Cardiovascular system Flashcards
what are the clinical features of angina?
Typical symptoms include: chest pressure or squeezing lasting several minutes, provoked by exercise or emotional stress, relieved by GTN.
usually described as a central, crushing, retrosternal chest pain.
what are the risk factors for angina?
smoking hypertension hyperlipdaemia isolated HDL cholesterol diabetes inactivity obesity family history of CHD males illicit drug use
what are the differential diagnosis for chest pain?
acute MI prinzmetal's angina acute pericarditis MSK pain GI reflect Pleuritic chest pain aortic dissection PE oesophagitis, oesophageal spasm anxiety
what is prinzmetals angina?
angina caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest. ECG during pain show ST elevation
what is decubitus angina?
occurs on lying down
what investigations would you perform for stable angina?
CT coronary angiography is the gold standard diagnostic investigation.
resting ECG - often normal but may reveal ST-T changes suggestive of ischemia or Q wave indicative of riot infarction
Haemoglobin levels
fasting lipid profile
fasting blood glucose or HbA1c
Also, consider
TSH
Stress exercise ECG -ST segment elevation elevation and depression identify ischaemia.
angiography
what would an ECG of a person with a stable angina show?
often normal but may reveal ST-T changes suggestive of ischaemia or Q wave indicative of riot infarction
may show ST segment depression and T wave flattening or inversion during an attack.
how is stable angina managed?
1st line - lifestyle education
PLUS - anti platelet therapy (aspirin or clopidogrel)
PLUS - statin e.g. atorvastatin
You can add prophylactic treatment:
Beta blockers (bisoprolol)
calcium channel blockers (amlodipine)
nitrates
revascularisation
GTN spray - sublingual glycerol trinitrate to terminate acute episodes of angina.
why should verapamil and BB not be prescribed together?
risk of complete heart block
how do Beta blockers work?
reduce heart rate and force of ventricular contraction, both of which reduce myocardial oxygen demand.
how do calcium channel blockers work?
block calcium influx into the cell and the utilization of calcium within the cell. They relax the coronary arteries and reduce the force of left ventricular contraction thereby reducing oxygen demand. The side effects (postural dizziness, headache, ankle oedema) are the result of systemic vasodilation
how do nitrates work?
Nitrates reduce venous and intracardiac diastolic pressure, reduce impedance to the emptying of the left ventricle and dilate coronary arteries
what is acute coronary syndrome?
it is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
there are three types
- unstable angina
- ST elevation myocardial infarction
- non-St elevation myocardial infarction
what are the risk factors for ischaemic heart disease?
unmodifiable - increasing age, male gender, family history
modifiable risk factors - smoking, diabetes mellitus, hypertension, hypercholesterolaemia, obesity
what is the pathophysiology of IHD?
- initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
- this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
- fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
- monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
- smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction
in ACS what are the features of the chest pain?
- typically central/left sided
- may radiate to the jaw or left arm
- often described as heavy or constricting
- certain patients e.g. diabetic/elderly may not experience any (silent MI)
other than chest pain, what symptoms do patients experience with ACS?
- nausea and vomiting
- sweating and clamminess
- feeling of impending doom
- shortness of breath
- palpitations
- pain radiating to jaw or arms
symptoms should continue at rest for more than 20 minutes - if they settle with rest consider angia
what ECG changes do you see in STEMI, NSTEMI and unstable angina?
STEMI:
ST segment elevation (>20 mins) in leads consistent with an area of ischaemia
New Left Bundle Branch Block also diagnoses a “STEMI”
NSTEMI:
ST segment depression in a region, Deep T Wave Inversion, Pathological Q Waves (suggesting a deep infarct – a late sign)
The ECG may be normal or show non-specific changes
unstable angina - The ECG typically shows ST-segment depression and T-wave inversion, but may be normal
How is ACS usually diagnosed?
it typically requires serial troponins(at baseline and 6 or 12 hours after onset of symptoms
a rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle however they are non-specific - meaning that a raised troponin does not automatically mean ACS
other than ACS what are some causes of raised troponins?
chronic renal failure sepsis myocarditis aortic dissection PE
what are the different cardiac markers?
