cardiology 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 between shoulder blades. Patient commonly hypertensive or Marfan-oid. Persistent, most severe at onset.
Describe the characteristic, and contrasting, features of chest pain resulting from pleural and respiratory disease
Sharp pain, worse on inspiration and coughing. Not relieved by GTN. Not central, may be one sided, no radiation. Often associated with breathlessness or cyanos
Describe the characteristic, and contrasting, features of chest pain resulting from gastro-oesophageal disease
GORD will cause a typical “heartburn”, a retrosternal burning sensation after food, relieved by antacids. Oesophageal spasm may be mistaken for MI/angina. It will be relieved with GTN after ~20 minutes, later than the 2 minute relief in angina. The pain will be severe, retrosternal and burning. Often associated with a history of dyspepsia or dysphagia
Describe the characteristic, and contrasting, features of chest pain resulting from musculo-skeletal disease
Localised to one location on the chest, tender to palpitation, more sensitive on when moving and respiring.
What is a typical history of a patient with acute coronary syndrome?
(symptoms)
- Sever crushing, gripping or heavy chest pain lasting longer than 20 minutes
- Not relieved by 3x GTN sprays at 5 minute intervals
- Radiates to the left arm, neck or jaw
- Associated dyspnoea, nausea, fatigue, sweatiness and palpitations in the elderly or diabetics, who can present later with a variety of symptoms
What are the clinical features of ACS?
(on examination)
Can be variable
- Sympathetic activation: tachycardia, hypertension, pallor, sweatiness
- Vagal stimulation: bradycardia, vomiting
- Myocardial impairment: hypotension, narrow pulse pressure, raised JVP, basal crepitations, 3rd heart sound
- Tissue damage: low grade pyrexia
Later a pericardial rub and peripheral oedema may develop, or pansystolic murmer due to papillary muscle rupture/ventriculo-septal defect
What are differential diagnosis of central chest pain from ACS?
(not an objective)
Cardiac:
- Coronary artery spasm
- Pericarditis/myocarditis
- Aortic dissection
Non-cardiac:
- PE
- Pneumothorax
- Oesophageal disease
- Mediastinitis
- Costochondritis
- Trauma
What does the spectrum of acute coronary syndromes cover?
ST-segment elevation myocardial infarction (STEMI)
Non-ST-segment elevation myocardial infarction (non-STEMI)
Unstable angina (UA)
What pathology do all acute coronary syndromes share?
- Atheromatous plaque formation in the coronary arteries
- Fissuring/ulceration of the plaque leading to platelet aggregation
- Localised thrombosis, vasocontriction and distal thromboembolism
- Myocardial ischaemia
What is unstable angina?
(aka crescendo angina)
- Angina occuring at rest, or sudden increased frequency/severity of existing angina
- Pathologically caused by fissuring of plaques, thus there is a risk of subseuent total vessel occlusion and progression to acute MI
What is the an acute myocardial infarction?
What are the two different types?
- Occurs followinf full arterial occulsion, with different patterns
- The diagnosis of MI requires elevations in serum cardiac troponin levels, with additional categorisation based on ECG changes:
- ST elevation/new left bundle branch block (LBBB) = STEMI
- No ST elevation/LBBB = NSTEMI (ECG often shows T wave inversion or ST depression)
What is the time course of an MI?
(not an objective)
0-12 hours
12-24 hours
24-72 hours
3-10 days
10 days - months
- 0-12 hours: infarct not visible, loss of oxidative enzymes
- 12-24 hours: infarct pale and blotchy , intercellular oedema
- 24-72 hours: infarcted area excites acute inflammatory response, with dead area soft and yellow with neutophilic infiltration
- 3-10 days: organisation of infarcted area by vascular granulation tissue
- 10 days-several months: collagen deposition, infarct replaced by collagenous scar
How does an ECG and serum troponin establish the diagnosis of an ACS?
STEMI:
- ST segment elevation, troponin elevated.
