Cardio Key Flashcards

1
Q

Unstable angina

A

Troponin normal

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2
Q

Acute Coronary Syndrome includes:

A

√ ST elevation myocardial infarction (STEMI).

√ Non-ST elevation myocardial infarction (NSTEMI).

√ Unstable angina

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3
Q

Acs ◙ Symptoms and signs

A

The classic and most common feature of ACS is chest pain.

Typically, central/left-sided/ substernal/ epigastric.

√ May radiate to the jaw, the left arm, the shoulder.

√ Often described as ‘heavy’ or constricting,

‘like an elephant on my chest’

  • It should be noted however in real clinical practice that patients present with

a wide variety of types of chest pain and patients/doctors

may confuse
ischaemic pain for other causes such as dyspepsia.

  • Certain patients e.g. diabetics/elderly may not experience any chest pain
    → Silent MI

◙ Other possible symptoms in ACS include:

Dyspnoea
▐ sweating

▐ nausea and vomiting
▐ may appear pale and clammy

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4
Q

◙ Risk Factors of Ischemic Heart Disease:

A

Modifiable risk factors

Obesity
Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia

Non modifiable

Increasing age
Family history
Male gender

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5
Q

Investigations

A

√ ECG

√ cardiac markers e.g. troponin
ECG in ST-elevation MI

→ elevated ST segment in certain leads gives a clue about the site and type
of the STEMI as follows:

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6
Q

ECG features of Left main coronary artery occlusion [LMCA]:

A

√ Wide spread ST depression.

√ ST elevation in aVR.

Do → Emergency coronary angiography.

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7
Q
A
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8
Q

STEMI

A

Elevated cardiac enzymes

More severe symptoms

ST elevation on ECG and new LBBB

Complete thrombus occlusion

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9
Q

NSTEMI

A

Occluding thrombus sufficient to cause tissue damage and mild myocardial necrosis

ST depression + /- T wave inversion on ECG

Elevated cardiac enzymes

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10
Q

Unstable angina

A

Non occlusive thrombus

Non specific ecg

Normal cardiac enzymes

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11
Q

Management of ST elevation MI (STEMI):

A

◙ In Acute Settings → MONA
(IV Morphine, O2, Nitrates, Aspirin 300 mg)

• If the patient presents within 12 hours of the onset of the symptoms

→ Primary PCI (Percutaneous Coronary Intervention) ‘’The gold standard’

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12
Q

PCI

A

In this procedure (PCI),

the blocked arteries are opened up using a balloon
(angioplasty)

following which a stent may be deployed to prevent the artery
occluding again in the future.

This is done via a catheter inserted into either the
radial or femoral artery

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13
Q

• If Not, or PCI is unavailable

A

→ Thrombolysis (Alteplase is preferred over Streptokinase).

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14
Q

• (Chronic) Long-term Management of MI:

A

1) Aspirin for life.

2) Ticagrelor or Prasugrel for 12 months ‘’or: Clopidogrel”.

3) Beta Blockers (for 12 months) “e.g. atenolol, bisoprolol ® concor, zebeta”.

4) ACE inhibitors (for life) “e.g. captopril, enalapril, ramipril”

[If intolerant to ACEi such as dry cough, use ARBs instead e.g. losartan,
valsartan, irbesartan]

5) Statins (for life) “e.g. Atorvastatin 80 mg PO OD”.

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15
Q

So, Long-term MI Rx = 5 Drugs:

Aspirin,
Clopidogrel,
BB,
ACEi,
Statins

A

AABC+S →

Aspirin, ACE inhibitors, Beta-blockers, Clopidogrel + Statins

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16
Q

Management of NSTEMI & Unstable Angina:

A

(based on the recent UK guidelines)
Important:

For all patients where the diagnosis of NSTEMI or Unstable Angina is
made →

Aspirin 300 mg (+) LMWH

e.g. Enoxaparin, Dalteparin “or
Fondaparinux” need to be given as soon as possible.

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17
Q

Antithrombin use?
Mi

LMWH
e.g. Enoxaparin,
Dalteparin “
or Fondaparinux

A

√ Aspirin 300 mg.

√ Nitrates or morphine to relieve chest pain if required.

√ Antithrombin:

be offered to patients who are not at a high risk of bleeding

and who are not
having angiography within the next 24 hours.

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18
Q

If angiography is likely within 24 hours or a patient’s creatinine is > 265
µmol/l, _____ should be given.

A

Unfractionated heparin

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19
Q

Mi

2nd antiplatatelet?

A

[Note: Fondaparinux and LMWH are given Subcutaneously, whereas
Unfractionated Heparin is given Intravenously].
√ Second antiplatelet: e.g. Clopidogrel, Prasugrel.

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20
Q

________ should be given to patients who have an intermediate or higher risk
of adverse cardiovascular events (predicted 6-month mortality above 3.0%),

and who are scheduled to undergo angiography within 96 hours of hospital
admission.

A

√ Intravenous glycoprotein Iib/IIIa receptor antagonists (eptifibatide or
tirofiban)

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21
Q

__________should be considered within 96 hours of first
admission to hospital to patients

who have a predicted 6-month mortality
above 3.0%.

It should also be performed as soon as possible in patients who
are clinically unstable.

A

√ Coronary angiography

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22
Q

[Example 1]
A patient presents with (acute chest pain radiating to jaw and shoulder
+ other features suggesting ischemic heart disease…)

However without , ST elevation on ECG. What to Do Next?

A

without st elevation
→ Measure Cardiac Enzymes, especially (Troponin)

√ If Troponin is high → NON-STEMI = Non-ST elevation MI

√ Immediate management
→ Give Subcutaneous LMWH OR Fondaparinux + Aspirin 300 mg

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23
Q

LMWH = Low Molecular Weight Heparin

A

Examples → Dalteparin, Enoxaparin

Fondaparinux (trade name Arixtra) is an anticoagulant medication chemically
related to low molecular weight heparin.

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24
Q

[Example 2]
A 60 YO man with Hx of smoking, HTN and DM presents to his GP
complaining of 25 minutes of left side dull aching chest pain radiating to his
jaw.

He was given Aspirin 300 mg by his GP and then sent to medical services
in a local hospital.

He is no longer in pain. The ECG is normal.
The troponin is
elevated 202 ng/L (Normal: < 5 ng/L).

What is the next step in management?

A

Since the ECG is normal, alteplase is wrong.
Since ECG is normal and Troponin is high → Non-STEMI

→ Anti-coagulation (LMWH e.g. Dalteparin, Enoxaparin or Fondaparinux).

