Cardiovascular Flashcards
Describe the characteristic, and contrasting, features of chest pain resulting from myocardial ischaemia.
Pain similar to angina (retrosternal, crushing, worse with exertion/cold/after food) but more severe and not relieved by GTN spray.
Associated with nausea, sweating and vomiting.
Patients may experience “angor animi”, a feeling of impending doom.
Describe the characteristic, and contrasting, features of chest pain resulting from aortic dissection.
Severe tearing pain, felt behind the shoulder blades. Persistent but worse at onset.
Patient likely to be hypertensive and Marfan-oid.
Describe the characteristic, and contrasting, features of chest pain resulting from pleural and respiratory disease.
Sharp pain which is worse on inspiration and coughing. Not central - may be one sided and does not radiate.
May be associated with breathlessness and cyanosis.
Not relieved by GTN spray.
Describe the characteristic, and contrasting, features of chest pain resulting from Gastro-oesophageal disease.
GORD presents with ‘heartburn’. Retrosternal burning sensation after food, relieved by antacids.
Oesophageal spasm may be mistaken for MI.
Pain relieved by GTN spray but takes 20 minutes, longer than 2 minute relief present with angina.
Often associated with a history of dysphagia or dyspepsia.
Describe the characteristic, and contrasting, features of chest pain resulting from musculoskeletal disease.
Pain localised to one point on the chest
Pain worse on respiring and movement.
Tender to palpation.
What is the levine sign?
Levine’s sign is a clenched fist held over the chest to describe ischemic chest pain.
Describe the typical history of a patient with ACS.
Severe crushing retrosternal pain of a longer duration than angina pectoris.
This may also be accompanied by autonomic symptoms (these may not be present in elderly patients or those with diabetes.)
Associated symptoms may include: N/V and syncope.
Atypical symptoms include: dyspnoea, plueritic chest pain and indigestion.
Describe the clinical features of ACS.
Examination may show systolic murmurs or pulmonary oedema as well as pallor, sweating and tachycardia.
CXR may be normal or show pulmonary oedema or a widened mediastinum (suggesting aortic dissection).
Killip 1 = no crackles and no 3rd heart sound,
Killip 2 = crackles in <50% of lung or 3rd heart sound, Killip 3 = crackles in >50% of lung fields,
Killip 4 = cardiogenic shock.
Describe the use of oxygen and analgesia in ACS.
Patients are given high flow oxygen, aspirin, clopidogrel, LMWH.
IV opiates may be administered if necessary, alongside oral/sublingual/IV nitrates.
Anti-emetic must also be administered if opiates used.
Beta-blockers may also be given.
Describe the spectrum of the acute coronary syndromes: ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation syndromes (non-STEMI) and unstable angina (UA).
STEMI:
Complete occlusion of coronary artery.
NSTEMI:
Patients have elevated troponin without ST segment elevation.
Subtotal occlusion of the artery and infarct occurs.
Unstable angina:
Chest discomfort caused by minimal exercise or rest.
Creatine kinase and troponin are normal.
ECG may show ST segment depression or T wave inversion.
Usually atheromatous plaque rupture causes platelet aggregation, lumen narrowing and ischaemia.
Describe the role of ECG findings and serum Troponin to establish the diagnosis.
STEMI:
ST segment elevation, elevated troponin.
NSTEMI:
T wave inversion or ST segment depression, troponin elevated. No ST segment elevation.
Unstable angina:
No ECG or troponin changes.
Troponin is released 4-6 hours after the event and peaks at 24 hours. CK-MB (Creatine Kinase Myocardial B fraction) may be a better early marker.
Following ST elevation, R waves decrease in amplitude and Q waves may develop in full thickness infarcts.
What is the order of ECG changes following an MI?
First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.
Describe the role of anti-platelet agents, thrombolysis (including indications and contra-indications), primary percutaneous coronary intervention (PCI) and ‘rescue’ PCI
Anti-platelet agents are first-line therapy in the treatment of occluded coronary vessels.
Fibrinolysis after 12 hours is not supported by evidence, however; if administered before then, it saves 30 lives per 1000 people treated.
