Cardiology Flashcards
Define atherosclerosis
A build up of fatty deposits leading to plaque formation in blood vessel walls causing the hardening and stiffening of the walls
What do the letters in ECGs stand for
P : atrial depolarisation
Pr interval : AVN conduction delay
QRS : septal depolarisation + apex depolarisation + outer depolarisation = whole ventricular depolarisation
St segment : isovolaemic ventricular relaxation
T : ventricular repolarisation
ECG paper / box sizes
Width :
0.2s = big square
0.04s per small box (5 small squares = 1 big square)
Height :
0.5mV = big square
0.1mV per small square
What chest leads give you an inferior view of the heart
AvF, lead II, lead III
Which artery supplies inferior portion of heart
RCA
What chest leads show anterior view of heart
V1 - V4
What leads show lateral view of the heart
V5-V6, lead 1, aVL
What do the 4 heart sounds show
S1 : mitral + tricuspid close
S2 : aortic + pulmonary close
S3 : heard straight after S2
rapid ventricular filling in early diastole
normal in pregnant
pathological in mitral regurgitation
AKA pathological “gallop”
S4 :heard straight before S4
due to blood forced into stiff hypertrophic ventricles
seen in LVH / aortic stenosis
Erbs point is where heart sounds best heard
Categories of ischamic heart disease
Angina
Myocardial infarction
What sign is seen as a result of myocardial ischaemia
“Angina” (Levine’s sign - fist over chest) central crushing chest pain due to decreased coronary artery blood flow ‘ increased O2 demand
3 characteristics / signs of stable angina pain
Central crushing chest pain radiating to the neck and jaw
Brought on by exertion
Relived by 5 mins of rest / GTN spray
Types of angina
Stable
Unstable
Prinzmetal
Dont need to know about angina pectoris - but Decubitus is a variant of this angina and it is induced by lying down
Define each type of angina
Stable: normal 3 part definition - i.e. about pain & / on exertion, relieved with rest / GTN spray
Unstable: Pain at rest, not relieved by rest or GTN spray
Prinzmetal: Due to coronary Vasospasm (not to do with atherogenesis —> ischaemia)
What can coronary vasospasm cause
Prinzmetal angina
What is seen in Px with Prinzmetal angina (ECG)
ECG : ST elevation
Seen in cocaine users
What is and when is QRISK score used
Predicts risk of CVD in the next 10 years
Score >10% indicates 10prevention - give statins
What should you do with QRISK score of >10%
Give statin - atorvastatin
primary prevention
What’s GRACE score and when is it used
Predictor of mortality from MI with the next 6months-3years
Used in ACS cases to help guide Tx
What is ACS
Umbrella term for :
Unstable angina - severe ischaemia
NSTEMI - partial infarction
STEMI - transmural infarction
Risk factors for IHD
Obesity
Smoking
Diabetes mellitus T2
Hypertension
Older age
Male
FHx
Pathophysiology for IHD
ATHEROGENESIS - endothelial injury induces cells to signal chemokines (IL-1,IL-6, IFN-¥) to produce…………..
Fatty streaks — intermediate lesions — fibrous plaques
Precursor of a plaque
Fatty streaks
What is the constituents of a fatty streak
T cells
+
Foam cells (lipid laden macrophages)
Fatty streaks can begin to form in less than 10y/o
Where can fatty streaks be found
In intima wall of vessel
What are intermediate lesions and its constituents
Essentially bigger fatty streaks as more lipids are taken up..
You see:
T cells +
Foam cells
Smooth muscle cells
platelets also aggregate at & adhere to site of lesions, inside vessel lumen
What are fibrous plaques and their constituents
Large lesions with the development of a fibrous cap over the lesion - lipid increased with a necrotic core
You see:
T cells +
Foam cells +
Smooth muscle cells +
Fibroblasts
Nature of the plaque in stable angina
Fibrous cap is strong & less prone to rupture
If plaque prone to rupture —> prothrombotic state; platelet adhesion + accumulation; progressive lumen narrowing
Percentage of lumen narrowing in stable angina
> 70% is when symptoms start to develop
Signs and symptoms of stable angina
Central crushing chest pain radiating to the neck & jaw
Dyspnoae
Fatigue
Sweating
Investigation & diagnosis of stable angina
1st line:
ECG : Resting - normal
Exercise induced (Ischaemic) - change
Gold standard:
CT angiography - stenoses atherosclerotic arteries (>70% occlusion)
1st line investigation for stable angina
1st line:
ECG : Resting - normal
Exercise induced (Ischaemic) - change
Gold standard investigation for stable angina
Gold standard:
CT angiography - stenoses atherosclerotic arteries (>70% occlusion)
Treatment for stable angina
Remember RAMP for stable angina management
Refer to cardiologist; Advise on lifestyle modification, Medical Tx, Procedural intervention
Medical Tx:
Immediate symptomatic relief -
GTN sublingual spray
Long term symptomatic relief -
All patients:
CCB (CI : heart failure) / BB (CI : asthma)
CCB + BB
CCB + BB + another anti-anginal (ivabradine / longacting nitrates)
Secondary prevention -
Aspirin
Atorvastatin
ACEi
What procedural interventions are there for stable angina
given if pharmacological intervention unsuccessful
Revascularisation
PCI - balloon stent via femoral artery to coronary artery
CABG - bypass graft (LAD bypassed using great saphenous vein)
Give a positive and negative for PCI
+ve : Less invasive
-ve : High risk of restenosis
What is restenosis
a gradual re-narrowing of the stented segment that occurs requiring further procedural treatment
What type of CCB is used in stable angina
Non-rate limiting one - Amlodipine
If others are used(verapamil / diltiazem), causes excessive bradycardia
Dihydropyridine CCBs have predominantly peripheral vasodilatory actions, whereas nondihydropyridine CCBs have significant sinoatrial (SA) and AV node depressant effects and possible myocardial depressant effects with lesser amounts of peripheral vasodilation.
