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Cardiology Flashcards

1
Q

Characteristics of myocardial infarction chest pain

A

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

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2
Q

Characteristics of aortic dissection chest pain

A

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

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3
Q

Characteristics of pleural disease chest pain

A

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

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4
Q

Characteristics of oesophageal disease chest pain

A

Retrosternal, dyspepsia, dysphagia
Exacerbated on bending over/lying supine
Oesophageal spasm can be relieved by GTN in 20mins, as oppose to 2mins with angina

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5
Q

Characteristics of MSK disease chest pain

A

E.g. costochondritis
Severe, associated with local tenderness
Worse with certain movements
History of trauma

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6
Q

Pathology of acute coronary syndrome

A

Atheromatous plaque formation in the coronary arteries
Fissuring/ulceration of the plaque leading to platelet aggregation
Localised thrombosis, vasoconstriction, distal thromboembolism
Myocardial ischaemia

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7
Q

Unstable angina definition and pathology

A

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

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8
Q

Describe the different patterns of acute MI

A 
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
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9
Q

Diagnosis of MI

A

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)

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10
Q

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?

A

Supplies RA, RV, posterior septum
Supplies AVN in 80% and SAN in 60%
Posterior/inferior MI
Leads II, III, aVF

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11
Q

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?

A

Circumflex and left anterior descending arteries
Massive anterio-lateral MI
Leads I, aVL, V5/V6

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12
Q

What areas does the circumflex artery supply, and where would a resulting occlusion cause an MI? What ECG leads would this be shown in?

A

Supplies LA, LV
Lateral MI
Leads I, aVL, V5/V6

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13
Q

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?

A

Supplies LV and anterior septum
Antero-septal MI
Leads V1-4

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14
Q

Changes to a necrotic area post-MI

A

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

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15
Q

What is death in IHD usually due to

A

VF

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16
Q

Acute coronary syndrome symptoms

A

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)

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17
Q

Acute coronary syndrome on examination:

A

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)

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18
Q

Differential diagnoses of chest pain

A

Cardiac: coronary artery spasm, pericarditis, myocarditis, aortic dissection, angina, MI
Non-cardiac: PE, pneumothorax, oesophageal disease, mediastinits, costochondritis, trauma

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19
Q

Acute coronary syndrome investigations

A

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

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20
Q

Changes in troponin in acute coronary syndrome

A

rise 4-8h after onset of symptoms
24h = peak
detectable for 10d
Raised in critically unwell patients with non-cardiac causes

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21
Q

ST changes in a non-reperfused STEMI

A

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

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22
Q

Immediate complications of acute MI

A

Arrhythmias: VT and VF common with reperfusion
AF
Brady/AV block if SAN/AVN affected

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23
Q

Short term complications of acute MI

A

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

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24
Q

Long term complications of acute MI

A

Heart failure: IHD –> LHF –> RHF
Dressler’s syndrome: immune-mediated pericarditis, high ESR, anti-myocardial antibodies
Ventricular aneurysm formation

