Cardiovascular Flashcards
Ischaemic Heart Disease: stable angina focus
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Condition due to narrowing or blockage of coronary arteries, most commonly due to atherosclerosis, resulting in a mismatch between myocardial oxygen supply and demand
Can manifest as:
- Stable Angina : only happens on exertion, rest or GTN stop symptoms
- ACS (unstable angina, STEMI, NSTEMI)
CLINICAL FEATURES
Angina- retrosternal chest pain, may radiate to left arm, neck or jaw. Angina is 1) chest pressure or squeezing lasting several minutes, 2) provoked by exercise or emotional stress, and 3) relieved by rest or glyceryl trinitrate.
For stable angina the examination is normal
INVESTIATIONS
ECG- in IHD will show Q wave which are negative deflections before QRS begins. Do troponin after ECG
1st investigations: resting ECG, bloods (glucose, lipids, FBC as RF for IHD)
1st line imaging for stable angina: Contrast enhanced CT coronary angiogram (to visualise coronary arteries and determine viability of PCl)
Cardiac Stress Testing (ECG whilst exercise)
MANAGEMENT
Lifestyle educations + BAGS
If no angina: just education, antiplatelet (aspirin/clopidogrel) and statin
If angina symptoms: BAGS
- Beta blocker (bisprolol or atenolol) OR CCB like verapimil or diltiazem- can only use both if one isnt working and have to use non cardioselective CCB like nifendimpine or amlodipine. If cant tolerate these CCB then ivabradine, isosorbide mononitrate, nicorandil or ranolazine
- Antiplatelet (aspirin or clopidogrel)
- GTN spray to stop angina attacks
- Statin
If cant control medically: PCl or CABG
Side effects of GTN
- Headaches
- Flushing
- Dizziness
- Hypotension
- Tachycardia
Acute coronary syndrome
-aetiology
-clinical features
-investigations
-management
-prognosis + complications
The term acute coronary syndrome (ACS) is applied to patients in whom there is a suspicion or confirmation of acute myocardial ischemia or infarction (sudden reduced blood flow to the heart). Non-ST-elevation myocardial infarction (NSTEMI), ST-elevation MI (STEMI), and unstable angina are the three traditional types of ACS.
Include : Unstable angina, NSTEMI, and STEMI
Indications of ACS to tell where the block is:
- Left Bundle branch block= down in V1 (W) and up in V5/6 (M) (WiLLiaM). Left bundle branch blocks are always pathological like MI, hypertension, aortic stenosis, cardiomyopathy or hyperkalaemia. If an LBBB is found investigation for ACS needed, if its an MI cause is usually anterior-anteroseptal MI
- Right Bundle Branch Block = MaRRoW. M/up in V1, W/up in V6. Can be normal due to old age, right ventricular hypertrophy or cor-pulmonale (inc right ventricular pressure). Right bundle bracnh in V1/Vs has rSr and scooped S complex, in V5/6 has a broad and deep S (so have QRS then scoops)
Clinical Features :
- Acute central chest pain: dull, squeezing/crushing, radiates to left chest, jaw, shoulder
- dyspnoea
- sweating
- Pallor
- Nausea and vomiting
- Dizziness and syncope
In diabetics it may be painless
Investigations:
1st: 12 lead ECG to check for STEMI (ST elevation over 2mm in V1-V6 or over 1mm in II,III,avF,avL with new LBBB or NSTEMI (ST depression + T wave inversion)
PAILi- (posterior-anterior-inferior-lateral) St elevations create reciprocal ST depressions in the next letter of mneumonic. every 15-30 mins in first 1hour
Urgent: Blood - cardiac troponin levels: show its a STEMI or NSTEMI. Repeat after 1-6 hours, they rise 3 hours after MI begins and stay raised for 10 days. CK-MB is raised for 3-4 days after infarction, but useful to check if theyve had a second reinfarction because troponin will stay high but CKMB wont.
MI Location
Anteroseptal MI: V1-4 affected, left anterior descending. Septal is V1-2, anterior is V1-4.
Lateral MI: I, avL, V5, V6, left circumflex
Inferior MI: II, III, avF, right coronary artery
Posterior: V7,V8,V9 ST elevation, ST depression in anterior leads and tall R waves in V1-2. left circumflex, or right coronary
If ST depression is deep and in many leads then = severe ischaamia, usually left anterior descending- gonna die
Management:
Acute ACS= MONA- morphine, oxygen if sats under 94%, nitrates (not if hypotensive), Aspirin 300mg
NSTEMI: calculate GRACE score
If Hb under 80g/L then transfusion of packed RBC’s
STEMI: FIRST Aspirin 300mg and then based on whether can get PCl within 2 hours
- If symptoms within 12h and can do a coronary angioplasty within 2h then:
Angiography,
Give: Prasugrel + unfractionated heparin + bailout glycoprotein 2b/3a inhibitor, angioplasty with drug eluting stent (AspirinPrasugrelUnfracheparinGlycoprotein)
If patient already on anticoagulent then clopidogrel instead of Prasugrel
If patient has pain or haemodynamic instability after then urgent CABG
Ideal insertion point for PCl (coronary angiplasty) is radial artery then femoral - If symptoms under 12h but PCl not possible in 2 hours then : Fibrinolysis route (A FAT : aspirin, fondaparinux, alteplase, ticagrelor )
Antithrombin like fondaparinux and then thrombolysis with alteplase
Give ticagrelor after this proceudure
If the fibrinolysis (altepase) is given then repeat ECG in 60-90 mins and tranfer or urgent cardiac angioplasty if ST elevation isnt resolved
-If after 12 hours then PCl if ongoing or cardiogenic shock
- If high bleeding risk swap Prasugrel for ticagrelor or ticagrelor for clopidogrel
NSTEMI/unstable angina
Aspirin 300mg and continue forever
Fondaparinux (activated antithrombin III). Dont give if immediate PCl is planned or if patient is a high bleeding risk use nother antithrombin or dose like swap to praugrel or ticagrelor or clopidogrel
THEN work out 6 month mortality GRACE score
- If low risk under 3% thn give ticagrelor with the lifelong aspirin (if high bleeding risk then clopidogrel) (total treatment = A F GRACE TA)
- If high risk (over than 3%) : PCl within 72 hours with drug eluting stent if needed, always give unfrationated heparin before PCl. Also give ticagrelor or prasugrel. A F GRACE HPClT
- If haemodynamically unstable: immediate PCl, unfractionated hparin with ticagrelor but NO FONDAPARINUX
+ PRASUGREL GOES WITH PCL
Long term management of MI
DABS
Dual antiplatelet therapy (aspirin + ticagrelor or clopidogrel) (clopidogrel if theyre already on an anticoag like warfarin)
ACEi (ramipril)
Beta Blocker (bisprolol) but can reduce awareness of hypoglycaemic events
Statin (primary prevention dose is 20mg, secondary prevention aka after MI is 80mg)
Cannot drive for 4 weeks
If had MI due to cocaine use then IV benzodiazepines like lorazepam
Prognosis
If patient has cardiogenic shock then 80% chance to die in a month.
Cardiogenic shock is when lung crackles head on auscultation because is a sign of pulmonary oedema due to heart failure
Killip class moretality classification system
- Killip class I: no signs of heart failure
-Killip class II: lung crackles + S3
-Killip class III: obvious pulmonary oedema (38% die in 30 days)
-Killip class IV: cardiogenic shock (tissue hypoperfusion, oliguria, systolic BP less than 90 with presentation of hypovolaemic shock)
Complication post MI:
Heart block: usually right coronary artery (infarction of AV node leads to loss of conduction for atria to ventricles)
Most common cause of death post MI:
Ventricullar fibrillation
What complications can ACS cause
MI can cause mitral regurgitation if the cords are ruptures so might see flash pulmonary oedema.
Can have abnormal s3+4 heart sounds if left ventricular aneurysm due to damage and weakening of the ventricular muscle. Patients will be breathless, tired and persistent ST elevation if its due to an MI.
