Cardio conditions Flashcards

1
Q

Cardio s1-s4 sounds

A

S1 - AV valves close - Tricuspid and mitral valves

S2 - Semilunar valves close - Aortic and pulmonary valves

S3 - Rapid ventricular filling (pathological in mitral regurgitation and heart failure)

S4 - Pathological gallop
- Blood forced into a stiff hypertrophic ventricle (LVH + aortic stenosis)

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2
Q

Which ECG leads would you see abnormalities in during a:

  • Right coronary artery pathology
  • Left anterior descending
  • Left circumflex artery
A

RCA - Inferior leads
II, III, aVF

LAD - anterior and septal leads
V1 - V4

Left circumflex - Lateral leads
V5,V6, aVL and I

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3
Q

What is the amplitude and time units on ECG paper of 1 big square (encompassing 5 small squares)?

A

Amplitude - 0.5mv

Time - 0.2s

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4
Q

Mitral stenosis

RF

Pathology
Symptoms
Investigations
Treatment

A

Narrowing of the mitral valve orifice, obstructing LV inflow, preventing proper filling during diastole.

RF - Rheumatic heart disease, post streptococcal infection, women

PATHOLOGY
RHEUMATIC CARDITIS is the predominant cause (fusion and thickening of the valve leaflets lead to narrowing of the valve orifice)

Other causes: calcification due to ageing, SLE, IE

2 consequences:
- Increased LA pressure is referred to the lungs where it leads to pulmonary congestion.

  • Limited filling of the LV, reducing CO

SYMPTOMS
- MALAR FLUSH
- Jugular vein distension (A wave)
- Dyspnoea
- Orthopnea
- Loud S1 snap (thick valve cusps slap each other)
- Rumbling low pitched, mid diastolic murmur (at the apex)
Best heard on expiration with patient lying on left side

INVESTIGATIONS
1st line - Chest X-ray –> Enlarged LA

ECG - Atrial fibrillation, P mitrale - broad, bifid P wave(indicates left atrial enlargements)

GS - Transthoracic echocardiography

Treatment
Surgical
- Percutaneous balloon valvotomy (stent open Mitral valve opening)
- Mitral valve replacement

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5
Q

Mitral regurgitation

RF

Pathology
Symptoms
Investigations
Treatment

A

Backflow of blood from the LV to the LA during systole (insufficient mitral valve)

RF - Mitral valve prolapse (valve flaps don’t fit), IE, Rheumatic heart disease

PATHOLOGY
Causes
- Myxomatous mitral valve
(Accumulation of connective tissue leading to thickened and redundant valve leaflets - which may lead to prolapse) - MAIN CAUSE
- Connective tissue disorders - Marfan’s, Ehler danlos

SYMPTOMS
- Exertional dyspnoea
- Fatigue
- Pansystolic blowing murmur radiating to the axilla
(Possible S3 sound- rapid ventricular filling to compensate for leaked blood)

INVESTIGATIONS
1st line - Chest X-ray
ECG

GS - Transoesophageal echocardiogram (assess severity of valve dysfunction, LV size and function)

TREATMENT
If not severe
Rate control - BB, CCB
+
Serial echocardiogram for monitoring
(IE prophylaxis)

Severe
Valve replacement surgery

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6
Q

Aortic stenosis

RF

Pathology
Symptoms
Investigations
Treatment

A

Narrowing of the aortic valve, obstructing blood flow out of the LV.

RF - >60 years (calcification of valve), congenital bicuspid aortic valve, RHD

PATHOLOGY
Mainly due to ageing calcification.
Also can be due to congenital bicuspid aortic valve.

As narrowing of valve gets more severe, LVH will develop –> overtime, LV will become less complication and will decline in function

SYMPTOMS
Triad (SAD)
- Syncope (Exertional)
- Dyspnoea (Exertional)
- Angina
(S4 heart sound)
Narrow pulse pressure + slow rising carotid pulse (Decreased systolic pressure caused by AS)

Ejection systolic, crescendo decrescendo murmur - radiating to the carotid arteries

S4 will be seen in LVH

INVESTIGATIONS
1st line - Chest X-ray, ECG

GS
Transoesophageal echocardiography

TREATMENT
Surgical
Young, clinically stable, healthy patient
- Surgical aortic valve replacement (IE prophylaxis)

Severe AS and clinically unstable, older patient
- TAVI - Transcatheter aortic valve implant

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7
Q

Aortic regurgitation

RF

Pathology
Symptoms
Investigations
Treatment

A

The diastolic leakage of bloodflow from the aorta into the LV due to inadequate coaptation of the valve leaflets (insufficiency)

RF - Bicuspid aortic valve, rheumatic fever, Marfans, ehler danlos

PATHOLOGY
Caused by congenital bicuspid aortic valve or connective tissue disorders (Marfan’s - results in aortic root dilation, causing valve leaflets to stretch resulting in incomplete coaptation)

