Cardiology Flashcards
1
Q
Describe the chest pain in stable angina.
A
- Brought on by exercise;
- Resolves with resting.
2
Q
Describe the pain in pulmonary embolism
A
- Pleuritic in nature;
- Dyspnoea;
- Cough
- Tachycardia;
- Hypoxia
- Haemoptysis
- Leg swelling & other features of DVT.
3
Q
Describe the pain in acute coronary syndrome.
A
- Pain for > 10min;
- Pain on rest or minimal exertion;
- Radiates to left arm and left jaw;
- Retrosternal pain (tightness, pressure);
- Diaphoresis;
- Dyspnoea;
- Nausea and vomiting.
4
Q
Describe the pain and other symptoms of aortic dissection.
A
- Sudden tearing chest pain irradiating to the back in between the scapulas;
- Diaphoresis;
- Hypontension;
- Tachycardia;
- Different blood pressures and pulses in between arms;
- Abnormal or absent periphereal pulses.
5
Q
Describe the symptoms of pericarditis.
A
- Pericardial friction rub
- Sharp pleuritic pain;
- Relieved by sitting forward;
- Worse with inspiration and body movements
- Fever;
- Cough;
- Similar to angina pain (but it changes with body position/movement unlike in angina).
6
Q
What are the causes of pericarditis?
A
- (Post) viral infections: Coxsackie virus;
- Post MI: Dressler’s syndrome;
- Tuberculosis;
- Uraemia
- Trauma
- Connective tissue disease;
1st two are most important for the exam.
7
Q
What is the ECG presentation in pericarditis?
A
Limb leads (I, II, III, aVL and aVF) and precordial leads (V2-V6)
* Concave ST elevation (saddle shape) of 0.5 - 1mm;
* PR depression
aVR lead
* ST depression
* PR elevation
8
Q
Describe what is acute mitral regurgitation after MI.
A
- Seen 2-10 days after MI;
- Caused by papillary muscle dysfunction or partial rupture;
- (More) associated with inferior MI;
9
Q
What are the symptoms of acute mitral regurgitation after MI?
A
- Dyspnoea;
- Haemodynamic instability.
10
Q
Acute MR after MI
What is the 1st line for diagnosis?
A
Echocardiogram.
11
Q
What is the treatment in pericarditis?
A
- NSAIDS: in most cases;
- Colchicine: prevents recurrence
12
Q
Describe the management of adult tachycardia.
A
- ABCDE
Haemodynamically unstable tachycardia:
* Synchronised DC (direct shock) cardioversion
Haemodynamically stable tachycardia:
1. QRS ≥0.12 s (broad)
2. QRS <0.12s (narrow)
Broad QRS
* Regular: VT (amiodarone IV)
* Irregular: VF, Torsades de pointes, polymorphic VT, Wolff-Parkinson-White syndrome
Narrow QRS
* Regular: SVT
* Irrgular: AF
13
Q
Describe ventricular tachycardia
A
- It is a broad complex (QRS) tachycardia;
- It impairs CO leading to hypotension, acute cardiac failure
- HR: 100 - 250 bpm
TREATMENT
1. With pulse:
Stable
* Amiaodarone
* Procainamide
* Lidocaine
* Flecainide
Unstable
Syncronised cardioversion
2. Without pulse:
Defribrillation
14
Q
What is the function of anticoagulants?
A
They disrupt the coagulation cascade, reducing the frequency and extent of clot formation.
15
Q
Describe the simplified coagulation cascade.
A
Intrisic pathway:
* Factor 9 ⟶9a
Extrinsic pathway:
* Factor 7⟶7a
Common pathaway:
* Factor 10⟶10a
* Prothrombin ⟶ Thrombin
* Fibrinogen ⟶ Fibrin
* CLOT FORMATION
16
Q
Describe the pharmacology of warfarin
A
Class:
* Vitamin K antagonist.
MOA:
* ↓ the synthesis of vit K dependent clotting factors.