Troponins (T or I)
Creatine kinase (CK, specifically CK-MB)
Myoglobin
how do you acutely manage ACS?
MONA - morphine, oxygen, nitrates, aspirin
what investigations other than ECG and troponin would you perform for ACS?
FBC U&E LFT lipid profile TFT HbA1C
plus echo, CXT and CT angiogram to assess for coronary artery disease
how should you manage acute STEMI?
> Primary PCI if available within 2 hours of presetation
> thrombolysis if PCI is not available in 2 hours (streptokinase, alteplase or tenecteplase)
how would you manage acute NSTEMI?
BATMAN
B- beta blockers unless contraindicated
A- aspirin 300mg stat dose
T- ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M - morphine titrated to control pain
A - anticoagulant: low molecular weight heparin at treatment dose
N - nitrates -GTN spray to relieve coronary artery spasm.
what score can be used to give a 6-month risk of death or repeat MI after having an NSTEMI
GRACE score
used to assess the need for PCI in NSTEMI
** if the GRACE score is greater that 3% in NSTEMI so you should do PCI
what are the complications of myocardial infarction?
DREAD
D-death R-rupture of the heart septum or papillary muscles E edema- heart failure A- arrhythmia and aneurysm D - dressler's syndrome
what is dressler’s syndrome?
aka post-MI syndrome.
usually occurs 2-3 weeks after an MI
caused by localised immune response and causes pericarditis
it presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation
It causes a pericardial effusion and rarely a pericardial tamponade
what investigations for Dressler’s syndrome and what will they show?
ECG - global ST elevation and T wave inversion
Echo - pericardial effusion
Inflammatory markers - CRP and ESR raised
how do you manage Dressler’s syndrome?
NSAIDs and in more severe cases steroids can be used
they may need pericardiocentesis to remove fluid from around the heart
what is the secondary prevention medical management for MI’s
6 As
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.
how do you manage unstable angina?
antiplatelet therapy statin BB ACE i lifestyle
what is heart failure?
when cardiac output is inadequate for the body’s requirements
what are the causes for low output heart failure?
cardiac output is decreased and fails to increase with exertion
Pumps failure -> systolic and or diastolic failure as well as arrhythmias (bradycardia, heart block, tachycardia and anti-arrhythmic (e.g.beta blockers, verapamil)
excessive preload -> aortic or mitral regurgitation, fluid overload
excessive afterload ->aortic stenosis, hypertensions
what are the causes of high output heart failure?
there is right ventricular failure followed by left ventricular failure
causes are:
anaemia, thyrotoxicosis, thiamine deficiency (beri beri), pregnancy, paget’s
what is systolic and diastolic heart failure?
systolic is the inability of the ventricles to contact resulting in decreased cardiac output (heart failure with reduced ejection fraction)
causes: IHD, MI, cardiomyopathy
Diastolic - inability of the ventricles to relax and fill normally - HF with preserved ejection fraction.
Causes: constrictive pericarditis, tamponade, restrictive cardiomyopathy
what are the causes, symptoms and signs of right ventricular failure?
causes - LVF, pulmonary stenosis and lung disease (cor pulmonale)
symptoms and sigs ->peripheral oedema, ascites, nausea, anorexia, facial engorgement, increased JVP, hepatomegaly
what are the causes, symptoms and signs of left ventricular failure?
causes - IHD, idiopathic dilated cardiomyopathy, systemic hypertension, mitral and aortic valve disease, specific cardiomyopathies
symptoms and signs - dyspnoea, poor exercise tolerance, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea, nocturnal cough (plus pink frothy sputum), wheeze, nocturia,cold peripheries, weight loss, muscle wasting
what is acute heart failure ?
new onset or decompensation of chronic
it is characterised by peripheral and/or pulmonary oedema with or without signs of peripheral hypo perfusion
what is chronic heart failure?
Develops/progresses slowly
venous congestion common
arterial pressure maintained until late