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25
[Example 3] A 62 YO man with Hx of smoking and HTN presents complaining of 25 minutes of left side constricting chest pain radiating to his left shoulder. He was given Aspirin 300 mg and trinitrates for the pain. ECG was then done and showed ST elevation in leads V1-V4. What is the most appropriate next step in management?
→ PCI “Percutaneous Coronary Intervention”. If not among the choices, pick → Alteplase “Thrombolysis”
26
Example 4] A 59 YO hypertensive patient presents to the A&E complaining of dull central chest pain for around 4 hours. His vitals are as follows: HR: 99, BP: 155/95, RR: 21, O2 sat on room air: 97% Chest X-ray is normal. Troponin level is pending. He was given IV morphine for his chest pain. The ECG is as follows: Chest pain + T wave inversion suggests → myocardial ischemia.
In this case, 2 drugs should be given immediately: √ Aspirin 300 mg. √ LMWH or Fondaparinux. Pick the one that is given in the choices. “low-risk patients can be treated conservatively. However, if subsequent ischemia develops → coronary angiography with PCI”.
27
What if the ECG shows features of left main coronary artery occlusion (Wide spread ST depression + ST elevation in aVR)
? → Emergency coronary angiography.
28
[Example 5] A 61 YO patient presents to the A&E complaining of dull central chest pain for around 4 hours. His vitals are as follows: HR: 75, BP: 135/85, RR: 21, O2 sat. on room air: 97% He was given IV morphine for his chest pain. The ECG is as follows: Widespread st depression This ECG shows the typical features of • Widespread ST depression, and • ST elevation in aVR.
Do → Emergency coronary angiography.
29
Atrial Myxoma
o 75% in the left atrium. o Benign tumours o Tend to grow on the wall (inter-atrial septum). o 10% are inherited → Familial myxoma
30
Features: of cardiac tamponade Dx → → Echo —Pedunculated heterogenous mass typically attached to the region of fossa ovalis (inter-atrial septum
◙ Obstruction of Mitral valve → Mid-diastolic murmur, Dyspnea, Syncope, Congestive HF. ◙ Small pieces may break off and travel to arteries causing (ischemia) of different parts of the body such as: ♦ Lung → Can cause PE (Pulmonary Embolism) →Can cause Stroke → Clubbing and Blue fingers. ◙ Atrial Fibrillation
31
If acute limb ischemia develops “sudden painful swollen limb with a loss of pulse” → we could save the limb by performing an urgent catheter
Embolectomy
32
A patient was hit by a car into his chest and is brought to the emergency department. His neck veins are distended, Heart sounds are faint, hypotensive and tachycardic.
The likely Diagnosis → Cardiac Tamponade. The most appropriate management → Pericardiocentesis • Beck’s Triad: Hypotension, Muffled Heart Sounds, High JVP (Distended neck veins).
33
Axis Deviation
o If QRS in lead I is up (+ve) and in lead II is down (negative) → Left axis deviation o If QRS in lead I is down (-ve) and in lead II is up (+ve) → Right axis deviation
34
These causes are important! Causes of Left Axis Deviation
Inferior MI Wolff Parkinson White Syndrome Left Ventricular Hypertrophy Left Anterior Fascicular block (or hemiblock) Obese
35
Causes of Right Axis Deviation
Pulmonary Embolism Right Ventricular Hypertrophy Chronic Lung Disease Lateral MI Left Posterior Fascicular Block (or hemiblock) Thin, Tall, Children
36
Causes of EXTREMER Right Axis Deviation (No man’s land) = (North west axis):
o Congenital Heart Disease. o Left Ventricular Aneurysm.
37
Types of heart block
P R interval > 0.2 seconds (Only prolonged PR intervals). (i.e., PR interval occupies more than 1 large square (or 5 small squares).
38
Second degree heart block • type 1 (Mobitz I = Wenckebach)
→ Progressive prolongation of the PR interval until a dropped beat occurs
39
• type 2 (Mobitz II)
→ PR interval is constant but the P wave is often not followed by a QRS complex.
40
Third degree (complete) heart block
• There is no association between P waves and QRS complexes.
41
Management of AV Heart Block:
◙ 1st Degree Heart Block and Mobitz type 1 usually → do not require treatment (as long as the patient is Asymptomatic). ◙ Mobitz type 2 and Complete heart block (3rd degree heart block) → require permanent pacemaker • Initially → Atropine (first choice for all symptomatic bradycardia). • Then → Transcutaneous pacing. (Used to buy time until transvenous pacing is done). • Then → Transvenous pacing. • Then → Permanent pacing (Pacemaker).
42
Small and large squares ecg
For your knowledge: • 1 small square • 1 large square contains 5 small squares = 0.04 sec. X 5= 0.2 sec.
43
44
• Atrial fibrillation is a common arrhythmia after surgery. So, if it develops after surgery → Continue to observe and monitor vital signs. • If it does not resolve on its own or if it worsens → Intervene (eg, bisoprolol).
45
• Atrial Flutter management →
• Atrial Flutter management → Cardioversion (Shock)
46
Ventricular tachycardia
√ Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus. √ It can develop into ventricular fibrillation and therefore requires urgent treatment. √ P wave might be present or absent.
47
N.B: • ECG showing broad complex tachycardia in a (still) conscious patient even if semiconscious ± atrial activity and “haemodynamically STABLE”
→ Ventricular tachycardia → Give Amiodarone He is stable!
48
• ECG showing ventricular tachycardia in a haemodynamically unstable (e.g. SBP ≤ 90) patient
→ DC cardioversion = shock. He is unstable but has a pulse.
49
• If the patient is Unconscious, Collapsed, or Not breathing + No Pulse!
→ Ventricular Fibrillation → Defibrillation = Asynchronized shock
50
VT and VF
[As the patient is still conscious and with a felt pulse, it is likely ventricular tachycardia; not ventricular fibrillation. However, remember that ventricular tachycardia is managed by amiodarone if the patient is stable and by cardioversion if unstable]. If No pulse → Immediate Defibrillation.
51
• ______ is the most important shockable arrhythmia. • _______ is the most important cause of ventricular tachycardia (VT) clinically.
• Ventricular fibrillation is the most important shockable arrhythmia. • Hypokalemia (↓ K+) is the most important cause of ventricular tachycardia (VT) clinically.
52
Polymorphic (Broad-Complex) Ventricular Tachycardia = Torsades De Pointes (TDP)
◙ Beat-to-beat variations with no uniform pattern of ventricular contractions. ◙ Broad QRS (except in resting status), Prolonged QT, Fainting episodes, Patient might be a young athlete, Recurrent. ◙ Treatment → IV Magnesium Sulphate.
53
Narrow-complex ◙ Usually in young patients Supraventricular ◙ Presents with Palpitations, Light-headedness, tachycardia (SVT)
◙ Usually in young patients ◙ Presents with Palpitations, Light-headedness, Recurrent , Young ♠ Initial line → Valsalva manoeuvre, Carotid massage. ♠ Not improved? → Intravenous adenosine
54
WPWS
Delta wave on the ECG
55
Sinus Bradycardia
Lightheadness, hypotension, vertigo, syncope, dizziness. N.B. Sinus bradycardia is normal in young athletes. ◙ The first drug of choice for Symptomatic Bradycardia (Dizziness, feeling unwell) → Atropine
56
Sinus Tachycardia
Physiological situation (exercise, stress, anger). Hx of infection.
57
Ventricular Older adult, Sudden collapse, Not breathing, Unconscious No pulse
VF Immediate defibrillation
58
59
Atrial Flutter
‘’Fluttering Feeling in the chest’’, Sawtooth waves on the ECG → Synchronized ardioversion.
60
Ventricular Tachycardia
Regular and Fast rhythm. Ongoing lightheadness, Palpitations, Chest pain. → Give Amiodarone. If unstable (SBP <90, ↓ consciousness) → Immediate synchronized Cardioversion. Immediate defibrillation. If Pulseless VT → Defibrillation = Unsynchronized cardioversion “high”
61
Atrial Flutter
‘’Fluttering Feeling in the chest’’, Sawtooth waves on the ECG → Synchronized ardioversion.
62
Atrial Fibrillation
Palpitation, Tachycardia, Dyspnea, Fibrillatory waves on the ECG, Irregularly irregular rhythm → Give Beta-Blocker. If Asthmatic → Give Calcium Channel Blocker. If with hypotension → Cardioversion / IV amiodarone.
63
Management of Congestive Heart Failure
While loop diuretics (furosemide, bumetanide) and nitrates are important in the management of acute or decompensated cardiac failure, they have no effect on long-term survival.
64
◙ The following medications have all been shown to reduce mortality in patients with left ventricular failure:
• ACE-inhibitors • Beta-blockers • Angiotensin receptor blockers (ARBs) • Aldosterone antagonists (e.g. Eplerenone, Spironolactone) • Hydralazine with nitrates
65
How to manage CHF? (Important) •
How to manage CHF? (Important) • For all patient, for symptomatic relief and to reduce the volume overload → Diuretics (e.g., Furosemide ▐ Lasix ™) or (Bumetanide).
66
Heart failure
• Start with either an ACE inhibitor or Beta blocker (one drug at a time). • If the symptoms persist → Add the other one (ACEi or BB). • If the symptoms still persist → Add Spironolactone
67
√ Spironolactone is a potassium-sparing diuretic and an aldosterone antagonist . √ (Important) If the patient of congestive heart failure is already on FUROSEMIDE, Beta blocker, and ACEi and still has lower limb edema → This means that the diuretic is not efficient (the furosemide) → Therefore, one of the following is needed:
• Increase the dose of the furosemide. • Switch the furosemide to either bumetanide or torsemide. • Consider admission for IV loop diuretics.
68
V. Imp. Note: If the patient has Diabetes, we start with ACE inhibitors (e.g. Ramipril) instead of Beta-Blockers
ACE inhibitors are reno-protective and thus beneficial for diabetic patients.
69
• If HF + AF
• If HF + AF → Digoxin
70
N.B. One might ask “Won’t Furosemide + ACE inhibitors lead to hyperkalemia?
The answer is → No! • Thiazide and Loop Diuretics (e.g. Furosemide) → HypOkalemia. • ACEi (e.g., Ramipril) and Spironolactone → HypeRkalemia.
71
The Summary of STEMI (ST-Elevation MI) Management
◙ In Acute Settings → MONA (Morphine, O2, Nitrates, Aspirin 300 mg) + Heparin (either unfractionated or LMW such as enoxaparin/ fondaparinux)
72
MI mng
• If the patient presents within 12 hours of the onset of the symptoms → PCI (Percutaneous Coronary Intervention) ‘’The gold standard’’ • If Not, or PCI is unavailable → Thrombolysis (Alteplase).
73
◙ (Chronic) Long-term Management of MI
Aspirin for life, Ticagrelor or Prasugrel for 12 months ‘’Clopidogrel previously’’, Beta Blockers (for 12 months), ACE inhibitors , Statins So, Long-term MI Rx = 5 Drugs: Aspirin, Clopidogrel, BB, ACEi, Statins AABC+S → Aspirin, ACE inhibitors, Beta-blockers, Clopidogrel + Statins
74
Patent Foramen Ovale
√ The foramen allows blood to pass from the right atrium to the left atrium. √ The opening is supposed to close soon after birth, but sometimes it does not. In about 1 out of 4 people, the opening never closes. If it does not close, it is called a PFO. √ In most of these individuals, the PFO causes no problems and remains undetected throughout life.
75
Patent foramen ovale
√ PFO has long been studied because of its role in paradoxical embolism (an embolism that travels from the venous side to the arterial side). This may lead to a stroke or transient ischemic attack . √ Transesophageal echocardiography is considered the most accurate investigation to demonstrate a patent foramen ovale. √ A patent foramen ovale may also be an incidental finding.
76
Gold standard for diagnosing for foramen ovale
The important point to remember is: Trans-oesophageal Echocardiography (TOE) with bubble contrast is the gold standard in diagnosing Patent Foramen Ovale (PFO)
77
78
Important Complications of Myocardial Infarction (MI) Cardiac arrest
• This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. • Patients are managed as per the ALS protocol with defibrillation.
79
Mi complication Chf mng . Management ◙ For all patient for symptomatic relief and to reduce the volume overload → Loop Diuretics (e.g., Furosemide) ◙ Start with either ACEi or BB. (One drug at a time) (Remember that ACEi and ARBs is delt with as similar in effect). ◙ If the symptoms persist → Add the other one (ACEi or BB). ◙ If the symptoms still persist → Add Spironolactone (Aldosterone Antagonist). [Important: If a patient is already on an ACE inhibitor (eg, lisinopril) or is already on ARBs (eg, losartan, candesartan) and he needed an additional medication for his chronic heart failure, pick a beta-blocker eg, bisoprolol]. If he is already on an ACEi or ARBs + BB → go for spironolactone.
Chronic heart failure If the patient survives the acute phase, their ventricular myocardium may become dysfunctional resulting in chronic heart failure
80
Tachyarrhythmias Complication of mi
Tachyarrhythmias ◙ Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other arrhythmias can also occur e.g. ventricular tachycardia. ◙ Management: 1) Check the patient’s pulse, if no pulse, commence the arrest protocol immediately (and deliver immediate defibrillation) 2) Administer O2.
81
Pericarditis “important √” ◙ Occurs within 48 hours (i.e. 2 days) after MI. ◙ Features → Pleuritic chest pain that is worse on lying flat and during inspiration ± Fever ± Pericardial rub. ◙ Pericardial effusion may develop leading to enlarged globular heart on chest X-ray and is confirmed by echocardiogram. ◙ ECG → Widespread Saddle Shaped ST Elevation with upward concavity + PR Depression.
◙ Management of Pericarditis (imp): √ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800 mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days. √ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence)
82
Acute Tricuspid regurgitation (MR):
Similar to mitral regurgitation but the pan-systolic murmur is heard over the lower left sternal border.
83
Acute mitral regurgitation (MR): “important √” pansystolic murmur ◙ Occurs 2-15 days after the MI (Mostly inferior MI). ◙ Treatment → vasodilators, but often requires emergency surgical repair.
◙ Due to → Ischemia or rupture of the papillary muscles of the mitral valve. ◙ An early-to-mid systolic or Pansystolic murmur is typically heard at Apex. ◙ May present with Hypotension, Tachycardia, and Pulmonary edema. If with Pulmonary Edema → SOB (Dyspnea), Bi-basal Crackles, Tachycardia. ◙ To diagnose MR → Echocardiogram.
84
Ventricular septal defect (VSD)
◙ Rupture of the interventricular septum usually occurs in the first week after a MI attack and is seen in around 1-2% of patients ◙ Features: acute heart failure associated with a pan-systolic murmur best heard at the left lower sternal border + Heart Failure (eg, bibasilar crackles) + Shock (hypotension, tachycardia). ◙ An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. ◙ Urgent surgical correction is needed.
85
Dressler’ s syndrome “important √” ◙ Similar to pericarditis in features but it tends to occur 2-6 weeks following a myocardial infarction.
◙ The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. ◙ It is characterised by a combination of fever, pleuritic chest pain that worsens on inspiration and lying flat , pericardial effusion and a raised ESR. ◙ It is treated with NSAIDs. ◙ ECG: Widespread Saddle Shaped ST Elevation ± PR Depression
86
Left ventricular aneurysm ◙ The ischaemic damage sustained during a MI episode may weaken the myocardium resulting in a thin muscular layer; thus, aneurysm formation. ◙ This usually occurs 4-6 weeks post MI.
◙ This is typically associated with persistent ST elevation and left ventricular failure. ◙ A thrombus may form within the aneurysm increasing the risk of stroke . Patients are therefore anticoagulated. ECG → Persistent ST Elevation + Left Ventricular Failure. CXR → Enlarged heart with a bulge at the left heart border . Echo → Paradoxical movement of the ventricular wall.
87
Dressler’ s syndrome “important √
” ◙ Similar to pericarditis in features but it tends to occur 2-6 weeks following a myocardial infarction. ◙ The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. ◙ It is characterised by a combination of fever, pleuritic chest pain that worsens on inspiration and lying flat, pericardial effusion and a raised ESR. ◙ It is treated with NSAIDs. ◙ ECG: Widespread Saddle Shaped ST Elevation ± PR Depression.