Give a positive and negative of CABG procedure
+ve: Good prognosis
-ve: more invasive + longer recovery time
Clinical classification of unstable angina
Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
New onset angina
Occlusion for unstable angina
partial occlusion of minor coronary artery (>90%)
Type of infarction in unstable angina
None - ischaemia only
ECG finding in unstable angina
Normal
May show some ST depression / T wave inversion
Troponin levels in unstable angina
Normal
Level of occlusion for NSTEMI
Major partial occlusion (>90%) / total occlusion of minor coronary artery
Type of infarction in an NSTEMI
Subendothelial infarct
I.e. area furthest away from the occlusion dies
ECG finding for NSTEMI
ST depression
T wave inversion
no Q waves! - seen in STEMI, only after some time
Troponin levels for NSTEMI
Raised
Due to infarct obviously
Level of occlusion in STEMI
Complete occlusion of major coronary artery
Type of infarction in STEMI
Transmural infarction
ECG finding of STEMI
ST segment elevation
Pathological Q waves - develop after some time
Troponin levels seen in STEMI
Raised
Signs and symptoms of ACS
Same as stable (more severe) - dyspnoea, chest pain radiating to neck and jaw, sweating + nausea
+
Pain at rest, prolonged with no relief
often described as - ’impeding doom’ +
Palpitations
What is a silent MI
Diabetic patients may not experience typical chest pain during an acute coronary syndrome
Due to diabetic neuropathy; don’t feel the anginal pain so could miss the diagnosis and Px could die with sudden collapse
Investigations & diagnosis of ACS
ECG
Bio markers
CT coronary angiogram
Treatment for ACS
_Acute - remember MONAC_
- Morphine
- Oxygen (if SATs <94%; COPD: 88-92%)
- Nitrates (GTN spray)
- Aspirin
- Clopidogrel
Then…
For unstable / NSTEMI = GRACE score
- low risk : monitored
- high risk : coronary angiogram - may need PCI
For STEMI
- PCI if within 12hr Sx onset / <2hr of first medical contact
- Thrombolysis using alteplase / streptokinase if >12hrs of Sx onset, then consider PCI
_Long-term prevention_
Aspirin
Aatorvastatin (life)
ACEi (life)
Beta blocker (life)
Role of alteplase
Thombolytic agent - activates plasmin to break down fibrin
In what conditions is troponin elevated in…
MI
But also…
Myocarditis
PE
Aortic dissection
Sepsis
Chronic renal failure
Complications of ACS
Acutely (<2 weeks)
H.F - due to ventricular fib
Mitral incompetence
LV wall rupture
Cardiogenic shock
>2 weeks
Dressler’s syndrome (autoimmune pericarditis)
H.F
LV aneurysm (heart becomes saggy)
Define heart failure
Inability for the heart to pump sufficient Oxygen in order to meet the demand of the tissue metabolism
A syndrome not a diagnosis
Causes of heart failure
IHD - most common
Hypertension
Valvular heart disease (aortic stenosis)
Arrythmias (AF)
Risk factors for heart failure
Age (>65y/o)
Smoking
Obesity
Previous MI
Male > female
Pathophysiology of heart failure
Normally…
Increased preload = increased afterload (frank starlings law)
But, in failing heart…
Decreased cardiac output due to dysfunctional frank starling law so
1) Compensatory mechanism activation: RAAS + SNS (to temporarily increase BP) - increased aldosterone — increased ADH ; increased Ad/NAd
2) compensation then fails as heart undergoes cardiac remodelling. (Decreasing C.Output)
• Heart becomes less adapted to function so increased RAAS +SNS causes fluid overload
• In response to the increased work of the heart, both left and right circuits are affected - Congestive heart failure
Classification of heart failure
Time classified: acute / chronic
Ejection fraction (normal EF = 50-70%)
> 40% ejection fraction suggests what
Preserved ejection fraction
(Heart pump function is preserved)
Diastolic failure
- Filling issues due to stiffness
E.g. hypertrophic cardiomyopathy, Ventricular hypertrophy
What can cause diastolic heart failure
hypertrophic cardiomyopathy, ventricular hypertrophy
What does < 40% ejection fraction suggest
Reduced ejection fraction
Heart pumping has failed
Systolic heart failure
- reduced C.Output due to inability to pump
E.g. IHD
Give a cause for Systolic heart failure
IHD
Left sided heart failure causes what
Results in pulmonary vessel backlog
- therefore, pulmonary oedema
What does right sided heart failure cause
Causes backlog in systemic venous system
- leading to peripheral oedema
Cardinal signs of heart failure
Dyspnoea
Fatigue
Ankle oedema
Signs / symptoms of heart failure
Oedema
3, 4 heart sound
Increased JVP (backlog in jugular veins) - i.e. RHF
Orthopnoea (worse when lying flat) / paroxysmal nocturnal dyspnoea
Bibasal crackles** (pul. Oedema) - i.e. LHF
Hypotensive + tachycardic
What classification describes severity of heart failure
NY heart association class 1-4 of HF severity:
1) No limit on physical activity
2) Slight limit on moderate activity
3) Marked on moderate / gentle activity
4) symptoms even at rest
Key marker found in Heart failure
BNP
B type- natriuretic peptide
(> 400µg/mL)
Inactive BNP = NT-proBNP
it is x5 higher than BNP so (> 2000µg/mL) is high level indicating HF
Investigation / diagnosis of heart failure
Bloods - Raised BNP
ECG - Abnormal: may show signs of LVH
Chest X-ray - ABCDE
•Alveolar ‘batwing’ oedema
• kerley B-lines
•Cardiomegaly
•Dilated upper lobes
• pleural Effusion
Echocardiogram - shows dimension of heart chambers
Types of treatment available for heart failure
Conservative
Pharmacological
Surgical
Type of conservative treatment for HF
Lifestyle ∆’s
(Reduce BMI, exercise, diet, smoking + alcohol cessation)
Pharmacological treatment for HF
L.A.B.A - first line medical Tx
ACEi - ramipril
ß Blocker - atenolol
+
Aldosterone antagonist - Spironolactone
Loop diuretic - Furosemide
Consider cardiac resynchronisation therapy (to improve AV conduction)
Surgical treatment for heart failure
Consider revascularisation, valve surgery
Heart transplant = last resort
Role of BNP
Released by ventricular myocardium - opposes affect of RAAS
BNP act on blood vessels, causing them to dilate, or widen.
They also work on the kidneys, causing them to excrete more salt and water.
Reduce the production of adrenaline, angiotensin, and aldosterone.
BNP is therefore secreted when there’s increased pressure on heart - elevated in heart failure
Define Cor pulmonale
Right sided heart failure caused by respiratory disease.
Cause of Cor pulmonale
Remember it is RHF due to a resp disease
• COPD - most common cause
• PE
• Interstitial lung disease
• CF
Pathophysiology of cor pulmonale
Increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries.
This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.
Signs / symptoms of cor pulmonale
Raised JVP
Cynosis
peripheral oedema
3rd Heart sound
Murmurs : Tricuspid regurg - Pan systolic
Define abdominal aortic aneurysm
Permanent aortic dilation exceeding 50% where diameter > 3cm
> 5.5cm is urgent (significant rupture risk)
Rupture - surgical emergency!