Can lead to left ventricular thromboemolism which leads to other embolic strokes/blockages
s3- the left ventricle is larger than normal
s4- left ventrical is too stiff
Combined= left ventricle is larger than usual and stiff walls causing pulmonary congestion
Persistant ST elevation in V1-6
Left Ventricular free wall rupture
- raised JVp
-pulsus paradoxus - drop in BP over 10mmHg
- diminished heart sound
urgent pericardiocentesis and thoracotomy needed
What are the side effects of ramipril, and what class of drugs is it
ACEi
Side effects include:
Angioedema
Cough
High potassium (especially if using amiloride a potassium sparing diuretic)
1st dose causes hypotension
Cardiac arrest
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Sudden circulatory failure as loose systolic function
Four cardiac arrhythmias that cause :
- Ventricular fibrillation (shockable)
- Pulseless Ventricular tachycardia: sinus tachy but pulseless (shockable)
- Pulseless electrical activity: no pulse but sinus rhythm (non shockable)
- Asytole: non shockable
VT and VF usually caused by IHD and acute MI
Reversible causes: 4H+4T
hypoxia, hypothermia, hper/hypokalaemia, hypovolamia
thrombosis, tension pneumothorax, tamponade, toxins
CLINICAL FEATURES
Unresponsive patient
Not breathing
No pulse (no circulation)
INVESTIGATIONS
Continuous cardiac monitoring: find wherther the rhythm is shockable (VT and VF) or non-shockable (Asystole+PEA)
ECG after pulse returns
FBC- check if due to hypovolaemia
Serum elctrolytes- check if due to high or low potassium
MANAGEMENT
IF SHOCKABLE:
- unwitnessed attack
1) Defibrillate (shock)
2) CPR for 2 mins then assess rhythm
3) If no pulse then IV adrenaline 1mg after third shock and then every other cycle (3, 5, 7 etc) or 3-5 mins
4) If persisting after 3rd shock, give IV amiodarone 300mg (one off dose)
- witnessed attack (e.g patient on a monitor)
3 successive shocks (rather than 1 shock followed by CPR) - if cant achieve IV then drugs should be given via the intraosseous access in the proximal tibia
- if Torsades then give manesium
IF NON SHOCKABLE
1) CPR for 2 mins, then reassess
2) IV adrenaline 1mg ASAP (after 1st cycle), then every other cycle (or every 3-5 mins)
3) Atropine (once) if rate goes below 60bpm
AFTER RESCUSSCITATION:
o2 sats of 94-98%- give oxygen
IF DUE TO 4H + 4T
warm slowly if hypothermia
if hypo or hyperkalaemia, correct electrolytes
hypovolaemia give IV colloids, crystalloids and blood products
tamponade- pericardiocentesis
tension pneumothorax- aspiration or chest drain
Thromboembolism- treat as PE or MI
Toxin- antidote
PROGNOSIS
if sudden usually poor outcome
TO IMPROVE SURVIVAL RATE OUTSIDE OF HOSPITAL need early CPR, including compression only from bystanders
How is Left and Right axis deviation differentiated between
LAD = Lead 1 positive and avF negative (L in LAD is for Lead 1). A lad has no avFemales
RAD= Lead 1 negative and avF positive (if ur RAD u get females)
Cardiac Failure
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Inability of the cardiac output to meet the body’s demands, despite normal venous pressures. Usually over 65 years old
Heart failure categorised into:
1) Acute
2) Chronic
3) Low (cardiac) output state
4) High (cardiac) output state: normal heart unable to meet metabolic needs e.g. caused by anaemia, Beri-beri (thiamine deficiency), pregnancy, hyperthyroidism.
Left Heart Failure: can be systolic or diastolic.
- systolic : HFrEF when LVEF less than 40%.
Caused by dilated cardiomyopathy, arrythmias, myocarditis, IHD. Hear S3 usually due to mitral regurg, atria has more blood so when opens blood rapidly empties
- diastolic: HFpEF >50%, heart can’t relax and properly fill with blood. Causes: hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, constrictive pericarditis, cardiac tamponade. S4 is heard when atria trying to force more blood into stiff ventricle
Right Heart Failure:
secondary to Left heart
infarction
pulmonary hypertension
tricuspid regurgitation
Congestive Heart Failure: Left and right heart failure
CLINICAL FEATURES
LEFT HEART: dyspnoea, orthopnea, paroxymal nocturnal orthynopea, inspiratory bibasal crackles, prink frothy sputum due to pulmonary oedema, wheeze, cyanosis, S3 gallop rhythm. Features of Left more associated with LUNGS as blood comes from lungs and pumped to rest of body so if cant pump out moves back into lungs
Clinical features of high output:
HF with fluid overload, acute breathlessness but no pain, bilateral pitting oedema, elevated JVP
RIGHT HEART: swollen ankles, riased JVP, hepatomegaly , ascites, swollen because right heart takes used blood from body so if fails pushes back on that
INVESTIGATIONS:
BNP - raised in cardiac failure, sensitive test not specific as drugs can cause falsely lower such as ACEi, ARB, BB, diuretics, aldosterone antagonists. (BNP raised if has to pump harder due to failure so if have pressure lowering drugs heart load is eased so even if failing wont have to pump as hard)
Troponin raised
CRP raised
If suspect PE do D dimer
Transthroacic echocardiogram- DIAGNOSTIC TEST. done after BNP to confirm. Can calculate EF from this test. less than 40%= HF systolic, over 50% =HF diastolic
Chest X-ray: ABCDE
- alveolar shadowing (oedema)
- Kerley B lines (horizontal lines in lungs periphery that extend to pleural surface (can see extending to cardiophrenic angle). Thinkened interlobular septa for pulmonary oedema too
- Cardiomegaly
- Dilated upper lobe vessels (blood pushed back itno atria
- Effusion (pleural): see notching of costophrenic angles
ECG
ABG
Bloods- rule out anaemic, check for TFT as hyperthyroidism can lead to hypervolaemic hyponatraemia. Need fluid restriction
DIAGNOSIS
framingham criteria 2 majors and 1 minor
Majors- paroxymal nocturnal dyspnoea, bibasal crepitations, S3, cardiomegaly, increased central venous pressure, weight loss, neck vein distension, pulmonary oedema, HJP reflex.
Minor- bilateral ankle oedema, dyspnoea on exertion, tachycardia, decrease in vital capacity by 1/3, nocturnal cough, hepatomegaly, pleural effusion, tachycardia
MANAGEMENT
Acute HF
treat pulmonary oedema: sit patient up, oxygen, morphine, IV furosemide (loop diuretic, can cause hypokalaemia).
If patient in cardiogenic shock (hypotension): give inotropes (dobutamine). If doesnt work vasopressor (norepinephrine).
Only give nitrates if HF due to MR/AR or have hypertension
if RHF do fluid challenge
not responding- CPAP
Once stabilised
LVEF under 40% think SABA: SGLT2 (flozin), ACEi (ramipril), Beta blockr (bisprolol), aldosterone antagonist (spirinolactone)
If get gynaecomastia then eplerenone
LVEF over 40 then SGLT2 and consider all other medications
Interventions:
annual influenza and one time pneumococcal vaccine
Conservative management:
Daily weights, fluid restriction, catheter/fluid balance
PROGNOSIS
50% die in 2 years
NYHA Classification
Stage I: no limitation on activity
Stage II: ordinary physical activity causes breathlessness
Stage III: normal at rest but breathlessness for smaller tasks
Stage IV: symptoms at rest
What medication is contraindicated in heart failure
CCB like verapimil or diltiazem
Aortic Aneurysm
- aetiology: define, pathophysiology, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Focal dilatation of the abdominal aorta to >1.5x its normal diameter or >3cm
Primary event is loss of intima and loss of fibres from media (associated with high proteolytic activity and lymphocytic infiltration)
Aneurysms are dilation of all layers of the arterial wall
Often occur below renal arteries (infrarenal)
Affects Males 60-70
Screening populations are males over 65 with a single USS
Risk Factors: Smoking most important
FHx, older, male, connective tissue disorder like marfans, atherosclerosis, high cholesterol
CLINICAL FEATURES
Usually asymptomatic and only found incidentally on USS or CT.
If ruptured: life threatening
- severe, central abdominal pain radiates to back
- pulsatile and expansile abdomial mass
- signs of shock: hypotension + tachycardia
INVESTIGATIONS
Aortic Ultrasound: dont delay diagnosis and management of ruptured AAA while waiting because US wont tell u if ruptured
CT Angiogram: visualise ruptured AAA, only if haemodynamically stable
US Screening for men over 65 in UK
MANAGEMENT
Regular US surveillance
- If 3-4.4cm then every year
- If 4.5-5.4cm then every three months
Surgical management
Refer within 2 weeks to vascular surgery for repair if rapidly enlarging (more than 1cm per year) or 5.5cm+
if ruptured of symptomatic then urgent surgery. They will do an open repair or EVAR (endovascular aneurysm repair)
PROGNOSIS + COMPLICATION
Ruptured - patients usually dont reach theatre in time
Complications: Endo-leak if stent fails to exclude blood from aneurysm, presents asymptomatically on routine follow ups
Aortic Dissection
- aetiology: define, pathophysiology, classification, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Tear in the aortic wall intima, causes blood to from into a false lumen in the intima-media space. Can cause formation of a haematoma and rupture which occuludes vessels.
Normally ascending aorta
Normally 60-80 year olds, or marfans syndrome age 30-50 years (predisposed to aortic aneurysm and dissection)
Standford Classification
A: ascending aorta
B: Descending aorta (below left subclav artery)
DeBakey Classification
I- ascending and descending aorta (Stanford A+B)
II- only ascending aorta up to brachiocephalic artery (Stanford A)
III- only abdominal aorta distal to left subclav (Stanford B)
Risk Factors: Hypertension most important
other RF: trauma, marfans syndrome, smoking
CLINICAL FEATURES
- sudden and severe tearing chest pain
- Intercapsular pain radiating to the back
- aysmmetrical BP and pulse between limbs- usually arms: see weak or absent carotid, brachial or femoral. See radio-radial delay, radio-femoral delay
- Early diastolic murmur (aortci regurg): austin-flint murmur where mid diastolic best heard at the apex. Is a sign of severe aortic regurg
- focal neurological defiits - horners syndrome
-hypertension
-marfans syndrome or ehlers danlos syndrome signs
INVESTIGATIONS
1st CAP CT Angiogram: will visualise false lumen.