Patients who fail to reperfuse after 60-90 minutes (as demonstrated by ECG), may be re-thrombolysed or sent for rescue coronary angioplasty.
PCI is the preferred treatment, within 90 minutes if possible.
PCI can be administered after thrombolysis.
Contraindications to thrombolysis include haemorrhagic stroke (however old), ischaemic stroke (within 6 months), CNS damage, neoplasm and trauma (within 3 months), GI bleed (within last month), any known bleeding disorder or aortic dissection.
Relative contraindications include: Pregnancy, liver damage, refractory hypertension, endocarditis, traumatic CPR, oral anticoagulant therapy.
Which anti-platelets are used in ACS?
Aspirin or if allergic clopidogrel.
Ticagrelor in combination with low-dose aspirin is recommended for up to 12 months as a treatment option in adults with acute coronary syndromes (ACS) that is, people:
with ST-segment-elevation myocardial infarction (STEMI)
defined as ST elevation or new left bundle branch block on electrocardiogram.
that cardiologists intend to treat with primary percutaneous coronary intervention (PCI) or
with non-ST-segment-elevation myocardial infarction (NSTEMI).
Describe the causes and pathological consequences of ACS.
Atheromatous plaques may fissure, leading to thrombus formation, or bleeding into the plaque.
Complete occlusion of coronary arteries, resulting in ischaemia leads to full thickness ischaemia, unless collateral blood supply is established or lysis occurs.
Such circumferential subendocardial infarction may occur in hypoperfused cardiac tissue, due to stenosed arteries.
Describe the difference in prognosis between STEMI, non-STEMI and UA with respect to mortality and morbidity.
6 month mortality in the GRACE registry was 13% for NSTEMI and 8% for UA.
1 month mortality in a community STEMI may be as high as 50%, with 50% of these deaths occurring within 2 hours.
Early death may be due to arrhythmia.
Of those who reach hospital, 80% survive up to 28 days. Prognosis is worse for anterior infarcts than inferior. Morbidity is likely to be related to the level of ischaemia and myocardial damage sustained.
Describe the potential complications of ACS: rhythm abnormalities, cardiac failure, ventricular septal defect, ruptured chordae tendineae, haemopericardium, Dressler’s syndrome, ventricular aneurysm and reinfarction.
Rhythm abnormalities (AF, VF, bradyarrhythm),
Cardiac failure (shock),
VSD (Usually occurs in the first week post MI, present with new onset murmur, patients lie flat),
Ruptured chordae tendinae (mitral regurgitation, may present with sudden pulmonary oedema or death),
Haemopericardium (cardiac tamponade),
Dressler’s syndrome (immune mediated pericarditis. Present with frisction rub, chest pain and fever (post-infection/MI)),
Ventricular aneurysm (5-7% of patients following STEMI. Bulging of ventricle, can result in death),
Reinfarction,
Post-infarct angina.
Describe the pathway of care developed within the hospital for STEMI/nonSTEMI/UA.
Aspirin 300mg + Clopidogrel 300mg.
Sublingual GTN.
Oxygen (*if <94%, check NICE guideline).
Brief history. IV access and bloods (troponin, FBC, lipids, biochemistry, glucose).
12-lead ECG.
IV opiate and antiemetic.
Beta-blocker if not contraindicated. GPIIb/IIIa inhibitor if PCI available.
“MONA” - Morphine, oxygen, nitrates, aspirin
“BROMANCE” - Beta-blocker, reassurance, oxygen, morphine, aspirin, nitrates, clopidogrel, enoxiparin.
What is the TIMI score?
An assessment of morbidity and mortality in MI.
TIMI for STEMI:
age>65,>75, Hx of angina, Hx of hypertension, Hx of DM, systolic BP<100, HR>100, Killip II-IV, weight>67kg, Anterior MI or LBBB, delay to Rx>4hrs.
TIMI for NSTEMI/UA:
age>65, >3 CAD RFs, known CAD (stenosis>50%), aspirin use in last 7 days, severe angina, ST deviation, elevated cardiac markers.