(Aortic regurgitation –> Increase LV volume and pressure –> increase LA pressure –> backlog of blood to pulmonary vasculature –> pulmonary oedema and cardiogenic shock)

SYMPTOMS
Dyspnoea, fatigue, pallor, cysnosis
- Early diastolic, high pitched blowing murmur (right 2nd ICS)
- Widened pulse pressure
- Collapsing corrigan’s pulse / water hammer pulse
- Quincke’s sign - Capillary pulsation upon compression of nailbed
- De Muset’s sign - Head bobbing with heart beat

INVESTIGATIONS
1st line - Chest X-ray, ECG

GS - Transoesophageal echocardiogram (possible aortic root dilation, evaluate severeity of regurgitation + LV function)

TREATMENT
Chronic - IE prophylaxis (serial echocardiogram to monitor patients)

(For Acute - surgical aortic valve replacement) - Rare

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8
Q

Stable angina

RF

Pathology
Symptoms
Investigations
Treatment

A

Chest pain caused by insufficient blood supply to the myocardium and induced by physical exertion or emotional stress.

RF - Advancing age, smoking, hypertension, diabetes, obesity, males

PATHOLOGY
Primarily caused by atherosclerosis (narrowing of coronary arteries resulting in ischemia)

SYMPTOMS
1) Central crushing chest pain that radiates to the arm, neck or jaw
2) Chest pain provoked by exercise or emotional stress (or cold weather)
3) Chest pain relieved by Glyceryl trinitrate or with 5 mins of rest
(palpitations, dyspnoea, syncope)

INVESTIGATIONS
1st line - Resting ECG - Normal

GS - CT coronary angiography - Shows stenosed atherosclerotic arteries (narrowing of artery)

TREATMENT
Symptomatic - GTN spray
Lifestyle modification –> Increase physical activity, smoking cessation, healthy diet

Pharmacological
1st line - Beta blockers (CI in asthma) in which case you give CCB (CI in heart failure)

2nd line - CCB + BB

(Consider: Antiplatelets, statins)
If symptoms not controlled –> Revascularisation with :
PCI - Balloon stent coronary artery
or CABG - bypass graft (more invasive, better prognosis)

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9
Q

Acute coronary syndrome

RF

Pathology
Symptoms
Investigations
Treatment

A

Umbrella term for unstable angina, NSTEMI, STEMI

RF - Old age, diabetes

PATHOLOGY
STEMI - Complete and persistent blockage of coronary artery resulting in myocardial necrosis with ST elevation

Unstable angina + NSTEMi - Partial blockage of coronary artery usually resulting in myocardial necrosis in NSTEMI, but NOT in Unstable angina (which you differentiate with serum troponin)

SYMPTOMS
- Central crushing, heavy chest pain that can occur at rest with radiation to the arm, jaw or neck (feeling of impending doom)
- More severe Diaphoresis, dyspnoea, syncope, palpitations

INVESTIGATIONS
1st line - 12 lead ECG
UA - usually no changes (possible ST depression)
NSTEMI - T wave inversion + ST depression
STEMI - ST elevation in at least 2 contiguous ECG leads

Serum troponin
UA - Normal
NSTEMI - Elevated
STEMI - Elevated

GS - CT coronary angiogram - shows extent of occlusion

TREATMENT
Acute - MONA
IV Morphine
Oxygen if SATS <94%
GTN spray
Aspirin (+ clopidogrel)

Based on the Grace score - (risk of death within 6 months of discharge in patients with ACS)

If NSTEMI/UA –>
Low risk - Dual antiplatelet therapy - clopidogrel and aspirin
High risk - Immediate angiogram + consider PCI

STEMI –>
PCI - If within 12 hours of symptom onset
Thrombolysis with alteplase if >12 hours of symptom onset

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10
Q

What do you give for long term prevention of ACS

A

Beta blocker

Aspirin + clopidogrel

Statin (Atorvastatin)

Ace-inhibitor - Enalapril

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11
Q

What is prinzmetal (variant) angina briefly

A

It results from coronary artery spasm often occuring at rest.

Spasms cause temporary narrowing of arteries leading to reduced blood flow to the heart

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12
Q

Abdominal aortic aneurysm

RF

Pathology
Symptoms
Investigations
Treatment

A

Permanent pathological dilation of the aorta >3cm.
This is typically infrarenal (below the renal arteries)

RF - Old men who smoke, marfan’s, ehler danlos

PATHOLOGY
Occurs due to smooth muscle, elastic and structural degradation in the aorta. (Involves all 3 layers)
1) Proteolytic degradation of aortic wall
2) Inflammation and immune responses - Leukocyte infiltrate

> 3cm is AAA
5.5cm is considered emergency with increased risk of rupture

SYMPTOMS
Non ruptured –> Palpable pulsatile abdominal mass (PPAM)
Ruptured –> PPAM + Sudden epigastric pain radiating to the flank/back
- Hypotension + Tachycardia

A DDX is acute pancreatitis but pancreatitis has a NON PULSATILE mass.