If unstable then Transoesophageal echocardiography
Chest X-Ray: widened mediasteinum
ECG- to rule out STEMI (always have to rule out for acute chest pain)
Tranthoracic echocardiography- see intimal flap and two lumens
Bloods - troponin to exclude MI
MANAGEMENT
Type A:
opioid + Beta blocker labetolol and surgery
Surgical management: ASS- aortic root replacement and surgery.
Type B:
uncomplicated : bed rest, IV beta blockers (labetolol) for lowering BP,opioid Analgesia (same as type A but no surgery)
complicated (end-organ ischaemia): IV labetelol, opioid and open surgery/endovascular repair
If hypotensive: IV fluids and analgesia, vasopressors (end in phrine or in)
PROGNOSIS
left untreated fatal in 50-60% within 24 hours
COMPLICATIONS
cardiac tamponade
aortic incompetence
aneurysmal rupture
myocardial infarction
What are the clinical features of Marfans syndrome and the pattern of inheritance
Tall and high arched palate
Pectus excavatum
Joint hypermobility
is autosomal dominant
Aortic Valve Disease
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
AORTIC STENOSIS : narrowing. ventricle to aorta is impared
Causes of aortic valve disease:
1) Aortic valve stenosis : calcification and fibrosis of aortic valve leaflets, pts over 65
2) Bicuspid aortic valve: fusion of 2/3 aortic valve leaflets (turbulent blood flow- more likely to calcify) , younger pts under 65. Associated with coarctation of the aorta (hypertension in adults, HF in infants, radio-femoral delay, mid-systolic murmur maximal over back)
3) Rheumatic fever : not common bcs ABs given from streptococcal phraryngitis
AORTIC REGURGITATION : doesnt close reflux from aorta to ventricle
Acute aortic valve disesase
- Infective endocarditis
- Aortic dissection type A
Chronic aortic valve disease
- congenital bicuspid aortic valve
- rheumatic heart disease
- aortic dilation form connective tissue disorders
CLINICAL FEATURES
1) AORTIC STENOSIS (ASS)
- Exertional syncope
- Angina/ chest pain
- Dyspnoea
SAD: syncope, angina, dyspnoea
- Narrowing pulse pressure (systolic + diastolic similar)
- Slow rising pulse
- Soft S2
- signs of left heart failure
- Harsh crescendo-decrescendo (diamond shaped) louder on expiration in 2nd ICS on right sternal edge
- Late ejection systolic murmur that radiates bilaterally to the carotids (aka ejection click murmur)
2) AORTIC REGURGITATION (ARmED) aortic regurgitation is mid-diastolic (austin flint if severe) or early diastolic
- Dyspnoea
- Rapid cardiac decompensation secondary to heart failure
- Signs of left heart failure
- Pulmonary oedema
- Quincke’s signs- nailbed pulsation
- De Musset’s sign- Head bobbing
- Widening pulse pressure (PP) (valve is loose so larger difference between sytolic and diastolic)
- Collapsing pulse (Corrigan’s pulse/water-hammer pulse)
- High-pitched, decrescendo early diastolic murmur
- Austin flint murmur (mid-diastolic murmur at the apex) if severe
INVESTIGATIONS
Aortic Stenosis:
ECG
Transthoracic echocardiography : see calcification and narrowing of aortic valve in stenosis
Chest X-Ray to check for pumonary oedema
Aortic Regurgitation:
ECG
Transthoracic echocardiography : see calcification and narrowing of aortic valve in stenosis
Chest X-Ray to check for pumonary oedema
Colour flow Doppler: specific and sensitive for severity
MANAGEMENT
Aortic Stenosis:
Clinically stable: asymptomatic:
- not severe: statin and hypertension management, annual ECG
- severe (less than 50% EF, high BNP, progressing rapidly, abnormal exercise test) then WASABi ( warfarin, AVR, statin, ABx, BP management)
Clinically Stable: symptomatic:
WASABi ( warfarin, AVR, statin, ABx, BP management)
- if cant tolerate surgery: transcatheter
Aortic Regurgitation:
Mild to moderate= yearly ECG
Severe, asymptomatic
- LVEF over 55%, LVESD under 50mm yearly ECG
- LVEF under 55%, LVESD over 50mm = AVR or aortic repair,, if comorbidities then transcatheter aortic valve implantation
Severe, symptomatic= aortic valve replacement or repair,, if comorbidities then transcatheter aortic valve implantation
After operation:
Metallic valves are at high risk of thromboemoblic event so need long term anticoagulation with warfarin
Dont give: Nitrates (can cause hypotension)
If have pulmonary oedema/LHF sign= furosemide
Prophylactic ABx if high risk of infective endocarditis after valve replacement
PROGNOSIS
dont give ACEi in mod to severe AS as can vasodilate, reduce coronary perfusion pressure= ischaemia
Mitral Valve Disease
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Mitral Stenosis:
- Structural anomaly of the mitral valve, resulting in a decreased cross-sectional area of the valve
- Impairing blood flow from the left atrium to the left ventricle
- Commonly due to rheumatic fever
Mitral Regurgitation:
- Leakage of blood from the left ventricle into the left atrium due to incomplete closure of the mitral valve during systole
- Second most common valve issue after AS
- Can be primary or seconary
Primary Mitral Regurgitation: direct involvement of the valve leaflets. Caused by rheumatic fever, infective endocarditis and mitral valve prolapse (MVP in young females)
Secondary Mitral Regurgitation: Changed of the left ventricle leading to valvular incompetence. Caused by coronary artery disease (common after MI due to papillary wall rupture) and dilated cardiomyopathy
RISK FACTORS:
Collagen disorders- Marfans dyndrome and Ehlers-Danlos syndrome (if have joint hypermobility and stria/stretch marks think collagen disorder)
Polycystic kidney disease- associated with mitral valve prolapse and mitral valve regurgitation
CLINICAL FEATURES
1) Mitral Stenosis:
Dyspnoea
Hoarseness (compression of recurrent laryngeal as atrium enlarged)
Dysphagia (enlarged atrium compressed oesophagus)
Malar flush
Symptoms of RHF
Haemoptysis
Auscultation: mid diastolic murmur best heard on left lateral side. Loud S1. If severe then length of murmur increases so becomes closer to S2
2) Mitral Regurgitation
- Dyspnoea
- Fatigue
- Palpitations
- Left-sided heart failure
- Pulmonary oedema
- Auscultation: pan systolic heard at apex and radiates to left axilla. Quiet S1
- In post MI mitral pegurg can get flah pulmonary oedema (frothy sputum, breathlessness, coarse bilateral lung crackles developed over a few hours)
INVESTIGATIONS
Mitral Stenosis:
- Transthoracic echocardiography: TTE will show reduced mitral valve are, left atrium enlargement, pulmonary hypertension
- Chest X-Ray
in mitral stenosis: left atrium enlargement
- ECG
in mitral stenosis: right ventricular hypertrophy and p-mitrale if moderate severe (p wave becomes m shaped/biphasal) ( mitrale is indicative of left atrial enlargement
Mitral Regurgitation:
- Transthoracic echocardiography
- ECG :left ventricular hypertrophy and p mitrale
MANAGEMENT
1) Mitral Stenosis:
- asymptomatic: monitor with regular ECG
- symptomatic: baloon valvotomy or valve replacement. If have pulmonary oedema furosemide
- severe: percutaneous mitral valve commissurotomy
2) Mitral Regurgitation
Valve repair or replacement.
If acute give nitroprusside before surgery
If not fit fot surgery then transcatheter or continue HF management
Heart failure: nitrates and diuretics (furosemide) Nitrates not routinely given but if HF with severe hypertension of MR/AR then do. Do not give nitrates in hypotension
COMPLICATIONS:
M Stenosis: atrial fibrillation (all patients require anticoagulation with warfarin to target INR of 2.5), stroke, congestive heart failure
M Regurg: heart failure, pulmonary oedema, cardiogenic shock (Tx with inotropes - dobutamine), atrial fibrillation
Treatment for rheumatic fever and how it clinically presents
prodromal illness + erythema marginatum (annular/ring like rash affecting trunk and inner arms and legs, face okay- rings arent raised much and not itchy
Treatment: IM benzylpenicillin or oral penicillin V
What protein is mutated in Marfans syndrome
Fibrillin- 1
Right heart valve diseases
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Tricuspid Stenosis : rheumatic fever causes, usually causes mitral or aortic too
CLIN FEATURES:
- Fatigue
- Ascites
- Oedema
- Early diastolic murmur
Tricuspid Regurgitation : RV dilatation (pulmonary hypertention), rheumatic fever, IV drug users infective endocarditis, congenital
CLIN FEATURES:
- Fatigue
- Ascites
- Oedema
- Elevated JVP
- Hepatomegaly, hepatic pain and jaundice
- Pansystolic murmur- loudest at 4th intercostal left parasternal region on inspiration
Pulmonary Stenosis : congenital (tetralogy of fallot). PS is associated with carcinoid heart disease (hedinger syndrome)
CLIN FEATURES:
- Fatigue
- Ascites
- Oedema
- Dyspnoea
- Ejection systolic murmur
Pulmonary Regurgitation: pulmonary hypertension
CLIN FEATURES:
Decrescendo murmur in early diastole
INVESTIGATIONS
Tricuspid Stenosis:
ECG- peaked p wave, atrial fib
Transthoracic Echocardiogram (2D+ doppler)
Chest X ray
Tricuspid Regurg:
Transthroacic Echocardiography: RV dilation, tricuspid enlargement
ECG- atrial fib or flutter
Chest X ray
Pulmonary Stenosis:
ECG
Chest X-ray
Transthroacic Echocardiography with Doppler
Pulmonary Regurg:
ECG
Chest X ray
Transthoracic Echocardiography with doppler
MANAGEMENT
Tricuspid stenosis: fluid and sodium restriction and loop diuretics, if severe (RHF) then surgical repair
tricuspid regurg: treat the cause
- if symptomatic: tricuspid valve replacement or annuloplasty
- if have HF symptomc: diuretics, beta blocker, angiotensin inhibitor
pulmonary stenosis: if severe (HF symptoms, peripheral cyanosis) Pulmonary valvuloplasty or percutaneous balloon
Pulmonary Regurgitation:
treatment of cause and HF treatment
What are the features of rheumatic fever
- Recent sore throat
- Chorea- sudden uncontrollable jerky movements of arms, legs, facial muscles
- Polyarthralgia- pain in multiple joints
- Erythema marginatum
What sided heart murmurs are louder on inspiration and what sided on expiration
RILE
right inspiration
left expiration
Arrythmias: Atrial Flutter and Fibrillation
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Atrial fibrillation: Superventricular tachycardia characterised by uncoordinated atrial activation that results in irregular ventricle response. Common in older patients
- Acute AF= less than 48 hours
- Paroxymal AF= if AF terminates randomly, and terminates with in 7 days
- Persistent AF= Over 7 days but cardioversion fixes
- Permanent AF= cannot achieve sinus rhythm, cannot be cardioverted
Causes of Atrial Fibrillation
- Ischaemic heart disease
- Heart failure
- PE
- Valve disease
- Hypertension
- Hyperthyroidism
- Pneumonia
- Alcohol
Atrial Flutter: Supraventricular tachycardia characterised by succession of rapid atrial depolarisation.