Use:
* Requires monitoring of INR;
* In VTE/PE requires rapid loading so bridge gap cover with LMWH until INR > 2 on two consecutive days.
* In AF slow loading so no bridge gapping with LMWH needed.
* Many interacion with medicines, food and herbals.
Reversal agent
* Vitamin K
* Prothrombin factor
* Fresh frozen plasma
17
Q
Describe the pharmacology of DOAC’s:
-Apixaban
-Rivaroxaban
-Edoxaban
A
MOA: Factor Xa inhibitor.
Use:
* Baseline renal & liver function tests to start the administartion;
* No INR monitoring;
* Rivaroxaban needs to be taken with food to ↑ bioavailability.
Reversal agent:
* Andexanet alfa
18
Q
Describe the pharmacology of DOAC’s:
* Dabigatran
A
MOA: Thrombin inhibitor
Use:
*Baseline renal & liver function tests to start the administartion;
* No INR monitoring;
* Needs to be taken with food to ↓ GI side effects.
Reversal agent:
* Idarucizumab
19
Q
Describe the pharmacology of unfractioned heparin (UFH):
A
MOA:
* Inactivation of factor Xa
* Inactivaction of thrombin
* Inactivation of factor IXa
* Inactivation of 7a
Use:
* Imediate action after administration
* Short life
* Immediate reversibility
* Preferred on those at risk of bleeding
Reversal agent:
* Protamine
20
Q
Describe the pharmacology of LMWH:
* Enoxiheparin
* Dalteparin
* Tinzaparin
A
MOA:
* Inactivation of factor Xa
* Inactivaction of thrombin
Use:
* Can be used SC
* Easier than UFH in terms of monitoring
* Can be used in pregnancy (doesn’t cross the placenta)
* Low risk of HIT
* Contraindicated in renal impairment (eGFR < 30 ml/min)
Reversal agent:
* Protamine
21
Q
Name the causes of aortic stenosis.
1st world causes
A
- Degenerative calcification (older patient > 65YO);
- Bicuspid aortic valve (younger patients).
3rd world: Rheaumatic heart disease.
22
Q
Symptoms of aortic stenosis
A
- Angina: ↓EF causing ↓ myocardial perfusion;
- Syncope: ↓EF causing ↓ cerebral perfusion
- Dyspnoea: fluid buildup
23
Q
Describe the murmur of aortic stenosis
A
- Ejection systolic murmur
- Heard at 2nd intercostal space (right sternal border)
- Louder in expiration
- Radiates to the carotids
24
Q
What is the investigation of choice in aortic stenosis?
A
Echocardiogram.
25
Describe the step by step classification of **ACS**
**Ischaemic chest pain present**
* Left sided, substernal or central;
* Radiates to the left arm, shoulder or jaw
* Can be silent MI in diabetic patients (without pain)
* Sweating
* Hypotension
**12 lead ECG**
**ST elevation**
* ST elevation MI (STEMI)
**No ST elevation**
* Measure troponin
**Raised troponin**
* Non-ST elevation MI (NSTEMI)
**Normal troponin**
* Unstable angina
26
Treatment for **ACS** upon arrival and confirmation
**Dual antiplatelets aggregation**
* AAS 300 mg
* Clopidogrel 300 mg
**Anticoagulation**
* Fondaparinux SC
* *If on DOAC's use LMWH (dalteparin/enoxiheparin) instead of fondaparinux*
**Antihypertensives**
* ACEI
* Beta blockers
**Statins**
* Atorvastatin 80mg
27
**STEMI**: Describe the different ECG changes.
**Inferior wall MI**:
* ST elevation in lead II, III and aVF
* *Coronary artery affected*: Right Coronary Artery (80%) and Left Circumflex (20%)
**Anterior wall MI**
* ST elevation in leads V1-V4
* *Coronary artery affected*: LDA
**Lateral wall MI**:
* ST elevation in leads I, aVL, V5-V6
* *Coronary artery affected*: LCX
**Posterior wall MI**
* ST elevation in leads V7-V9
* *Coronary artery affected*: LCX and RCA
28
Describe the ***initial / immediate*** management for **STEMI**.