88
Cardiac tamponade Vs Pericarditis
◙ Pericarditis (Can occur as a Complication of MI, may develop shortly after MI within 2 days) and Dressler’s syndrome (presents 2-6 weeks after MI) both have the same features: → Pleuritic chest pain that worsens on lying flat and during inspiration, and improves on upright sitting forward. ± Pericardial rub, ± Widespread Saddle shaped ST elevation on the ECG. ◙ They can also lead to Pericardial effusion (Enlarged globular heart on chest X-ray) and if severe enough, Cardiac Tamponade can also develop (also enlarged globular heart of the X-ray + Beck’s Triad: Hypotension, Muffled Heart Sounds, High JVP).
89
Wide spread ST depression (+) ST elevation in aVR
→ Left main coronary artery [LMCA] occlusion → Emergency coronary angiography
90
For Theoretical Exams: ◙ Any patient presents with STEMI
TEMI: → Give MONA (Morphine, O2, Nitroglycerin, Aspirin) and then: → Send immediately for (Percutaneous Coronary Intervention). • If PCI is not obtainable → alteplase ie thrombolysis • If PCI and Alteplase are not given, pick →Streptokinase. [i.e. thrombolysis].
91
◙ Any patient presents with NSTEMI or Unstable angina: → After giving morphine, 2 medications should be given immediately:
√ Oral Aspirin 300 mg ◙ Any patient presents with NSTEMI or Unstable angina: → After giving morphine, 2 medications should be given immediately: (+) √ SC Low molecular weight heparin “or” SC Fondaparinux.
92
• If left main coronary artery occlusion:
i.e. (widespread ST depression + ST elevation in aVR): after giving morphine → Emergency coronary angiography.
93
The first drug of choice for Symptomatic Bradycardia (Dizziness, feeling unwell) is
→ Atropine Given 0.5 mg IV push and may be repeated up to a total dose of 3 mg). What if he was given atropine but no response? Next step would be → Temporary transcutaneous pacemaker. ◙ 2nd Line → Dopamine. ◙ 3rd Line → Epinephrine. ♠ N.B. If the question was “the next best step” (or) “the initial line”, the Answer will be → O2 (ABCD).
94
Beck’s Triad: √ Hypotension, √ Muffled “faint = weak” Heart Sounds , √ High Jugular Venous Pressure [JVP] (= Distended neck veins).
→ Cardiac Tamponade. → Echo for Dx and Pericardiocentesis for Rx
95
Infective Endocarditis (IE) New Murmur + Fever → IE think of ± Malaise, Rigors.
The initial step → Blood Culture √ Then → Echo Example: 6 weeks following MI, a 59-year-old patient presented with a 10-day history of intermittent fever and a new-onset of a soft high-pitched murmur at the apex. His ECG is normal. Fever + New-onset murmur, Think → infective Endocarditis
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• Risk Factors:
◙ A previous episode of endocarditis → the strongest risk factor. ◙ Rheumatic valve disease. ◙ Prosthetic valves. ◙ Congenital heart defects. ◙ Intravenous drug users (IVDUs: typically causing tricuspid lesion).
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• The Causative Organisms
: - Staph. Aureus is the commonest cause of IE in general . - Staph. Epidermidis is the commonest cause after prosthetic valve surgery. - Strept. Viridans (especially sterpt. Mitis and strept. Sanguinis) are the commonest cause in people with poor dental hygiene or following a dental procedure.
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• Features and Diagnosis → Modified Duke criteria Infective endocarditis is diagnosed in any of the following situations: • 2 major criteria, or • 1 major and 3 minor criteria, or • 5 minor criteria
Major criteria 1) Positive blood cultures ◙ Two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, (Or) ◙ Persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis Not to be confused, it is true that staph. Aureus is the commonest pathogen in IE; however, it is not specific for IE as it causes many other inflammations. 2) Evidence of endocardial involvement (i.e. +ve Echo for IE) ◙ Positive echocardiogram ( oscillating structures Abscess formation , new valvular regurgitation or dehiscence of prosthetic valves). (Or) ◙ New valvular regurgitation
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Minor criteria
1. Predisposing heart condition or intravenous drug use. 2. Microbiological evidence that does not meet the major criteria. 3. Fever > 38°C. 4. Vascular phenomena → Major emboli, Splenomegaly, Clubbing, Splinter haemorrhages, Janeway lesions, Petechiae or purpura. 5. Immunological phenomena → Glomerulonephritis, Osler’s nodes, Roth spots. N.B. - Osler’s Nodes: painful, red nodules on the hands or feet that can persist for hours to days. - Janeway lesions: Non-tender, small, erythematous or hemorrhagic macular or nodular lesions on the soles or palms. they occur due to septic micro- emboli that deposit the bacteria under the skin).
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Endocarditis: initial “Empirical” “Blind” therapy
• Native valve endocarditis → - Amoxicillin + low-dose Gentamicin. (Or), - Vancomycin + low-dose Gentamicin ( If Penicillin allergic or MRSA Methicillin-Resistant Staph. Aureus” is suspected or Severe Sepsis). • If Hx of prosthetic valve endocarditis→ Vancomycin + low-dose Gentamicin + Rifampicin
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IE
The most important note to remember is that in any patient presenting with Fever + a new heart Murmur → suspect Infective Endocarditis and order Blood Culture until proven otherwise.
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Example 1: A man who had dental extraction a few days ago presents with petechia. His vitals are stable except his body temperature which is 38.9. On examination (O/E): He has petechiae, painful nodules on his palms, and a cardiac murmur.
The likely Dx → The underlying cause of this condition → The next investigating step → Answers Infective Endocarditis. (Fever + New Murmur). infection. blood culture ( followed by Echo).
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Example 2: A man presents with Fever, confusion, petechiae. This is a picture of his soles
What is the most appropriate investigation? → Blood Culture These lesions are likely endocarditis). ♦ Likely → → Do Blood culture Janeway lesions (minor criteria of infective Infective endocarditis then Echocardiogram
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In a patient with Atrial Fibrillation → We use the CHA2DS2-VASc Score
“To determine the need to anticoagulants” . ◙ Give Warfarin or DOAC (Direct-Acting Oral AntiCoagulants, such as Apixaban, Rivaroxaban, Edoxaban, Dabigatran) To: √ All patients with score ≥ 2. √ Consider giving Warfarin or DOAC to Men who score ≥ 1.
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DOAC uses and disadvantage
Advantages of DOAC: o No need for INR Monitoring, o Faster Onset of Action (2-4 hours Reduces the risk of intracranial Hemorrhage. Disadvantages of DOAC: o No Antidote o Require strict compliance by the patients.
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Important Scoring Systems to Know
◙ The CHA2DS2-VASc score is used to determine the need to anticoagulants in a patient who has atrial fibrillation. √ important ◙ The ABCD2 score (Prognostic) is used to identify the risk of future stroke in patients who have had a suspected TIA in the following 7 days . √ Not advised to be used now according to the recent 2019 CKS guidelines. ◙ The HAS-BLED score estimates the risk of major bleeding for patients on anticoagulation for atrial fibrillation. ◙ The DRAGON score predicts the 3-month outcome in ischaemic stroke patients receiving tissue plasminogen activator (tPA) e.g. alteplase. The QRISK2 score is used to determine the risk of a cardiovascular event in the next 10 years
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Pulmonary edema
Mechanism: Often caused by congestive heart failure. When the heart is not able to pump efficiently → blood may return into the veins → then to the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. Features: Desaturation (Low O2 Sat.), Dyspnea (SOB), Orthopnea (SOB worsens when lying down), Auscultation → Crepitations “Crackles = rales”. Mostly bi-basal. Tachycardia.
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Investigations: : While chest X-ray usually shows features of pulmonary edema The single most appropriate Investigation), the underlying cause requires
Echocardiogram to be identified (e.g. Congestive Heart Failure, Complication of MI → Acute Mitral Regurgitation due to papillary rupture, Ventricular aneurysm, …etc.)
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Pulm oedema Investigation First line And to find cause
Therefore, pay attention to the question words! ◙ The Most Appropriate Investigation → Chest X-Ray. “imp √” ◙ The Investigation Needed to Identify the Underlying Cause → Echo. “imp √”
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Pulmonary oedema mng
Management: MONA (But the last A -Aspirin- is replaced by F -Furosemide-): → Morphine, O2, Nitrates, Furosemide (Lasix). 1) Sit the patient up (Popup position) and give O2 (aim for O2 saturation of ≥ 95%, or ≥ 90% in COPD patients). 2) Spray 2 puffs of sublingual GTN (Glyceryl TriNitrates). 3) Give Furosemide (Lasix) 40 mg IV (Slowly). 4) Give Diamorphine ( 2.5-5 mg IV slowly) or Morphine (5-10 mg IV slowly) to relieve pain, anxiety and distress.
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Pulm oedema and embolism
N.B. A good difference between Pulmonary Edema and Pulmonary Embolism is that Pulmonary Oedema can be diagnosed by Chest X-ray while Pulmonary Embolism needs CTPA (CT Pulmonary Angiogram).
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Pulmonary Oedema → X-ray findings Kerley Lines (Expansion of the interstitial space by fluid
Pulmonary Oedema → Kerley Lines + Bat’s wing hilar shadow
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20 days after MI, a patient developed sudden Dyspnea. O/E → Tachycardia, Desaturation (88% on Room Air), Hypotension and Bilateral Chest Crackles.
◙ The likely Dx → Pulmonary Oedema. ◙ The appropriate Initial investigation → Chest X-Ray. ◙ The best investigation to identify the cause → Echocardiography. ◙ Treatment → MONF (Morphine, O2, Glyceryl Trinitrates, FUROSEMIDE). Pulmonary Oedema → Kerley Lines (Expansion of the interstitial space by fluid)
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Pulm oedema medications in existing heart failure patients
Important: If pulmonary edema is cuased by existent hear failure, the patient needs to be discharged on either ACE inhibitor or a beta blocker (one drug at a time). If asthmatic → ACE inhibitor is preferred over BB as BB may worsen asthma
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The Typical Presentation of Acute MI (75% of cases):
◙ Central Chest Pain or Epigastric pain or Substernal pain that is severe, sudden, crushing, pressuring, squeezing, constricting or burning. ◙ Radiates to arms, shoulders, neck or jaw. ◙ ± Sweating (Diaphoresis), Nausea, Vomiting, Fatigue and/or Palpitations. ◙ SOB “Shortness of breath”.
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Important DD: [Dissecting Aneurysm] Aortic dissection
Although Dissecting aortic Aneurysm may have more or less a similar presentation to MI, to be chosen as an answer, there should be other clinchers pointing towards dissecting aneurysm such as: √ Unequal pulses in upper limbs. √ Hx of Marfan Syndrome (tall, long slender limbs and fingers). √ Hx of Ehlers-Danlos syndrome/ turner syndrome. √ Severe tearing chest pain that radiates to the Back. √ HTN is the most important risk factor. √ The patient presents with Hypotension, SOB, tachycardia, sweating.
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Points on Aortic Dissection
• Aortic dissection is a rare but serious cause of chest pain. • Pathophysiology → tear in the tunica intima of the wall of the aorta. • Injury of the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart. • In most cases, this is associated with a sudden onset of severe chest or back pain, often described as “tearing” in character. Also, vomiting, sweating, and lightheadedness may occur. • Other symptoms may result from decreased blood supply to other organs, such as stroke or mesenteric ischemia. • Aortic dissection can quickly lead to death from not enough blood flow to the heart or complete rupture of the aorta. • The transoesophageal echocardiogram (TEE) is a good test in the diagnosis of aortic dissection, with a sensitivity up to 98% and a specificity up to 97%. It has become the preferred imaging modality for suspected aortic dissection. • Other good investigations → CT scan with contras/ MRI. • In emergency settings → US or CT scan.
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Classification of aortic dissection
Stanford classification of Aortic Dissection: type A: ascending aorta, 2/3 of cases type B: descending aorta, distal to left subclavian origin, 1/3 of cases
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◙ Management od Aortic Dissection
• Type A → surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention. • Type B → conservative management, bed rest, reduce blood pressure: IV labetalol to prevent progression
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Cardiac Tamponade Accumulation of pericardial fluid under pressure • Beck’s Triad: Hypotension ▐ Muffled Heart Sounds ▐ High JVP (Distended neck veins). • Others: Dyspnea, Pulsus Paradoxus, Tachycardia.
• Cardiac Tamponade can develop as a complication of MI After MI → Acute pericarditis → Pericardial effusion → Cardiac Tamponade • Trauma is the most important cause of cardiac tamponade
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Cardiac tamponade
N.B. Chest X-ray that shows → Think of either enlarged globular heart Pericardial effusion (OR) Cardiac Tamponade. • Dx: Echocardiogram is diagnostic • Rx: Urgent pericardiocentesis.
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Cardiac tamponade hypovolemia Initial management?
Important! If the patient is in hypovolemic shock (severely low BP) and the question asks about the [INITIAL] treatment line and IV fluids is within the option, pick it! Cardiac Tamponade: Oxygenation and ventilation → 1 to 2 L IV fluid NS → bedside Pericardiocentesis
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Left Bundle Branch Block (LBBB)
In the context of chest pain, new LBBB is significant as it is an indication for thrombolysis / percutaneous coronary intervention (PCI). LBBB features on ECG: ◙ Notched (M shaped) broad complex QRS: usually in Lead (I), aVL and V6 but not always. ◙ Deep inverted (Negative) QRS: usually in lead (V1). ◙ Left Axis Deviation (Not always) Important Note → A new onset LBBB is characteristic for Myocardial Infarction (MI)
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Ruptured Abdominal Aortic Aneurysm (AAA
◙ The classical picture: a triad of: Pain, Hypotension, pulsatile tender abdominal mass. - Sudden onset severe abdominal ± Lower back ± Flank pain. - Shock (Hypotension, Sweating, Fainting) - Absent Lower Limb Pulse, mottled skin. ◙ It is a surgical emergency; therefore, immediate Ultrasound is the most appropriate initial investigation. ◙ If no U/S in the options, go for CT scan abdomen.
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◙ Screening for Abdominal Aortic Aneurysm (AAA) in the UK
: √ Men only. √ Once only. √ In 65th year. √ by Ultrasound.
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Management of Chronic Heart Failure In a patient with Heart Failure [LL Edema, Dyspnea, Orthopnea, Ejection fraction less than 40%],
The management would be: • For symptomatic relief and to reduce the volume overload, all patients should receive → Diuretics (e.g. loop diuretics e.g. Furosemide) • Start with either ACEi or BB. (one drug at a time) • If the symptoms persist → Add the other one (ACEi or BB). • If still symptomatic → Add spironolactone “potassium sparing diuretics”. • V. Imp. Note: If the patient with Heart Failure has Diabetes , we start with ACE inhibitors (e.g. Ramipril) instead of Beta-Blockers.