- Troponin is released at 4-8 hours and peaks at around 24 hours. dectectable for 10 days
- A release of CK-MB may be an earlier enzyme sign.
NSTEMI:
- No ST segment elevation, troponin elevated.
Unstable angina:
- No ST segment elevation, troponin normal.
What is the management of unstable angina and NSTEMI?
(normal A-E)
(asses patient using GRACE score)
BROMANCE
- Beta-blocker
- Reassurance
- Oxygen
- Morphine
- Aspirin
- Nitrates/GTN spray
- Clopidigrel
- Exoparin
What is the management of STEMI?
MONA
- Morphine
- Oxygen
- Nitrates (GTN spray)
- Aspirin
Percutaneous coronary intervention (PCI) is gold standard treatment if available in a timely fashion: door to ballon in 90 minutes, patient transfer advised if intervention can occur within this window
GRACE score as well
What if PCI are contra-indicated for a STEMI?
What are the conta-indications?
Thrombolysis is indicated if PCI not available or there are significant co-morbidities
What are contra-indications for thrombolysis?
- haemorrhagic stroke at any time
- ischaemic stroke within 6 months
- CNS damage or neoplasm
- recent trauma (3 weeks)
- GI bleed within last month
- known bleeding disorder or aortic dissection.
- Relative contraindications include pregnancy, liver disease, endocarditis, traumatic CPR, oral anticoagulant therapy, refractory hypertension.
What is the GRACE score for ACS?
Takes into account age, heart rate, blood pressure, class of CHF, renal function, ST segment changes, troponin elevation and whether there was an arrest at admission to give a mortaily risk at various time intervals (usually one for 6 months)
Describe the difference in prognosis between STEMI, non-STEMI and unstable angina 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.
What are the potenital short term complications of ACS?
Pulmonary oedema:
- Left heart fails to pump effectively, with poor systolic emptying leading to dilation: ‘a dilated chamber is a failing chamber’
- The backpressure in the pulmonary veins is reflected into the capillaries, leading to extravasation of low-protein fluid into the alveolar sacs
- This is a life-threatening emergency, characterised by extreme breathlessness, with sweating and anxiety
- There may be a cough producing frothy, blood-stained sputum
- On examination there are signs of acute heart failure with crackles
- Arterial PO2 falls, and initially PCO2 falls also due to overbreathing, but later the PCO2 rises due to impaired gas exchange
Cardiogenic shock:
- Carries a high mortality due to the vicious cycle of hypotension causing further reduction in coronary flow, and thus further pump failure ect.
Thromboembolism:
- Mural thrombus formation over the inflamed area of endocardium can cause emboli to the brain, kidney, gut, lower limbs ect. causing infection
Venticulo-septal defect:
- Intracardiac rupture may occur through the septum, causing left-right shunt and development of severe LVF if severe
Ruptured chordae tendiae:
- Leads to mitral valve incompetence
Rupture of ventricular wall:
- Usually occurs 2-10 days after the infarct, due to re-organisation and softening of the wall
- This leads to haemopericardium (blood in pericardial sac), cardiac tamponade (compression of the heart due to fluid in pericardium) and rapid death
What are the potential long term complications of ACS?
Heart failure:
- IHD is the most common cause of left heart failure
- Often leads to right heart failure
Dressler’s syndrome
- Immune-mediated pericarditis, associated with a high ESR and sometimes anti-myocardial antibodies
- Rare, develops 2-10 months after infarction
- Pericarditis gives a sharp chest pain, exacerbated by movement and lying down - relieved by sitting forward
- May be a pericardial effusion, leading to dyspnoea if it compresses adjacent bronchi
Ventricular aneurysm formation:
- Gradual distension of the infarcted part of the ventricular wall, which has been replaced by a collagen scar
- Aneurysmal rupture will lead to cardiac tamponade and death
Describe the pathway of care developed within the hospital for STEMI/non-STEMI and unstable angina
- 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.