**MONA**
* Morphine IV
* O₂
* Nitrates (avoid in low BP and inferior wall MI)
* Antiplateletes (AAS 300 mg & consider clopidogrel 300mg)
29
Describe the ***definitive / GOLD standard*** management for **STEMI**.
**Percutaneous coronary intervention**:
* Within 12 h of symptoms onset
**Thrombolysis**:
* If PCI in not available within 120 min
* Perform within 12h of symptoms onset
* Alteplase or tenecteplase
**Angiography with follow up rescue PCI**: if persistent ST ↑ after thrombolysis.
30
Describe the ***long term*** management for **STEMI**.
* AAS for **life**
* Statins for **life**
* ACEi's or ARB's for **life**
* Beta blockers for **12 months**
* Clopidogrel/Ticagrelor/Prasugrel for **12 months**.
31
Define what is the **CHA₂DS₂-VASc** score
* It's a score used to assess a person's stroke risk.
* It used in AF to determine the most appropriate anticoagulation strategy.
32
Based on **CHA₂DS₂-VASc** score, when to offer anticoagulation treatment?
1. When score is ≥ 2 (both men and women).
2. When score is = 1(in men).
33
# **CHA₂DS₂-VASc** score
≥ 65 YO or at least 1 comorbidity
Give DOAC.
34
# **CHA₂DS₂-VASc** score
<65 and no comorbidities
Don't give DOAC.
35
What is the management of **AF with unstable vitals**?
| Signs of shock, syncope, acute cardiac failure or ischaemia.
Electric cardioversion.
36
What is the management of **AF with stable vitals**?
1. Rate control (B-blockers)
2. Rhythm control / chemical cardioversion
3. Anticoagulation (CHA₂DS₂-VASc 1st)
37
# Management of **AF with stable vitals**
Describe how **rate control** is done.
**1st line**:
* *B-blockers*: metoprolol/atenolol
*OR*
* *(Rate limiting) Calcium channel blocker* : Verapamil/Diltiazem
**2nd line**
*If rate is refractory to 1st line*
* Add digoxin
* If patient has heart failure digoxin is 1st line (or calcium channel blocker).
## Footnote
If patient has **asthma** choose calcium channel blockers
38
# Management of **AF with stable vitals**
Describe how **rhythm control** (chemical cardioversion) is done.
* Amiodarone
* Flecainide
## Footnote
If patient on **AF >48h**, rate control and LMWH instead.
39
# Management of **AF with stable vitals**
When to choose/do **rhythm control** (chemical cardioversion)?
| *Flecainide / Amiodarone*
*Patients that are:*
- Symptomatic
- Young
- Presenting with lone AF for the 1st time.
40
# Management of **AF with stable vitals**
When to choose/do **rate control**?
*Patients that are:*
* > 65 YO
* Stable and AF started > 48h *(chemical cardioversion might cause thromboembolism)*
* History of multiple failed cardioversions.
41
# Management of **AF with stable vitals**
Anticoagulation (medications lines)
**1st line:**
* DOAC
**2nd line**
* Warfarin *(if DOAC contraindicated)*.
42
What are the features of **atrial myxoma**?
**Obstruction of MV**
* Mid-diastolic murmur
* Dyspnoea
* Syncope
**Embolisation**
**Arrhythmias**
43
What is the *Gold standard investigation* in **atrial myxoma**?
Echocardiography.
44
What is the *management* of **atrial myxoma**?
**Without embolisation**
* Surgical removal
**With embolisation**
* Embolectomy
45
What are the **symptoms of heart failure**?
1. Dyspnoea / orthopnoea / Paroxystic nocturnal dypnoea
2. Fluid retention (ankle swelling)
3. Fatigue
46
What are the **causes** of heart failure?
* Hypertension
* Valvular disease
* Alcohool
* MI
47
What are the **investigations** in heart failure?