INVESTIGATIONS
1st line + GS - Abdominal ultrasound

TREATMENT
Asymptomatic + unruptured –> Manage RF: Stop smoking, decreased BP, decrease BMI

Growing rapidly ,>5.5cm + unruptured –> EVAR (Endovascular aneurysm repair) or open surgery - laparotomy(more invasive)

Ruptured –>
STABILISE - ABCDE (resuscitate)
+
EVAR
SURGICAL EMERGENCY (100% mortality if not treated immediately)

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13
Q

Heart failure

RF

Pathology
Symptoms
Investigations
Treatment

A

A clinical syndrome that can result from a structural or functional cardiac disorder, impairing the ability of the ventricles to fill with blood, reducing pre-load and cardiac output –> (Cardiac output is not sufficient to meet demands of the body)

RF - previous MI, hypertension, smoking, valve disorder, cor pulmonale, >65

PATHOLOGY
Main cause - Ischemic heart disease

Frank starling law (Normally) - Increased preload –> increased afterload –> increased cardiac output

Failing hearts have a decreased cardiac output –> initial compensatory mechanism via RAAS and sympathetic nervous system –> compensatory mechanisms fail and heart undergoes CARDIAC REMODELLING –> RAAS + SNS leads to fluid overload –> Heart failure

Can be classified into 2
1) HF with reduced ejection fraction
2) HF with preserved ejection fraction

SYMPTOMS
3 cardinal signs

1) Dyspnoea/orthopnea (difficulty breathing when lying flat)/paroxysmal nocturnal dyspnoea (patients must stand up or sit up in the middle of the night to relive discomfort)

2) Fatigue

3) Ankle swelling (oedema)

(3rd+4th heart sound, increased JVP, bibasal crackles - pulmonary oedema)

INVESTIGATIONS
1st line - Bloods
BNP levels - elevated (released from stressed ventricles)

ECG - abnormal, possible signs of LVH

Chest X-ray -
A - Alveolar oedema
B - Kerly B lines - interstitial oedema
C - Cardiomegaly
D - Dilated vessels
E - Pleural effusion

GS - Echocardiogram

TREATMENT
Conservative
- Lifestyle changes - Decrease BMI, exercise, stop smoking

Pharmacological (ABAL)
1st line - Ace inhibitor
- Beta blocker
- Aldosterone antagonist
- Loop diuretic

(Chronic heart failure/worsening heart failure - Ivabradine)

Last resort
Surgery
- Revascularise
- Heart transplant

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14
Q

What are some types of heart failure, explain them briefly

(Just have an idea no need to know in depth)

A

Left sided heart failure - Occurs when the LV is unable to effectively pump blood to the body, leading to inadequate perfusion of organs and tissues.

Cor pulmonale which leads to right sided heart failure –> Pulmonary hypertension leading to increased resistance, causes the right ventricle to work harder to pump blood to the lungs, eventually leading to RVH and later right sided heart failure

Ischaemic heart failure - resulting from coronary artery disease and reduced blood supply to the heart

Myopathic - Cardiomyopathy due to intrinsic muscle dysfunction e.g. sarcomere/cytoskeleton

Hypertensive - due to increased BP –> LVH –> impaired relaxation and compliance –> decreased preload and cardiac output

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15
Q

What are the 2 categories of heart failure, name some causes of each

A

Can be classified into 2
1) Heart failure with preserved ejection fraction –> LV ejection fraction >50%
(Inability to relax and fill, issue is with filling so reduced preload)

Caused by: LVH, Constrictive pericarditis, cardiac tamponade

2) Heart failure with reduced ejection fraction –> LV ejection fraction <40%
(Failure to contract, issue with the pump itself)

Caused by: IHD, MI, (Because of damage to the heart muscle)

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16
Q

What is the classification system used for determining the severity of heart failure?

A

NEW YORK HEART ASSOCIATION CLASSIFICATION

1 - No limit on physical activity
2 - Slight limit on moderate activity
3 - Marked limit on moderate activity
4 - Inability to carry out physical activity without discomfort.

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17
Q

Aortic dissection

RF

Pathology
Symptoms
Investigations
Treatment

A

A tear in the intima layer of the aorta, resulting in blood flowing into the media at high pressure, dissecting the media and creating a false lumen.

RF - Marfan syndrome, Ehler-Danlos syndrome, smoking, hypertension

PATHOLOGY
With a false lumen
1) Blood from the false lumen can flow back up the aorta and cause a cardiac tamponade.

2) Blood can puncture a hole through the tunica media and adventitia, bleeding into the mediastinum

3) Blood in the false lumen can compress branches of the aorta, decreasing blood flow to organs –> causing shock.