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Coronary Artery Dominance
Right coronary artery (RCA) gives off the PDA • The artery that supplies the Posterior Descending Artery (PDA) determines the coronary dominance. of the population, the (Right Dominant). of the population, the • In 85% • In 15% left circumflex gives off the PDA (Left Dominant). ◙ Hence, the artery that has artery dominance is the (RCA), as it gives off the PDA in 85% of people.
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Dressler’s syndrome ◙ It tends to occur around 2-6 weeks following a MI. ◙ The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers.
It is characterised by a combination of fever, pleuritic pain worsens on inspiration and on lying flat, pericardial effusion and a raised ESR. ◙ ECG → Widespread Saddle Shaped ST Elevation + PR Depression ◙ It is treated by NSAIDs. ◙ Its features are more or less similar to acute pericarditis
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Hypokalemia ◙ Muscle weakness and cramps + U wave on the ECG ◙ One important reason for hypokalemia is Thiazide like Diuretics (e.g. Bendroflumethiazide) and Loop diuretics (e.g. Furosemide) But not Potassium-sparing diuretics (e.g. Spironolactone) which causes HypeRkalemia.
◙ Spironolactone, ACE inhibitors, ARBs → ◙ Loop diuretics, Thiazide like diuretics → HypeRkalemia. HypOkalemia. ◙ The ECG changes in HypUkalemia → U Wave
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Hypokalemia RX
U wave (hypokalemia) → an additional wave after (T-wave) Management of hypokalemia 1) Oral or IV potassium chloride (based on severity), e.g. 2) Stop/ Treat the cause (e.g. stop furosemide, thiazide like diuretics).
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HypOkalemia causes
Loop Diuretics (e.g. Furosemide • Thiazide-like diuretics( e.g. bendroflumethiazide, indapamide) • Villous Adenoma Conn’s disease (1ry hyperaldosteronism) Vomiting and Diarrhea • Renal tubular failure • Cushing Syndrome
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HypeRkalemia
ACE inhibitors (e.g. enalapril) • ARBs (e.g. losartan). Potassium-sparing diuretics Eg. Spironolactone/ Eplerenone) • Congenital Adrenal Hyperplasia (CAH Addison’s (1ry Adrenal Insufficienc • CKD/ Acute renal failure
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Hypokalemia
Remember: √ Severe vomiting can cause hypokalemia. √ Hypokalemia features include muscle weakness and cramping.
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Paroxysmal Supraventricular Tachycardia = (Narrow-Complex SVT) ◙ Usually in young patients ◙ Presents with Palpitations, Light-headedness, Recurrent, Young Mng?
Management: imp √ ♠ Initial line → Valsalva manoeuvre, Carotid massage. ♠ Not improved? adenosine → Intravenous (6mg Rapid IV Bolus), still not improved? → give additional 12mg adenosine, still not improved? → give another 12mg adenosine
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Asthma and. svt
N.B. Adenosine is contraindicated in asthmatics → Verapamil (CCB) is the preferred option in SVT in a patient with Asthma. ♠ Still not improved? → Electrical DC “Cardioversion” • Prevention of future episodes → ß-Blockers or Radio-frequency ablation. IMPORTANT NOTE: If the patient is hemodynamically unstable (eg, hypotension, chest pain, shock, and or altered mental status) Proceed immediately to → electrical synchronised cardioversion. In summary: → Carotid Massage and Valsalva Manoeuvre → IV Adenosine 6 mg → IV Adenosine 12 mg → IV Adenosine 12 mg → Cardioversion (Shock). [ Important Note: Start with this step if chest pain, hypotension, and or altered mentation ie, hemodynamic unstable patient]
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Polymorphic (Broad-Complex) Ventricular Tachycardia = Torsades De Pointes (TDP
) ◙ Beat-to-beat variations with no uniform pattern of ventricular contractions. ◙ Broad QRS (except in resting status), Prolonged QT, Fainting episodes, Patient might be a young athlete, Recurrent. ◙ Treatment → IV Magnesium Sulphate. N.B. Verapamil should NOT be used in VT.
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Drug causing prolong QT
◙ Quick Important Note to Remember: High doses of can lead to Citalopram, (a SSRI), can cause prolonged QT intervals, which Torsade De Pointes
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PCI For patients who present with STEMI, give MONA (Morphine, O2, Nitroglycerin, Aspirin) and send immediately for (Percutaneous Coronary Intervention). What if PCI is not given in the options?
Pick → i.e. Alteplase “preferred” or Streptokinase (Tissue Plasminogen Activator) Thrombolysis.
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MI (Acute chest pain radiating to jaw, shoulder…) BUT on ECG. No st elevation What to Do Next?
→ Request Cardiac Enzymes, especially (Troponin) If Troponin is high → NON-STEMI Elevation MI → Give LMWH OR Fondaparinux + Aspirin 300 mg
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6 weeks after MI, a patient returns with SOB when walking long distance and his ECG shows ST elevation in V1-V5 leads.
The likely cause → Left Ventricular Aneurysm. (Persistent ST elevation post-MI → Think of: Left Ventricular Aneurysm) Left ventricular aneurysm ◙ The ischaemic damage sustained during a MI episode may weaken the myocardium resulting in a thin muscular layer; thus, aneurysm formation. ◙ This usually occurs 4-6 weeks post MI. ◙ This is typically associated with persistent ST elevation and left ventricular failure. ◙ A thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated. ECG → Persistent ST Elevation + Left Ventricular Failure. CXR → Enlarged heart with a bulge at the left heart border. Echo → Paradoxical movement of the ventricular wall.
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Hypertension Management Hypertension classification Stage Criteria 1 and 2
Stage 1 Clinic BP ≥ 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP ≥ 135/85 mmHg Stage 2 Clinic BP ≥ 160/100 mmHg and subsequent ABPM daytime or hypertension HBPM average BP ≥ 150/95 mmHg
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Stage 3 htn
Stage 3 “Severe Clinic systolic BP ≥ 180 mmHg, hypertension” or clinic diastolic BP ≥ 110 mmHg
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Abpm Hbpm
Keys: ABPM → Ambulatory Blood Pressure Monitoring. HBPM → Home Blood Pressure Monitoring. N.B. Clinic BP is usually higher than ABPM and HBPM because some people get stressed or feared while at a clinic → a slight increase in BP. Management of hypertension Lifestyle advice should not be forgot
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Lifestyle advice
Low salt diet. • Caffeine intake should be reduced. • Stop smoking. • Drink less alcohol. • Eat a balanced diet rich in fruits and vegetables. • Exercise more. • Lose weight.
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Many of type 2 and 1 hypertension
♠ When to Treat Stage 1 Hypertension? • Treat if the patient’s age is < 80 years AND + any of the following: Target organ damage, established cardiovascular disease, renal disease, diabetes (DM) or a 10-year cardiovascular risk equivalent to ≥ 10%. ◙ Note: If a patient is completely free and has a stage 1 Hypertension → Lifestyle and Diet Modification + review (Follow up). ◙ Note: In a patient with stage 2 hypertension at a clinic (Clinic BP ≥ 160/100) → Before commencing antihypertensive drugs, record either ABPM or HBPM.
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◙ Note: For patients < 40 years and with stage 2 hypertension or higher
→ Consider a specialist referral to exclude secondary causes of the HTN
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If ABPM or HBPM ≥ 150/95 mmHg (i.e., confirmed stage 2 or higher hypertension) → -________
If ABPM or HBPM ≥ 150/95 mmHg (i.e., confirmed stage 2 or higher hypertension) → Always treat.
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Htn mng
The Steps of The Management of Hypertension Step 1 • Patients < 55-years-old → start with ACE inhibitor (A) or ARBs. • Patients ≥ 55-years-old of Afro-Caribbean origin “of any age” → start with Calcium channel blocker. or In other words: • White + < 55 YO • —- ace inh or arb White + > 55 YO → start with ccb Afro-Caribbean + any age → start with ccb as a step 1 management of HTN.
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Step 2 (still hypertensive after step 1)
• Both: ACE inhibitor + Calcium channel blocker (A + C)
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◙ However, if this diabetic patient is Afro-Caribbean, Hypertension mng?
→ start with both ACE inhibitor + Calcium Channel Blocker as a first step.
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Why ACE inhibitor is used for Diabetic Hypertensive patients?
- It is reno-protective (unless eGFR is low; <30; in advanced CKD). - It has protection against diabetic retinopathy. - It has +ve effect on glucose metabolism.
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Before commencing ACE inhibitor for any patient
→ If eGFR (Glomerular Filtration Rate) is low ; <30 as in advanced Chronic Kidney Disease → ACEi and ARBS should be avoided in this case.
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Always treat hypertension in a DIABETIC patient with regardless of the age ____\\ as it is reno-protective “Unless if the eGFR is <30”.
Ace inh
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Q] An elderly man feels dizzy when he stands and loses balance and falls. He is on a number of medications: ramipril for hypertension, zopiclone insomnia, cetirizine for allergy of hay fever, metformin for diabetes, and lithium for bipolar disorder. He has postural hypotension (his diastolic BP while standing is > 10 mmHg lower than his diastolic BP while sitting). Which medication is the most likely reason for his recurrent falls?
→ ACE inhibitors (Ramipril). They can cause postural hypotension → thus falls. Anti-hypertensive medications as ACE inhibitors and Calcium channel blockers can cause postural hypotension → dizziness on standing → Falls. if there was no postural hypotension, we would suspect Zopiclone (Although rare, it can lead to falls by balance impairments).
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Again, any patient of any age and any ethnic group presents with Hypertension and he is a Diabetic patient
Start with → (e.g. Enalapril). ACE inhibitor (Note, if the eGFR is 30 or below, ACEi and ARBS should be avoided).
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Absent “P” wave on ECG + Irregularly Irregular Rhythm + Palpitation
Diagnosis? → Atrial Fibrillation. beta-blockers. Management? √ First line → beta blocker √ If asthmatic → Avoid beta-blockers and give √ ccb If the patient has associated HF → give digoxin
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Examples of DOAC “Direct-Acting Oral AntiCoagulants” -important √-
Apixaban, Rivaroxaban, Edoxaban, Dabigatran”
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Af in hypotension
If haemodynamically unstable Cardioversion √ If the patient with AF is unstable (eg, SBP ≤ 90) → (Shock). (eg, hypotension) and the AF has just started and no cardioversion in the options, Pick → IV amiodarone. Imp √
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Fever + New Murmur → Infective Endocarditis “until proven otherwise”
Be careful, the reason of IE is → Infection “infective” endocarditis. - Staph. Aureus is the commonest cause of IE in general. - Staph. Epidermidis is the commonest cause after prosthetic valve surgery. - Strept. Viridans (especially sterpt. Mitis and strept. Sanguinis) are the commonest cause in people with poor dental hygiene or following a dental procedure.
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Ventricular Ectopics = Three-beat patterns = Ventricular Trigeminy.
◙ A sense of a missed/skipped beat, unsustained palpitation ± Dyspnea and Dizziness due to immature discharge of a ventricular ectopic focus which produces → an early and broad QRS complex. ◙ Causes → Ischemic heart disease (MI), Cardiomyopathy, Stress, Alcohol, Caffeine, Cocaine, Medications OR Naturally. ◙ Over half the population have silent, or asymptomatic ventricular ectopics which are discovered incidentally on a routine ECG. ◙ If there is No underlying Heart disease (e.g. IHD, Cardiomyopathy) → Benign; no clinical significance. ◙ If these ventricular ectopics are due to IHD or Cardiomyopathy → May precipitate to more life-threatening arrhythmias like Ventricular Fibrillation
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The Typical Presentation of Acute MI (75% of cases) ◙ SOB “Shortness of breath”. ♠ Keep in mind that some patients may present with additional Atypical feature such as Abdominal Pain, Jaw pain or Altered mental status.
◙ Central Chest Pain or Epigastric or Substernal pain that is severe, sudden, crushing, pressuring, squeezing or burning and radiates to arms, shoulders, neck or jaw. ◙ ± Sweating (Diaphoresis), Nausea, Vomiting, Fatigue and/or Palpitations.
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A patient with chronic heart failure developed gout. A medication for his gout is prescribed. A few days later, the patient came back to the hospital complaining of worsening of his Heart Failure symptoms (SOB, Orthopnea).
- The likely cause of this patient’s gout → Thiazide like diuretics (e.g. bendroflumethiazide) or Loop Diuretics (Both can cause hyperuricemia (Gout) and both can be used to treat volume overload caused by Heart Failure) - The likely cause of this patient’s worsening of SOB and Orthopnea → NSAIDs (e.g. Ibuprofen) that was prescribed to treat his gout.
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Rationale for avoiding nsaids and cox 2 inh in heart failure
Never give NSAIDs (e.g. Ibuprofen) nor selective COX-2 inhibitors (e.g. Celecoxib) to the following patients: CKD, CHD, IHD (Chronic Kidney Disease, Chronic Heart Failure, Ischemic Heart Disease). ◙ These drugs can worsen the HF (worsening the SOB and Orthopnea) and also the renal function. ◙ Remember that NSAIDs inhibit the synthesis of prostaglandins → thus, decrease the eGFR, retain more salt and water (risk factor for HF). ◙ N.B. Thiazide like diuretics and Loop diuretics decrease the clearance of Uric Acid → leading to Gout (Hyperuricemia) ◙ N.B. NSAIDs such as Ibuprofen are used for the treatment of Gout. If given to a patient with chronic heart failure, they would worsen the HF symptoms (Orthopnea and Dyspnea).
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In-Hospital Cardiac Arrest algorithm If No Signs of Life (i.e. No breathing, No detectable Pulse):
Ring the emergency bell and call resuscitation team (Code Blue) first. Then → Start CPR 30:2. Then → Get defibrillator. Then → ALS when the resuscitation team arrives.
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In STEMI patient, what if PCI is not given in the options?
“preferred” or Pick → = i.e. Alteplase Streptokinase (Tissue Plasminogen Activator) Thrombolysis.
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Diabetic patients may develop “Silent MI” i.e. painless MI. Thus, they may die suddenly and silently without feeling any chest pain ( They won’t feel chest pain → They won’t seek medical help).
This is because they may not feel chest pain due to autonomic neuropathy.
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An elderly male presents with Palpitations and Shortness of breath on exertion. The ECG is as follows. What is the likely diagnosis and management? Fine fibrillation waves Absent p wave Irregularly irregular
AF Beta blocker Ccb if asthmatic
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Svt mng
Remember: ◙ In → We firstly perform If this fails → We give Supraventricular tachycardia Carotid Massage (Narrow QRS Complex, absent p waves) and Valsalva Manoeuvre. IV Adenosine. IMPORTANT NOTE: If the patient is hemodynamically unstable ( eg, hypotension, chest pain, shock, altered mental status) Proceed immediately to → electrical synchronised cardioversion.