STEMI - “MONA” = Morphine, Oxygen, Nitrates, Aspirin NSTEMI/UA - “BROMANCE” = Beta-blocker, Reassurance, Oxygen, Morphine, Aspirin, Nitrates (GTN), Clopidogrel and Enoxoparin
What is the TIMI scoring system?
In patients with UA/NSTEMI, the TIMI risk score is a simple prognostication scheme that categorizes a patient’s risk of death and ischemic events and provides a basis for therapeutic decision making.
- age>65
- >3 Cornary artery disease risk factors
- known CAD (stenosis>50%)
- aspirin use in last 7 days
- severe angina
- ST deviation
- elevated cardiac markers.
Define stable angina
Episodic pain that takes place when there is increased myocardial demand, usually upon exercise, in the presence of impaired perfusion by blood. relieved by rest. Usually fades within minutes
Describe the typical history of a patient with stable angina
- Ischaemic pain of the myocardium, varying from a mild ache to a severe pain that provokes sweating and fear
- The pain is provoked by exercise, especially after meals, in the cold, and if the patient is angry/excited
- It fades quickly with rest, and in some patients the pain occurs predictably at certain levels of exertion
- There may be associated breathlessness
Usually no abnormal findings on examination, occasionally a 4th heart sound
What are the potenial underlying causes of angina?
- Coronary artery disease
- causes a decrease in blood flow reaching areas of myocardium
- Valvular heart disease
- increases cardiac workload
- Cardiomyopathy
- interferes with cardiac contractility
- Anaemia
- reduces oxygenation
What are the causes myocardial ichaemia?
- Reduced perfusion:
- Atheroma
- Embolus
- Thrombosis
- Spasm or inflammation of coronary arteries
- Generalised hypotension
- Reduced blood oxygenation
- Anaemia
- Carboxyhaemoglobinaemia
- Increased tissue demands
- Increased CO
- Cardiac hypertrophy
What clinical signs may be present in chronic stable angina pectoris?
- Xanthelasmata (cholesterol deposits around the eyes)
- tendon xanthoma (cholesterol deposits in the hands/skin)
- hypertension
- anaemic signs
- hyperthyroidism signs
- aortic stenosis (ejection systolic murmur radiating into neck)
List recognised risk factors for coronary artery disease
- Increasing age
- Male gender
- Family history
- Smoking
- Diet: high fat, low fruit and veg
- Obesity
- Hypertension
- Hyperlipidaemia
- Diabetes Mellitus
- type A personality
- haemostatic factors
What is coronary heart disease?
Also known as ischemic heart disease (IHD), is a group of diseases that includes: stable angina, unstable angina, myocardial infarction, and sudden cardiac death. It is within the group of cardiovascular diseases of which it is the most common type.
Define arteriosclerosis?
- Non-specific thickening and hardening of the walls of arteries causing a loss of contractility and elasticity, and decreased blood flow
- Often due to prolonged hypertension in smaller arteries
What is atheroma?
- Specific degenerative disease affecting large/medium sized arteries
- When this leads to thickening and hardening of the arterial wall, it is termed atherosclerosis: most common cause of arteriosclerosis affecting large/medium arteries
- Atherosclerosis reduces tissue perfusion, as well as predisposing to thrombus and aneurysm formation
Describe the pathology of atheroma formation
- Damage to the endothelium due to a variety of risk factors allows entry of LDLs into the intima
- This lipid is taken up by macrophages in the intima, and accumulates excessively as it is able to bypass normal receptor mediated uptake, forming a ‘fatty streak’
- As the macrophages take up more and more lipid, they release free lipid into the intima
- The macrophages also stimulate cytokines, which leads to collagen deposition by inflammatory cells, and the intimal lipid plaques becomes fibrotic
- At this stage it appears raised and yellow, and leads to pressure atrophy of the media and disruption of the elastic lamina
- Increased secretion of collagen forms a dense fibrous cap to the plaque, which is now hard and white
- Advanced places also show free lipid as well as lipid in macrophages
- The endothelium is fragile and often ulcerates, allowing platelet aggregation
What investigations would you do on a patient with suspected angina?