1. BNP (b-type natriuretic peptide)
2. Echo (if BNP⬆︎).
48
What is the **management of chronic heart failure** with ⬇︎EF?
► **1st line**
* ACE inhibitors / ARBs
OR
* B-blockers
then add
► **2nd line**
* Aldosterone antagonist (spironolactone)
then add
► **If refractory to all of the above meds**
* SGLT₂ inhibitor (Dapagliflozin)
➜ **If fluid overload**
* Loop diuretics (furosemide)
➜ **If atrial fibrillation**
* Digoxin
49
# **Heart murmurs**
Aortic stenosis
* Ejection systolic murmur
* 2nd intercostal space of right sternal border.
## Footnote
Ejection systolic because the LV is forcing blood through a stenotic valve **during systole** (the valve should be opened).
50
# **Heart murmurs**
Aortic regurgitation
* Early diastolic murmur
* **Left** upper sternum border.
## Footnote
The LV pumps blood (ventricular systole) throught an opened AV, then the valve closes and ventricular diastole begins. *The valve doesn't close properly*, hence the regurgitation in **early diastole**.
51
# **Heart murmurs**
Mitral stenosis
* Mid-late dyastolic murmur
* Opening snap
* Apex
## Footnote
The LV receives blood from the atrium **during dyastole** *(it needs to be relaxed to receive the volume)*. The inital stage of ventricular filling is passive, in **mid to late dyastole, the atrium kicks** (contracts) to deliver the rest of its volume. But there's a stenotic valve that won't completely open to let the blood flow normally. Hence a loud murmur in mid dyastole.
52
# **Heart murmurs**
Mitral regurgitation
* Pan-systolic murmur
* Apex
* Radiates to the axilla
| Pan-systolic means persisting through systole.
## Footnote
Systole begings when the MV closes, so that the LV can eject its content through the AV and not back through the MV.
So, *in MR, the valve is somehow opened*, during systole you will hear the **back flow of blood through the MV**.
53
# **Heart murmurs**
Pulmonary stenosis
* Ejection systolic murmur
* 2nd intercostal space of left sternal border.
## Footnote
The **RV contracts in systole** *to a stenotic valve* (it should be opened). Hence the murmur being heard during systole.
54
# **Heart murmurs**
Pulmonary regurgitation
* Early diastolic murmur
* 2nd intercostal space of left sternal border.
## Footnote
The RV relaxes in dyastole, **the pressure drops**. The valve doesn't close properly, there's *no more pressure proppeling the blood flow forward* so **it backflows as soon as dyastole begins**.
55
# **Heart murmurs**
Tricuspid stenosis
* Diastolic rumble
* Lower left sternal edge
## Footnote
The RV receives blood from the atrium **during diastole** *(it needs to be relaxed to receive the volume)*. The inital stage of ventricular filling is passive, in **mid to late diastole, the atrium kicks** (contracts) to deliver the rest of its volume. But there's a stenotic valve that won't completely open to let the blood flow normally. Hence a loud murmur in diastole.
56
# **Heart murmurs**
Tricuspid regurgitation
* Pan-systolic murmur
* Lower left sternal edge
## Footnote
Systole begings when the TV closes, so that the RV can eject its content through the PV and not back through the TV.
So, *in TR, the valve is somehow opened*, during systole you will hear the **back flow of blood through the TV**.
57
# **Heart murmurs**
Ventricular septal defect
* Pan-systolic murmur
* Left lower sternal border
58
# **Heart murmurs**
Patent ductus arteriosus
* Continuous machinnery murmur
* Left infraclavicular area
59
Atrial flutter
* Sawtooth pattern of the P wave
* Regular R waves
* Treatment is the same is AF
60
Management of V-tach
►**Stable patient** (pulse present)
✿ *Pharmacological cardioversion* (amiodarone, flecainide, lidocaine)
➜ *If above failed:* synchronised cardioversion
►**Unstable patient**
✿ *Pulse present:* Electrical cardioversion
✿ *No pulse:* Defibrillation
## Footnote
Broad QRS / Regular / No P waves
61
Management of V-fib
Defibrillation.