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In polymorphic ventricular tachycardia (i.e. torsade’s de pointes)
→ IV magnesium sulfate.
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Beck’s Triad in Cardiac Tamponade
Hypotension, Muffled Heart Sounds, High JVP (Distended neck veins). • Trauma (e.g. stab in the chest) is the most important cause for cardiac tamponade. • Dx: Echocardiography is diagnostic. • Tx: Urgent pericardiocentesis.
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In → Breakdown of small emboli from the mass that can travel down the blood and cause ischemia in multiple sites, leading to → (e.g. Pulmonary Embolism, Stroke, Clubbing, Blue fingers)
◙ In Atrial Myxoma → Mitral valve obstruction → Mitral Stenosis → Early or Mid-diastolic murmur, Dyspnea, Syncope
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Therefore, in a patient with Hx of syncope, SOB, Pulmonary Embolism and early-mid diastolic murmur → Think of
Atrial myxoma
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Points on alcohol
Points on Alcohol UK guidelines recommend that a person should drink - No more than 14 units a week, - No more than 3 units a day, - with at least 2 alcohol-free days a week.
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Example: If someone drinks 7 units of alcohol a week and smoke 20 cigarette a day, we should refer him to
→ Smoking Cessation Clinic. This is because his alcohol intake is insignificant as per NICE whereas his smoking is significant.
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scenario to test your knowledge on a previous topic 4 days after MI, an elderly patient presents with Fatigue and Dyspnea. On Auscultation → Pansystolic murmur at the apex and radiates to the axilla was heard.
→ The likely Dx → → The likely Cause → Mitral Regurgitation. Rupture of Papillary Muscles. Acute mitral regurgitation (MR): “important √” pansystolic murmur ◙ Occurs 2-15 days after the MI (Mostly inferior MI). ◙ Due to → Ischemia or rupture of the papillary muscles of the mitral valve. ◙ An early-to-mid systolic or Pansystolic murmur is typically heard. ◙ May present with Hypotension, Tachycardia and Pulmonary edema. ◙ Dx → Echocardiogram. ◙ Treatment → vasodilator therapy but often requires emergency surgical repair
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A scenario to test your knowledge on a previous topic 2 days after MI, an elderly patient presents with fever and chest pain. ECG shows ST elevation with upward concavity.
→ Acute Pericarditis. Post-MI Pericarditis “important √” ◙ Occurs within 2-3 Days after MI. ◙ Features → Pleuritic chest pain that is worse on lying flat and during inspiration ± Fever ± pericardial rub ◙ Pericardial effusion may develop leading to enlarged globular heart on chest X-ray and is confirmed by echocardiogram. ◙ ECG → Widespread Saddle Shaped ST Elevation with upward concavity + PR Depression. ◙ Management of Pericarditis (imp): √ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800 mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days. √ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence).
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For Acute Myocardial Infarction patients, the analgesic that can be used while in the ambulance is still
→ IV Morphine. ◙ Remember the initial management for acute MI → (MONA): Morphine, Oxygen, Nitrates, Aspirin.
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MI Analgesia while in an ambulance (Pre-Hospital)
1) Glyceryl Trinitrate (GTN) sublingual or spray. 2) ± Opioids (INTRAVASCULAR): 2.5-5 mg Diamorphine or 5-10 mg Morphine. - N.B. Around 1/3 of the patients with MI have nitrate-resistant chest pain; therefore, morphine is given additionally to relieve chest pain. √ IM absorption is unreliable + √ If the patient receives thrombolysis later on, the site of IM injection might bleed.
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Old adult, Sudden collapse, Not breathing, Unconscious → Shock ‘’defibrillation’’
Ventricular Fibrillation Old adult, Sudden collapse, Not breathing, Unconscious → Shock ‘’defibrillation’’
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Broad Complex Tachycardia ◙ Tachyarrhythmia is one of the complications of MI.
♠ An ECG showing broad complex tachycardia in a (still) conscious patient ± atrial activity → Ventricular tachycardia → IV Amiodarone. ♠ If the patient is hemodynamically unstable; i.e. unconscious, collapsed, not breathing → Ventricular Fibrillation → 1) Check the patient’s pulse, if no pulse, commence the arrest protocol immediately. 2) Administer O2. 3) If the patient is hemodynamically unstable: Shock followed by IV Amiodarone followed by further Shocks if needed. ◙ N.B. HypOkalemia is the most important cause of ventricular tachycardia (VT) clinically.
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Treatment of Cardiac Tamponade
→ Pericardiocentesis.
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◙ Tall Tented T-wave → HypeRkalemia. ◙ U-wave → HypOkalemia.
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45 Y/O African patient has BP 160/90 on three separate occasions. What is the initial line of treatment?
→ Calcium Channel Blocker (CCB) (First Step Management of hypertension in African-Caribbean patients is CCB regardless of the age).
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Any ethnicity + Any age + Diabetes → start with ______ as a step 1 management of HTN
Any ethnicity + Any age + Diabetes → start with ACEi/ARBs as a step 1 management of HTN
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Heart Murmurs Defect AS
Aortic stenosis Ejection systolic Right 2nd ic lateral to sternum Radiates to carotid artery Dyspnea on activity Angina chest pain Syncope
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Aortic Regurgitation
Early Diastolic left lower sternal border around the 3rd to 4th intercostal spaces Symptoms of Heart Failure
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Pulmonary Stenosis
Ejection Systolic Left 2nd ICS just lateral to sternum, radiates to left shoulder of infraclavicular area Systemic cyanosis
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Pulmonary regurgitation
Early-Diastolic Left 2nd ICS just lateral to sternum Symptom of right heart failure
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Mitral stenosis
Mid diastolic or late diastolic Apex left 5th ics mid clavicular line Symptoms of heart failure
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Mitral regurgitation
Pansystolic Apex( left 5th ics midclavicular Radiates to axilla) Symptoms of chf oedema ascites
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Tricuspid stenosis
Diastolic rumble 4th to 5th ics over left sternal border Fluttering Discomfort in the neck
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Tricuspid regurgitation
Pansystolic 4th -5th ics on left sternal border Symptoms of right sided heart failure
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Example: A patient with a history of MI presents with Orthopnea (Cannot lie down flat), Bibasilar crepitations , Pan-systolic murmur.
→ Mitral Regurgitation. → Request Echocardiogram.
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A scenario to test your knowledge on a previous topic A Young adult presents with frequent fainting attacks since childhood and prolonged QT. There are sinus rhythm and normal P-R interval. No FHx of arrhythmias or sudden death.
The likely Dx→ Polymorphic Ventricular Tachycardia (Torsades de pointes) Polymorphic (Broad-Complex) Ventricular Tachycardia = Torsades De Pointes (TDP) ◙ Beat-to-beat variations with no uniform pattern of ventricular contractions. ◙ Broad QRS (except in resting status), Prolonged QT, Fainting episodes, Patient might be a young athlete. Recurrent. ◙ Treatment → IV Magnesium Sulphate. N.B. Verapamil should NOT be used in VT.
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An elderly patient with a Hx of stroke presents with exertional dyspnea. ECG shows Atrial Fibrillation. Chest X-ray shows Straight left heart border.
→ Mitral Stenosis. The most common cause of mitral stenosis → rheumatic fever, rheumatic fever and rheumatic fever. Pathogenesis of Mitral Stenosis: Mitral stenosis impedes left ventricular filling → increased left atrial pressure (Which will lead to left atrial hypertrophy; therefore, CXR shows Straight left side heart border) → Blood returns Back to lungs → Pulmonary Congestion → Right Ventricular Failure (Hepatomegaly, Ascites, Oedema) Features • Mid-late diastolic murmur (best heard on expiration) ‘’low pitched’’ • Loud S1, opening snap • Low volume pulse • Malar flush • Atrial fibrillation
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Right and left heart murmurs
Note: ◙ Left heart murmurs (Mitral and Aortic) are best heard during expiration ◙ Right heart murmurs (Tricuspid and Pulmonary) best heart in inspiration
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Ext chest X-ray echo findings of MS
Chest x-ray in MS • Left atrial enlargement (often) → Straightening the left border of the heart. ECG (may show): - Signs of Right ventricular hypertrophy - P mitrale (bifid P wave) - AF Echocardiography → (Thickening of Mitral valve leaflets)
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First line treatment in AF (if no asthma)
→ ß-Blockers (e.g. Metoprolol)
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↓ Ejection Fraction (+) ↓ Septal Wall Thickness →
Dilated Cardiomyopathy
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◙ ↑ Ejection Fraction (+) ↑ Septal Wall Thickness →
Hypertrophic Cardiomyopathy.
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Dilated cardiomyopathy
Dilated Cardiomyopathy (DCM) Basics (For READING ONLY) • Dilated heart leads to systolic (± diastolic) dysfunction • All 4 chambers are affected but the Left Ventricle is more affected than the Right Ventricle. • Features include arrhythmias, emboli, mitral regurgitation • Absence of congenital, valvular or ischaemic heart diseas
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◙ Causes often considered separate entities • alcohol: may improve with thiamine • postpartum • hypertension Inherited causes?
• inherited • previous MI • infections e.g. Coxsackie B, HIV, diphtheria, parasitic • endocrine e.g. Hyperthyroidism • infiltrative e.g. Haemochromatosis, sarcoidosis • neuromuscular e.g. Duchenne muscular dystrophy • nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency • drugs e.g. Doxorubicin
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◙ Causes often considered separate entities for dilated cardiomyopathy
• alcohol: may improve with thiamine • postpartum • hypertension ◙ Other causes
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Inherited cardiomyopathy
• inherited • previous MI • infections e.g. Coxsackie B, HIV, diphtheria, parasitic • endocrine e.g. Hyperthyroidism • infiltrative e.g. Haemochromatosis, sarcoidosis • neuromuscular e.g. Duchenne muscular dystrophy • nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency • drugs e.g. Doxorubicin ◙ Inherited dilated cardiomyopathy • around a third of patients with DCM are thought to have a genetic predisposition • a large number of heterogeneous defects have been identified • the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen
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A Summary on Arrhythmias Management ◙ In Supraventricular tachycardia (Narrow-Complex) (SVT):
If the patient is → start with Valsalva manoeuvre and Carotid massage to stimulate the vagal tone (Parasympathetic which decreases the heart rate). - If still ill? → Give Adenosine 6 mg IV bolus. - If no response? → give another Adenosine double dose (12 mg). - If still no response? → give another Adenosine double dose (12 mg). - Unsuccessful yet? → Cardioversion. ♠ If the patient is haemodynamically Unstable → start with Cardioversion.
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In Polymorphic Ventricular Tachycardia (Broad-Complex) = (Torsade De Pointe) → Give IV MgSO4 (Magnesium Sulphate)
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AF
In AF: - Start with ß-Blockers (e.g. Metoprolol). - If Asthmatic patient → Calcium Channel Blockers. - If Associated Heart Failure → Digoxin.
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In Ventricular Tachycardia →
If stable patient → IV Amiodarone. If unstable → Synchronized cardioversion (Shock)
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Inherited dilated cardiomyopathy
Inherited dilated cardiomyopathy • around a third of patients with DCM are thought to have a genetic predisposition • a large number of heterogeneous defects have been identified • the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen
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In Supraventricular tachycardia (Narrow-Complex) (SVT):
If the patient is → start with Valsalva manoeuvre and Carotid massage to stimulate the vagal tone (Parasympathetic which decreases the heart rate). - If still ill? → Give Adenosine 6 mg IV bolus. - If no response? → give another Adenosine double dose (12 mg). - If still no response? → give another Adenosine double dose (12 mg). - Unsuccessful yet? → Cardioversion. ♠ If the patient is haemodynamically Unstable → start with Cardioversion.
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In Polymorphic Ventricular Tachycardia (Broad-Complex)
= (Torsade De Pointe) → Give IV MgSO4 (Magnesium Sulphate)
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Af
◙ In AF: - Start with ß-Blockers (e.g. Metoprolol). - If Asthmatic patient → Calcium Channel Blockers. - If Associated Heart Failure → Digoxin.
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◙ In Ventricular Tachycardia →
If stable patient → IV Amiodarone. If unstable → Synchronized cardioversion (Shock)
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Falls
Analysis and Causes of Falls. Causes are usually: 1) Cardiac cause (e.g. Arrhythmia). 2) Postural (Orthostatic) Hypotension. 3) Hypoglycemia. 4) Seizure.
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An elderly patient suddenly fell unconscious, he recovered completely within a few minutes, he remembers the event very well, he did not trip, he felt hot and flushed after the episodes but he did not feel dizzy or sweaty before the fall ECG 12 lead Stoke Adams
If the cause was hypoglycemia, he would have felt sweaty and dizzy before the episode. Plus, he would not have recovered until Glucose is administered. ◙ If it was a seizure, the stem has to include an eyewitness to describe the episode. Also, in seizure, there are usually post-ictal features such as confusion and drowsiness. However, the patient in the above stem did not feel any of these, he rather recovered completely. ◙ If it was Postural hypotension (Orthostatic hypotension), the fall usually follow a standing from a sitting position. In addition, the patient would have felt dizziness before the fall, Hx of difficult mobilisation, which are not mentioned here.
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Long term medications post-Myocardial Infarction = 5 Drugs
Long term medications post-Myocardial Infarction = 5 Drugs AABCS → Aspirin, ACEi, BB, Clopidogrel, Statin (e.g. Atorvastatin)
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An elderly patient fell and collapsed “syncope”. He was transferred to the A&E and now he is fully conscious. ECG shows irregular rhythm. What is the next best investigation
? → Echocardiogram. ◙ A Holter ECG (24-hour ECG) will not be beneficial as the ECG already shows Irregular Rhythm; hence, there is no point of using it again. Echo should be done to identify the underlying cause of this irregular rhythm so the treatment can be decided accordingly.
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Dc cardioversion in vt