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25
Define angina
Episodic pain that takes place when there is increased myocardial demand, usually upon exertion, in the presence of impaired perfusion by blood
26
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
27
Most common cause of stable angina
Low flow in atherosclerotic coronary arteries | Stenosis >70% in main coronary artery
28
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
29
Atheroma pathology
Specific degenerative disease affecting large/medium arteries Thickening & hardening = atherosclerosis Reduces tissue perfusion; predisposes to thrombus and aneurysm formation
30
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
31
Atheroma risk factors
``` >Age Male Family history (IHD<50) Smoking High fat, low fresh fruit + veg diet Obesity (abdominal) Hypertension Hyperlipidaemia DM ```
32
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
33
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 ```
34
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
35
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')
36
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 ```
37
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
38
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
39
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.
40
Congestive cardiac failure definition
Right heart failure that results from pre-existing heart failure
41
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
42
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
43
Left heart failure presentation
Fatigue, exertional dyspnoea, paroxysmal nocturnal dyspnoea, orthopnoea Cardiomegaly, displaced apex beat 3rd heart sound, gallop rhythm if tachycardic Bibasal course crackles
44
Right heart failure presentation
Fatigue, breathlessness, anorexia/nausea (hepatomegaly), pitting oedema, raised JVP, ascites, pleural effusions Cardiomegaly, gallop rhythm
45
Cardiac cachexia presentation
Hepatomegaly (nausea & decreased appetite) and increased metabolic demands leading to potentially life-threatening weight loss
46
NYHA classification of CCF
Stage I: disease present, no dyspnoea with normal activity Stage II: dyspnoea with normal activity Stage III: limiting dyspnoea Stage IV: dyspnoea at rest
47
CCF investigations
Bloods: FBC, LFTs, U&Es, TFTs, cardiac enzymes BNP: normal level excludes heart failure CXR: cardiomegaly and pulmonary oedema ECG: signs of ischaemia, hypertension, arrhythmias Echo: if ECG/BNP are abnormal. Gold-standard for diagnosis (ejection fraction <45%) Cardiac MRI Cardiac catheterisation: measure pressures Functional testing: Stress MRI/echo
48
Infective valvular disease pathology
Left-sided heart valves are more commonly the site of endocarditis (bacterial/fungal) Staph. aureus, Strep. Candida albicans Inflammation leads to collagen exposure and thrombus formation Post-inflammatory scarring, long-term functional impairment
49
Rheumatic valvular disease pathology
Rheumatic fever: immune disorder in children following tonsillitis/pharyngitis caused by group A beta-haemolytic strep (GAS). GAS antibodies cross-react with cardiac antigens to cause self-limiting myocarditis/pericarditis Damage heals by progressive fibrosis of valve leaflets and chordae tendinae Shrunken, fibrotic valves with secondary calcification 'Post-inflammatory scarring' if no rheumatic fever
50
Ischaemic valvular disease pathology
Mitral regurgitation caused by papillary muscle dysfunction post-infarction
51
Causes of mitral stenosis
Post inflammatory scarring | Rheumatic fever history in >50%
52
Mitral stenosis pathophysiology
LA unable to empty --> pulmonary hypertension LA becomes dilated and hypertrophied Pulmonary hypertension --> RHF 'cor pulmonale' AF develops due to muscular hypertrophy
53
Mitral stenosis presentation
``` Dyspnoea & haemoptysis: pulmonary HTN Fatigue, weakness, oedema: RHF Palpitations: secondary AF Malar flush: plum-red discolouration of cheeks due to vascular stasis Weak pulse, or irregularly irregular AF Raised JVP: RHF Left parasternal heave: RV hypertrophy Auscultation ```
54
Mitral stenosis presentation
Dyspnoea & haemoptysis: pulmonary HTN Fatigue, weakness, oedema: RHF Palpitations: secondary AF Malar flush: plum-red discolouration of cheeks due to vascular stasis Weak pulse, or irregularly irregular AF Raised JVP: RHF Left parasternal heave: RV hypertrophy Auscultation: mid-diastolic murmer, loud 1st sound, opening snap
55
Causes of mitral regurgitation