SIDENOTE atrial fibrillation is random firing so lots of spikey p wave. Atrial flutter is fast depolarisation so sharp downward slide on sawtooth
CLINICAL FEATURES:
- Irregularly irregular pulse
- Palpitations
- Chest pain
- Dyspnoea
- Faintness
Acute AF: HF (SOB), pulmonary and peripheral oedema
INVESTIGATIONS
ECG
Atrial Fibrillation: absent p wave, irregular small QRS complexes, irregularly irregular RR intervals.
Broad complex tachycardia= 100bpm+ and QRS wider than 3 squares)- cause is atrial fibrillation with a bundle branch block, stable patients usually present with.
Atrial Flutter: sawtooth pattern and 2:1 P wave: QRS
Bloods: should be normal
Holter monitor: to investigate palpitations
- if holter monitor confirms dysrhythmia then ECG
- if holter monitor is normal but patient symptomatic then external loop recorder considered
Transthoracic Echocardiogram: to rule out underlying cardiac structural disease e.g valvular
TFT: check for hyperthyroidism
MANAGEMENT
Favouring rate control:
o less symptomatic;
o hypertension;
o no history of HF; and
o persistent AF
o over 65
Rate control drugs: Beta blockers and Calcium Channel blockers. If have Heart Failure or CAD use beta bockers. Second like is Digioxinif patient is sedentary or BB and CCB unsuitable.
Favouring rhythm control:
o newly detected AF;
o age younger than 65 years; and
o no previous antiarrhythmic drug failure
Rhythm control drugs: pharmacological cardioversion : Flecainaide or Amiodarone. Choose Amiodarone if have an abnormal heart condition
1- Hameodynamically unstable aka faint/ <90/<60, MI= emergency electrical cardio version, don’t delay trying to achieve anticoagulation.
2- Haemodynamically stable under 48 hours= rate control first i think
rhythm control. Start pre-cardioversion anticoagulation. If patient is already taking anticoagulant check adherence for last 3 weeks if on DOAC, or INR if on warfarin then proceed with cardio version. If not on anticoagulation (check ORBIT score) then choose a low molecular weight heparin (LMWH), such as enoxaparin; or unfractionated heparin. Then have cardioversion either electrical or pharmacological with amiodarone or flecainide. Amioradone preferred if have structural heart issue
3- Hamodynamically stable over 48 hours= Rate control with beta blockers like bisoprolol, metoprolol, or a CCB like diltiazem or verapamil. Second line is digoxin.
If not on anticoagulants plan for anticoagulation for 3 weeks ((check ORBIT score) then choose DOAC like rivaroxaban, apixaban, edoxaban, or dabigatran; or a low molecular weight heparin (LMWH), such as enoxaparin; or unfractionated heparin) then an elective electrical or pharmicalogical.
If on anticoagulants, go ahead with cardioversion
4- Paroxysmal or Persistent Hamodynamically unstable= direct current cardioversion
5- Paroxysmal or Persistent Hameodynamically Stable= Long term oral anticoagulation according to CHA2DS2VASc score, usually a DOAC such as dabigatran, rivaroxaban, apixaban, or edoxaban. Rate control too with a beta-blocker, diltiazem, verapamil, or digoxin. Consider cardioversion
6- Atrial flutter recurrent= catheter ablation and long term anticoagulants
Use ORBIT score when patients being considered for anticoagulation to assess bleeding risk
After surgery use CHA2DS2VASc score to work out risk of stroke and decision about longer term anticoagulation. Should be on anticoagulants for at LEAST 4 weeks after, if DOAC contraindicated then warfarin but INR needs to be monitoring. DOACs include:
- Apixaban
- dabigatran
- edoxaban
- rivaroxaban
CHA2DS2VASc Score calculates risk of stroke
* If men has 1 or more, or women have 2 or more then anticoagulant long term
* Use a DOAC, but if contraindicated then heparin but DOAC preferred as doesn’t need monitoring
PROGNOSIS
Chronic AF in a diseased heart wont return to sinus
COMPLICATIONS
thromboembolism
List the side effects of amiodarone
- Bradycardia
- Hyper/hypothyroidism
- Pulmonary fibrosis
- liver fibrosis/pneumonitis
- jaundice
- taste disturbance
- persistent slate grey skin discolouration
- raised serum transaminases
- nausea
- constipation (particularly at the start of treatment)
Combination of what two medications can lead to Heart Block
Beta blocker + CCB like verapamil or diltiazem
Arrythmias: Supraventricular Tachycardia
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
A regular, narrow-complex tachycardia with no P waves and supraventricular origin. Has a REGULAR rhythm unlike AF.
Atrioventricular nodal re-entry tachycardia AVNRT is a local re-entry circuit within the AV node
Atrioventricular re-entry tachycardia AVRT is where a circuit forms between atria and ventricles due to presence of accessory pathways
Wolff Parkinson White syndrome also has accessory pathways but have delta waves once SVT is terminated. in WPW there is a slope up to the QRS called the delta wave, short PR intervals of less than 3 squares, wide QRS of more than 3 squares. WPW usually caused by AVRT. WPW will axis deviate to the opposite side of the accessory pathway
CLINICAL FEATURES
- Syncope
- Palpitations
- Chest Pain
- SOB
- Light-headedness
- Tachycardic on physical examination
INVESTIGATIONS
Do ECG once SVT is terminated and have normal rate and rhythm.
AVNRT will look normal on ECG (might have retrograde p wave, might not have p wave but bp will be 151-250bpm so can differentiate from sinus tachy which is 100-150bpm)
AVRT will have delta waves, no pwave - WPW, has more downsloping of ST segment compared to flat line in AVNRT
MANAGEMENT
1) Hameodynamically stable SVT:
1st Vagal manouvres- carotid sinus massage and valsalva manouvre (exhalation against closed airway like blowing into syringe).
2nd- Cardioversion with IV adenosine as a rapid bolus 6mg then 12mg then 18mg . Adenosine causes transient heart block in AV node, patient will feel like theyll die- causes intense brief chest pain, bronchospasm and flushing). Is short acting less than 10 seconds.
In asthmatics use verapamil.
2) Haemodynamically unstable SVT: DC cardioversion
3) AVRT/WPW: radiofrequency ablation of accessory pathway. NO BB or CCB
4) if recurring consider long term bblocker or ccb
Complications → haemodynamic collapse, DVT, systemic embolism, cardiac tamponade
Prognosis → normally good
Compare findings in all the arrhythmias
AF- Irregular tachycardia : flutter has sawtooth, fibrillation has shaky p waves
SVT- narrow QRS (less than 3 squares)
VT- broad QRS (more than 3 squares), conscious, large lines and regular
Torsades de Pointes- broad QRS that crescendo and decrescendo in amplitude
VF- broad QRS, patient unconscious/collapsed, smaller QRS amplitude than VT
Arrythmias: Ventricular Tachycardia
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
A regular broad-complex tachycardia originating from a ventricular ectopic focus. Rate usually over 120. SHOCKABLE RHYTHM
Risk Factors:
- CHD
- Structural heart disease
- Hypokalaemia
- Cocaine
CLINICAL FEATURES
- Chest pain
- Palpitations
- Dyspnoea
- Syncope
INVESTIGATIONS
ECG shows: large, broad squiggly lines
- Rate >100bpm
- Broad QRS complexes
- No P waves
- AV dissociation
Torsades De Pointes is a polymorphic VT which will gradually look like VT but crescendo and decrescendo. Has long QT interval before suddenly getting very messy .