Haemodynamically Unstable → e.g. √ Hypotension (SBP < 90), √ Loss of Consciousness, Others: √ HR > 150. √ Severe dizziness or syncope. √ Ongoing chest pain. √ increasing SOB. → Synchronized DC Cardioversion. [Any arrhythmia in an unstable patient → DC Cardioversion]
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An elderly patient suddenly fell unconscious, he recovered completely within a few minutes, he remembers the event very well, he did not trip, he felt hot and flushed after the episodes but he did not feel dizzy or sweaty before the fall
The best Investigation → 12-lead ECG
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Stoke adams
Therefore, the likely cause here is arrhythmia (Cardiac cause), likely (Stokes Adam attack). This is also supported by the fact that the patient felt hot and flushed after recovery, which means that the blood has been, rapidly, pumped back to the already dilated vessels. ( Dilated due to hypoxia caused by the irregular rhythm) → 12-lead ECG monitoring is required. Stokes Adam attack [For Reading]: Sudden collapse into unconsciousness due to a disorder of heart rhythm in which there is a slow or absent pulse resulting in syncope (fainting) with or without convulsions. In this condition, the normal heartbeat passing from the upper chambers of the heart to the lower chambers is interrupted. This results in a condition called a “heart block.” When a heart block occurs, the heart rate usually slows considerably. This can cause inadequate blood flow to the brain and result in fainting.
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Murmurs in Paediatrics
- Preterm baby with continuous or machinery murmur → PDA (Patent Ductus Arteriosus).
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Cyanotic baby with ejection systolic murmur
→ TOF (Tetralogy of Fallot). Ejection systolic murmur here is due to pulmonary stenosis which is one of the four major features of TOF.
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Progressive (Severe) Cyanosis + Poor feeding + Holosystolic “pansystolic” murmur along the left sternal border
→ Tricuspid Atresia.
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Acyanotic + Pan-systolic murmur
→ VSD (Others: Poor feeding and poorly gaining weight)
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Acyanotic heart disease
ASD VSD PDA COARCTATION KF AORTA
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Congenital Cyanotic heart disease
TRUNCUS ARTERIOSIS TRANSPOSITION OF GREAT ARTERIES TRICUSPID ATRESIA TETRALOGY OF FALLOT TOTAL ANOMOLOUS PULMONARY VASCULAR RETURN
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It is important to remember that:
√ PDA, ASD, VSD → Acyanotic. √ TOF, Tricuspid Atresia → Cyanotic. √ Pansystolic murmur = MR or TA or VSD.
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Patent Ductus Arteriosus (PDA)
• A form of congenital heart defect • generally classed as ‘acyanotic’ . (√) • connection between the pulmonary trunk and descending aorta • more common in premature (Preterm) babies. (√) • May close spontaneously
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Features investigation Of PDA
• left subclavicular thrill (sometimes rough systolic murmur along the left sternal border) • Continuous ‘machinery’ murmur (√) • large volume, bounding, collapsing pulse • wide pulse pressure Diagnosis → Echocardiogram
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RX of PDA
Management • Indomethacin / ibuprofen (NSAIDs) (ind=end=closes the duct) (inhibits prostaglandin synthesis) closes the connection in the majority of cases. (√) • If associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair. Indomethacin or ibuprofen → closes the duct. Prostaglandin → keeps the duct ope
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14 days old baby is Cyanosed, Desaturated with Ejection systolic murmur
. → Tetralogy of Fallot. The cause of ejection systolic murmur here is → pulmonary stenosis (one of the four criteria of TOF).
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Tetralogy of Fallot (TOF)
) Tetralogy of Fallot (TOF) is the most common cause of Cyanotic congenital heart disease **however, at birth, transposition of the great arteries is the more common lesion as patients with TOF generally present at around 1-2 months. ** It typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old TOF is a result of anterior malalignment of the aorticopulmonary septum.
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The severity of the right ventricular outflow tract obstruction determines the degree of cyanosis and clinical severity. In TOF
1) Ventricular septal defect (VSD) 2) Right ventricular hypertrophy (RVH) 3) Right ventricular outflow tract obstruction “pulmonary stenosis” (PS) → ejection systolic murmur 4) Overriding aorta
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Features of TOF
• cyanosis • causes a right-to-left shunt • ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur) • a right-sided aortic arch is seen in 25% of patients • chest x-ray shows a ‘boot-shaped’ heart. • ECG shows right ventricular hypertrophy
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Management of TOF
• Surgical repair is often undertaken in two parts. • Cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm.
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Familial Hypercholesterolemia It is Autosomal Dominant First degree relatives: Parents and siblings. Second degree relatives: Grandparents, aunts, uncles
Q) When to highly suspect it? 1) If Cholesterol is > 7.5 (Normal: <5 mmol/L) 2) Family History of “MI” in a first degree relative before the age of 60 or 2nd degree below 50
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Ventricular Fibrillation
Sudden collapse Not breathing Unconscious No pulse Defibrillation
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While in a hospital, an elderly patient was found unresponsive, no pulse and no breathing (No signs of life). Management?
→ Ring the emergency bell and call the resuscitation team. First → Start CPR 30:2. → Get Defibrillator. → Commence ALS when the resuscitation team arrives.
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Pan-Systolic murmur could be:
◙ MR → Mitral Regurgitation. ◙ TR → Tricuspid Regurgitation. ◙ VSD → Ventricular Septal Defect.
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VSD (Ventricular Septal Defect):
◙ If small hole → Asymptomatic ± Left sternal pan-systolic murmur with systolic thrill. ◙ If large hole → • Pan-systolic murmur along the left sternal border. • Left sternal heave, and systolic thrill. • Pulmonary HTN → Dyspnea, Fatigue. • May develop a right-to-left shunt → Cyanosis
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Myocardial Infarction (Weak dead part of the cardiac muscle) can cause → Congestive Heart Failure
→ Backflow of the blood to the lungs → Pulmonary Oedema → Desaturation, Dyspnea, Orthopnea, Crepitations → Perform → Perform → chest X-ray to Diagnose —- to identify the Underlying cause of the Pulmonary Oedema we do, Echo MONF (Morphine, Oxygen, Nitrates, Furosemide is RX
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On ECG, if there is no connection between P waves and QRS complexes
→ Complete heart Block (3rd degree heart block).
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A 57 YO hypertensive patient is on Enalapril (ACE inhibitor) for hypertension developed annoying dry cough. What is the most appropriate action?
→ (Give ARBs e.g., Losartan instead -important-). Other ARBs (Angiotensin II receptor blockers) that could be the valid answer → Losartan, Valsartan, Candesartan. √ One of the important and common side effects of ACE inhibitors is dry cough. If developed, shift to ARBs. √ Another side effect of ACEi to remember is → Hyperkalemia (↑ serum K+).
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Pansystolic murmur at the apex + Hx of Rheumatic fever
→ Mitral Regurgitation (MR). Notes: ◙ MR can occur 2ry to MI (Rupture of papillary muscles). ◙ MR can occur 2ry to Rheumatic fever. ◙ MR may lead to → Right-sided (Congestive) heart failure (Ascites, LL oedema). ◙ MR may lead to → Pulmonary oedema ◙ Rheumatic fever can lead to either Mitral Regurgitation or Mitral Stenosis. We can decide based on clinical features.
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Ms and MR
Mitral Stenosis Mid-Late Diastolic murmer with opening click Symptoms of heart failure 5th ics mcl at apex MR Pan-Systolic murmur At the Apex (left 5th ICS MCL), radiates to Axilla Symptoms of congestive Heart Failure; edema, Ascites
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Scenario A 60 Y/O patient with Hypertension, Previous MI and Asthma presents complaining of recurrent falls. He is on Salbutamol inhaler as needed, Aspirin, Corticosteroid inhaler (Beclomethasone), Indapamide, Enalapril and Amlodipine.
The likely underlying cause of the recurrent falls → Postural Hypotension. The patient is on multiple anti-hypertensive medications (CCB → Amlodipine ▐ Thiazide-like diuretics → indapamide ▐ ACEi → Enalapril). These Blood Pressure Lowering agents are known to cause orthostatic “Postural” hypotension. → Blood Pressure Monitoring + Review the patient’s medications.
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An elderly patient fell and collapsed “syncope”. He was transferred to the A&E and now he is fully conscious. ECG shows irregular rhythm. What is the next best investigation?
→ Echocardiogram. ◙ A Holter ECG (24-hour ECG) will not be beneficial as the ECG already shows Irregular Rhythm; hence, there is no point of using it again. ◙ Echo should be done to identify the underlying cause of this irregular rhythm so the treatment can be decided accordingly. ◙ The most common Valvular heart disease that causes is →AS (ejection systolic murmur at the 2nd right ICS + Angina ± Dyspnea). Syncopal attack ◙ Syncope during or shortly after exertion → Exercise ECG.
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An elderly patient fell and collapsed “syncope”. He was transferred to the A&E and now he is fully conscious. ECG shows irregular rhythm. What is the next best investigation? → Echocardiogram.
This patient likely has AF causing TIA (syncope + irregular rhythm), and to determine the cause of his Atrial fibrillation, do Echo. ◙ Causes of AF: √ Endocardium → Endocarditis, Mitral valve disease. √ Myocardium → Cardiomyopathy. √ Pericardium → Constrictive pericarditis . √ HF, HTN, MI. √ Hyperthyroidism, excessive alcohol intake, chronic lung disease.
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Aortic Stenosis
Ejection Systolic murmur Right 2nd ICS just lateral to sternum, radiates to Carotid artery Dyspnea on activity, Anginal chest pain, syncope
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A 6-week-old baby presents with the features of progressive cyanosis, poor feeding and SOB since the age of two weeks. Holosystolic murmur is heard.
→ Tricuspid Atresia
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Preterm, continuous murmu
r → PDA
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Cyanotic baby with ejection systolic murmur (due to pulmonary stenosis)
→ TOF (Tetralogy of Fallot).
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- Progressive (Severe) Cyanosis + Poor feeding + Holosystolic murmur along the left sternal border
→ Tricuspid Atresia.
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Acyanotic, Pan-systolic murmur →
Acyanotic, Pan-systolic murmur → VSD ( Others: Poor feeding and poorly gaining weight)
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Before prescribing amiodarone
Request → Serum Electrolytes and Urea Amiodarone Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential.
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Monitoring of patients taking amiodarone
• TFT (Thyroid), LFT (Liver), U&E (Serum electrolytes and Urea), CXR, ECG prior to treatment • TFT, LFT every 6 months • ECG every 12 months
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Adverse effects of amiodarone use
• Thyroid dysfunction: both hypothyroidism and hyperthyroidism • Corneal deposits • Pulmonary fibrosis (The most serious)/pneumonitis • Liver fibrosis/hepatitis • Peripheral neuropathy, myopathy • Photosensitivity • ‘Slate-grey’ appearance (Grey skin) • Thrombophlebitis and injection site reactions (So, usually given via central veins) • Bradycardia • Prolonged QT interval
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• A racing heart or palpitation is a common phenomenon in Alcoholics which is not serious or harmful.
→ Reassurance.
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Pulmonary Regurgitation
Early- Diastolic Left 2nd ICS just lateral to sternum Symptoms of Right-Sided Heart Failure
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PR can occur after correction of PS in TOF
After surgical correction of Tetralogy of Fallot early in life, the corrected pulmonary stenosis (one of the four criteria of TOF) can be complicated into Pulmonary regurgitation (diastolic murmur at the left upper sternal border) that can manifest many decades late
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A man who had cardiac surgery when he was a child presents with diastolic murmur.
(stenosis as a child – due to TOF) Suspect pulmonary regurgitation (on top of the corrected pulmonary stenosis)
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A patient who underwent surgery 2 days ago developed high fever, rigors, night sweats and systolic murmur
. New murmur + Fever → Investigation → Infective Endocarditis. Blood Culture then Echocardiogram.
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Young Adult + Recurrent Palpitations + Light-headedness + Tachycardia
→ Think of SVT (Paroxysmal Supraventricular Tachycardia) = Narrow Complex. → Valsalva manoeuvre and Carotid massage → IV Adenosine: 6 mg → 12 mg → 12 mg → Cardioversion N.B. Adenosine is contraindicated in asthmatics → Verapamil (CCB) is the preferred option in SVT in a patient with Asthma.
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◙ 1st Degree Heart Block and Mobitz type 1 usually
→ do not require treatment (as long as the patient is Asymptomatic).
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◙ Mobitz type 2 and Complete heart block (3rd degree heart block)
→ require permanent pacemaker
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Symptomatic bradycardia
. • Initially → Atropine (first choice for all symptomatic bradycardia). • Then → Transcutaneous pacing. (Used to buy time until transvenous pacing is done). • Then → Transvenous pacing. • Then → Permanent pacing (Pacemaker).
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Aortic Stenosis → Aortic Stenosis. The most appropriate investigation → Echocardiogram.
- The commonest valvular disease in the elderly (Over 65). - Usually Asymptomatic apart of exercise intolerance (often mild). - It can cause syncopal fainting. - Ejection systolic murmur at the right 2nd ICS, louder on sitting upright and during expiration, and radiates to carotid. A scenario of an elderly presents with mild exercise intolerance or is asymptomatic but visiting for the purpose of check-up is found to have ejection systolic murmur.
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Investigations following Syncope Patients who have unannounced loss of postural tone leading to a period of unconsciousness need to be investigated for 4 main causes
: 1) Irregular rhythm (Cardiac syncopal events): Usually abrupt, with rapid recovery and flushing → 12 Lead ECG. 2) Low blood pressure or postural drop → frequent falls, dizziness while trying to stand from a sitting position, Hx of taking multiple medications → Measure BP while lying and 3 minutes after standing (i.e. Blood Pressure Monitoring). 3) Seizures → need eyewitness to confirm, as there is usually post-ictal drowsiness or confusion. 4) Hypoglycemia → Hx of excessive alcohol intake, sweating, tachycardia, hypotension, confusion before falling → Check blood glucose