SYMPTOMS
- Sudden onset severe tearing/ripping chest pain (back pain if descending aorta involved)
- Absent peripheral pulse
- Difference in BP between 2 arms (>10mm Hg difference) – also pulse difference

INVESTIGATIONS
1st line - Chest X-ray –> Widened mediastinum

GS - CT angiogram

(TROPONINS, CT angiogram)

Classify AD as type A or B via Stanford classification
A - Ascending aorta affected before the left subclavian artery
B - Descending aorta distal to the left subclavian artery

Treatment
Type A - Open surgery
Type B - Endovascular aneurysm repair

Medical prevention
+ Special Beta blocker - Labetolol
or if BB doesn’t work - Sodium Nitroprusside.

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18
Q

Where does aortic dissection most commonly occur?

A

Areas of high pressure.
Commonly:
At the sinotubular junction (where the aortic root transitions to the ascending aorta) or distal to the left subclavian artery.

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19
Q

What are the differential diagnosis of Tachycardia?

(Hint: Regards to the ECG)

A

Narrow QRS + Regular rhythm - Sinus tachycardia

Narrow QRS + Irregular rhythm - Atrial fibrillation

Wide QRS + Regular rhythm - Ventricular tachycardia

Wide QRS + Irregular rhythm - Polymorphic ventricular tachycardia

(Seems like Wide QRS - ventricles pathology)

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20
Q

Path of electrical conduction in the heart

A

SAN –> AVN –> Bundle of his –> purkinje fibres

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21
Q

What are the 2 shockable and 2 non shockable rhythms?
(In cardiac arrest)

A

Shockable
- Ventricular tachycardia
- Ventricular fibrillation

Non Shockable
- Pulseless electrical activity
- Asystole

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22
Q

Atrial fibrillation

RF

Pathology
Symptoms
Investigations
Treatment

A

A supraventricular tachyarrhythmia - occurs when abnormal electrical signals start firing, overriding the normal signals from the sinoatrial node (primary pacemaker)

RF - Hypertension, heart failure, mitral stenosis, alcohol abuse, smoking, advancing age, males

PATHOLOGY
(Can be caused by: Hyperthyroidism, IHD, hypertension, mitral valve pathology)
Rapid re-entrant ectopic signals typically from the pulmonary veins cause Atrial spasm –> Atrial blood pools rather than entering the ventricles
- Decreased CO and increased risk of thromboembolism

SYMPTOMS
- Palpitations
- Irregularly irregular pulse
- May present with a stroke as a complication (thromboemboli)
- Fatigue

3 types of AF - Paroxysmal, Persistent, Permanent

INVESTIGATIONS
1st line + GS - ECG
Absent P waves + irregularly irregular QRS complex + Narrow QRS complex

TREATMENT
If Acutely, haemodynamically unstable (new onset AF within 48 hours, heart failure, chest pain) –> SYNCHRONISED DC (direct current) CARDIOVERSION

For stable, long term treatment (RATE CONTROL)
- Beta blockers (bisoprolol)
OR CCB (Verapamil)
+
DOAC if CHADSVASC score more or equal to 2 (Apixaban)

Last resort: radiofrequency ablation (permanent)

23
Q

What are the 3 types of Atrial Fibrillation?

A

Paroxysmal - AF that occurs and terminates spontaneously within 7 days

Persistent - AF occurring longer than 7 days

Permanent - Sinus rhythm can’t be restored/maintained (doctor accepts A.fib as final rhythm)

24
Q

What are the 2 pointers in CHADSVASC score?

A

CHA2DS2-VASC

Congestive heart failure
Hypertension
Age >75 (2 points)
Diabetes
Previous stroke/TIA (2 points)

Vascular disease
Age 65-74
Sex category - Female

25
Q

2 complications of atrial fibrillation

A

Ischemic stroke

Heart failure

26
Q

Atrial flutter

RF

Pathology
Symptoms
Investigations
Treatment

A

A supraventricular tachycardia with atrial rates 250-300bpm.

PATHOLOGY
(Fast atrial ectopic firing)
Re-entrant rhythm with Abnormal signals typically arise from the tricuspid annulus

SYMPTOMS
- Palpitations
- Fatigue
- Dyspnoea

INVESTIGATIONS
1st line + GS - ECG
Saw toothed pattern (F wave?), often with a 2:1 block (2 P waves for 1 QRS) - atrial rate at about 300bpm

TREATMENTS
Acutely unstable (Shock, syncope, MI) –> Synchronised DC cardioversion

Stable -
1st line - rate control
BB - Bisoprolol
+
DOAC depending on CHADSVASC score

(Permanent - Radiofrequency ablation)