Caused by macrolides like azithromycin/clarithromycin, or low potassium, magneium, calcium or hypothermia. Can also be secondary to subarachnoid haemorrhage
May lead to VF and sudden death
MANAGEMENT
VT: first ABC, check if has a pulse. If in cardiac arrest then difibrillation
Stable VT: Chest X Ray first to check for risk of pulmonary fibrosis/pneumonitis then IV amiodarone 300mg, (If have a identifiyable reversible cause like drugs, MI ect then adenosine first line, amiodarone second)
Haemodynamically Unstable: DC Cardioversion
Stable Torsdaes de Points: IV magnesium sulphate
Unstable Torsades de Points: DC cardioversion.
in VT dont give CCB like verapamil, diltiazem or amlodipine
Arrythmias: Ventricular Fibrillation
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death.
Due to ventricular fibres contracting randomly causing complete failure of ventricular function. Usually in patients with an underlying heart disease
CLINICAL FEATURES
- Sudden collapse and unconscious (unconscious improtant to differentiate between VT and VF)
- Pulseless
- Noisy or irregular breathing
INVESTIGATIONS
ECG- ventricular tachycardia is regular looking but ventricular FIBRILLATION is smaller squiggly lines. Fibrillation has smaller amplitude of QRS complexes than VT
MANAGEMENT
1) if no pulse= ALS:
- unwittnessed attacks = 1 shock then 2 mins of CPR
- witnessed attack= up to 3 shocks then CPR then amiodarone 300mg and 1mg adrenaline. Repreat 1mg of adrenaline very 3-5 mins, give another amiodarone 150mg after 5 shocks
If amiodarone isnt available then use lidocaine.
2) With VF : Urgent defribrillation and cardioversion.
If survive need implantable cardioverter defribrillator
PROGNOSIS
depends on time between onset and medication. Early defribrillation within 4-6 mins is ideal
What condition are implantable cardioverter defribrillators used in and what other condition are these patients at risk of
Hypertrophic obstructive cardiomyopathy
- Left ventricular hypertrophy
- Deep T wave inversion
- S4 heart sound
There is considerable risk of sudden cardiac death due to ventricular tachycardia or ventricular fibrillation
What is arrhythmogenic right ventricular dysplasia, how it would present on ECG and what makes this condition worse
Autosomal dominant inherited cardiac arrhythmia that is a common cause of sudden cardiac death in people under 65 years old
on ECG
- Epsilon wave (after S in QRS goes up and forms a separate tiny peak
- Widened QRS
- T wave inversion
- Prolonged S upstroke in V1-3
Exercise makes worse
Arrythmias: Heart Block
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
1st degree AV block = prolonged conuction through AV node (fixed PR prolongation)
2nd degree AV block=
- Mobitz Type I: progressive prolongation of AV node conduction resulting in one atrial impulse failing to conduct through. Continuous prolongation of PR until one dropped
- Mobitz Type II: Intermittent/regular failure of conduction through AV node. Fixed PR prolongation then randomly drops a QRS
3rd degree/complete AV block= no relationship between atrial and ventricular contraction. P waves and QRS both regular but not with eachother
Causes of Heart Block:
Drugs (digoxin)
Metabolic (high potassium)
MI- right CA occlusion (inferior MI) blocks the AV node
CLINICAL FEATURES
1st and 2nd degree usually asymptomatic
2nd degree Mobitz II and 3rd degree can show signs of reduced cardiac output like hypotension but also cause Stokes-Adams attacks which involve:
- Syncope
- Dizziness
- Palpitations
- Chest pain
- On ECG have wide and large inverted T waves
3rd degree:
- JVP may show cannon A waves
- Syncope
- Regular bradycardia → 30-50 bpm
ECG INVESTIGATIONS
1st degree AV block- fixed prolonged PR interval (more than 3-5 square).
- If has a fixed prolonged PR and a U wave before a plattened T wave and ST segment depression could be hypokalaemia (due to diuretic like thiazide)
2nd degree AV block Mobitz I: Progressively prolonged PR interval, then eventually dropped beat
2nd degree AV block Mobitz II: PR interval is constant but intermittently a P wave is not followed by a QRS
3rd degree/complete Av block- No relationship between p waves and QRS complexes- complete AV dissociation
MANAGEMENT
Chronic block (Mobitz II)= Permanent pacemaker. On ECG pacemakers cause a vertical line before QRS
Acute block= IV atropine, used for bradycardias to speed up if patient is symptomatic or has low BP. Max dose of atropine is 3mg, after that try transcutaneous pacing then transvenous pacing
Mobits II and 3rd degree pts that have a broad QRS are at risk of asystole in bradycardia. Give transvenous pacing
PROGNOSIS
usually have serious underlying cardiac issue
For palpitations what monitoring should be done after bloods and ECG
Palpitations ⇒ holter monitoring (24hr continuous ECG) should be done after initial bloods and ECG.
Arterial Thrombosis
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Blood clot in an artery. Symptoms only begin when blood flow is blocked
Main cause= atherosclerosis
Other causes: Atrial fibrillation, Antiphospholipid syndrome
Clinical Features: can cause four different conditions
1) Myocardial Infarction- chest pain, SOB, dizziness
2) Stroke: unilateral face paralysis + weakness, slurred speech
3) Transient ichaemic attack: blood flow to brain is temporarily blocked, causes short lived stroke symptoms
4) Acute limb ischaemia: blood supply to limb is blocked so get:
- Pain
- Pallor
- Poikilothermia or perishingly cold
- Pulselessness
- Paraesthesia
- Paralysis
MANAGEMENT
Prevention : reduce antherosclerotic risk.
- Improve lifestyle- stop smoking, improve diet, lose weight, reduce alcohol, exercise
- Medications: statin, antihypertensive, anticoagulation (warfarin), antiplatelets (aspirin/clopidogrel)
Already blocked:
1) Thrombolysis
2) Embolectomy
3) Angioplasty (widen affected artery)
4) CABG (divert blood around blocked
Arterial Ulcers
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Localised area of damage and breakdown of skin due to inadequate blood supply. Seen on feet of patients with severe atheromatous narrowing of arteries
Risk Factors:
- PAD (peripheral artery disease)
- CHD (coronary heart disease)
- History of stroke or TIA
- Diabetes
- Obesity
- Smoking
- High cholesterol
CLINICAL PRESENTATION
- often distal: heel, lateral malleolus, tips of toes
- severe pain, elevation makes worse
- punched out appearance
- well defined borders
- hair loss, shiny, cold and pale skin
- absent pulses
- night pain (pain worse when lying down because blood flow reduced even further, better when dangling off the end of the bed
INVESTIGATIONS
Duplex ultrasonography of lower limbs: assess patency of arteries and potential for revascularisation or bypass surgery
Ankle-brachial pressure index: will be low
Over 1.3= vessel calcification
0.8-1.3= normal
0.5- 0.79= moderate arterial disease (claudation) (arterial ulcers usually here)
less than 0.5= critical limb ischaemia
Bedside- capillary refill
MANAGEMENT
Lifestyle- stop smoking and reduce cholesterol in diet
Wound- clean ulcer and change dressing
Surgical intervention
- skin grafting
- Revascularisation : restore blood flow through bypass or angioplasty. Improves healing
Deep Vein Thrombosis
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Development of a blood clot in a major deep vein in the leg, thigh, pelvis or abdomen. more likely in legs due to blood stasis and gravity
RF:
- COCP
- Post-surgery
- Prolonged immobility
- Pregnancy
- Malignancy
- Smoking
- Polycythaemia
CLINICAL FEATURES
- Calf swelling
- Warmth and erythema
- Dull pain (may also be painless)
- Oedema- worse on leg with suspected DVT
- Homan’s sign= calf pain on dorsiflexion
INVESTIGATIONS
Wells criteria : wells score of 2 or more means imaging is necessary (proximal leg US within 4 hours + d dimar test + DOAC and a scan within 24 hours)
less than 2 means just do a d-dimer, can do anticoagulation whilst waiting. If d-dimer is positive do the same as if they had a wells score over 2, if not consider another diagnosis.
if patient has a headache then d dimer is first test
if cant get a scan or d dimer start DOAC
if imaging is negative stop DOAC and repeat scan in 7 days
Gold Standard investigation= Proximal leg doppler ultrasound. Will find
- Inability to fully compress lumen of vein using ultrasound transducer
- Reduced or absent spontaneous flow
- Lack of respiratory variation
- Intraluminal echoes
- Colour flow abnormalities
MANAGEMENT
LMWH or DOAC
heparin over DOAC is eGFR less than 15ml/min or patient pregnant
- If DVT doesnt extend beyond knee then 3 months DOAC/LMWH
- if DVT extends beyond the knee then 6 months DOAC/LMWH
- If recurrent DVT then long term warfarin
if anticaogulation contraindicated and risk of embolism then : IVC filter- to prevent PE
Prevention:
- Compression stockings
- Mobilisation
- Prophylactic heparin if high risk aka hospital patients
PROGNOSIS
Good. Proximal DVt have greater risk of embolisation.
COMPLICATION
PE
Bleeding during intial treatment
Post thrombotic syndrome
- Painful heavy calves
- Pruritus
- Swelling
- Varicose veins
- Venous ulceration
need graduated compression stockings
Gangrene
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Complication of necrosis characterised by the decay of body tissues.