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Vasovagal syncope Usually in a YOUNG FEMALE ( with NO chest pain, palpitation and with Normal ECG) Unconscious + Hx of prolonged standing, straining, pooping, heavy weight lifting or after visual stimuli
B. A vasovagal attack is usually due to overwarm environment, or prolonged standing period, or after visual stimuli e.g. seeing blood. The patients usually feel dizzy and ‘’tunnel vision’’ before the attack.
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DDx of Sudden Falls.
• Drop attacks → Sudden falls without losing consciousness. • Stokes Adam → Unconscious + Abnormal ECG. • Hypoglycemia → Unconscious (or) ↓ level of consciousness + Sweating, do not recover unless given glucose. • Vasovagal attacks → Unconscious + Hx of prolonged standing, straining, pooping, heavy weight lifting or after visual stimuli e.g. seeing blood. The patients usually feel dizzy and ‘’tunnel vision’’ before the attack . Usually in a YOUNG FEMALE (with NO chest pain, palpitation and with Normal ECG) • Epilepsy → Unconscious ± Post-seizure confusion
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Digoxin Toxicity Features and mng
• GIT (Commonest): Nausea, Vomiting, Anorexia. • Neurological: Hallucination, Confusion. • Visual: Yellow green vision, (Yellow haloes), blurred vision. • Arrhythmias: Bradycardia, V tach, Premature contractions. Management: • Order Digoxin level • Digibind [DigiFab] = (digoxin immune FAB). • Correct Arrhythmia • Monitor Potassium
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Aspirin Toxicity → Ringing in the ears √ The earliest symptoms of acute aspirin poisoning may include (tinnitus) and impaired hearing. √ More clinically significant signs and symptoms may include rapid breathing (hyperventilation), vomiting, dehydration, fever, double vision, and feeling faint.
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Thiazide-like diuretics ◙ Thiazide-like diuretics work by inhibiting ______reabsorption at the beginning of the _____ part of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive. ______symporter. ◙ The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other _________such as indapamide and chlortalidone. ◙ Remember that: ___________– inhibit the ______cotransporter in the thick _____ limb of the loop of Henle.
◙ Thiazide-like diuretics work by inhibiting sodium reabsorption at the beginning of the proximal part of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+ -Cl− symporter. ◙ The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone. ◙ Remember that: Furosemide and Bumetanide (Loop diuretics) – inhibit the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle.
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Common adverse effects Thiazide like diuretics
• Postural Hypotension. √ • HypOkalemia and HypOnatremia. √ • Gout (Hyperuricemia). √ • dehydration • impaired glucose tolerance • impotence • Thiazide diuretics can cause hypercalcaemia and hypocalciuria
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A patient with hypertension on treatment presents complaining of recurrent falls especially when trying to get up.
→ Postural hypotension likely due to thiazide being used for hypertension.
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A patient who is hypotensive (90/70), but is still conscious and the pulse is felt, his ECG shows a pattern between Ventricular tachycardia and Ventricular fibrillation. What is the treatment
As the patient is hemodynamically unstable (Hypotensive) → Cardioversion. If there was No pulse (Hypotensive) → Defibrillation. Remember: Defibrillation = Asynchronized cardioversion In 2 conditions: √ Ventricular Fibrillation. √ Pulseless Ventricular Tachycardia.
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2 weeks post MI, a patient was readmitted due to Hypotension, Tachycardia and Pulmonary edema. What is the likely underlying cause?
→ Acute Mitral Regurgitation. Acute mitral regurgitation (MR): “important √” pansystolic murmur Occurs 2-15 days after the MI (Mostly inferior MI). ◙ Due to → Ischemia or rupture of the papillary muscles of the mitral valve. ◙ An early-to-mid systolic or Pansystolic murmur at cardiac apex is typically heard. ◙ May present with Hypotension, Tachycardia and Pulmonary edema (SOB and bibasilar crackles). ◙ Dx → Echocardiogram. ◙ Treatment → vasodilator therapy but often requires emergency surgical repair
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Stable Angina.
√ In the case of stable Angina, the pain is precipitated by predictable factors such as exercise and emotional stress. This is because while exercising, the Oxygen demand is more than the Oxygen supply. √ Stable Angina is relieved by Rest and GTN “Glyceryl Trinitrates”.
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Unstable Angina
Occurs mostly at rest, unpredictable, random. It is an emergency.
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◙ A baby with Progressive (Severe) Cyanosis + Poor feeding + Holosystolic murmur along the left sternal border
Tricuspid atresia
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◙ A baby who does not have cyanosis, presents with Poor feeding and poor weight gaining + Holosystolic murmur along the left sternal border →
VSD Tricuspid Atresia → Cyanotic. VSD → Acyanoti
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A patient known to have hypertension presents with Chest discomfort and Nausea. His ECG is as follows:
The ECG shows → (Likely 2ry to Tall Tented T-Waves → Hyperkalemia ACE inhibitors being used to control his Hypertension)
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Diuretics and K imbalance
Remember that: ◙ Spironolactone and ACE inhibitors and ARBs → hyperkalemia ◙ Loop diuretics, Thiazide diuretics → Hypokalemia
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Different waves and diagnosis
J wave (Osborn wave) in → Hypothermia U wave in → “HypUkalemia”, an additional wave after T wave. Hypokalemia Tall Tented T-wave [Peaked T-wave] in → Hyperkalemia Delta wave in → WPW syndrome (Wolff Parkinson White Syndrome) Widespread Saddle Shaped ST Elevation with upward concavity + PR Depression in → Pericarditis
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ACS medically treated mi Mng
Acute coronary Syndrome Aspirin (lifelong) & Ticagrelor or clopidogrel (12 months)
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Per cutaneous coronary intervention (PCI)
Aspirin (lifelong) & prasugrel or ticagrelor (12 months)
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TIA
Aspirin 300 mg 2 weeks then Clopidogrel 75 mg (lifelong)
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Ischaemic stroke
Aspirin 300 mg 2 weeks then Clopidogrel 75 mg (lifelong)
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Ischemic stroke + AF
Aspirin 300 mg for 2 weeks then start Anticoagulation ( e.g. Warfarin or DOAC- apixaban, rivaroxaban)
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Peripheral arterial disease
Clopidogrel (lifelong)
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Who should receive a statin
? • All people with established cardiovascular disease ( stroke, TIA, ischaemic heart disease, peripheral arterial disease).2ndary prevention 80mg Primary prevention 20mg • following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk ≥ 10% should receive statin. • patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins. • patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy Statins should be taken at night as this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins.
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Atrial fibrillation in an unstable patient
→ Cardioversion If not in the options → IV amiodarone (or IV flecainide) not oral! If stable → BB, (or CCB if he is asthmatic), ( or digoxin if associated heart failure)
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Scenario, A 70 YO female presents to the ED after a fall at home. She is confused, pale, with irregularly irregular pulse and cold peripheries. Her BP is 80/50 and HR is 150 bpm. ECG is done and shows narrow QRSs and absent P waves.
The next step in management is → Immediate DC Cardioversion ◘ The patient has AF (Irregularly irregular rhythm, Tachycardia, Absent P waves). ◘ Since she is unstable (Confusion, severe Hypotension) → cardioversion.
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A man was hit by a car and sent to the ED. He is hypotensive with distended neck veins and faint heart sounds. His blood pressure is 82/47 and HR is 120
. The most appropriate management → [Pericardiocentesis]. Cardiac Tamponade Accumulation of pericardial fluid under pressure • Beck’s Triad: Hypotension ▐ Muffled Heart Sounds ▐ High JVP (Distended neck veins). • Dx: Echocardiogram is diagnostic • Rx: Urgent pericardiocentesis
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Ventricular Fibrillation
Old, Sudden collapse, confusion, severe hypotension, Not breathing, Unconscious ‘’defibrillation’’ → Deliver immediate Shock
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AF
Atrial fibrillation in an unstable patient → Immediate shock If stable → BB, (or CCB if he is asthmatic), ( or digoxin if associated heart failure)
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A 70 YO female presents to the ED after a fall at home. She is confused, pale, with irregularly irregular pulse and cold peripheries. Her BP is 80/50 and HR is 150 bpm. ECG is done and shows narrow QRSs and absent P waves
The next step in management is → Immediate DC Cardioversion ◘ The patient has AF (Irregularly irregular rhythm, Tachycardia, Absent P waves). ◘ Since she is unstable (Confusion, severe Hypotension) → cardioversion. If cardioversion is not given, pick → IV amiodarone.
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MI (Acute chest pain radiating to jaw, shoulder…) BUT No elevation on ECG. What to Do Next
? without ST elevatuon → Order Cardiac Enzymes, especially (Troponin) √ If Troponin is high → NON-STEMI Elevation MI √ Immediate management → give LMWH or fondaparinux + Aspirin 300 mg.
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A patient’s ECG shows SVT [Supraventricular Tachycardia].
→ Adenosine. (Remember that Valsalva maneuverer and Carotid massage are tried initially and IV Adenosine is then given). IMPORTANT NOTE: If the patient is hemodynamically unstable (eg, hypotension, chest pain, shock, and or altered mental status) Proceed immediately to → electrical synchronised cardioversion.
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Loop diuretic Furosemide Bumatenide
Gout Hyponatremia Hypokalemia
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K sparing diuretic Eplerenone Spirinolactone
Hyponatremia Hyperkalemia Gynaecomastia
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Thiazide like diuretic Bendroflumethiszide Indapamide
Hyperglycaemia Hyponatremia Hypokalemia Gout Postural hypotension
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What is the most appropriate investigation? A man presents with Fever, confusion, petechiae. This is a picture of his sole!! Jane ways lesions
These lesions are likely endocarditis). Janeway lesions (minor criteria of infective ♦ Likely → Infective endocarditis → Do Blood culture then Echocardiogram.
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give Calcium Chloride (or Calcium Gluconate) (or Calcium carbonate)
This is likely a case of Hyperkalemia (Tall Tented T waves are seen on the ECG To prevent cardiac arrhythmia
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Calcium carbonate in severe hyperkalemia with _____
Note, If severe hyperkalemia (> 6.5), and there is no hyperkalemic ECG changes, we still give Calcium carbonate as a next step to protect the heart.
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◙ An elderly female with a history of Atrial Fibrillation presents to the A&E with speech disturbance and asymmetric weakness of face and arm. These symptoms started 3 hours ago. CT scan of the head shows no hemorrhage. The “long-term” management of this patient would involve:
→ Rivaroxaban (or any other DOAC e.g. Apixaban, Rivaroxaban, Edoxaban, Dabigatran) “Now preferred over Warfarin” This patient with TIA/ ischemic stroke will need to take Aspirin 300 mg for 2 weeks, then rivaroxaban (DOAC) and atorvastatin 80 mg for long-term management. If he did not have AF, clopidogrel will be given instead of DOAC.
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◙ In patients with Hx of ischemic stroke, the long-term medications:
√ with Atrial Fibrillation → DOAC (eg, apixaban) + Statins (eg, Atorvastatin). √ Without Atrial Fibrillation → Clopidogrel + Statins (eg, Atorvastatin). Important: What if a patient with a history of stroke is already on warfarin and presents with a new onset atrial fibrillation? Since he is already on an anticoagulant, he should continue on warfarin and should not be switched to DOAC (eg, Edoxaban) unless his INR is increased.
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2ry Prevention (Long-term management) of Ischemic Stroke/ TIA:
√ Control Blood Pressure. [To prevent further stroke in the future]. Remember, if he has DM, pick or add ACEi eg, ramipril. √ Statins (for All patients regardless of their cholesterol baseline level). √ Ani-platelets (or) Anti-coagulation: ( Based on presence or absence of AF): → Anticoagulants: Warfarin [or] DOAC (Dabigatran/ Apixaban/ Rivaroxaban/ Edoxaban). DOAC is now preferred. (Warfarin is almost obsolete nowadays. DOAC is recommended instead) → Antiplatelets: Clopidogrel 75 mg OD. Absense of AF • If there is Atrial Fibrillation • If No Atrial Fibrillation Important: What if a patient with a history of stroke is already on warfarin and presents with a new onset atrial fibrillation? Since he is already on an anticoagulant, he should continue on warfarin and should not be switched to DOAC (eg, Edoxaban) unless his INR is increased.
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A patient has recovered form TIA. What score is helpful to determine the risk of a stroke in the following week? Just in case qn
→ ABCD2 Score. ◙ The ABCD2 score (Prognostic) is used to identify the risk of future stroke in patients who have had a suspected TIA in the following 7 days. √ IMPORTANT: ABCD2 score is Not advised to be used now according to the recent 2019 CKS guidelines. Therefore, it will not be a valid answer anymore. Thus, this question is to not be considered. We have added it just in case!
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A Diabetic patient with heart failure on beta-blockers, ACE inhibitors, insulin and furosemide was found to have hypokalemia. What is the likely cause?
→ Furosemide. (Loop diuretics such as furosemide can cause hypokalemia).
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A patient with hypertension on treatment presents complaining of ankle swelling/ edema. The likely cause of this ankle oedema is:
(a calcium channel Blocker). → Amlodipine √ This patient is likely taking CCB for his HTN. √ CCB can cause ankle swelling as it causes vasodilatation.
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Before prescribing amiodarone, what investigation should be ordered?
→ Serum Electrolytes and Urea.
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(Do not mix thing up): The 2 most important tests to be done before initiating lithium are:
(TFTs) Thyroid Function Tests, and: (KFTs) Kidney Function Tests.
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The following ECG is done for a 58 YO man who presents with palpitation. He is otherwise healthy. What is the most appropriate line in Rx?
→ Beta-blockers (eg, metoprolol, atenolol) ◙ Agents used to control rate (Rate Control) in patients with Atrial Fibrillation (AF): o Beta-blockers (eg, atenolol 50-100 mg PO OD, bisoprolol, metoprolol) → First line but Contraindicated in Asthma. o Calcium channel blockers [non-dihydropyridine = rate-limiting CCB] (eg, diltiazem, verapamil) → if Asthmatic patient.