Risk factor for aortic aneurysm
Idiopathic
Connective tissue disorder — Marfan syndrome, Ehler danlos synderom
Smoking(biggest RF), obesity, HTN (those RF for atherosclerosis)
Pathophysiology for aortic aneurysm
Smooth muscle, elasticity and structural degeneration in all 3 layers of vascular tunic (intima, media, adventitia) with leukocyte infiltration
If not all 3 layers affected - pseudoaneurysm
Note: Most aortic aneurysm = Abdominal (infrarenal), but
Can occur as thoracic
• Main cause = Marfan syndrome / Ehler’s Danlos / Atherogenesis
• Monitor with CT / MRI
• Any Sx: surgery immediately
Signs / symptoms of AAA
Asymptomatic till increased rupture risk / ruptured
Sudden epigastric pain radiating to flank
Pulsatile mass in abdomen
Hypotensive + tachycardic
Differential diagnosis for AAAneurysm
Acute pancreatitis
• Non-pulsatile + more associate with Grey turner (flank discolouration) / Cullen Sx (superficial oedema/bruising)
Investigation & diagnosis of AAA
1st line + diagnostic
ABDO USS
Tx for AAA
Conservative management - ∆ modifiable risk factors
aSx and <5.5cm : monitor
Sx, >5.5cm &/ rapidly expanding : Surgery
• Endovascular repair - stent inserted through femoral artery (less invasive)
• Open surgery (more invasive)
Complication of abdominal aortic aneurysm
Rupture
Stabilise: ABCDE, fluids + transfusions
Then, consider surgery
• AAA graft surgery; replacing weakened walls with graft
• 100% mortality if not treated immediately
Define aortic dissection
Tear in the intima of the aorta resulting in blood dissecting through the media of the aorta, separating the layers apart - due to mechanical wall stress; surgical emergency
Who is aortic dissection most commonly seen in
50-70y/o men
Risk factors for aortic dissection
HTN (most common)
Connective tissue disorder - Marfan syndrome, EDS
FHx
AAA
Trauma
Smoking
Common locations of aortic dissection
1) Sinotubular junction - where the aortic root becomes tubular; near aortic valve. (Ascending aorta)
• Aortic dissection A
2) Distal to left subclavian artery - thoracic descending aorta. (Descending aorta)
• Aortic dissection B
Types of aortic dissection + the classification
Stanford’s classification
Type A : Ascending aorta
Sinotubular junction - 2/3 (more common)
Type B : Descending aorta
Distal to left subclavian artery - 1/3
Debakey system
Type I : ascending + descending aorta
Type II : ascending aorta
Type III : descending aorta
Pathophysiology of aortic dissection
Blood dissects media + intima, where it pools in a false lumen which can propagate forwards (anterograde) and backwards (retrograde; towards aortic root)
Decreased perfusion to end organ —> organ failure + shock
Signs and symptoms of aortic dissection
Sudden onset ripping/tearing chest pain
Anterior pain - ascending
Posterior pain - descending
Hypotension/shock
Syncope
Diastolic murmur
Radial pulse deficit
Differential diagnosis of aortic dissection
MI
Central crushing chest pain with gradual worsening intensity
Investigation & diagnosis of aortic dissection
CXR shows widened mediastinum (> 8cm = suspicious)
Gold standard -
TOE (Transoesophageal echocardiogram) : shows intima flap / false lumen - more invasive than TTE but is more specific to aortic dissection + v.sensitive;
then classify AD as A / B
OR
CT angiogram : shows intima flap / false lumen / leak or rupture (also v. Specific & sensitive) - used more when Px is haemodynamically stable
Treatment for aortic dissection
Surgery - open surgery (type A) / endovascular aortic repair (type B)
— if they’re hypotensive: consider IV fluid, blood transfusion, adrenaline
Medical (prevention) -
1) Special beta blocker : esmolol / labetolol
— ß-Blocker and partial ∂-blockers prevent reflex tachycardia + decrease BP
• Aim: systolic BP (100-120) + HR: ≈ 60
2) Vasodilator : Sodium Nitroprusside
Give 3 complications of aortic dissection
(Haemorrhagic) Cardiac tamponade
Ischaemic stroke
Pre-renal AKI
Types of beta blockers used in aortic dissection
Esmolol / labetolol
Define hypertension
Abnormally high BP
≥ 140/90 mmHg (clinical)
≥ 135/85 mmHg (ambulatory / home readings)
Types of hypertension
Primary (Essential) - idiopathic HTN (95% of cases)
Secondary - known underlying cause
Causes of hypertension
Primary = idiopathic
Secondary = Remember ROPE
Renal disease
Obesity
Pregancy / eclampsia
Endocrine disorder:
- Conn’s (most common cause of HTN)
- Phaemochromocytoma
- Cushing’s
Risk factors for hypertension
Older age
Obesity
Black ethnicity
Smoking
Diabetes
Increased salt intake
FHx
Describe the different stages of HTN
1) 140/90 … 135/85
2) 160/100 … 150/95
3) 180/120 - start immediate Tx
Pathophysiology of HTN
Ultimately all mechanisms stimulate RAAS + SNS (increasing cardiac output) + TPR … Increasing BP
Signs / symptoms of HTN
Mostly aSx
May have pulsatile headaches
Malignant hypertension :
180/120 (usually marked more by diastolic BP ≥ 120)
Px : typically seen in 30-40y/o black males
M.HTN causes:
Heart failure
Blurred vision
Haematoma
Headache
Consider signs of 2º cause
Investigation & diagnosis of hypertension
BP reading in hospital (≥140/90)
— Then ABPM for 24hr to confirm diagnosis (≥135/85)
Assess end organ damage
— Fundoscopy (papilloedema)
— eGFR (renal function + risk of diabetes)
— Echo/ECG (heart function; check for LVH)
Treatment for hypertension
——— < 55y/o / T2DM ——— ≥ 55y/o / black African———
1 —————ACEi————or———— CCB—————
2 —————————ACEi + CCB—————————
3 ———— ACEi + CCB + Thiazide diuretic —————
4 —— ACEi + CCB + Thiazide ± diuretic + K+ sparring——
What do you give if ACEi is contraindicated
ARB - Candesartan
4th line for HTN has you add which drug and what drug is given if contraindicated
In 4th line, the 4th drug given is K+ sparring diuretic
But if K+ > 4.5, give ∂/ß blocker
If Px is Black & has T2DM, what is 1st line treatment
ACEi
Because T2DM takes precedence over being black
A 60y/o black man has hypertension and T2DM, what is the first line treatment
ACEi
Having T2DM takes precedence
Complications for hypertension
Heart failure
CKD
IHD
Cerebrovascular accident risk increases
Define DVT and a PE
DVT
- Thrombus formation in deep leg vein
When in calf, less concerning - more common
When in thigh, life threatening - less common
PE
- When DVT emobolise and lodges in pulmonary artery circulation
Risk factors for DVT ± a PE
Remember Virchow’s Triad:
• Hypercoagulability
Pregnant
Antiphospholipid syndrome
DIC
• Venous stasis
Immobility
Long haul flights
Surgery
• Endothelial injury
Trauma / Surgery
Smoking
HTN
What can a PE cause / lead to
Cor pulmonale
(Right sided heart failure due to a resp condition);
Increased PVR —> increased right ventricle strain to overcome it —> RVH —>R.Ventricle fails, 2º to Pulmonary artery pressure
Give 3 conditions that present with pleuritic chest pain
PE
Pneumothorax
Pneumonia
Differential diagnosis between: PE, Pneumothorax, Pneumonia
Do CxR:
PE - normal
Pneumonia + pneumothorax - diagnostic
Signs / symptoms of DVT
Unilateral, swollen, warm + oedematous calf with dilated superficial veins.