Categorised into:
- Infections gangrene (wet) : caused by necrotising fasciitis and gas gangrene (clostridium perfringes)
- Ischaemic gangrene (dry): caused by peripheral artery disease (critical limb ischaemia) due to atheroscleosis or venous obstruction
Risk Factors:
Diabetes, Atherscleosis. Smoking, likely to caogulate, alcohol, malnutrition
CLINICAL FEATURES
- Painful black tissue
- Feeling of heaviness in affected area
- Oedema and swelling
WET: sudden onset of pain, low grade fever and chills, poorly demrcated necrotic area
GAS: darkened skin, crepitus may be heard from escaping gas, infective area STANKY, might see gas on radiograph
DRY: diminished pulses and ABPI, no sign of infection, well demarcated necrotic area, history of chronic claudication (pain when walking in limbs)
INVESTIGATIONS
suspect wet/ infective= Blood cultures
Doppler ultrasonography - to detect presence and severity of artery or venous obstruction
DIAGNOSIS NEEDS: surgical exploration and skin biopsy
MANAGEMENT
Infectious/Wet: surgical debridement and broad spectrum antibiotics
Ischaemic/Dry: IV heparin, surgical revascularisation.
- If limb is non-viable then amputation
PROGNOSIS
to improve outcome needs to be early recognition and aggressive antibiotic and surgical management
COMPLICATIONS
sepsis, shock, loss of limb, acute renal failure, haemolysis
Peripheral Vascular Disease
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Disease characterised by narrowing and occlusion of the peripheral arteries due to atherosclerotic plaques
Risk Factors
- Smoking- main one
- Diabetes
- Hypertension
- Hyperlipidaemia
- Physical inactivity
- Obesity
- CAD
Fontaine Classification:
Stage I- asymptomatic PAD
Stage II- IIA claudation after walking over 200m, IIB claudation after walking less than 200m
stage III- ischaemic pain at rest
Stage IV- Necrosis, ulcers or gangrene
Claudation is pain on exertion due to inadequate blood flow during exercise, causing fatigue discomfort or pain
Critical limb ischaemia : compromise of blood flow to an extremity , causeds limb pain at rest worse at night for at least 2 weeks. pts develop arterial ulcers and gangrene
Acute limb ischaemia: sudden decrease in limb perfusion that threatens limb viability. 6 Ps pain, paralysis, paraesthsia, pulseless, pallor, perishingly cold. AF is a risk factor for. Give IV heparin
CLINICAL FEATURES
- Most patients are asymptomatic
- Intermittent claudication- Cramping pain of leg which is worse upon exertion, relieved by rest
- Diminished or absent pulse
- Erectile Dysfunction (impotence)
- Thigh or buttock pain when walking
calf pain- femoral artery
buttock pain- iliac artery
Red Flags indicating critical limb ischaemia
Resting pain
Skin changes- ulcers or gangrene
INVESTIGATIONS
1st ankle-brachial pressure index ABPI (systolic ankle BP to systolic brachial BP. PAD is less than 0.8, critical limb ischamia is less than 0.5
If have intermittent claudations
1st line = duplex ultrasound scan, determine site, severity and length of stenosis
If acute limb ischaemia
1st line = bedside handheld arterial doppler scan. Then Lower limb CT angiography to quantify occlusion extent
Buergers test: lie patient flat, lift leg to 45 degrees. If limb becomes pale = arterial insufficiency
less than 20 degree angle indicates severe limb ischaemia
when patient swings legs over bed should see reactive hyperaemia
MANAGEMENT
Intermittent claudation
- lifestyle- stop smoking, exercise training
- meds: antiplatelet therapy (clopidogrel or aspirin), statins (atorvastatin) , antihypertensive
- if exercise s ineffective and doesnt want angioplasty or bypass: Naftidrofuryl oxalate which is a vasodilator that can allieviate pain in PVD
- if risk factor mod and exercise hasnt improved then refer for surgical revascularisation
Critical limb ischaemia (pain at rest, tissue loss, gangrene)
Urgent referral to vascular MDT for revascularisation
Endovascular Revascularisation/angioplasty if small stenosis under 10cm
Surgical Revascularisation/bypass if large over 10cm
If gangrene then amputation: a non-viable limb shows signs of tissue loss, nerve damage, sensory loss, skin mottling, plantar fasciitis
Acute limb ischaemia
IV heparin
Analgesia+ fluid + oxygen
Refer to vascular surgery for embolectomy, bypass or amputation
PROGNOSIS
claudation- stable and good prognosis
critical limb ischaemia- poor prognosis
COMPLICATIONS
Arterial ulcers, gangrene, permanent limb pain/weakness
What is leriche syndrome
Aortoillac occlusive disease
- Buttock claudication
- Impotence
- Absent/weak distal pulses
Venous Ulcers
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Large, shallow, sometimes painful ulcers usually found superior to the medial malleoli. Caused by incompetent valves in the lower limbs leading to venous stasis and ulceration . Venous hypertension
Risk Factors → obesity, immobility, recurrent DVT, varicose veins, previous injury or surgery to the leg, increasing age
CLINICAL FEATURES
- Frequently occur just above the medial malleolus & typically painless
- Shallow ulcers with irregular borders
- Itchy
- Usually only mild pain- less painful when elevated
- Features of venous insufficiency: oedema, brown pigmentation (haemosiderin deposition), lipodermatosclerosis (skin hardening), eczema
- Exudative
INVESTIGATIONS:
Duplex USS of lower limbs
ABPI to exclude arterial ulcer (normal is 0.8-1.3)
Swab for microbiology cultures if signs of infection
Biopsy: In any non-ischaemic wound that fails to improve after 3 months of treatment
MANAGEMENT
- Compression bandaging : to reduce venous stasis (DONT DO IN ARTERIAL DISEASE, make sure ABPI is cleared first)
- Debridement and cleaning
- skin graft if large or refractory ulcers
- ABx if infected
- Topical steroids to help with surrounding dermatitis
PROGNOSIS
Good, results are better if patients are mobile with few comorbidities
COMPLICATION
recurrance, infection
What are the side effects of ACEi and when is it contraindicated
Angioedema (swollen areas with hives usually)
Cough (if get cough switch to ARB
Elvated potassium
ACEi are the most common cause of drug induced angioedema
Contraindicated in renal artery senosis as ACEi may cause renal impairment (affecting U&Es).
Consider if patient has risk factors or has atherosclerotic vascular disease
Side effects of statins
Ankle swelling (peripheral oedema
Headache
Flushing
What are the side effects of thiazide like diuretics and in what condition are they contraindicated
Contraindicated in gout
Side Effcts:
Hypercalcaemia (stones, bone pain, abdo pain, constipation, polyuria, muscle weakness, depression)
Hyponatraemia
Hypokalaemia (on ECG low potassium flattens T waves and causes ST depression, causes U waves after T waves, long QT, prlonged PR interval
Impaired glucose tolerance
Erectile dysfunction
What are the stages of hypertensive retinopathy
- Grade 1 → arteriolar narrowing and tortuosity. Silver wiring.
- Grade 2 → Arteriovenous nicking
- Grade 3 → flame haemorrhage and cotton wool exudates
- Grade 4 → papilloedema (poorly defined margins of optic disc on fundoscopy)
Side effects of calcium channel blockers and which is preferred in HF
Ankle swelling
Amlodipine less likely to exacerbate HF than verapamil
What is buergers disease- IDK if this is needed
Small and medium vessel vasculitis associated with smoking and causes Raynauds phenomenon
On angiogram see corkscrew shaped collateral blood vessels
Intestinal Ischaemia
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Obstruction of mesenteric vessel leading to bowel ischaemia and necrosis
Three types
1) Acute mesenteric ischaemia: Acute inadequate blood flow to the small intestine. Affects SMA, associated with arterial thrombosis and embolus (can lead to atrial fib)
2) Chronic mesenteric ischaemia: Constant or episodic hypoperfusion of the small intestine, usually due to atherosclerosis
3) Ischaemic colitis: Hypoperfusion of the large bowel. Affects IMA, area near splenic flexure and 2/3 of transverse colon at high risk as those are watershed areas.