27
Q

4 differentials of a Narrow Complex Tachycardia

A

Sinus tachycardia - Normal P wave, QRS complex and T wave

Supraventricular tachycardia (AVNRT, AVRT, atrial tachycardia) - (in AVNRT - QRS followed immediately by T waves (with P waves buried - P wave and QRS occurs at same time)

Atrial fibrillation - Absent P waves, irregularly irregular ventricular rhythm

Atrial flutter - Saw toothed pattern with mostly 2:1 conduction

28
Q

Atrioventricular re-entry tachycardia (AVRT) - Wolff-Parkinson White syndrome

RF

Pathology
Symptoms
Investigations
Treatment

A

A supraventricular tachycardia caused by electrical signals re entering the atria

AVRT - Re entry through an accessory pathway called the BUNDLE OF KENT
- A pre excitation syndrome - which allows for electric signals to prematurely enter the ventricles (leading to delta waves in the QRS complex)

SYMPTOMS
- Palpitation
- Dizziness
- Dyspnoea

INVESTIGATIONS
1st and GS - ECG
- Short PR interval
- Delta waves (in QRS complex) - slurred upstroke
- Wide QRS

TREATMENT
1st line - Vagal maneuvers
- Carotid massage
- Valsalva maneuver

2nd line - IV adenosine CI asthma give CCB - verapamil

Definite - last resort - Radiofrequency ablation of bundle of Kent.

29
Q

Atrioventriculae nodal reentrant tachycardia (AVNRT)

Investigation
Treatment

A

Paroxysmal supraventricular tachycardia due to the presence of a re-entry circuit within the AV node

MOST COMMON SVT

ECG - Absent P waves as p wave is buried within QRS complex

TREATMENT
1st line - Vagal maneuvers
- Carotid massage
- Valsalva maneuver

2nd line - IV adenosine

Definite - last resort - Radiofrequency ablation

30
Q

What are the 4 broad complex tachycardias?

What are their treatments

A

Ventricular tachycardia - Wide QRS + regular rhythm –> IV amiodarone

Polymorphic ventricular tachycardia (e.g. Torsades de pointes) - Wide QRS + irregular rhythm –> IV magnesium

Atrial fibrillation with BBB –> Treated like normal A fib.
Unstable - Synchronised DC cardioversion
Stable - BB + DOAC if needed (CHADSVASC)

Supraventricular tachycardia with BBB (treated like SVT)

1st line - Vagal maneuvers
- Carotid massage
- Valsalva maneuver

2nd line - IV adenosine

Definite - last resort - Radiofrequency ablation of bundle of Kent.

31
Q

LONG QT SYNDROME

Causes

A

Caused by electrolyte imbalance (Hypokalemia, hypocalcemia, drugs - amiodarone, SSRIs, Romano Ward syndrome - Autosomal dominant)

Takes the heart longer than usual to recharge between beats
QT interval >440 milliseconds

32
Q

Torsades de pointes briefly

A

A form of polymorphic ventricular tachycardia.

Recurrent contractions of the ventricles (before proper repolarisation) leading to faster contractions than the atria.

Treat with correcting the underlying cause e.g. Electrolyte imbalance
otherwise –>
MAGNESIUM INFUSION

33
Q

Hypertension

RF

Pathology
Symptoms
Investigations
Treatment

A

RF - Obesity, physical inactivity, alcohol, black ethnicity, diabetes

PATHOLOGY
Primary/essential hypertension - Idiopathic (90% of cases)

Secondary causes: ROPED
Renal disease
Obesity
Pregnancy induced
Endocrine (Phaechromocytoma, conns, cushings)
Drugs – NSAIDS

RAAS + SNS increase in activity
Hypertension can lead to atherosclerosis and end organ damage.

SYMPTOMS
Mostly asymptomatic
Pulsatile headaches
Fever

In malignant hypertension (phaeochromocytoma)
- Blurred vision
- Heart failure
- Renal failure

INVESTIGATIONS
If BP in hospital >140/90 mmHg, do Ambulatory blood pressure monitoring to confirm diagnosis (135/85 mmHg throughout the day)

Assess for end organ damage
- Fundoscopy - Papilloedema
- Urinalysis + eGFR - Kidney function
- Echo - LVH

TREATMENT
If <55 YO or T2DM (Not a black African)
1) Ace inhibitor
NO MATTER WHAT AGE/ETHNICITY, if patient has T2DM give Ace-Inhibitor

If >55 YO or Black African
1) CCB

2) Ace inhibitor + CCB
3) Ace inhibitor + CCB + Thiazide

34
Q

Deep vein thrombosis

RF

Pathology
Symptoms

A

Development of a blood clot in a major deep vein in the leg, thigh, pelvis or abdomen

RF - Major surgery, bedridden for 3 days or more, active cancer, increased age, plaster immobilisation

PATHOLOGY
Mostly caused by Virchow’s triad: venous stasis, hypercoagulability, Endothelial damage

SYMPTOMS
- Unilateral calf swelling with veins that are warm and oedematous
- May be red

35
Q

What condition is it when a venous thromboembolism completely occludes a large vein?