What is phlegmasia cerulea dolens
Complete occlusion of a large being —> severe DVT
Severe ischaemia —> presents a s cyanosis (blue, not red like DVT)
Which scoring system is used in DVT / PE
Wells score
Diagnosis + investigation of DVT
Wells score ≥ 2 is likely of DVT
If D-dimer - elevated (1st line) —>
Do Duplex USS (Gold standard - diagnostic)
If D-dimer not elevated - not a DVT/PE
Is D-dimer specific or sensitive
Sensitive (95%)
Not specific
Measures clot burden - a small protein released into the blood when a clot is fibrinolysed
- Will always (95% of the time) be seen in DVT/PE - sensitive
but can also be raised in other conditions - not specific
Conditions D-dimer can be elevated in
DVT / PE
Heart failure
Pneumonia
Pregnancy
Malignancy
Treatment for DVT
DOAC
- Rivaroxaban / Apixaban
LMWH - if DOAC is contraindicated (e.g in renal impairment )
+ mobilisation, compression stockings (unless contraindicated - Peripheral Arterial Disease)
Differential diagnosis for DVT
Cellulitis
• Skin infection
Typically Staph. Aureus / Strep. Pyogenes
• Tender, inflamed, swollen calf with pronounced demarcation (Bullae: fluid-filled blisters + golden-yellow crust - indicate a staphylococcus aureus)
Typically show leukocytosis - sign of infection on FBC
BUT
Not seen in DVT : D-dimer and D.USS used for DVT diagnosis
Complication of DVT
PE
Signs and symptoms of PE
Sudden onset pleuritic chest pain
Dyspnoea ± haemoptysis (streaky blood)
Tachycardic + tachypnoea (respiratory alkalosis), hypotensive, increased JVP
+ evidence of DVT : swollen, red, oedematous & tender leg
Prophylaxis for VTE: DVT/PE
LMWH - Enoxaparin
Warfarin
DOAC
Diagnosis + investigation of PE
Wells score ≥ 4 : PE likely
If likely —> CT Pulmonary Angiogram (CTPA - Gold standard) = Diagnostic
This is because CTPA is specific for Pulmonary Embolism
If unlikely (Wells score < 4) —> D-dimer (1st line)
- if raised, do CTPA
- if not raised, not PE
Treatment for pulmonary embolism
If massive PE (hypotensive:< 90 systolic BP):
Thrombolytics - Alteplase
If non-massive PE:
1st line - DOAC (Rivaroxaban / Apixaban)
• if contraindicated (renal impairment) - give LMWH
Define pericarditis
Inflammation of the pericardium ± effusion; typically acute, can be chronic
Cause / aetiology of pericarditis
Idiopathic
Viral - Coxsackie virus (most common cause)
Bacterial - TB
Autoimmune - SLE, Rheumatoid.A (common)
Dressler’s syndrome (>2 weeks post MI)
Pathophysiology of pericarditis
• Inflamed pericardial layer rub against each other - because of narrowed pericardial space due to the inflammation
• Further exacerbating inflammation
Can either present as:
• Dry - no extra fluid; not as bad because friction doesn’t need to be overcome
• Effusive - extra fluid needed to compensate for friction
Signs and symptoms of pericarditis
sharp severe pleuritic chest pain with referral to left shoulder tip (at trapezius ridge)
Relieved sitting forward
Worse laying flat or on inspiration
Pericardial friction rub on auscultation - heard when patient leans forward squeaky leather to and fro sound
May show signs of right sided HF (constrictive pericarditis) —> SoB, peripheral oedema, tachycardia (chronic inflammation of pericardium)
What is constrictive pericarditis
Late complication of acute pericarditis + there’s a sign of poor heart prognosis.
Granulation tissue formation in pericardium —> impaired diastolic filling.
Investigation and diagnosis of pericarditis
ECG (diagnostic):
- Widespread saddle shaped ST elevation
- PR depression
CXR:
- “Water-bottle” heart (cardiomegalic)
- Pneumonia commonly seen (bacterial pericarditis - TB)
Increased ESR
- Seen in autoimmune pericarditis
Increased WCC
- in infective pericarditis
Treatment of pericarditis
Idiopathic + viral:
NSAID’s (aspirin)
+
Colchicine (anti inflammatory - used in gout too)
+ antibiotic if bacterial (R.I.P.E Abx for TB)
Complication of pericarditis
Pericardial effusion
Cardiac tamponade
Myocarditis
Constrictive pericarditis
Define pericardial effusion
Pericardial effusion
When the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart).
Cardiac tamponade
Where the pericardial effusion is large enough to raise the intra-pericardial pressure. This increased pressure squeezes the heart and affects its ability to function. It leads to reduced filling of the heart during diastole, resulting in decreased cardiac output during systole
Types of effusion and their causes
Transudative effusion:
Due to increased hydrostatic pressure
Less protein
Transparent fluid
••• Congestive heart failure
••• Pulmonary hypertension
Exudative effusion:
Occur in any inflammatory process; via infection / malignancy
More protein
Cloudy fluid
••• Infection; pneumonia / pancreatitis
••• PE
••• Medication - methotrexate
Signs and symptoms of pericardial effusion & cardiac tamponade
Sx related to pericarditis (chest pain)
Phrenic nerve compression can cause hiccups
Oesophageal compression may cause dysphagia (difficulty swallowing)
Recurrent laryngeal nerve compression may cause a hoarse voice
For cardiac tamponade:
Beck’s triad - hypotension, increased JVP, muffled s1-s2 sound
Pulses paradoxicus - fall in systolic BP of 10+ mmHg on inspiration (good indicator of cardiac tamponade) —> kussmaul’s sign
Investigation and diagnosis of pericardial effusion + cardiac tamponade
ECG : may show electrical
CxR : big globular heart
Echo : diagnostic
Treatment of pericardial effusion + cardiac tamponade
Pericardial effusion - Tx underlying cause (NSAIDs + Colchicine —> pericarditis)
Cardiac tamponade - urgent pericardiocentesis
Define Peripheral vascular disease
Essentially IHD of lower limb arteries.