62
Management of **supraventricular tachychardia**
► **It is managed by RATE CONTROL**
◘ *Stable patients*
➜ **1st line:**
Valsava manoeuvres or carotid massage
➜ **2nd line:**
-*Adenosine* 6mg IV bolus
-If failed: repeat 12mg adenosine IV
-If failed: repeat 18mg adenosine IV
➜ **3rd line:**
Verapamil or B-blockers
➜ **4th line**
Electrical cardioversion
◘ *Unstable patients*
➜ ELECTRICAL CARDIOVERSION
| Prevention of episodes: B-blockers or radio ablation.
## Footnote
If asthmathic patient do not use adenosine or b-blockers. Only verapamil.
63
What are the causes of **Torsades de Pointes**?
* Long QT syndrome
* Electrolyte abnormalities:
-Hypomagnesemia
-Hypokalaemia
-Hypocalcaemia
* Erhytromicin
* Antipsychotics
64
What is the management of **Torsades de Pointes**?
* **Magnesium sulphates IV**
* Correction of electrolyte abnormalities
* Stop the causative drug
* If it progresses to Vfib ➝ defibrillation.
65
What is **familial hypercholesterolaemia**?
Genetic inherited condition resulting in high levels of cholesterol in the blood.
66
When to suspect **hypercholesterolaemia**?
- Cholesterol > 7.5 mmol
- Personal of family history of premature coronary heart disease *(before 60yo)*.
67
Describe **1st degree heart block**
* PR interval > 0.2 sec (>5 small squares).
* There is conduction delay without interrumption from atria to ventricules.
## Footnote
**Normal PR interval:** 0.12 - 0.2 sec (3 to 5 small squares).
68
Name the causes of **1st degree heart block**
* Increased vagal tone
* Electrolyte disturbances (**hyperkalaemia**)
* Inferior MI
* AV nodal blocking drugs (*B-blockers, calcium channel blockers, digoxin, amiodarone)*
* MV surgery
* Athlets
## Footnote
* As an isolated finding it is a benign entity that does not cause haemodynamic instability.
* No specific treatment is required for 1st degree heart block.
69
Name the types of **2nd degree heart block**.
* Mobitz type I AV block (Wenckebach)
* Mobitz type II AV block
70
Describe the 2nd degree heart block **Mobitz I (Wenckebach)**.
* Progressive prolongation of the PR interval, culminating in a non-conducting P wave.
71
What are the causes of **Mobitz I (Wenckebach)** AV block?
◉ **Drugs**:
* Beta-blockers
* Amiodarone
* Digoxin
* Calcium channel blockers
◉ **↑ vagal tone:**
* Athletes
◉ **Inferior MI**
◉ **Post cardiac surgery:**
* MV repair
* Tretalogy of fallot repair
◉ **Myocarditis**
72
What is the treatment for **Mobitz I (Wenckebach) AV block**?
◉ **Symptomatic:**
* Atropine
◉ **Asymptomatic:**
* No treatment required
73
Describe the 2nd degree heart block **Mobitz II**.
* PR interval is constant
* P waves that do not conduct can be seen (dropped QRS).
74
What is the treatment for **Mobitz II AV block**?
➜ **Initial treatment:**
* Atropine
➜ **Most appropriate treatment:**
* Temporary pacing (until treated with a pacemaker)
75
Describe the **3rd degree (complete) heart block**.
* No association between P waves and QRS complex.
* Atria and ventricles contract independently.
76
What are the causes of the **3rd degree (complete) heart block**?
* Inferior MI
* Lyme disease
* AV nodal blocking drugs (b-blocker, calcium channel blockers, amiodarone, digoxin).
77
What is the treatment for **3rd degree (complete) heart block**.
