms and EF)