Males
Risk factor for Peripheral vascular disease
Smoking
HTN
Ageing
Obesity
CKD
T2DM
Pathophysiology for peripheral vascular disease
Intermittent claudication (least severe) —>
Atherosclerotic, partial lumen occlusion, pain on exertion as blood flow < demand
Critical limb ischaemia (more severe) —>
Occlusion is V. Big; blood supply barely adequate to meet metabolic demand
Pain at rest + increased risk of gangrene / infection
Limb ischaemia can be acute / chronic!!
Define peripheral arterial disease
Peripheral arterial disease (PAD) refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas
Define intermittent claudication
Intermittent claudication is a symptom of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock
Reduced blood to muscle —> reduced O2 —> ischaemia —> this causes cells to release adenosine (signalling molecule for nerve cells) —> feel the signal as pain —> pain = claudication
Define critical limb ischaemia
Critical limb ischaemia is the end-stage of peripheral arterial disease
Pain at rest; non-healing ulcers + gangrene
Difference between PVD & PAD
Pretty much the same thing
Risk factors for PVD
Same as atherosclerosis:
Smoking
HTN
Ageing
Obesity
CKD
T2DM
Define acute limb ischaemia
rapid onset of ischaemia in a limb.
Typically, this is due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.
Define gangrene
the death of the tissue, specifically due to an inadequate blood supply.
Features of limb ischaemia
Remember 6P’s - found in both acute and critical (chronic is more limb threatening)
Pain
Pallor
Perishingly cold
Paralysis
Paraesthesia
Pulselessness
In critical limb ischaemia - causes burning pain. It is worse at night when the leg is raised
Mention 3 things that can occur if blood vessels to a region is occluded in PVD
1) Irreversible nerve damage (within 6hrs)
2) Irreversible muscle damage (6-12hrs)
3) Skin ∆’s are last to appear therefore likely to be gangrenous
Investigations and diagnosis of PVD
Ankle brachial pressure index (ABPI) = 1st line
[•] < 0.9 indicates PVD
[•] 0.9 - 1.3 = Normal;
[•] 0.5 - 0.9 = intermittent claudication;
[•] < 0.5 = critical limb ischaemia;
[•] When absent / v. Low = high risk of Acute limb ischaemia
Ratio / comparison of systolic BP of lower limb * upper limb
Duplex ultrasound scan
[•] Assesses degree of stenosis
CT Angiography = Gold standard
[•] Highlights arterial circulation
Buerger’s test
[•] +ve
[] Elevate leg 45˚ for a minute; Pallor.lower the leg; reactive hyperaemia (blue initially, then red)
What classification used in PAD/ PVD
Fontaine’s classification (stages 1-4):
Classification of the pain experienced after a particular distance.
1) Asymptomatic
2) Intermittent claudication:
• 2a - > 200m pain free walking
• 2b - < 200 m
3) Critical limb ischaemia (pain at rest)
4) Ischaemic ulcers —> gangrene formation
Treatment for PVD
Intermittent claudication
- RF management
Critical limb ischaemia
- Revascularisation surgery (PCI if small; CABG if big occlusion)
Acute limb threatening ischaemia
- Surgical emergency (do within 4-6hrs) —> risk of amputation
Complications of PVD
Amputation
Permanent limb weakness
Rhabdomyolysis (increased ca2+ and k+ release in blood - Arrhythmias / AKI)
Risk of Cerebrovascular accident + CKD
Define virulence
Ability of microbe to cause damage to host
Define infective endocarditis
Inflammation of the endocardium
- causative bacteria; colonise abnormally in the endothelium (leading to vegetation)
Cause of infective endocarditis
Staph. Aureus - most common; IVDU / T2DM / Surgery
Strep. Viridans - Poor dental hygiene; Gram +ve haemolytic Optochin resistant strep.
Staph epidermidis - Prosthetic valve / infected IV catheters
Types of infective endocarditis
Acute
S. Aureus; high virulence. Sx onset days-weeks
Subacute
S. Viridans; lower virulence. Sx onset weeks-months
Risk factors for infective endocarditis
Male, elderly; with prosthetic valves
Young IVDU
Young with congenital heart defect
Rheumatic heart disease
Pathophysiology of infective endocarditis
Abnormal / damaged endocardium have increased platelet deposition; bacteria adheres to this & causes vegetation.
- Around valves - typically mitral valve (highest turbulence; more damage), but in IVDU more so tricuspid valve is affected\
- causes regurgitation (+ left side more affected so get aortic & mitral insufficiency; increased risk of HF)
Signs and symptoms of infective endocarditis
FEVER + NEW MURMUR = I.ENDOCARDITIS
Symptoms: vague; fever, fatigue, SoB
Signs:
ROTH SPOTS
JANEWAY LESIONS
SPLINTER HAEMORRHAGES
OSLER NODES
What criteria is used in infective endocarditis
DUKE criteria
Investigation and diagnosis of infective endocarditis
Diagnosis made using a DUKE criteria
ECG (prolonged PR —> aortic root abcess)
Increased ESR / CRP + neutrophilia
TOE = gold standard
Blood culture —> over 3 sites over 24hr
- 2 major / 1 major + 2 minor
— Major:
≥2 +ve blood cultures
echo TOE - shows vegetations
— Minor:
IVDU
1 +ve blood culture
Pyrexia
Immunological signs
Treatment of infective endocarditis
Staph Aureus: vancomycin + rifampicin
Strep Viridans: Benzylpenicillin + gentamicin
For 4 - 6 weeks
Surgery —> remove valve if incompetent & replace with prosthetic
Complication of infective endocarditis
Heart failure
Aortic root abscess
Septic emboli (± sepsis)
The effects of regurgitation of heart muscle
Insufficiency + proximal chamber dilation
(Regurgitation - defective valve, floppy)
• Loss of structural chamber integrity + strength
Stenosis causes increase upstream pressure + proximal chamber hypertrophy
(Stenotic - narrowed valve lumens)
• Heart becomes huge and rigid; poorly compliant
When are murmurs best heard
Remember “RILE”
Right side valve defect —> Inspiration
Left side valve defect —> Expiration
A.R-M.S - Diastolic murmur
A.S-M.R - systolic murmur
Most common valve disorder
Aortic stenosis
Normal area of aortic valve vs. Pathological
3-4cm normal
Sx at 1/4 lumen size
Effects of aortic stenosis on heart
Results in LV dilation + hypertrophy
What causes aortic stenosis
Ageing calcification
Rheumatic heart disease
Signs / symptoms of aortic stenosis
Remember S.A.D
Syncope (exertional)
Angina
Dyspnoea (related to heart failure)
- Murmur: Ejection systolic crescendo decrescendo radiating to carotids
- Prominent S4: seen in LVH
- narrow pulse pressure + slow rising pulse (NOT collapsing corrigan’s pulse)
Investigation and diagnosis of aortic stenosis
ECG
CXR
ECHO (Gold standard) - shows LV size + function, aortic valve area (Doppler derived)
Treatment of aortic stenosis
Surgical (if Px = symptomatic);
*Healthy Px — open repair / valve replacement (definitive)
In a risky Px (>75y/o) — TAVI; transcutaneous aortic valve implant = less invasive; just a stent valve open
Type of sound heard in a hypertrophic cardiomyopathy
Causes S4 (sound just before S1)
Associated with sudden death in young men