What does it present with?

A

Phlegmasia cerulea Dolens –>

Significant pain, cyanosis and swellling

INVESTIGATIONS
If Wells Score is 1 or less (Unlikely DVT) –> Do a D-dimer test
- If its normal - DVT excluded
- If its elevated do a venous duplex ultrasound - where a reduced or absent spontaneous flow CONFIRMS the diagnosis

If Wells score is 2 or more (likely DVT) –> Do a venous duplex ultrasound (Diagnostic)

TREATMENT
1st line - DOAC (Apixaban, rivaroxaban)
LMWH if CI (renal impairment)

Non pharmacological treatment
- Physical activity - mobilisation, walking exercises
- Compression stockings

36
Q

Pulmonary embolism

RF

Pathology
Symptoms
Investigations
Treatment

A

Life threatening condition resulting from a dislodged thrombi occluding pulmonary vasculature

RF - Age, hormone replacement therapy (estrogen increases risk of thrombus formation)

PATHOLOGY
- Complication of DVT
- Thrombus trapped in pulmonary vasculature –> increases pulmonary vascular resistance –> can cause Cor pulmonale where RVH is caused by increase strain on the RV to overcome pulmonary vascular resistance –> eventual RV failure

SYMPTOMS
- Sudden onset pleuritic chest pain
- Dyspnoea (with possible haemoptysis)
- Evidence of DVT (swollen calf, immobilisation)
(increased JVP)

INVESTIGATIONS
1st line
If Wells score >4 (likely PE) –> CT pulmonary angiogram (diagnostic)

If Wells score <4 (unlikely PE) –> D-dimer test :
- If raised –> CTPA
- If not raised –> Not PE

ECG - Sinus tachycardia + S1Q3T3 (also sign of cor pulmonale)
T wave inversion of anterior and inferior leads + new RBBB

Chest X-ray - normal

TREATMENT
Non massive PE (usually this)
1st line
DOAC - Apixaban
LMWH if CI (renal impairment)

Massive PE
Thrombolytics e.g. alteplase, streptokinase

37
Q

Peripheral vascular disease

RF

Pathology
Symptoms
Investigations
Treatment

A

Range of syndromes caused by obstruction of vessels of the lower extremity

RF - Smoking, diabetes, hypertension, obesity, ageing

PATHOLOGY
Mostly caused by thrombus from an atherosclerotic plaque

Increasing stages of severity (Fontaine classification)
- Asymptomatic
- Intermittent claudication (divided into pain free walking >/< 200m.
- Ischemic rest pain - Chronic limb ischemia
- Ulceration or gangrene

Intermittent claudication (least severe) –> inadequate blood flow on exertion leading to crampy pain

Critical/chronic limb ischaemia (most severe) –> results in SYMPTOMATIC reduced blood supply to the limbs –> caused by atherosclerosis –> ischemic rest pain

SYMPTOMS
Generally
- Intermittent claudication
- Ischemic rest pain
(pulseless on palpation of extremities or bruits - pulsatile regions)
–> may develop to Acute limb ischaemia in which cause 6 P symptoms.

Skin changes on the leg - cooler + ulcerations

INVESTIGATIONS
First line - Ankle brachial pressure index. (ratio of BP)
<0.9 = intermittent claudication
<0.5 = Chronic limb ischemia

Buerger’s test - elevate leg at 45 degree angle for 1-2 minutes, if there is pallor, test is positive

TREATMENT
Intermittent claudication
- Graded exercise therapy
- RF modification - Stop smoking, balanced diet, increase physical activity
- Pharmacological: Atorvastatin, clopidogrel

Chronic limb ischaemia
- Revascularisation surgery
PCI - if small
Bypass surgery - if bigger

38
Q

Acute limb ischemia

Pathology
Symptoms
Treatment

A

A complication of peripheral vascular disease (main difference with CLI is that onset is sudden)

There is a sudden decrease in limb perfusion threatening the viability of the limb –> Rapid onset ischemia due to occlusion of arterial supply (by thrombus/embolus)

SYMPTOMS
Pain
Pallor
Paraesthesia
Paralysis
Perishingly cold
Pulselessness

TREATMENT
If non viable limb (Sign of tissue loss, nerve damage or significant sensory loss)
–> Amputate

If limb is viable on assessment –> Urgent revascularisation
within 4-6 hours (Endovascular thrombolysis/thrombectomy, bypass surgery)

39
Q

Pericarditis

RF

Pathology
Symptoms
Investigations
Treatment

A

Inflammation of the pericardium characterised by a triad of chest pain, pericardial friction rub and serial electrocardiogram changes