➜ **Initial treatment:**
* Atropine
➜ **Most appropriate treatment:**
* Temporary pacing (until treated with a pacemaker)
➜ **Definitive treatment:**
* Pacemaker
78
Name and describe the classification **stages of hypertension**.
◉ **Stage 1 hypertension**
- *Clinic BP:* >= 140/90 mmHg
**AND**
- *Ambulatory or home blood pressure monitor:* >= 135/85 mmHg
◉ **Stage 2 hypertension**
- *Clinic BP:* >= 160/100 mmHg
AND
- *Ambulatory or home blood pressure monitor:* >= 150/95 mmHg
◉ **Stage 3 hypertension / Severe hypertension**
- *Clinic:* **Systolic** >= 180 mmHg
OR
- *Clinic:* **diastolic** >= 120 mmHg
79
Describe the management treatment for **stage 1 hypertension**.
◉ **Healthy patient**
- Lifestyle changes only.
◉ **Patient < 80 y.o.**
➜ *Treat if presenting with ≥1 of the following:*
- Target organ damage
- Cardiovascular disease
- Renal disease
- DM
- A 10 year cardiovascular risk >= 10%.
80
Describe the management treatment for **NON DIABETIC stage 2 hypertension**.
◉ **STEP 1**
- **< 55 yo:** ACEi / ARB
- **≥ 55 yo:** CCB (calcium channel blocker)
- **African / afro-Caribbean:** CCB
➜*If BP still > 140/90, advance to step 2*
◉ **STEP 2**
- ***< 55 YO:*** ACEi / ARB + CCB or thiazide-like diuretic.
- ***≥ 55 YO:***CCB + ACEi / ARB or thiazide-like diuretic.
- ***African / afro-Caribbean:*** CCB + ACEi / ARB or thiazide-like diuretic.
◉ **STEP 3**
- ACEi / ARB + CCB + thiazide-like diuretic.
81
Describe the management treatment for **stage 2 hypertension with DIABETES**.
◉ **STEP 1:**
1. ACEi / ARB
2. ***If black:*** ARB (*less angiodema risk*)
◉ **STEP 2**
- Add CCB or thiazide-like diuretic
◉ **STEP 3**
- ACEi / ARB + CCB + thiazide-like diuretic
82
Describe the **BP targets** on patients *on antihypertensives*.
**Clinic BP targets:**
- < 80 YO: < 140/90
- > 80 YO: < 150/90
**DM**
- Same as clinic
**CKD + DM**
- < 130/80
83
Describe the *management* of **ABPM / HBPM** results.
**Stage 1 hypertension (*BP ≥ 135/85*)**
- Offer lifestyle changes.
**Stage 2 (BP ≥ 150/95)**
- Start Rx
84
Describe the *management* of **clinic BP results**.
**Stage 1 hypertension ≥ 140/90**:
- Offer ABPM
NO STAGE 2
**Stage 3 ≥180/120**:
- *Signs of target organ damage present:* same day hospital referral.
- *Absent signs of organ damage:* start Rx.
85
Describe the presentation and symptoms of **infective endocarditis**.
➜ **Fever + New murmur**
* Congestive cardiac failure
* **Janeway lesions:** painless, erythematous lesions on palm or sole.
* **Osler nodes:** raised and tender nodes on the fingers.
* **Roth spots:** white spots on retina surrounded by hemorrhage.
* **Splinter hemorrhage:** on the nail beds.
86
What are the risk factors for **infective endocarditis**?
* Valvular heart disease
* Valve replacement
* IV drug user
* Dentristy procedures
87
What are the **pathogens** associated with causing **infective endocarditis**?
◉ **Most common pathogens**:
* S. aureus
* Streptococous
➜ *Mitral valve is affected*
◉ **Injection drug users:**
* S. aureus
➜ *Tricuspid valve affected*
88
What is the **initial step** on the *management* of **infective endocarditis**?
➜ **1st:** Blood culture
➜ **2nd:** Echo
89
Describe how the **diagnosis** of **infective endocarditis** is made.