Post-inflammatory scarring/rheumatic Post-infarction papillary muscle dysfunction LV dilation Mitral prolapse: floppy mitral valve syndrome
56
Mitral regurgitation presentation
Palpitations: increased stroke volume/AF Dyspnoea/orthopnoea: pulmonary HTN Fatigue Features of RHF/CCF Laterally displaced apex beat with systolic thrill Auscultation: pansystolic murmur at apex radiation into the axilla. Soft 1st sound + prominent 3rd sound Signs of LHF/RHF develop later into disease AF less common
57
Causes of aortic stenosis
Calcification of congenital bicuspid valve Post-inflammatory scarring/rheumatic fever Senile calcific degeneration
58
Aortic stenosis pathophysiology
``` Progressive outflow obstruction leads to left ventricular hypertrophy, may lead to angina Risk of sudden cardiac death due to arrhythmias Poor prognosis (2-3y) without surgical intervention ```
59
Aortic stenosis presentation
Exercise induced syncope, angina, dyspnoea Pulse: small volume, slow rising carotid pulse BP: narrow pulse pressure (small stroke volume) Palpation: normal apex beat (LVH but no dilation), systolic thrill in aortic area, thrusting apex beat Auscultation: ejection systolic murmer with crescendo, radiates to carotids, S2 soft Signs of LVF, then CCF
60
Causes of aortic regurgitation
Post-inflammatory scarring Infective endocarditis Senile calcific degeneration Dilation of aortic root due to inflammatory disease (syphilis, aortic stenosis)
61
Aortic regurgitation presentation
Usually asymptomatic until acute LVF Angina pectoris (low diastolic BP), dyspnoea Bounding/collapsing pulse Wide pulse pressure Auscultation: early diastolic murmer with decrescendo Signs of LVF Quinke's sign: capillary pulsation in nail beds De Musset's sign: head nodding with each heartbeat Duroziez's sign: murmer on femoral arteries if pressure applied distally Pistol shot femorals: sharp bang in time with heartbeat if femorals auscultated
62
Common causes of right sided valve disease
Post-inflammatory scarring in rheumatic heart disease, endocarditis associated with IVDUs Carcinoid syndrome may lead to pulmonary stenosis
63
Tricuspid stenosis presentation
Symptoms of RHF Pre-systolic liver thrill Mid-diastolic murmur
64
Tricuspid regurgitation presentation
Symptoms of RHF Systolic liver thrill Pan-systolic murmur Classic in cor pulmonale
65
Pulmonary stenosis presentation
Symptoms of RHF RV heave Ejection systolic murmur
66
Pulmonary regurgitation presentation
Usually asymptomatic Diastolic murmur Can occur secondary to pulmonary hypertension
67
Who is at risk of infective endocarditis
Patients with a cardiac structural abnormality: insidious onset, caused by GI/skin commensals that cause bacteraemia, then become enmeshed in platelet aggregates on abnormal endocardium Patients with structurally normal heart valves: acute fulminating presentation with pathogens that directly invade the valve (IVDUs, post-cardiac surgery, post-septicaemia)
68
Most common organisms causing infective endocarditis
Strep. viridans Staph. aureus Strep. epidermis
69
Infective endocarditis presentation
Pyrexia & a new murmur is IE until proven otherwise Insidious illness: malaise, lethargy, anorexia, arthralgia Distal infarction/AKI (immune complex deposition)
70
Infective endocarditis presentation
``` Pyrexia & a new murmur is IE until proven otherwise Insidious illness: malaise, lethargy, anorexia, arthralgia Distal infarction/AKI (immune complex deposition) Microscopic haematuria (70%) Splenomegaly (40%) Osler's nodes (15%) Clubbing (10%) Splinter haemorrhages (10%) Roth spots (5%) Janeway lesions Petechial rash Digital infarcts ```
71
Infective endocarditis investigations
Bloods: FBC, CRP/ESR (raised), U&E Cultures x3 at different times Urinalysis: proteinuria & microscopic haematuria ECG: MI due to emboli/conduction defects CXR: evidence of heart failure, abscesses, emboli Transthoracic echo: negative echo doesn't rule out IE
72
Infective endocarditis Duke's major and minor criteria
MAJOR +ve culture: typical organism in 2 cultures Endocardial involvement on echo: vegetations, abscesses, new regurg. MINOR Predisposition Fever >38 Vascular/immunological signs Culture/echo +ve not sufficient for major Diagnosis = 2 major OR 1 major + 3 minor
73
Acute infective endocarditis morphology
Bacterial proliferation in the valve leads to necrosis of valve tissue, rapid perforation of valves, acute cardiac failure
74
Subacute infective endocarditis morphology
Gradual onset destruction of valves Stimulation of thrombus formation leads to systemic embolisation Persistent low grade inflammation leads to immunological phenomena