Clinical assessment alone can be sufficient to confirm stable angina
- Exclude other causes: FBC, glucose, lipids, thyroid function test
- Resting 12-lead ECG: usually normal, may be signs of previous MI (consider aortic stenosis if LVH/LBBB)
- Then use clinical assessment and ECG findings to estimate the likelihood of CAD using NICE tool:
- If >90% treat as stable angina
- If 61-90%, coronary angiography is indicated
- If 31-60% functional imaging is indicated
- SPECT myocardial perfusion scan, exercise echo, stress MRI
- If 10-30% CT calcium scoring is used
- If <10% investigate for another cause
What drugs are used to treat angina?
Symptomatic treatment:
- GTN spray + B-blocker or calcium inhibitor as first line
- Combination therapy, or nicorandil for refractory disease
Secondary prevention:
- Statin
- Low dose aspirin
- ACE inhibitor if co-morbid diabetes
What combination therapy is used for refractory disease (doesn’t respond to the 1st line treatment - in this case of GTN spray and b-blocker or calcium channel blocker) of angina?
What shouldn’t never be used?
B-blockers and dihydropyridines such as amlodipine are the combination used
NEVER combine a rate-limiting calcium channel blocker and a B-blocker, this can cause asystole (heart stops beating)
How should nitrates be used to treat angina?
Mechanism of action?
Side effects?
- Sub-lingual spray is first line for symptom relief
- spray under tongue, wait 5 minutes and spray again. If pain after 10 minutes call 999
- Can be used prior to performing activities that provoke angina
- They cause marked venorelaxation, thus reducing pre-load on the heart
- This can cause venous pooling on standing, thus can cause postural hypotension and dizziness
- They also affect large muscular arteries, reducing aaortic pressure and cardiac afterload, as well as dilating coronary vessels
- Decreased pre-load and after-load decreases the oxygen requirement of the myocardium and coronary vasodilation leads to increased oxygen delivery
How do B-blockers treat angina? - mechanism of action
Side effects?
- ß1 adrenoceptors are found mainly on the heart, acting to increase heart rate and stroke volume
- ß2 adrenoceptors act to cause smooth muscle relaxation in many organs, e.g. the trachea
- In ischaemic heart disease, ß1 selective ß-blockers are used to reduce cardiac rate and force (reduce myocardial oxygen consumption) with little broncho-constrictive effect as possible
- They also have an anti-hypertensive effect by reducing cardiac output, and decrease renin release from juxta-glomerular cells
- They also have class two anti-arrhythmic effects
Side effects:
- Bronchoconstriction: contradiction in asthma, caution in COPD
Cardiac depression/bradycardia: can be critical if combined with other rate limiting agents - Hypoglycaemia: impair the sympathetic warning signs of hypo’s
- Fatigue
What are types of calcium channel blockers? -examples
How do they work?
Side effects?
- Dihydropyridines (amlodipine/nifeipine) or rate-limiting agents (verapamil/diltiazem)
- All work to prevent smooth muscle contraction, reducing afterload and causing coronary vasodilation
- The rate-limiting agents also act on cardiac calcium channels in the AV node to control heart rate, exhibiting class IV anti-arrhythmic effects
- Side effects are:
- flushing
- headache
- Ankle swelling
- Constipation (GI smooth muscle inhibition)
What is Nicorandil and how does it work?
- Causes marked vasodilation
- It is combinded NO donor and also an activator of ATP-sensitive K-channels on vascular smooth muscle cells, leading to hyperpolarisation
What is the framingham risk score?
The Framingham Risk Score is a gender-specific algorithm used to estimate the 10-year cardiovascular risk of an individual.
Assessment for primary prevention of CHD
What is QRISK 2?