Define aortic regurgitation
Leaky aortic valve, insufficient
What causes aortic regurgitation
Congenital bicuspid valve
Rheumatic heart disease
Connective tissue disorders; Marfan’s / Ehler’s Danlos
INFECTIVE ENDOCARDITIS
Signs and symptoms of aortic regurgitation
Murmur: Early diastolic blowing murmur (@ right sternal border)
Severe form = Austin flint murmur - a mid diastolic low pitched rumble; Heard when regurgitation is so severe the blood bounces off mitral valve cusps + makes sound
Collapsing corrigon pulse with wide pulse pressure
Investigation and diagnosis aortic regurgitation
ECG
CXR
Echo (Gold standard) - evaluate aortic valve, root and dimension
Treatment of aortic regurgitation
Consider IE prophylaxis
Surgical valve replacement is symptomatic
Differential diagnosis for aortic regurgitation
Infective endocarditis
Define mitral stenosis
Mitral lumen 4-6cm
Symptoms appear at < 2cm
Risk factors for mitral stenosis
Rheumatic fever Hx
men
ageing
Causes of mitral stenosis
Rheumatic heart disease - most common, post strep. Pyogenes infection
Valve calcification - seen in older Px
Infective endocarditis
Pathophysiology of mitral stenosis
Rheumatic heart disease causes mitral reactive inflammation; over the years its exacerbated with calcification —> leading to left atria hypertrophy
Signs / symptoms of mitral stenosis
Malar flush
Dyspnoea
A wave on JVP
Associated with AFib - M. Stenosis leads to LA hypertrophy so more chance of embolisation as blood being pumped out harder
Murmur: low pitched, mid-diastolic murmur
- loudest at apex
- best heard on expiration (lying on LHS)
*Loud S1 snap *
Investigation and diagnosis for mitral stenosis
ECG - may show AFib / p mitrale - ‘m’ shaped p wave seen in LA enlargement
CXR - LA enlargement
(Gold standard) - echocardiogram
Treatment for mitral stenosis
Surgical
- Percutaneous balloon valvotomy (a stent)
- Mitral valve replacement
Define mitral regurgitation
Insufficient mitral valve function
Causes of mitral regurgitation
myxomatous mitral valve (most common; mass of cells in valves connective tissue making leaflet heavier & prolapse)
Connective tissue disorders; Marfan / Ehlers Danlos
Risk factors for mitral regurgitation
Females
Older
Decreased bmi
Prior MI
Connective tissue disorder
Signs / symptoms of mitral regurgitation
Exertion dyspnoea (pulmonary hypertension, from back log of blood)
Murmur - pan-systolic murmur - radiating to axilla
- soft S1, prominent S3 if prolonged and lead to heart failure (severe form)
Investigation and diagnosis of mitral regurgitation
ECG
CXR
Gold standard - Echocardiogram
Treatment for mitral regurgitation
ACEi, BBlockers + monitoring using Echo
If severe - valve replacement / repair
Mitral stenosis murmur
Mid diastolic low pitched ‘rumbling’ murmur
Loud S1
What might malar flush indicate
Mitral stenosis
Which valvular heart disease might cause atrial fib
Mitral stenosis
Which valvular disease might cause congestive heart failure
Mitral regurgitation
Mitral regurgitation murmur
Pan-systolic high pitched whistling murmur
Radiates to axilla
With S3 heart sound
Aortic stenosis murmur
Ejection systolic high pitched crescendo-decrescendo murmur
Radiates to the carotids
Slow-rising pulse with narrow pulse pressure
Aortic regurgitation murmur
Early diastolic ‘rumbling’ murmur
With collapsing pulse (aka corrigans pulse)
Austin flint murmur heard best at apex of the heart (severe for of aortic regurgitation)
Where are the 4 valve murmurs heard from
Pulmonary: 2nd I.C.S left sternal border
Aortic: 2nd I.C.S right sternal border
Tricuspid: 5th I.C.S left sternal border
Mitral: 5th I.C.S mid clavicular line (apex area)
Define tachycardia
> 100 bpm
Types of tachycardia
Supraventricular tachycardia (SVT)
Atrial fib
Atrial flutter
AVRT (non-junctional) - wolff-Parkinson’s white syndrome
AVNRT
Ventricular tachycardia
prolonged QT syndrome
Ventiricular fibrillation
What is the most common SVT
AVNRT
- re-enterant pathway goes through AVN
Difference between AVRT and AVNRT
AVRT - re-enterant pathway through accessory pathway
(Bundle of kent)
AVNRT - re-enterant pathway goes through AVN
Define bradycardia
< 60 bpm
Types of bradycardia
Bundle branch block
- RBBB / LBBB
1˚/2˚/3˚ heart blocks
Atrial fib rhythm
Irregularly irregular
Causes of atrial fibrillation
Heart failure, HTN
2˚ to mitral stenosis
Idiopathic
Risk factors for atrial fibrillation
60+
Valvular heart defect
Hx of MI
T2DM
HTN
Pathophysiology of atrial fib
Rapid re-entrant ectopic foci (over 300 beats) causes atrial spasm - not coordinating contraction like normal .
This leads to atrial blood pooling instead of pumping efficiently to the ventricles
So, decreased CO and increased risk of thromboembolic events
Signs / symptoms of atrial fibrillation
Palpitations
Irregularly irregular pulse
Chest pain
Syncope
Hypotensive
Sx can be paroxysmal (episodic), persistent (> 7 days), permenant - sinus rhythm unrestorable
Investigation and diagnosis of atrial fibrillation
ECG (diagnostic) - irregularly irregular, narrow QRS complex
No P waves
Treatment of atrial fibrillation
Acute / unstable - (syncope, shock, chest pain, heart failure):
DC synchronised cardioversion
If stable (/prevent further episodes) - ß-blockers/CCB (like verapamil) + anticoagulant
Surgical radiofrequency ablation - restores normal rhythm by targeting misfiring heart tissue and killing it
Which scoring system is used in Atrial Fib
CHA2DS2 VASc score is used
Because high stroke risk + anticoagulation needed
HASBLED score
Assesses risk of major bleeds in AF patients on anticoagulant
≥ 3 score (max 9) - regular reviews required
What does CHADS VASc stand for
Congestive heart failure
HTN
Age > 75y/o (2 points)
DM type2
Stroke (2 points)
Vascular disease
Age 65-74y/o
Sex category = female
Complication of atrial fibrillation
Heart failure
Ischaemic stroke
Define atrial flutter
Irregular regular atrial firing
Less common and less severe that atrial fib
Risk factor of atrial flutter
Same as atrial fib:
60+
Valvular heart defect
Hx of MI
T2DM
HTN
Causes of atrial flutter
Similar to atrial fibrillation -
Heart failure, HTN
2˚ to mitral stenosis
Idiopathic
Pathophysiology of atrial flutter
Fast atrial ectopic firing causes atrial spasm but not as uncoordinated as A. Fib
Pathway typically from around tricuspid annulus (opening of valve)
Signs and symptoms of atrial flutter
Dyspnoea, palpitations…
Irregularly regular
Investigation and diagnosis of atrial flutter
ECG (diagnostic) - F wave ‘Saw-tooth’ pattern
Often seen with 2:1 block (2 P waves for every QRS )
Treatment of atrial flutter
Acute: unstable —> DC synchronised cardioversion
Stable —> rhythm / rate control (ß-blocker) with oral anticoagulation (prevent thromboemboli)
Radiofrequency ablation
Define Wolff Parkinson’s white (AVRT)
AVRT - means an accessory pathway exists for impulse conduction, not re-entry though the AVN.