What is the GRACE score?
Similar to the TIMI score.
GRACE score is based on age, heart rate, systolic blood pressure, serum creatinine and Killip score.
Define stable angina.
Angina is chest discomfort which is precipitated by exercise and relieved with rest.
Usually lasts minutes.
Angina = Strangling.
Describe the typical history of a patient with stable angina.
Chest pain relieved by rest.
Pain may be tight, heavy or gripping and is usually located retrosternally but may radiate to the jaw and/or arms.
Cold weather, anger, excitement and food may all provoke angina.
May also cause angor amini, sweating and SOB.
Discuss the potential underlying causes of angina 4
Coronary artery disease reduces blood flow to cardiac muscle.
Valvular heart disease puts increased strain on cardiac muscle.
Cardiomyopathy disturbs contractility of cardiac muscle.
Anaemia reduces oxygenation of blood reaching cardiac muscle.
Describe relevant clinical features of angina 7
Xanthelasmata - Cholesterol deposits around the eyes, indicating high levels of cholesterol in the blood.
Tendon xanthoma - Appear as slowly enlarging subcutaneous nodules related to the tendons or ligaments. Most commonly found on the hands, feet, and Achilles tendon. Associated with severe hypercholesterolaemia and elevated LDL levels.
HTN
Anaemia
Hyperthyroidism causing tachycardia and irregular rhythm
Aortic stenosis - Ejection systolic murmur heard between heart sounds 1 and 2, may radiate into neck.
List recognised risk factors for coronary artery disease. 11
Obesity, smoking, male, hypertension, high cholesterol, hyperlipidaemia, diabetes, low exercise levels, age, family history, type A personality.
Describe the pathology of the coronary arteries in patients presenting with angina.
Fatty streaks develop in areas of stress or turbulence.
Damage to endothelium causes inflammatory cells to migrate to the area.
Macrophages ingest lipid, and release cytokines which stimulate smooth muscle cells to migrate to the intima and lay down hyaline fibrous matter.
Macrophages may also release TNF-alpha and IL1 which may lead to the destruction of this fibrous cap and subsequent thrombus formation.
Describe the investigation of a patient with suspected angina.
CV examination, resting ECG, FBC, exercise test ECG, scintigraphy, angiography
List the classes of drugs used to treat angina, mechanism of action and their common side effects.
Nitrates can relieve angina fairly quickly and are used when required. They cause vasodilation and side effects include headache and hypotension.
B-blockers have negative inotropic and chronotropic effects, reducing the strain on the heart. Side effects include fatigue, cold extremities and weight gain.
Calcium channel blockers inhibit the excitability of cardiac muscle. Rate limiting blockers such as verapamil and diltiazem inhibit conduction through the AV node and cause a bradycardia, dihydropyridine blockers may reduce contractility but may cause reflex tachycardia so are best used in combination with beta-blockers. Other side effects include dizziness, flushing, headache and peripheral oedema.
Nicorandil, a potassium channel agonist, acts similarly to nitrates to reverse angina pain.
Use the Framingham/QRISK tools to estimate cardiovascular risk.
The QRISK tools collate risk factor information and estimate a 10 year risk of heart attack or stroke.
Outline the ECG changes that may develop during an exercise stress test.
Down sloping ST segment depression, T wave inversion. False positives and false negatives are common (20%), though these patients will have good prognosis.
Describe the typical history of pulmonary oedema and its common causes.
SOB, especially when lying down.
Paroxsymal nocturnal dyspnoea - patients will wake up in the middle of the night totally out of breath due to fluid shift from interstitium to vascular compartments.
Cheynes-stokes respiratory cycles may also occur, due to impaired response of central chemoreceptors to carbon dioxide levels.
Common causes include: left sided heart failure, pulmonary hypertension, fluid overload, acute respiratory distress syndrome (causes including: pneumonia, aspiration, sepsis, severe trauma), both acute and chronic kidney disease, hypoalbuminaemia, morphine overdose, tumour, and altitude.