QRISK2 (the most recent version of QRISK) is a prediction algorithm for cardiovascular disease (CVD) that uses traditional risk factors (age, systolic blood pressure, smoking status and ratio of total serum cholesterol to high-density lipoprotein cholesterol) together with body mass index, ethnicity, measures of deprivation, family history, chronic kidney disease, rheumatoid arthritis, atrial fibrillation, diabetes mellitus, and antihypertensive treatment.
(better than framingham)
What ECG changes may develop during an exercise stress test for patient with angina?
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
Give symptoms for acute pulmonary oedema as well
- Dysponea (SOB)
- Paraxysmal noctural dysponea
- Orthopnea (SOB when lying down): due to increased venous return on lying down, and can be measured objectively by number of pillows required to sleep
- Cough: producing frothy, blood stained sputum
Acute presentation:
- Severe dyspnoea
- Productive cough
- Anxiety and perspiration
- Cheyne-Stokes respiration in LVF: cycling apnoea/hyperventilation due to impaired response of respiratory centre to CO2
Describe the pathophysiolgy of pulmonary oedema
(not an objective)
- Pulmonary oedea is due to an increase in fluid in the alveolar wall (pulmonary interstitium), which then affects the interstitial spaces
- The most common cause is left ventricular failure, which causes increased pressure in the alveolar capillaries and leakage of fluid into the interstitium
- This leads to subjective dyspnoea, but can remain stable for some time
- Severe LVF causes leakage of fluid from the interstitium into the alveolar spaces, leading to a severe acute impairment of respiratory function
- Capillary rupture can lead to leakage of red cells also, which are up taken by macrophages and broken down: macrophages containing iron pigment in the alveoli/interstitium are thus termed ‘heart failure cells’
What are the common causes of pulmonary oedema?
- Increased capillary pressure:
- Cardiogenic: LVF, valve disease, arrhythmias, ventricular septal defect, cardiomyopathy, negatively inotropic drugs
- Pulmonary venous obstruction
- Iatrogenic fluid overload
- Increased capillary permeability
- Acute respiratory distress syndrome (ARDS)
- Infection: pneumonia/sepsis
- Disseminated intravascular coagulation
- Inhaled toxins
- Reduced plasma oncotic failure
- Renal/liver failure: hypoalbuminaemia
- Lympathic obstruction:
- Tumour/parasitic infection
- Others:
- Neurogenic: raised ICP/head injury
- PE
- Altitude
What are the clinical feature on examination of pulmonary oedema?
- Tachypnoea
- Tachycardia, with gallop rhythm
- Raised venous pressure
- Peripheral shutdown
- Widespread crackles/wheezes on auscultation
What are differiential diagnosis for pulmonary oedema?
- If no cardiac cause for pulmonary oedema is present, Acute respiratory distress syndrome should be suspected
- Chest infection may similarly produce a cough but is less likely to give pink frothy sputum and breathlessness
- Pulmonary embolism typically presents with pleuritic chest pain, cough and shortness of breath
Outline the general principles of management of pulmonary oedema due to acute/decompensated heart failure
- Sit patient upright, administer 100% oxygen
- IV diamorphine 1.25-5mg
- IV furosemide 40mg-80mg
- GTN spray 2 puffs sublingual (unless systolic BP <90)
- Continue necessary investigations and history as above
- If SBP >100, start an IV infusion of nitrate
- Consider non-invasive ventilation (e.g. CPAP) if not improving
- If SBP <100, treat as cardiogenic shock, alert ICU
- May require invasive ventilation
What investigations would you do in a patient with acute pulmonary oedema?
What would you expect to find?
- ABG:
- Initial type 1 respiratory failure due to hyperventilation, with later type 2 respiratory failure due to impaired gas exchange
- Bloods:
- FBC, U&E, glucose, D-dimer, CRP
- CXR:
- diffuse haziness (‘bat wing oedema’) with Kerley B lines and upper zone vessel enlargement, cardiomegaly pleural effusions
- ECG:
- tachycardia, arrhythmia, signs of a cardiac cause
- Echocardiography:
- to demonstrate a cardiac cause, e.g. MI/valvular disease