75
Infective endocarditis complications
``` Systemic emboli Pulmonary abscess in right sided disease Valvular incompetence CCF glomerulonephritis ```
76
What pathologies can a T wave inversion represent?
STEMI/NSTEMI Ventricular hypertrophy: in leads looking at the involved ventricles BBBB Digoxin (also sloped ST segment)
77
What can ST elevation indicate
``` STEMI Myocardial injury (e.g. pericarditis) ```
78
What can ST depression indicate
NSTEMI | Sign of ischaemia rather than infarction
79
RBBB on an ECG
Septum depolarisation: R wave in V1, small Q wave in V6 Excitation of left ventricle: S wave in V1, R wave in V6 Delayed excitation of right ventricle: R1 in V1, deep S wave in V6 RBBB best seen in V1: RSR1 + T wave inversion MarroW: M in V1, W in V6
80
RBBB differentials
Underlying ASD/PE
81
LBBB on an ECG
Septum depolarisation: Q wave in V1, R wave in V6 Excitation of right ventricle: small R wave in V1, S wave in V6 Delayed excitation of left ventricle: S wave in V1, another R wave in V6 T wave inversion in lateral leads LBBB best seen in V6: broad 'M' complex + T wave inversion WilliaM: W in V1, M in V6
82
LBBB differentials
Asymptomatic: consider aortic stenosis | Consider MI
83
PR interval >220ms
Heart block
84
Significant ST elevation
>2mm in a chest lead >1mm in a limb lead on 2 leads
85
Prolonged QT interval causes
Drugs, electrolyte abnormalities | May lead to ventricular tachycardia
86
Cardiac axis deviation
Right axis deviation: RVH | Left axis deviation: LVH
87
Tall R waves
``` V1 = RVH V6 = LVH ```
88
Clockwise rotation
Transition point (where R & S waves are equal, thus at right angles to depolarisation) shifts from V3/4 (normal) to V5/6
89
First degree heart block ECG sign and indications
SAN depolarisation spreads to ventricles with delay PR interval >0.22s Indicates: coronary artery disease, acute rheumatic fever, electrolyte disturbances, digoxin toxicity
90
Second degree heart block variations
'Mobitz type 2' phenomenon: Constant PR interval, sometimes atrial contraction without ventricular contraction 'Wenckebach'/'Mobitz type 1' phenomenon: Progressive PR lengthening until an atrial beat isn't conducted, then repeats 2:1/3:1 conduction: 2/3x more P waves as QRS complexes (may need pacing)
91
Third degree/complete heart block
Normal atrial contraction P wave dissociated from QRS complex Ventricles excited by a 'slow escape mechanism' from a depolarising focus within the ventricles = wide QRS Causes: MI/conducting tissue disease
92
Sinus bradycardia associations
HR<60bpm | Athletic training, syncope, hypothermia, hypothyroidism, immediately following an MI
93
Sinus tachycardia associations
HR>100bpm | Exercise, fear, pain, haemorrhage, thyrotoxicosis
94
P waves in supraventricular rhythms
Sinus = normal Atrial = abnormal Junctional (AVN) = absent
95
Bradycardia physiology
Rhythm controlled by wherever is spontaneously depolarising quickest (usually SAN at 70bpm) SAN failure results in atrial focus or AVN control (50bpm) If these fail or blocked conduction --> ventricular focus (30bpm) = escape rhythms Singular/normal rhythm return = escape beats
96
Extrasystole physiology
Extra beat Extrasystole comes early wheras escape beat comes late If they occur early in T wave of preceding beat they can induce VF
97
Tachycardia physiology
Find P wave to determine origin Atrial (>150bpm) P waves may be superimposed on previous T waves >200bpm = atrioventricular block - some P waves not followed by QRS complexes Ventricular tachy = wide QRS in all 12 leads. May require cardioversion
98
Ventricular fibrillation on ECG and presentation
No QRS identified, disorganised ECG | Unconscious patient, manage as cardiac arrest
99
Atrial fibrillation on ECG and presentation
Irregular baseline with no P waves Irregular ventricular contraction 450-600 atrial contractions per minute Asymptomatic, dyspnoea, palpitations, syncope, chest pain, stroke/TIA 24h ambulatory ECG to detect paroxysmal AF
100
Atrial flutter on ECG
Atrial rate >250/min | Saw tooth baseline
101
Hyperkalaemia on an ECG
Tall tented T waves, widened QRS, prolonged PR interval
102
Hypokalaemia on an ECG
T wave flattening | U wave on the end of the T wave
103
Hypercalcaemia on an ECG
QT shortnening
104
Hypocalcaemia on an ECG
QT prolongation
105
Wolff-Parkinson-White sydrome
Short PR interval QRS delta wave Sinus rhythm, right axis deviation Can cause paroxysmal tachycardia

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