Cardiology Flashcards
What is the most likely cause of an irregular broad complex tachycardia in a stable pt?
Atrial fibrillation with right bundle branch block
What is the management of stable aegina?
all patients should receive aspirin and a statin in the absence of any contraindication
sublingual glyceryl trinitrate to abort angina attacks
NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on ‘comorbidities, contraindications and the person’s preference’
if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)
if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine
if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
What is the cause long QT syndrome
Long QT interval is important as it may deteriorate into VF and lead to sudden death
Erythromycin Chloroquine Myocarditis Hypothermia Sub arachnoid haemorrhage Amiodarone Tricyclic antidepressants Antipsychotics
How do you treat long QT syndrome?
IV magnesium sulphate
What Ix should you do for angina and what is the gold standard?
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes)
CT coronary angiogram
What is the medical management of angina?
Secondary Prevention
Immediate symptomatic relief- GTN spray
Long Term Symptomatic Relief is with either (or used in combination if symptoms are not controlled on one):
Beta blocker (e.g. bisoprolol 5mg once daily) or; Calcium channel blocker (e.g. amlodipine 5mg once daily)
Secondary prevention Aspirin (i.e. 75mg once daily) Atorvastatin 80mg once daily ACE inhibitor Already on a beta-blocker for symptomatic relief.
What procedures can you do for stable angina?
PCI
CABG
What is the pathophsyiology of ACS?
Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets. This is why anti-platelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.
What coronary arteries supply which part of the heart?
The Left Coronary Artery becomes the Circumflex and Left Anterior Descending (LAD).
Right Coronary Artery (RCA) curves around the right side and under the heart and supplies the:
Right atrium Right ventricle Inferior aspect of left ventricle Posterior septal area Circumflex Artery curves around the top, left and back of the heart and supplies the:
Left atrium
Posterior aspect of left ventricle
Left Anterior Descending (LAD) travels down the middle of the heart and supplies the:
Anterior aspect of left ventricle
Anterior aspect of septum
What are the three types of ACS?
Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)
How do you diagnose ACS?
When a patient presents with possible ACS symptoms (i.e. chest pain) perform an ECG:
If there is ST elevation or new left bundle branch block the diagnosis is STEMI.
If there is no ST elevation then perform troponin blood tests:
If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain
What are the symptoms of ACS?
Central, constricting chest pain associated with:
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 angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”.
What are the ECG changes in
A) stemi and
B) nstemi
STEMI:
ST segment elevation 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)
What causes raised troponin?
Troponins are proteins found in cardiac muscle. The specific type of troponin, the normal range and diagnostic criteria vary based on different laboratories (so check your policy). Diagnosis of ACS typically requires serial troponins (e.g. 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. They are non-specific, meaning that a raised troponin does not automatically mean ACS.
There are alternative causes of raised troponins:
Chronic renal failure Sepsis Myocarditis Aortic dissection Pulmonary embolism
What Ix do you do for ACs?
Perform all the investigations you would normally arrange for stable angina:
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes) Plus:
Chest xray to investigate for other causes of chest pain and pulmonary oedema
Echocardiogram after the event to assess the functional damage
CT coronary angiogram to assess for coronary artery disease
Stemi management?
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:
Primary PCI (if available within 2 hours of presentation)
Thrombolysis (if PCI not available within 2 hours)
The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor).
Percutaneous Coronary Intervention (PCI) involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast to identify the area of blockage. This can then be treated using balloons to widen the gap or devices to remove or aspirate the blockage. Usually a stent is put in to keep the artery open.
Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.
What is acute NSTEMI management?
B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. <95%).
What are the complications of MI?
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
Dressler’s Syndrome
This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced.
It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function).
A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).
Management is with NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.
What is secondary prevention of ACS?
Secondary Prevention Medical Management (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.
