Cardiology Flashcards
Characteristics of myocardial infarction chest pain
Crushing, gripping, heavy
Retrosternal
Radiates to neck, shoulder, jaw (rarely teeth, back, abdomen)
Associated with parathesia/heaviness in one/both arms
Provoked by exercise, relived by nitrites
Associated with dyspnoea, nausea and sweating
Comes on in minutes
Levine’s sign +ve
Characteristics of aortic dissection chest pain
Severe central pain, radiating to the back and down the arms
Patient may be shocked + neurological symptoms secondary to spinal cord hypoperfusion
Distal ischaemia/absent peripheral pulses
Comes on in seconds
ECG may be normal
More common in Marfan’s/hypertensives
Characteristics of pleural disease chest pain
Localised sharp pain exacerbated with deep breathing and coughing
Not central, dyspnoea, cyanosis
Associated with costo-chondral tenderness
Pain in shoulder tip suggestive of diaphragmatic pleural irritation
Characteristics of oesophageal disease chest pain
Retrosternal, dyspepsia, dysphagia
Exacerbated on bending over/lying supine
Oesophageal spasm can be relieved by GTN in 20mins, as oppose to 2mins with angina
Characteristics of MSK disease chest pain
E.g. costochondritis
Severe, associated with local tenderness
Worse with certain movements
History of trauma
Pathology of acute coronary syndrome
Atheromatous plaque formation in the coronary arteries
Fissuring/ulceration of the plaque leading to platelet aggregation
Localised thrombosis, vasoconstriction, distal thromboembolism
Myocardial ischaemia
Unstable angina definition and pathology
Angina occuring at rest, or sudden increased frequency/severity of existing angina
Caused by fissuring of plaques, thus risk of total vessel occlusion –> AMI
Can be ischaemic ST depression but no troponin rise
Describe the different patterns of acute MI
Regional MI (90%): infarct of 1 segment of ventricular wall (thrombus formation on an atheromatous plaque) Regional subendocardial infarction: lysis of thrombus/strong collateral supply limits infarct to subendocardial zone Circumferential subendocardial infarction (10%): general hypoperfusion of coronary arteries (hypotensive episode) in artherosclerotic arteries - no Q wave
Diagnosis of MI
Elevation in serum cardiac troponin levels
ST elevation/new LBBB = STEMI (generally full thickness myocardial infarct)
No ST elevation/LBBB, no Q waves = NSTEMI (partial thickness lesion)
What areas does the right coronary artery supply, and where would a resulting occlusion cause an MI? What ECG leads would this be shown in?
Supplies RA, RV, posterior septum
Supplies AVN in 80% and SAN in 60%
Posterior/inferior MI
Leads II, III, aVF
What areas does the left coronary artery supply, and where would a resulting occlusion cause an MI? What ECG leads would this be shown in?
Circumflex and left anterior descending arteries
Massive anterio-lateral MI
Leads I, aVL, V5/V6
What areas does the circumflex artery supply, and where would a resulting occlusion cause an MI? What ECG leads would this be shown in?
Supplies LA, LV
Lateral MI
Leads I, aVL, V5/V6
What areas does the left anterior descending artery supply, and where would a resulting occlusion cause an MI? What ECG leads would this be shown in?
Supplies LV and anterior septum
Antero-septal MI
Leads V1-4
Changes to a necrotic area post-MI
0-12h: loss of oxidative enzymes
12-24h: infarct pale & blotchy, intercellular oedema
24-72h: infarct area excites acute inflammatory response - soft and yellow with neutrophilic infiltration
3-10d: vascular granulation tissue organisation
10d-months: collagen deposition, infarct replaced by collagenous scar
What is death in IHD usually due to
VF
Acute coronary syndrome symptoms
Severe crushing chest pain >20mins
Not relieved by 3x GTN at 5min intervals
Radiates to left arm, neck, jaw
Dyspnoea, nausea, fatigue, perspiration, palpitations, angor animi
Silent infarct: presents without chest pain (elderly and diabetic)
Acute coronary syndrome on examination:
Sympathetic activation: tachy, HTN, pallor, sweating
Vagal stimulation: brady, vomiting
Myocardial impairment: hypotension, narrow pulse pressure, raised JVP, basal creps, 3rd heart sound (blood hitting ventricle wall)
Tissue damage, low grade pyrexia
Later: pericardial rub & peripheral oedema, pansystolic murmur (papillary muscle rupture/ventriculo-septal defect)
Differential diagnoses of chest pain
Cardiac: coronary artery spasm, pericarditis, myocarditis, aortic dissection, angina, MI
Non-cardiac: PE, pneumothorax, oesophageal disease, mediastinits, costochondritis, trauma
Acute coronary syndrome investigations
ECG: continuous to identify arrhythmias
Bloods: FBC, U&E, clotting, glucose (lowered), lipids (raised), cardiac enzymes (troponin)
CXR: consider for evidence of cardiomegaly, pulmonary oedema, widened mediastinum in dissection
Transthoracic echo: if in doubt
Changes in troponin in acute coronary syndrome
rise 4-8h after onset of symptoms
24h = peak
detectable for 10d
Raised in critically unwell patients with non-cardiac causes
ST changes in a non-reperfused STEMI
5mins: tall pointed T waves
30mins: ST elevation
2+h: T wave inversion, Q waves develop
Days: ST returns to normal
Weeks: T wave may return to normal, Q wave remains
Immediate complications of acute MI
Arrhythmias: VT and VF common with reperfusion
AF
Brady/AV block if SAN/AVN affected
Short term complications of acute MI
Pulmomary oedema: left heart failure –> extravasation of low-protein fluid into alveolar sacs –> frothy blood stained sputum. pO2 + pCO2 fall, then pCO2 rises.