RF - male, transmural MI, cardiac surgery

PATHOLOGY
Causes:
- idiopathic
Main cause - VIRAL INFECTIONS - coxsackie viruses, EBV, adenovirus
- TB (bacterial),
- Autoimmune - SLE, Sjorgen’s
- Dressler syndrome - when pericarditis develops post MI

Due to causes mentioned, the inflamed pericardial layers rub against each other and exacerbate further inflammation

SYMPTOMS
- Sharp, pleuritic chest pain that may radiate to the trapezius ridges or left shoulder
- Pain is worse on inspiration and a supine position and is relived on leaning forward
- Pericardial friction rub on ausculation

INVESTIGATIONS
FBC - ESR elevated, leukocytosis
GS - ECG - Localised PR depression + Global Saddle shaped ST elevation

TREATMENT
NSAIDS + colchicine

40
Q

Complication of constrictive pericarditis

SYMPTOMS, INVESTIGATIONS, TREATMENT

A

Due to pericardial layers rubbing against each other, it can lead to PERICARDIAL EFFUSION

Pericardial cavity fills with fluid, creating an inward pressure on the heart, making it difficult to expand during diastole.

This can in turn lead to CARDIAC TAMPONADE

When pericardial effusion is large enough to raise intrapericardial pressure –> It can squeeze the heart, reducing filling during diastole –> reducing CO –> Leading to Shock and DEATH

Cardiac tamponade will present with PULSUS PARADOXUS (a fall in BP >10mmHg on inspiration)

SYMPTOMS of cardiac tamponade
BECK’s Triad
- Hypotension
- Increased Jugular venous pressure
- Muffled S1+S2 heart sounds
+
Pulsus paradoxus

INVESTIGATIONS
1st line - ECG

Chest X-ray - Big heart
GS - Transoesophageal echocardiogram

Treat pericardial effusion with NSAIDS + colchicine

Treat cardiac tamponade with URGENT PERICARDIOCENTESIS

41
Q

Describe all the degrees of AV block

A

1st Degree - Slow conduction through AV node
- PR interval is prolonged (>200ms)

2nd degree
MOBITZ 1 (WENCKEBACH)
- Progressively longer PR interval till a non conducted P wave/QRS drop (AV node completely fails)

MOBITZ 2 (HAY)
- Intermittent non conducted P wave
- Constant PR interval
(higher risk of progression to 3rd degree AV block)

3rd degree
- No association between atria and ventricles
- P waves not correlated with QRS complex
(more P waves than QRS)

42
Q

Causes of 1st, 2nd and 3rd degree AV blocks

A

1st degree - Drugs (e.g. BB, CCB, Digoxin)

2nd degree - Drugs (above), inferior MI, rheumatic fever

3rd degree - Acute MI, structural heart disease

43
Q

Symptoms and treatments of 1st, 2nd and 3rd degree AV blocks

A

1st degree
Sx - Usually asymptomatic
Tx - Asymptomatic so no treatment (Mobitz 1 also no treatment unless very symptomatic then give PACEMAKER)

2nd and 3rd degree
Sx - Syncope, fatigue, hypertension, chest pain, dyspnoea

MOBITZ 2 Tx–> Pacemaker

3rd degree
Tx –> IV atropine and pacemaker

44
Q

Infective endocarditis

RF

Pathology
Symptoms
Investigations
Treatment

A

An infection involving the endocardial surface of the heart, including valvular structure and chordae tendinae.

RF - Presence of artificial prosthetic valves, IV drug abusers, rheumatic HD

PATHOLOGY
Bacteria can be introduced endogenously (bacteria within body enters bloodstream) or exogenously (bacteria introduced by contaminated objects)
–> Leads to vegetations forming on heart valves. (Bacteria adhere to platelet deposition)

Main bacteria:
1) S.aureus (MC) - IVDU, prosthetic valves
2) S.viridans - alpha haemolytic strep associated with poor dental hygiene
3) Pseudomonas aeruginosa - contaminated water
(Enteroccocus)

SYMPTOMS
- Fever
- Malaise
- Sweating
- Headache
- Osler nodes - finger nodules
- Janeway lesions - painful marks on palms
- Splinter haemorrhages - on fingernails
- Roth spots - Retinal haemorrhage

INVESTIGATIONS
1st line - 3 sets of blood cultures at 3 different sites over 24 hours
FBC
Urinalysis

GS - Transoesophageal echocardiogram

DIAGNOSIS MADE WITH MODIFIED DUKES CRITERIA
(2 major, 1 major 3 minor, 5 minor)

TREATMENT
S.viridans (S.bovis) - Benzylpenicillin (Pen G) + Gentamicin

S.aureus - Flucloxacillin

Enterococci –> Amoxicillin + Gentamicin

45
Q

Which heart valve does IE affect most commonly?

A

Tricuspid

46
Q

What is the criteria used to diagnose Infective Endocarditis? What are the factors of the criteria?