Risk Factors
Age, AF, smoking, hypertension and diabetes
CLINICAL FEATURES
- Colicky abdomen pain
- Post prandial/food abdominal pain. (in CMI this is due to atherosclerosis causing intestinal angina)
- Diarrhoea
- Fever
- Rectal bleeding: most common in ischaemic colitis
Acute mesenteric ischaemia: Sudden, severe abdominal pain out of keeping with physical exam findings
Chronic mesenteric ischaemia: severe colickly post prandial pain, abdo bruit and weight loss
Ischaemic colitis: abdo pain can be colicky, rectal bleeding, urgency
INVESTIGATIONS
VBG: see high lactate due to metabolic acidosis
D dimer: can exclude MI but low sensitivity if positive
CT with contrast
CT Angiogram
Abdo C ray- thumbprint on barium enema for ischaemic colitis
MANAGEMENT
acute mesenteric ischaemia:
- Fluid resus
- Antibiotics
- Urgent embolectomy or arterial bypass+ bowel resection
CMI: systemic mesenteric bypass
Ischaemic colitis:
- Fluid resus
- antibiotics
- Conservative management
- Segmental colectomy if intial management doesnt resolve
Infective Endocarditis
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Infection of the endocardium that typically affects 1 or more heart valves. Usually affects males over 60
Valves from most to least likely to be affected
MATP: Mitral, Aortic, Tricuspid, Pulmonary
If due to IV then most likely is tricuspid
- Most common cause= stapylococcus aureus (prosthetic valves and IV drug use are risk factors for staph a infective endocarditis)
- Most common cause if less than 2 months after valve surgey = staphlococcus epidermidis
- Most common cause of subacute infective endocarditis streptococcus viridans= mainly affects predamaged native valves and a common cause is dental procedures
-Streptoococcus bovis - predisposes to IE and colorectal cancer
Risk Factors:
Prosthetic heart valves, (heart defects and post heart surgery)
Dental procedures
IV drug use (if IV usually right sided problem)
CLINICAL FEATURES
- Fever/chills
- New heart murmur
- Dyspnoea on exertion (HF feature)
On examination:
- Splinter haemorrhages (under fingernails)
- Janeway lesions (painless macule on palms and soles)
- Osler nodes (painful nodules on finger and toes)
- Clubbing
- Roth spots (white centred retinal haemorrhage on fundoscopy caused by septic emboli)
INVESTIGATIONS
3 sets of blood cultures 30 mins apart before antibiotics, repeat 4-72 hours after started ABx treatment too
Trans-thoracic echocardiogram- most sensitive : will show valvular, mobile vegetations. Do trans-oesophageal echocardiogram if TTE is negative or if have a prosthetic heart valve
Dukes criteria= determines whether unlikely, possible or likely to have IE and determines the next imaging choice
Definite IE: 2 majors OR 1 major + 3 minor OR 5 minors
Definite Next Step: CT Angiography, brain or whole body imaging CT +/- MRI
Possible IE= 1 major + 1 minor OR 3 minors
Possible IE Next Step: repeat blood cultures, echocardiography in 5-7 days, MRI or CT whole body or brain
MAJOR CRITERIA
1) Blood culture positive for IE
- Typical microorganisms consistent with IE from two separate blood cultures: oral streptococci, Streptococcus gallolyticus (formerly S treptococcus bovis), HACEK group, Staphylococcus aureus, Enterococcus faecalis.
- Microorganisms consistent with IE from continuously positive blood cultures:
≥2 positive blood cultures of blood samples drawn >12 hours apart
All of 3 or a majority of ≥4 separate cultures of blood (with first and last samples drawn ≥1 hour apart).
- Single positive blood culture for Coxiella burnetii or phase I IgG antibody titre >1:800.
2) Imaging positive for IE
Valvular, perivalvular/periprosthetic, and foreign material anatomic and metabolic lesions characteristic of IE detected by any of the following imaging techniques: TTE or TOE, CT, PET/CTA, WBC SPECT CT
MINOR CRITERIA:
1) Predisposing conditions (i.e., predisposing heart condition at high or intermediate risk of IE or people who inject drugs)
2) Fever defined as temperature >38°C (>100.4°F)
3) Embolic vascular dissemination (including those asymptomatic detected by imaging only):
Major systemic and pulmonary emboli/infarcts and abscesses
Haematogenous osteoarticular septic complications (i.e., spondylodiscitis)
Mycotic aneurysms
Intracranial ischaemic/haemorrhagic lesions
Conjunctival haemorrhages
Janeway’s lesions.
4) Immunological phenomena:
Glomerulonephritis
Osler nodes and Roth spots
Rheumatoid factor.
5) Microbiological evidence:
Positive blood culture but does not meet a major criterion as noted above
Serological evidence of active infection with organism consistent with IE
MANAGEMENT
Long term ABx for 6 weeks
- suspected IE= fluids + oxugen + broad spectrum ABx (amoxicillin if blind therapy and have native valve)
CONFIRMED IE
Blind therapy:
amoxicillin +/- gentamicin
if penicillin allergic or MRSA resistant or severe sepsis= vancomycin + gentamicin
prosthetic valve = vancomycin + rifampin + gentamicin
Staphylococci (IV drug) :
Flucloxacillin
If penicillin allergic or MRSA resistant (like epidermidis) = vancomycin + rifampicin
if prosthetic valve = flucloxacillin + rifampicin + gentamicin
if penicillin allergy and prosthetic valve= vancomycin + rifampicin + gentamicin
Streptococci (viridians):
Benzylpenicillin (+gentamicin if less sensitive)
If penicillin allergy Vancomycin + gentamicin
Surgery if PR interval prolongation because it can be due to aortic root abscess
Criteria for urgent valvular replacement in IE:
- Severe congestive failure
- Overwhelming sepsis despite Abx therapy
- Recurrent embolic episodes despite Abx therapy
- Pregnancy
PROGNOSIS
heart failure is the best predictor of prognosis
COMPLICATIONS
Ischaemic stroke as IE can cause vegetations which then may break away and circulate blocking other vessels.
What is atrial myxoma and how is it different form infective endocarditis
Atrial myxoma is a benign tumour usually in the left atrium.
clin features:
- Mitral valve obstruction (mid-diastolic murmur)
- Systemic embolisation
- Constitutional symptoms
Infective endocarditis wont have a mass on echocardiogram
Myocarditis
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Inflammation of the myocardium in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease
10% of sudden death in young adults, usually age 40
Causes:
- Idiopathic
- Viral : Coxsakie B, Parvovirus, Influenza A+B, Adenovirus
- Bacterial: Mycobacterial or streptococcal
- Fungal
- parasitic
- non-infectious: Connective tissue diseases (sarcoidosis or SLE), Toxic myocarditis( caused by cocaine, toxins, medication and alcohol), autoimmune
CLINICAL FEATURES
- Young patient with history of prodromal illness (viral): Fever, Myalgia- muscle pains, URTI symptoms around 2-3 weeks before initial presentation
- Chest pain : indicates perimyocarditis
- Cardiac Arrhythmias(palpitations)
- Dyspnoea
Pericarditis vs Myocarditis= In myocarditis theres acute pulmonary oedema
INVESTIGATIONS
- Endomyocardial biopsy (idk)
- 12 lead ECG: ST elevation and T wave inversion
- Bloods: High troponin, BNP, ESR
- Chest X-Ray: cardiac enlargement, pleural effusions, bilateral pulmonary infiltrates suggesting pulmonary oedema
- Echocardiogram
MANAGEMENT
Supportive: cardiac monitoring, Oxygen, Analgesics
- Antibiotics if bacterial, Antimycotics for fungal
LVEF affected: ACEi or ARB
Unstable: Nitroprusside
COMPLICATIONS
Congestive heart failure (diuretic+ Beta blocker), cardiac arrhythmias, dilated cardiomyopathy, pericarditis (can lead to cardiac tamponade)
PROGNOSIS
viral make full recovery may progress to dilated cardiomyopathy. Prognosis poor in infants
Pericardial Disease
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Inflammation of the pericardium (outer sac)- may be acute or chronic
Acute= new onset inflam lasting 4-6 weeks, usually viral infection
Chronic= lasts over 3 months, leads to constrictive pericarditis
Affects women more, 20-50 year olds
Risk Factors:
- Idiopathic
- Myocardial infarction
- Cardiac surgery
- Neoplasm
- Infections e.g. Coxsackie B virus
- Uraemia (high level of urea in blood)
- Systemic autoimmune disorders (RA, SLE)
CLINICAL FEATURES
Acute sharp and pleuritic chest pain- can radiate to left neck and shoulder- relieved sitting up or leaning forwards, worse lying down
Pericardial rub- superficial scratchy/squeak sound over left sternal border at end expiration when patient leaning formward
Fever and myalgia
Cardiac tamponade: fluid accumulates in pericardial space and constricts the heart, if stops contraction then cardiogenic shock (Beck’s triad: raised JVP, decreased BP, muffled heart sounds // also get pulsus paradoxus (large drops in BP on inspiration)) (on ECG of cardiogenic shock shows ECG with electrical alternans- diff sized QRS)
INVESTIGATIONS
ECG- saddle shaped ST elevation in all leads, no reciprocal changes, PR depression
Transthoracic echocardiography- pericardial effusion- cardiac tamponade potentially
Chest X-Ray: pericardial effusion
Bloods
- Troponin- shoildnt be elevated indicates myopericcarditis or other heart issues
- Urea- means its due to urea
- Blood culture- check for infective cause
MANAGEMENT
Often self-limiting
- NSAIDS can help alleviate symptoms (aspirin, ibuprofen, naproxen)
- PPI prophylaxis to protect against effects of high doses of NSAIDs
if patient has idiopathic or viral cause then add colchicine as reduces rate of recurrance but can cause diarrhoea
Surgical for cardiac tamponade or pericardial effusion- pericardiocentesis. If have a neoplastic disease then percutaneous balloon pericardiotomy
If recurrent then pericardectomy
PROGNOSIS
if large effusion over 20mm , high fever, subacute aka over several days but no clear onset or doesnt respond to NSAID is 7 days then poor prognosis
COMPLICATIONS
pericardial effusion with or without cardiac tamponade
What are the features of constrictive pericarditis
Constrictive pericarditis: dyspnoea, RHF (peripheral oedema), Kussmaul’s sign (rise in JVP on inspiration - inspiration reduces throacic cavity pressure so JVP should go down but because right ventricle not filling the bloods always pushed back, helps differentiate between constrictive pericarditis and cardiac tamponade), pulsus paradoxus
Chest X ray shows pericardial calcification
What is Dressler’s syndrome
Pericarditis several weeks after an MI that may occur with pleural effusion
- Acute pleuritic chest pain
- Fever
- Raised ESR
- SOB worse when lying down and better when sitting forward
ECG
- Widespread concave ST-elevation
- PR depression with reciprocal ST depression
- PR elevation in aVR
TREATMENT
- NSAIDs preferably
- Prolonged course of colchicine or steroids
Essential or Secondary Hypertension
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Blood pressure that is persistently ≥140/90 mmHg AND 24 hour blood pressure average reading (ABPM/HBPM) ≥135/85 mmHg
Primary is hypertension with no identifyable cause
Secondary is due to an identifyable cause such as:
- Most common cause = Conn’s syndrome (primary hyperaldosteronism)
- Renal stenosis
- Cushing’s syndrome
- Phaemochromocytoma
- Acromegaly
Risk Factors
- Age >65 years
- Alcohol intake
- Lack of exercise
- Obesity
- DM
- Black ancestry
CLINICAL FEATURES
Usually asymptomatic unless very high. Can present with headache, blurred vision and dizziness
Orthostatic hypertension= When there is a drop in SBP of at least 20 mmHg and/or a drop in DBP of at least 10 mmHg after 3 minutes of standing
INVESTIGATIONS
Ambulatory blood pressure measurement- measures BP over 12-24 hours and take an average.