Cardiogenic shock
Thromboembolism: emboli from inflamed endocardium to brain, kidney, gut, lower limbs
Venticulo-septal defect: left-right shunt
Ruptured chordae tendinae: mitral valve incompetence (LA–>LV)
Rupture of ventricular wall: haemopericardium, cardiac tamponade
Long term complications of acute MI
Heart failure: IHD –> LHF –> RHF
Dressler’s syndrome: immune-mediated pericarditis, high ESR, anti-myocardial antibodies
Ventricular aneurysm formation
Define angina
Episodic pain that takes place when there is increased myocardial demand, usually upon exertion, in the presence of impaired perfusion by blood
Causes of myocardial ischaemia
Reduced perfusion: atheroma, embolus, thrombosis, spasm, inflammation of coronary arteries, hypotension
Reduced blood oxygenation: anaemia, carboxyhaemoglobinaemia
Increased tissue demands: Increased CO, cardiac hypertrophy
Most common cause of stable angina
Low flow in atherosclerotic coronary arteries
Stenosis >70% in main coronary artery
Arteriosclerosis pathology
Non-specific thickening and hardening of the walls of arteries causing a loss of contractility and elasticity, and decreased blood flow
Cause: often prolonged hypertension in smaller arteries
Atheroma pathology
Specific degenerative disease affecting large/medium arteries
Thickening & hardening = atherosclerosis
Reduces tissue perfusion; predisposes to thrombus and aneurysm formation
Pathology of atheroma formation
Endothelium damage allows entry of LDLs into the intima
Lipid taken up by intima macrophages, accumulates as able to bypass normal receptor mediated uptake, forms fatty streak
Free lipids released into intima
Macrophages stimulate cytokines –> collagen deposition by inflammatory cells
Pressure atrophy of the media and disruption of elastic lamina
Increased collagen secretion forms fibrous cap on plaque
Endothelium ulcerates allowing platelet aggregation
Atheroma risk factors
>Age Male Family history (IHD<50) Smoking High fat, low fresh fruit + veg diet Obesity (abdominal) Hypertension Hyperlipidaemia DM
Variants of stable angina
Decubitus angina: precipitated by lying down as increased venous return to the heart, associated with LVF
Variant/Prinzmetal’s angina: occurs as a result of coronary artery spasm with ST elevation
Angina investigations
Clinical assessment Bloods: FBC, glucose, lipids, TFTs Resting 12-lead ECG Consider aortic stenosis if LVH/LBBB Stress lead ECG NICE tool to assess likelihood of CAD
Heart anatomy
Anterior: RV, RA, LV
Tricuspid valve: RA –> RV
Mitral valve: LA –> LV
Major branches of aortic arch: brachiocephalic trunk (common carotid/right subclavian); left common carotid; left subclavian
Pulmonary oedema pathophysiology
Increased fluid in pulmonary interstitium
Common cause = LVF
Subjective dyspnoea
Severe LVF causes leakage of fluid from interstitium into alveolar spaces
Capillary rupture can lead to leakage of red cells –> taken up by macrophages and broken down (therefore macrophages containing iron pigment in the alveoli termed ‘heart failure cells’)
Pulmonary oedema presentation
Dyspnoea Paroxysmal nocturnal dyspnoea Orthopnoea Cough: frothy blood stained sputum Anxiety + perspiration Cheyne-Stokes Tachypnoea Tachycardia Raised JVP Peripheral shut down Widespread creps & wheeze
Pulmonary oedema investigations
ABG: initial type 1 failure due to hyperventilation. Later type 2 failure due to impaired gas exchange
Bloods: FBC, U&Es, glucose, D-dimer, CRP
CXR: diffuse haziness (‘batwing oedema’), Kerley B lines, upper zone vessel enlargement, cardiomegaly, pleural effusion
ECG: tachycardia, arrhythmia, signs of cardiac cause
Echo: demonstrate cardiac cause
Pulmonary oedema causes
Increased capillary pressure: cardiogenic (LVF, valve disease, arrhythmias, VSD, cardiomyopathy, negatively inotropic drugs), pulmonary venous obstruction, iatrogenic fluid overload
Increased capillary permeability: ARDS, infection, DIC, inhaled toxins
Reduced plasma oncotic failure: hypoalbuminaemia due to liver/renal failure
Lymphatic obstruction: tumour, parasite
Neurogenic: raised ICP
PE
Altitude
TIMI score for likelihood of ischaemic events or mortality in patients with unstable angina or non–ST-segment elevation myocardial infarction (NSTEMI)
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.
Congestive cardiac failure definition
Right heart failure that results from pre-existing heart failure
Starling’s law
The stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant
Neurohormonal adaptation in chronic heart failure
Reduced cardiac output activates SNS and RAAS
RAAS activation –> vasoconstriction (increasing afterload), and Na+/H2O retention (increasing preload)
SNS activation: maintains cardiac output by increasing contractility, but prolonged stimulation leads to myocyte apoptosis and necrosis
Atrial natriuretic peptide (ANP): released in response to atrial stretch –> acts to antagonise effects aldosterone
Desensitization of the myocytes in the SNS and the ventricles enlarge