Hereditary
Most common example of AVRT = Wolff Parkinson’s white; accessory pathway for conduction I.e. via bundle of Kent.
- pre-excitation syndrome (excites ventricles earlier than typical pathway) - seen as delta waves
Signs / symptoms of AVRT
Palpitations, dyspnoea, dizziness
Investigation and diagnosis of AVRT
ECG
Slurred delta waves
Short PR interval
Wide QRS
Treatment of AVRT
1st line:
Valsalva (blow into syringe vs. Resistance) /
Carotid massage
2nd:
IV adenosine (will temporarily cease conduction) - warn patient as they will “feel like they’re dying”
3rd:
Consider surgical radiofrequency ablation of bundle of Kent
Define long QT syndrome
Ventricular tachyarrhythmia; usually congenital channelopathy disorder
Where mutations affects cardiac ion channels therefore heart conduction
- QT interval > 480ms
Causes of long QT syndrome
Romano ward syndrome (autosomal dominant)
Jarvell-Lange-Neilson syndrome (autosomal recessive)
Hypokalaemia + hypocalcaemia (non-inherited)
Drugs - Amiodarone, magnesium
Define Torsades de pointes
Polymorphic ventricular tachycardia in patients with prolonged QT
Rapid irregular QRS complex which ‘twist’ around baseline, can cease spontaneously or develop to ventricular fibrillation
Define ventricular fibrillation
Shapeless rapid oscillations on ECG
Px becomes pulseless + goes into cardiac arrest (no effective cardiac output)
1st line treatment for ventricular fibrillation
Electrical defibrillation
Non-synchronised as patient is pulseless
Define Primary AV block
PR prolongation (> 200ms) - every P wave is followed by a QRS
Asymptomatic / stable, therefore no Tx
Causes:
drugs (ß-blocker, CCB, Digoxin—> blocks AVN conduction)
Post MI
SLE
Complication: atrial fibrillation
Cause of primary av block
Drugs (ß-blocker, CCB, Digoxin—> blocks AVN conduction)
Post MI
SLE
Complication of primary AV block
Atrial fibrillation
Define secondary AV block
When some P waves conducted and others aren’t
2 types:
Mobitz 1 (Wenkebach’s)
Mobitz 2
Define Mobitz 1
Mobitz 1 (2˚ AV block)
PR prolongation until a QRS is dropped (PR interval progressively elongates)
Causes of AV block mobitz 1
Drugs - ß-blocker, CCB, Digoxin
Previous MI
SLE
Treatment for Mobitz type 1
No Tx unless v. Symptomatic
- syncope / reduced consciousness
Give Tx: Pacemaker
Define mobitz 2
Persistent PR interval prolongation with random dropped QRS
Causes of mobitz type 2
Drugs - ß-blocker, CCB, Digoxin
Previous MI
Rheumatic fever
Signs / symptoms of secondary AV block mobitz 2
Syncope
SoB
Chest pain
Treatment of mobitz 2
Pacemaker
Define tertiary AV block
Complete AV dissociation
I.e. atria and ventricles beat independently of each other
- ventricular escape rhythm is what sustains the heartbeat
SAN (best - 60-100)
—> AVN (then takes over: 40-60)
—> If dysfunctional, ventricular pacemakers take over (Worst firing rate: 20-40)
Cause of tertiary AV block
Acute MI
HTN
Structural heart disease
Tx for 3˚ AV block
IV atropine
+
Permanent pacemaker
Define bundle branch block
Blocking of the bundle of His
2 types:
RBBB
LBBB
Cause of RBBB
Pul emboli
IHD
Ventricular Septal Defect
RV later activated than LV
Dx of RBBB
ECG: MarroW
- “M” in V1 (RSR wave)
- “W” in V2 (deep S wave)
Hear: Wide physiological S2 splitting heart sound
Cause of LBBB
IHD
Valvular disease
LV is activated later than RV
Dx of LBBB
ECG: WilliaM
- “W” in V1 (RSR wave)
- “M” in V2 (deep S wave)
Hear: Reversed S2 splitting heart sound
Define cardiomyopathy
Disease of the myocardium (muscular / conduction defects)
Types:
Hypertrophic
Dilated
Restrictive
Which cardiomyopathy is most common cause of death in young people
Hypertrophic cardiomyopathy
Most common cardiomyopathy
Dilated
Cause of hypertrophic cardiomyopathy
Familial (inherited) - autosomal dominant mutation of sarcomere protein (troponin T, myosin B)
Exercise
Aortic stenosis
Pathophysiology for hypertrophic cardiomyopathy
Thick non-complaint heart = leads to impaired diastolic filling
Therefore, reducing C.O
Sx of hypertrophic cardiomyopathy
May present with sudden death
Chest pain
Palpitations
SoB
Syncope
Investigation and diagnosis of hypertrophic cardiomyopathy
Echocardiogram (definitive)
Abnormal ecg
Genetic testing
Treatment for hypertrophic cardiomyopathy
ß blocker
CCB
Amiodarone
Cause of dilated cardiomyopathy
Familial: Autosomal dominant - cytoskeleton gene mutation
IHD
Alcohol
Pathophysiology of dilated cardiomyopathy
Thin cardiac walls poorly contract therefore reduced CO
Sx of dilated cardiomyopathy
SoB
Heart failure
Atrial fib
Thromboemboli
Investigation and diagnosis of dilated cardiomyopathy
ECG
Echo (definitive)
Treatment for dilated cardiomyopathy
Treat underlying cause like AFib / HF
Cause of restrictive cardiomyopathy
Granulomatous disease (sarcoidosis / amyloidosis)
Idiopathic
Post MI
Pathophysiology of restrictive cardiomyopathy
Rigid fibrotic myocardium fills poorly + contracts poorly
Reducing CO
Sx of restrictive cardiomyopathy
If severe:
Dyspnoea, S3+4
Oedema, congestive heart failure
Narrow pulse pressure
Investigation + diagnosis of restrictive cardiomyopathy
ECG
Echo
Cardiac catheterisation (definitive)
Tx for restrictive cardiomyopathy
None;
Consider transplant
Px typically die within a year
Define shock
Medical emergancy - hypoperfusion, life threatening, due to acute circulation on failure
Leads to tissue hypoxia + risk of organ dysfunction
General Sx to recognise shock
Skin; pale, cold, sweaty
Reduced GCS
Increased capillary refill time
Decreased urine output
Prolonged hypotension
Define hypovolaemic shock
As a result of fluid loss — dehydration
Or
As a result of blood loss — trauma / GI bleed