◉ **Modified Duke criteria**
*Diagnosis is made if*:
➝ 2 major criteria
➝ 1 major + 3 minor criteria
➝ 5 minor criteria
► **Major criteria:**
* *Positive blood cultures* on 2 different occasions;
* *Echo*: showing abcess formation / new valve regurgitagion;
► **Minor criteria:**
* IV drug user / Predisposing heart condition;
* Fever ≥ 38ºC;
* *Vascular phenomenon:* embolus, splinther hemorrhage, janeway lesions;
* *Immunological phenomenon:* Roth spot, Osler's nodes;
* Positive blood culture not meeting major criteria.
90
Describe the **Rx** of infective **endocarditis**.
► **Native valve:**
* Amoxicilin + Gentamicin
* ***MRSA:*** Vancomycin + Gentamicin
► **Prosthetic valve:**
* Vancomycin + Gentamicin + Rifampin
91
Describe the **investigations** done after a **syncope** episode.
* ECG (arrhythmias)
* Blood pressure (supine and standing/sitting)
* Blood glucose
92
Name what other investigation can be done in **syncopal episodes** when the main 3 are incoclusive.
Tilt table test.
93
Describe the ECG features of **LBBB**.
► **Lead V6**
* Broad complex QRS
* "M" shape QRS
* (Can also be seen in lead I and aVL).
► **Lead V1**
* Deep S wave in V1
* "W" shape S wave
## Footnote
➜ V6 is more important.
➜ V6: when placing the electrodes on the chest, V6 is located to the far left so remember LBBB=V6.
94
Describe the ECG features of **RBBB**.
► **Lead V1**
* "M" shape QRS complex
## Footnote
➜ V1: when placing the electrodes on the chest, V1 is located to the center right so remember RBBB=V1
95
What are the **symptoms** of **Mitral regurgitation**?
◉ **Left ventricullar failure:**
* Dyspnoea
* Orthopnoea
* Paroxymal nocturnal dyspnoea
➜ *Signs of pulmonary congestion*
◉ **Right sided heart failure:**
➜ *With severe and chronic MR*
* Oedema
* Ascites
## Footnote
✿**Pansystolic/systolic murmur** at the apex radiating to the axilla.
96
What is the **cause** of **Mitral valve stenosis**?
➜ Most commonly due to ***rheumatic fever***.
97
What is the **non-surgical Rx** of **patent ductus arteriosus**?
* Indomethacin
* Ibuprofen
98
What is the investigation of choice on a **STABLE patient** with **Abdominal Aortic Aneurysm (AAA)**?
► **Gold standard:**
* CT angiography
99
What is the **investigation** of choice on an **UNSTABLE patient** with Abdominal Aortic Aneurysm rupture **(AAA)**?
* FAST scan.
100
What is the ***management*** of an **UNSTABLE patient** with Abdominal Aortic Aneurysm rupture **(AAA)**?
1. IV fluids
2. Emergency surgery / FAST SCAN
## Footnote
If surgery is an option than pick it, if not FAST.
101
Describe the 4 characteristics of **TOF**.
**Congenital cyanotic heart disease**
1. Pulmonary artery stenosis
2. Right ventricular hyperthrophy
3. Ventricular septal defect
4. Overriding of the Aorta (it overrides the VSD).
| Right to left shunt, hence the cyanosis.
## Footnote
* Ejection systolic murmur (VSD doesn't cause a murmur here).
* X-ray: boot shaped heart.
* Right to left shunt caused by the pulmonary stenosis.
102
Describe the management of **troponin levels**.
◉ **Less than 3h of symptoms onset:**
* > 30ng/L ⟶ treat as ACS
* < 12ng/L ⟶ repeat after 3h of symptoms onset
◉ **More than 3h of symptoms onset:**
* > 30ng/L ⟶ treat as ACS
* < 12ng/L ⟶ ACS unlikely ⟶Stable angina ⟶ Refer to cardiology outpatient