Describe the typical clinical features of pulmonary oedema
Tachycardia Gallop rhythm - Presence of 3rd heart sound, may be suggestive of stenosis or regurgitation. Bilateral basal crackles Other features may indicate a cause: Raised JVP in heart failure Jaundice in liver failure Hypo or hyper tension
Discuss the differential diagnosis for pulmonary oedema
If no cardiac cause for pulmonary oedema is present then ARDs should be suspected.
Chest infection may produce a cough but is less likely to produce pink frothy sputum and SOB.
Pulmonary embolism presents with SOB, pleuritic chest pain and cough.
Outline the general principles of management of pulmonary oedema including drugs used in treatment, their route of administration, mechanism of action and their common side effects.
High flow oxygen my be administered to reduce respiratory workload.
Obvs, sats and ECG and daily weights must be monitored.
Urinary catheter may be inserted and furesemide may be administered, initially IV, then switched to oral.
Furosemide is a loop diuretic (blocks Na/K/Cl ion channels in the thick ascending loop of Henle, thus decreasing water reabsorption.)
Common side effects include: numbness or tingling, headache, dizziness, blurred vision, low BP, dehydration.
Outline the investigations used in acute pulmonary oedema including ECG, CXR, Troponin, and echocardiography.
CXR is used to identify and quantify pulmonary oedema. It will show: Kerly B lines, fluid in the fissures, hazy hila and prominent vasculature (especially superiorly).
ECG, troponin and echocardiography will help determine the cause, be it cardiac.
FBC, U&Es, LFTs and urine dip are helpful in diagnosis of cause.
Define congestive cardiac failure and list common causes.
Congestive heart failure is the failure of both sides of the heart so that not enough blood is pumped out of the heart to adequately perfuse metabolically active tissues.
Common causes include ischaemic heart disease (30-35%), cardiomyopathies (30-34%) and hypertension (15-20%).
Other causes include: Infection, valvular heart disease, (poor ventricular filling (AV stenosis) or ventricular overload (regurgitation)), congenital heart disease (Septal defect), alcohol and drugs, arrhythmias (AF, tachymyopathy, CHB), pericardial disease and hyperdynamic circulation (anaemia, hyperthyroid, haemochromatosis).
Describe the typical history of a patient with CCF.
Exertional dyspnoea
Orthopnoea (SOB when lying flat)
Fatigue
Cachexia (from muscle dissuse, and reduced perfusion)
Describe the typical clinical findings in a patient with CCF
Most common clinical findings: RAISED JVP, cachexia, paroxsymal nocturnal dyspnoea, pulmonary oedema, s3 gallop, radiogrpahy cardiomegaly.
Less common: Hepatomegaly (causing ASCITES), PERIPHERAL OEDEMA, TACHYCARDIA.
What drugs are used to manage CCF?
Diuretcs - reduce water in system, reducing hypertension
Beta-blockers - used to reduce contraction force and tachycardia.
ACE-i - reduce BP
Digoxin
Vasodilators
Outline the common investigations used to define the cause of CCF.
CXR: Cardiomegaly Kerly B wings Bat wings Prominant upper lobe veins Fluid in fissures
BNP:
Raised in heart failure, if low, HF unlikely.
ECG:
Indicate cause eg MI, as well as ischaemia, hypertrophy or arrhythmias.
Echocardiography:
Able to visualise major causes and pathologies such as hypertrophy, valve defects etc.
What are the 5 main groups of causes of valvular heart disease?
Congenital (aortic bicuspid)
Rheumatic (reaction to group A strep, 50% mitral stenosis)
Degenerative
Endocarditis (erodes into valves causing insufficiency)
Cardiac remodelling
What are the congenital causes of valvular heart disease? (4)
Bicuspid aortic valve
Lutembacher’s syndrome (congenital atrial spetal defect or acquired mitral stenosis)
Ebstein Anomaly (tricuspid regurgitation)
Fallot’s tetralogy (Pulmonary stenosis)
How can degenerative causes lead to valvular heart disease?
Senile calcification of the aortic valve often occurs.
Rupture of chordate tendinae after MI may also occur.