Sx of hypovolaemic shock
Hypotension + tachycardia
Confusion
Clammy pale skin
Treatment for hypovolaemic shock
ABCDE
Airway
Breathing (give O2)
Circulation
Disability
Exposure
IV Fluids
Define Septic shock
Due to uncontrolled bacterial infection
Sx of septic shock
Pyrexia
Warm peripheries
Bounding pulse
Tachycardic
Treatment for septic shock
Broad spec antibiotics
Define cardiogenic shock
Due to heart pump failure; MI, cardiac tamponade, pulmonary embolism
Sx of cardiogenic shock
Sx of heart failure — (ankle) Oedema, SoB and fatigue
Increased JVP, S4
Treatment of cardiogenic shock
ABCDE
+
Treat underlying cause
Define anaphylactic shock
Due to IgE mediated type 1 hypersensitivity vs allergen;
Histamine release - constriction causes excess vasodilation and bronchoconstriction
Leads to decreased MAP and hypoxia
Sx of anaphylactic shock
Hypotension + tachycardia
Urticaria
puffy face + flushing of the cheeks
Dyspnoea
Treatment of anaphylactic shock
IM adrenaline - for SNS activation; stress response
Inflammatory response dampens down
Define neurogenic shock
Due to spinal cord trauma
E.g. RTA
- get disrupted SNS but intact PsNS
Sx of neurogenic shock
Hypotension + Bradycardia
Hypothermic
Treatment for neurogenic shock
ABCDE
+
IV Atropine (blocks fatal tone; allows more PsNS inhibition, more chance for SNS to work)
Which organs at highest risk of failure
Kidney
Lungs
Brains
Heart
Define rheumatic fever
A systemic response to ß haemolytic group A strep
- Almost exclusively I developing countries only
Causes of rheumatic fever
Post strep pyogenes infection (group A, ß haemolytic strep)
- typically pharyngitis
50% of cases affect the heart —> Rheumatic heart disease
Pathophysiology of rheumatic disease
M protein from S. Pyogenes reaches heart valve tissue; antibodies attack this ‘cross-link’ (molecular mimicry)resulting in autoantibody mediated destruction ± inflammation
- mitral valves most affected (70% just mitral; 25% mitral and aortic)
- typically thickens leaflets; mitral stenosis
Signs and symptoms of rheumatic fever
New murmur - mitral stenosis
Arthritis
Pyrexia
Syndentiams chorea - uncoordinated jerky movements
Investigation and diagnosis of of rheumatic fever
CXR - cardiomegaly / heart failure / mitral stenosis
Echo - details extent of valvular damage
Jones criteria: recent pyogenes infection
+
2 major
or
1 major + 2 minor
Treatment for rheumatic fever
Antibiotics:
IV benzylpenicillin then phenoxypenicillin for 10 days
For syndenhams chorea:
Haloperidol
What are Aschoff bodies
Histological finding for rheumatic heart disease from valves
What conditions make up tetralogy of Fallot
1) Ventricular Septal Defect
2) Over-riding aorta
3) Right ventricular hypertrophy
4) Pulmonary stenosis Right ventricular outflow obstruction
What does Px with tetralogy of Fallot present as
Cyanotic; VSD with RV outflow obstruction (therefore, oxygen systemically shunted)
Infants often seen in knee to chest squatting position - increases preload + afterload, therefore improves cyanosis
So can Px in clinic if put into the squat position they become less cyanotic
Investigation and diagnosis of tetralogy of Fallot
Echo
CXR - boot shaped heart
Treatment for tetralogy of Fallot
Full surgical repair within 2 years of life
Define coarctation of aorta
Aorta narrows at or just distal to ductus arteriosus
Blood is diverted massively through aortic arch branches, so increased upper body perfusion vs lower body
Sx of coarctation of aorta
Scapular bruits - HTN in collaterals
Upper body hypertension
Investigation and diagnosis of coarctation of aorta
CXR : Notched ribs - dilated intercostal vessels
CT angiogram
Treatment for coarctation of aorta
Surgical repair or stenting
What is the most common inherited heart defect
Bicuspid aortic valve
Typically tricuspid, Px ends up with bicuspid valve instead which degenerates quicker than normal + becomes regurgitative earlier
Define atrial septal defect
Aka patent foreman Ovale
Shunt of blood L—>R, therefore NOT CYNOTIC
May overload right side circulation; right ventricular hypertrophy (if severe; Eisenmenger syndrome)
What’s Eisenmenger syndrome
When pulmonary hypertension causes reversal shunt; R—>L shunt of blood
So deoxygenated blood is pumped systemically
In younger Px the heart is more compliant… but… in older, more shunting so causes dyspnoea
Investigation / test for atrial septal defect
ECHO
Tx for atrial septal defect
Spontaneous closure sometimes / surgical
Define ventricular septal defect
Shunt of blood L—R (non-cynotic; just like atrial septal defect)
Sx of ventricular septal defect
Small VSD: asymptomatic
Large VSD: exercise intolerant, failure to thrive, harsh pansystolic murmur
Investigation and diagnosis of ventricular septal defect
ECHO
Treatment for ventricular septal defect
Spontaneous closure / surgical
Define atrioventricular septal defect
Hole in the middle of the heart
Essentially, no atria
What is atrioventricular septum associated with
Down syndrome
Sx of atrioventricular septal defect
Shortness of breath
Exercise intolerance
Eventually leads to Eisenmenger syndrome
Define patent ductus arteriosus
When the ductus arteriosus fails to close post birth
Blood shunts from aorta —> pulmonary trunk; risk of pulmonary overload + Eisenmenger
Sx of patent ductus arteriosus
Dyspnoea
Failure to thrive
Machine like murmur
Investigation and diagnosis of patent ductus arteriosus
Echo
CXR
ECG
Tx for patent ductus arteriosus
Prostaglandin inhibitor - indomethacin
May induce closure
Otherwise consider closure
3 cardinal signs of aortic stenosis
Syncope
Angina
Dyspnoea