- If AMBP is declined then home blood pressure moitoring that the individual does at periodic intervals
If new BP is 180/120mmHg then investigate for end organ damage
- Fundoscopy : check for retinopathy
- Urine Dipstick : check for renal disease
- ECG : check for left ventricular hypertrophy
MANAGEMENT
Offer ABPM or HBPM:
if less than 135/85 not hypertensive just monitor.
Stage 1 HPT: clinical 140/90 and over AND ABPM/HBPM 135/85 and over: treat stage 1 HPT if less than 80 years old AND either has organ damage, CVD disease, renal disease, diabetes or 10 year CVD risk of 10% or more.
Stage 2 HTN: Clinical BP 160/100 and over and ABMP/HBMP 150/95 and over- treat all.
Stage 3- clinical systolic 180 or more OR diastolic 120 or more. Check for end organ failure or urgent admission depending on presentation.
Lifestyle Advice: weight loss, less dietary sodium, decrease alcohol, exercise, no smoking
If younger than 55 or diabetic or CKD patient with ACR over 30
1st= ACEi like lisinopril or enalapril or ARB
2nd= ACEi or ARB + CCB or thiazide-like diuretic (indapamide, hydrochlorothiazide, chlorthalidone)
3rd: combine all ACEi/ARB + CCB + thiazide like diuretic
4th: Alpha blocker if potassium over 4.5 OR spirinolactone if 4.5 or under
If over 55/ not diabetic or black ethnicity
1st CCB- Amlodipine/nifedipine
- also give a statin if QRISK score over 10%
2nd= CCB + ACEi or ARB OR thiazide-like diuretic (indapamide, hydrochlorothiazide, chlorthalidone)
- If black patient: ARB (losartan)
3rd: combine all ACEi/ARB + CCB + thiazide like diuretic
4th: Alpha blocker if potassium over 4.5 OR spirinolactone if 4.5 or under
If new BP over 180/120 and no worrying signs= urgent investigations for end organ damage: ECG, urine dipstick and bloods
If new Bp over 180/20 and worrying signs such as confusion, chest pain, HF signs, AKI then refer for acute medical admission
TARGETS
if under 80 : clinic of 140/90 and ABPM/HBMP of 135/85
if over 80: clinic 150/90 and ABPM/HBPM of 145/85
only systolic target changes by 10
PROGNOSIS
small reductions in BP decrease morbidity and mortality due to complications
COMPLICATIONS
CAD, Cerebral Vascular Accident, LVH, CHF, Peripheral Arterial Disease, CKD
Pulmonary Embolism
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
A thrombus which embolises to the lungs via the inferior vena cava and occludes the pulmonary vasculature
risk factors:
- Age
- DVT
- Recent surgery
- Bed rest over 5 days
- Malignancy
- Pregnancy
- COCP
- Antiphospholipid syndrome- puts the patient at an increased risk of thrombosis by increasing coagulability
- Virchows triad can lead to DVT and PE (vessel wall damage, venous stasis, hypercoagulability)
CLINICAL FEATURES
- Sudden sharp pleuritic chest pain when breathing deeply, normally on onse side- worse when coughing, swallowing or deep inspiration
- Dyspnoea
- Tachycardia and tachypnoea: tachypnoea most common
- Signs of DVT: unilateral painful leg swelling
- Cough, fever, haemoptysis
INVESTIGATIONS
Chest X Ray : will be normal, is used to rule out other causes of chest pain pneumothorax
CT pulmonary angiography (CTPA): preferred for definitive confirmation
- Do CTPA if Wells score over 4
- Patient should take DOAC whilst waiting for results
- If CTPA negative but still suspect then Proximal Leg Vein US is suspect DVT
ECG if haemodynamically unstable and cant have CTPA: sinus tachy and S1Q3T3
V/Q scan insteaad of CTPA if renal impairment, contrast allergy or pregnant. This scan identifies areas of ventilation and perfusion mismatch aka infarction
D dimer if wells score 4 or higher in non-pregnant patients (more sensitive than CTPA). If raised do CTPA, if negative stop anticaogulation and consider another diagnosis
ECG- sinus tachycardia and S1Q3T3 pattern. S wave deeper in lead one, Q wave deeper in lead 3 and inverted T in lead III.
ABG- hypoxaemia (type 1 resp failure)
Echocardiography Do if haemodynamically unstable so cant have CTPA
MANAGEMENT
IF STABLE:
1st DOAC (apixaban or rivaroxaban)
- if provoked PV aka due to a known event then 3 months meds
- if unprovoked then 6 months
- if cant have DOAC use warfarin, target INR of 3.5
- if pregnant LMWH instead of DOAC
IF UNSTABLE aka less then 90mmHg:
Thrombolysis (alteplase)
PROGNOSIS
mortality from cardiogenic shock secondary to right ventricle collapsing
COMPLICATIONS
acute bleeding, pulmonary infarction, cardiac arrest
Pulmonary Hypertension
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
An elevated mean pulmonary arterial pressure (mPAP) >20mmHg at rest
Cor pulmonale is right sided heart failure secondary to pulmonary artery hypertension (due to pulmonary disease)
Causes:
- Idiopathic pulmonary arterial hypertension
- Left heart disease: caused congestive heart failure and valvular heart diseases (aortic and mitral stenosis)
- Chronic lung disease- such as COPD, OSA, ILD
- Pulmonary artery obstruction e.g. chronic thromboembolic occlusion of pulmonary vessels
- Unclear multifactorial mechanisms
CLINICAL FEATURES
- Dyspnoea or syncope on exertion
- RHF symptoms: raised JVP, peripheral oedema, hepatomegaly
- Parasternal heave- enlarged right ventricle
- Loud S2
- Pasystolic murmur (tricuspid regurg) and early diastolic (pulmoanry regurg)
INVESTIGATIONS
1st line - Transthoracic echocardiogram
Confimatory test: Right heart catheterisation (mPAP over 20mmHg = PH)
ECG: right acis deviation, tall R wave in V1, if p pulmonale then peaked p wave
Chest X ray: right heart hypertrophy
MANAGEMENT
1st line if no signs of RHF: CCB
Also give warfarin
Lifestyle: exercise, less sodium, avoid pregnancy
PROGNOSIS:
2.8 years median survival
COMPLICATIONS
- cor pulmonale (RHF due to PH, usually due to COPD)
- Supraventricular tachyarrhythmias
Vasovagal Syncope
- aetiology: define, types, risk factors
- clinical features
- investigations
- management
- prognosis + complication
Loss of consciousness due to transient drop in blood flow to the brain caused by excessive vagal discharge
vagus nerve becomes too active, it can cause your heart rate and blood pressure to drop too much or too fast. then drop in blood flow= transient loss of consciousness
Most common cause of fainting in young people
Risk Factors
Emotions- fear, severe pain, blood phobia
Orthostatic stress- prolonged standing, hot weather
CLINICAL FEATURES
- Loss of consciousness lasting a short time
- Patients may experience vagal symptoms before passing out
- Dizziness
- Sweating
- Light-headedness
- Twitching of limbs during blackout
- Short post-ictal phase
INVESTIGATIONS
ECG: check for arrythmia. If have multiple episodes with loss of consciousness and quick recovery do 24h ECG
Echocardiogram: check for outflow obstruction
Lying/standing BP: orthoststic hypertension
Fasting blood glucose: check for DM/hypoglycaemia
MANAGEMENT
Patient Education and avoid triggers
Volume expansion : more salt in diet, electrolyte rich sports drinks
Fludrocortisone
PROGNOSIS
- Recurrences are common but often occur in clusters
- In the long term, the mortality risk is very low, but injury is a concern due to recurrent falls, especially in older people
COMPLICATIONS
injuries, fractures, extradural or cerebral haemorrhages