A

Modified Dukes Criteria

2 major
1 major + 3 minor
5 minor

Major
- Blood culture positive for organisms typical of IE in at least 2 samples
- Evidence of IE on TOE

MINOR
- Predisposing factors - Prosthetic heart valves, IVDU
- Fever
- Vascular phenomenon - Janeway lesion, septic emboli
- Immunologic phenomenon - Osler node, roth spots
- Blood culture positive - but not an organism constant with IE.

47
Q

Right and left bundle branch block

A

Right - Marrow
Causes: Lung pathology - esp PE (COPD), IHD, congenital heart disease

M in V1
W in V6
(Double R waves in V1, prolonged S wave in V6)

Left - William
Causes: MC - IHD, valve disorders

W in V1
M in V6

(Deep S in V1, Prolonged R in V6)

48
Q

Main cause of sudden cardiac death in young people

A

Hypertrophic cardiomyopathy

49
Q

Hypertrophic cardiomyopathy

RF

Pathology
Symptoms
Investigations
Treatment

A

Autosomal dominant genetic disease of sarcomere proteins (Troponin T/I) that results in myocyte hypertrophy and septal thickening.

–> You have a thick, non compliant heart - reduced ability to expans–> Impaired diastolic filling –> decreased CO

SYMPTOMS
- Syncope
- Dyspnoea
- Chest pain
–> May present with sudden cardiac death

INVESTIGATIONS
1st line - ECG –> Abnormal (LVH)

GS - Transeosophageal echocardiogram

Genetic testing (mutations in Troponin T and I)

TREATMENT
BB, CCB, amiodarone

50
Q

Dilated cardiomyopathy

RF

Pathology
Symptoms
Investigations
Treatment

A

Most common cardiomyopathy

Autosomal dominant mutation of the cytoskeleton gene
–> Results in thinning and stretching of cardiac walls leading to dilation and dysfunction –> reduced CO

SYMPTOMS
Dyspnoea
Heart failure
Atrial fibrillation

INVESTIGATIONS
ECG

GS - TOE

TREATMENT
Treat underlying condition - e.g. Heart failure, atrial fibrillation

51
Q

Restrictive cardiomyopathy

RF

Pathology

Investigations
Treatment

A

Caused by granulomatous disease e.g. Amyloidosis, sarcoidosis

Leads to a Rigid, Fibrotic myocardium that is stiff –> impaired ventricular filling –> decreased CO

INVESTIGATIONS
ECG
GS - ECHO

TREATMENT
- No curative treatment
- Heart transplant

52
Q

What are the 3 categories of shock?

Give examples of each

A

1) Distributive - Failure of vasoregulation (vasodilation/constriction)
e.g Sepsis, anaphylaxis

2) Cardiogenic - Pump dysfunction e.g. Post MI

3) Hypovolemic - Loss of intravascular volume e.g. GI bleed, trauma (generally haemorrhagic causes)

(Obstructive - Barriers to cardiac flow e.g. PE)

Take note for treatment
ABCDE

Hypovolemic - Oxygen, IV fluids
Septic - Broad spec antibiotics
Cardiogenic - IV fluids, diuretic
Anaphylactic - IM adrenaline

53
Q

Rheumatic fever

RF

Pathology
Symptoms
Investigations
Treatment

A

Autoimmune disease that occurs usually post strep pyogenes infection. (Pharyngitis)

50% lead to rheumatic heart disease

PATHOLOGY
M protein from S.pyogenes has regions sharing similarities with cardiac tissue (Molecular mimicry) –> When the immune system produces antibodies against the M protein, antibodies can cross react with cardiac myosin and other cardiac proteins –> auto-antibody mediated destruction
(MOSTLY AFFECTS MITRAL VALVE)

SYMPTOMS
- New murmur (mitral stenosis)
- Sydenham’s chorea (jerky uncoordinated movement)
- Arthritis
- Erythema nodosum - painful patches of darker skin

INVESTIGATIONS
1st line - Chest X-ray –> Cardiomegaly
(because of over working heart) - signs of mitral stenosis

GS - TOE - shows valvular damage

DIAGNOSE WITH JONES CRITERIA
Recent S.pyogenes infection + 2 major or 1 major 2 minor
Major - Polyarthritis, carditis, sydenham’s chorea, erythema nodosum, new murmur

Minor - fever, arthralgia, elevated ESR/CRP

TREATMENT
1st line - IV benzylpenicillin then phenoxypenicillin for 10 days

Haloperidol for sydenham’s chorea

54
Q

Difference between Right and left heart failure

A

Right heart failure
- Increased JVP
- Hepatomegaly
- Peripheral oedema (pedal oedema)
- Ascites

Left heart failure
- Paroxysmal nocturnal dyspnoea
- Orthopnea
- Pulmonary oedema (bibasal crepitation)
(nocturia, cold fingers)