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AF in heart failure
o Digoxin → (not considered first-line anymore as they are less effective at controlling the heart rate during exercise. However, they are the preferred choice if the patient has coexistent heart failure). √ If haemodynamically unstable Cardioversion √ If the patient with AF is unstable (eg, SBP ≤ 90) → (Shock). (eg, hypotension) and the AF has just started and no cardioversion in the options, Pick → IV amiodarone. Imp √
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A patient presented with chest pain and breathlessness. Pulse rate is 35 b/m. ECG shows broad complexes with atrioventricular dissociation. Most appropriate initial treatment?
◙ The first drug of choice for Symptomatic Bradycardia (Dizziness, feeling unwell) → Atropine (Given 0.5 mg IV push and may be repeated up to a total dose of 3 mg).
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A 76-year-old man was found outside by his carers this morning. He doesn’t remember what happened but denies history of pain. Temperature 35.1, BP: 102/70mmHg, PR: 108bpm, mucous membrane is dry. No stiffness of any limb, his heart sound is normal. His chest is grossly normal apart from some scattered coarse crackle in his Left Lower lung zone. He was catheterized and urinalysis showed Blood+++, Protein ++ and Ketone +, ECG showed peaked T wave and broad complex Tachycardia. Which of the following is the appropriate initial intravenous medication he should have?
A. Amiodarone B. C. Co- Amoxiclav D. Insulin- Glucose infusion E. Sodium Bicarbonate Peaked T wave suggesting Hyperkalemia (2ry to kidney injury in this case). → IV calcium gluconate (or calcium chloride) to protect the heart should be given initially.
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A question about a patient with unstable HR > 150, BP 80/60 and Having broad complex tachycardia. Most appropriate management was asked?
→ DC Cardioversion. Patient is unstable, SBP < 90 → (Cardioversion) Shock. ◘ Broad complex tachycardia + low BP (unstable) → Cardioversion ◘ Pulseless V. Tach or V. Fibrillation → Immediate Defibrillation.
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71-year-old man with 3 weeks history of fever, 1 month post inferior myocardial infarct, chest pain with soft systolic murmur, inverted Q waves in leads I, II & aVF. Temp- 37.5, BP- ?118/68 A. Pericarditis B. Costochondritis C. Pulmonary Embolism D. Infective endocarditis E. Papillary muscle rupture
New Murmur + Fever → IE. think of ± Malaise, Rigors, Fever The initial step → Infective Endocarditis (IE) Blood Culture. Then → Echo
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Patient with Hx of MI presented after a few days with chest pain which aggravates on inspiration and is relieved on bending forward. Most likely Diagnosis?
◙ Pericarditis Dressler’s syndrome (A Complication of MI that can develop shortly after the MI within 2 days) and (presents 2-6 weeks after MI) both have t’e same features → Pleuritic chest pain that worsens on lying flat and during inspiration, Pericardial rub, Widespread Saddle shaped ST elevation on the ECG. ◙ They can also lead to Pericardial effusion (Enlarged globular heart on chest X-ray) and if severe enough, Cardiac Tamponade can also develop (also enlarged globular heart on the X-ray). ◙ Management of Pericarditis (imp): √ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800 mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days. √ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence).
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A 60 YO man with Hx of smoking, HTN and DM presents to his GP complaining of 25 minutes left side dull aching chest pain radiating to his jaw. He was given Aspirin 300 mg by his GP and then sent to medical services in a local hospital. He is no longer in pain. The ECG is normal. The troIonin is elevated 202 ng/L (Normal: < 5 ng/L). What is the next step in management?
E) Alteplase. F) G) IV Glyceryl trinitrate (GTN). H) IV Morphine. Sc fondaparinux Since the ECG is normal, alteplase is wrong. Since ECG is normal and Troponin is high → Non-STEMI → Anti-coagulation (LMWH e.g. Dalteparin, Enoxaparin or Fondaparinux). + Oral Aspirin 300 mg.
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√ Ankle swelling and orthopnea → features of Heart Failure. √ Excessive alcoholism can lead to → Alcoholic Cardiomyopathy (Cardiac Enlargement on Chest X-ray) → which can cause Atrial Fibrillation.
The most common type of arrhythmia that develops in patients with alcoholic cardiomyopathy is → Atrial Fibrillation.
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AF
√ Acute alcohol intake can lead to → AF or flutter ((Holiday heart Syndrome)). √ AF presentation: Palpitation, Dyspnea, Dizziness or Syncope, Chest discomfort or pain, Stroke or TIC, Irregularly irregular pulse.
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A 59 YO hypertensive patient presents to the A&E complaining of dull central chest pain for around 4 hours. His vitals are as follows: HR: 99, BP: 155/95, RR: 21, O2 sat on room air: 97% Chest X-ray is normal. Troponin level was sent and still pending. He was given IV morphine for his chest pain. The ECG is as follows: What is the most appropriate next step in management? Chest pain + T wave inversion suggests → myocardial ischemia. In this case, 2 drugs should be given immediately
√ Oral √ SC Pick the one that is given in the choices. Aspirin 300 mg LMWH or Fondaparinux. “low-risk patients can be treated conservatively. However, if subsequent ischemia develops → coronary angiography with PCI”.
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What if the ECG shows features of left main coronary artery occlusion ( Wide spread ST depression + ST elevation in aVR)
? → Emergency coronary angiography.
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61 YO patient presents to the A&E complaining of dull central chest pain for around 4 hours. His vitals are as follows: HR: 75, BP: 135/85, RR: 21, O2 sat. on room air: 97% He was given IV morphine for his chest pain. The ECG is as follows:
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Overview: A 58-year-old man with a history of well-controlled hypertension on Ramipril (an ACE inhibitor) presents for a routine follow-up. Recent blood tests show a potassium level of 6.0 mmol/L (normal: 3.5-5.0 mmol/L), indicating moderate hyperkalemia. The patient is currently asymptomatic, with normal renal function and no significant past medical history. Next Step in Management:
arrange an ECG The most appropriate next step is to to check for any electrocardiographic changes that may indicate life-threatening arrhythmias due to hyperkalemia. Explanation: Even though the potassium level of 6.0 mmol/L represents moderate hyperkalemia, the patient is asymptomatic. An ECG is necessary to assess for changes such as: • Peaked T waves. • Widened QRS complex. • Prolonged PR interval. These changes can indicate a risk for life-threatening arrhythmias. If ECG abnormalities are present, urgent treatment with calcium gluconate may be required to stabilize the cardiac membrane.
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2. If ECG Shows Abnormalities (e.g., Peaked T Waves, Widened QRS, Prolonged PR Interval): • Administer intravenous calcium gluconate: This stabilizes the cardiac membranes and reduces the risk of arrhythmias.
Summary: First, arrange an ECG, then in both scenarios (normal or abnormal ECG): • Discontinue ACE inhibitors like Ramipril. • Avoid ARBs, as they also contribute to hyperkalemia. (So, both ACE inhibitors and ARBs can cause hyperkalemia). • Switch to safer alternatives such as calcium channel blockers or thiazide- like diuretics. • Continue monitoring renal function and potassium levels to ensure effective management of hyperkalemia and maintain blood pressure control.
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Hypertension Case Study Scenarios: Scenario 1: Patient: A 65-year-old man presents with a clinic blood pressure of 155/95 mmHg. He has a history of type 2 diabetes and is of Afro-Caribbean origin.
Answer: Start with an ACE inhibitor (e.g., Ramipril, Lisinopril) or an ARB (e.g., Losartan, Candesartan). Reasoning: For diabetic patients, ACE inhibitors or ARBs are the first-line treatment regardless of age or ethnicity due to their kidney-protective effects. The presence of diabetes takes precedence over ethnicity in this case.
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Scenario 2: Patient: A 45-year-old woman presents with a clinic blood pressure of 150/95 mmHg. She has no history of organ damage, cardiovascular disease, renal disease, or diabetes. She is otherwise healthy and does not smoke
. Answer: Recommend lifestyle modifications such as reducing salt intake, increasing exercise, and quitting smoking. Reasoning: In a healthy patient without risk factors or comorbidities, antihypertensive medication is not required for Stage 1 hypertension (clinic BP ≥ 140/90 mmHg but <160/100 mmHg). Lifestyle changes are the first recommendation unless there are additional risk factors like organ damage, diabetes, or cardiovascular disease.
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Scenario 3: Patient: A 50-year-old woman has been on Ramipril (ACE inhibitor) for 6 months for her Stage 2 hypertension (clinic BP ≥ 160/100 mmHg), but her blood pressure remains elevated at 160/95 mmHg. Her doctor added Amlodipine calcium channel blocker), but her blood pressure is still above 140/90 mmHg after another 3 months.
Answer: Add a thiazide-like diuretic (e.g., Indapamide, Chlorthalidone). Reasoning: After trying an ACE inhibitor and a calcium channel blocker (Step 1 and Step 2), adding a third drug, such as a thiazide-like diuretic, is the next step to achieve better blood pressure control.
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Scenario 4: Patient: A 40-year-old man presents with a clinic blood pressure of 170/100 mmHg. He has no significant medical history, no diabetes, and no organ damage.
Answer: Start with an ACE inhibitor (e.g., Lisinopril, Enalapril). Reasoning: For patients under 55 years with Stage 2 hypertension (BP ≥ 160/100 mmHg), the first-line treatment is typically an ACE inhibitor unless there are contraindications. His age and absence of other risk factors point toward this approach. Note: If the patient were ≥55 years or Afro-Caribbean of any age, the first-line treatment would be a calcium channel blocker (CCB).
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Scenario 5: Patient: An 82-year-old woman presents with a clinic blood pressure of 145/90 mmHg. She has mild frailty but no history of cardiovascular disease, diabetes, or renal impairment.
Answer: Individualized treatment based on overall health, considering her frailty. Reasoning: For patients over 80 years old, treatment decisions should be personalized. In this case, the patient's frailty means that the risks and benefits of medication need careful consideration, and lifestyle modifications might be a reasonable alternative if her health allows.
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Scenario 6: Patient: A 58-year-old man presents with a clinic blood pressure of 160/100 mmHg. He has no significant medical history and is of Afro-Caribbean descent
t. Answer: Start with a calcium channel blocker (e.g., Amlodipine, Diltiazem). Reasoning: For patients ≥55 years or Afro-Caribbean of any age, the first-line treatment for Stage 2 hypertension is a calcium channel blocker. This is because CCBs have been shown to be more effective in these populations compared to ACE inhibitors or ARBs.
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Scenario 7: Patient: A 52-year-old woman started on Ramipril (ACE inhibitor) for her Stage 2 hypertension. After 3 months, her blood pressure remained elevated, so her doctor added Amlodipine (calcium channel blocker). However, she developed significant ankle swelling after starting the CCB.
Answer: Stop the calcium channel blocker due to the side effects and replace it with a thiazide-like diuretic (e.g., Indapamide, Chlorthalidone). Reasoning: Ankle swelling (peripheral edema) is a common side effect of calcium channel blockers. In this case, the CCB should be discontinued and replaced with a thiazide-like diuretic. The four most common side effects of calcium channel blockers are: 1. Peripheral edema (ankle swelling). 2. Gingival hyperplasia (gum overgrowth). 3. Headache. 4. Flushing.
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Extra Question – Resistant Hypertension: What is the next step in managing resistant hypertension according to NICE UK guidelines if blood pressure remains uncontrolled after trying an ACE inhibitor/ARB, a calcium channel blocker, and a thiazide-like diuretic (ie, after trying all steps 1, 2, and 3 but hypertension remains uncontrolled)?
Answer: According to NICE UK guidelines (NG136), if blood pressure remains uncontrolled after steps 1, 2, and 3, the next step in managing resistant hypertension (Step 4) involves the following: 1. Add Low-Dose Spironolactone: o If the patient’s potassium levels are ≤ 4.5 mmol/L, add spironolactone at a dose of 25 mg once daily. 2. Alternative Option: o If the patient’s potassium levels are > 4.5 mmol/L or if spironolactone is not tolerated, consider using an alpha-blocker (e.g., Doxazosin) or a beta- blocker (e.g., Atenolol). 3. Referral to Specialist: o If the blood pressure remains uncontrolled despite these interventions, refer the patient to a hypertension specialist for further evaluation and management. 4. Monitoring: o Regular monitoring of potassium levels and renal function is necessary, especially when using spironolactone. This approach is based on the NICE NG136 guidelines for managing resistant hypertension in adults.
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Anti hypertensives
Common Antihypertensive Examples: • ACE Inhibitors: Ramipril, Lisinopril. • Angiotensin II Receptor Blockers (ARBs): Losartan, Candesartan. • Calcium Channel Blockers (CCBs): Amlodipine, Diltiazem. • Thiazide-like Diuretics: Indapamide, Chlorthalidone.
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Hypertension with diabetes and lifestyle advice
Key Notes: • Patients with diabetes: Start with ACE inhibitors or ARBs, regardless of age or ethnicity, to protect kidney function. • Lifestyle Modifications: Encourage lifestyle changes in all patients, including: o Salt reduction. o Regular exercise. o Stress management. o Limiting alcohol intake. o Smoking cessation.
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Stepwise Drug Treatment for Essential Hypertension in Non-Diabetic Patient
s: Step Patient Characteristics Treatment Options Step 1 Age <55 Start with ACE inhibitor. Age ≥55 or Afro-Caribbean origin Start with Calcium Channel Blocker (CCB). Step 2 BP uncontrolled in Step 1 Add a second drug: ACE inhibitor, CCB, or Thiazide-like diuretic . Step 3 BP uncontrolled in Step 2 Combine all three: ACE inhibitor + CCB + Thiazide-like diuretic.
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Stage 1 Hypertension Age < 80 years with risk factors Treatment?
Treat with antihypertensives if one or more of the following: - Target organ damage. - Cardiovascular disease. - Renal disease. - Diabetes. - 10-year cardiovascular risk ≥ 10%.
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Age > 80 years Stage 1 Hypertension
Individualized treatment based on overall health, frailty, and potential risks.
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No comorbidities ("completely healthy") Stage 1 Hypertension
Advice on lifestyle modifications (e.g., diet, exercise, no smoking); no antihypertensive treatment unless high risk
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Stage 2 Hypertension
Patients < 55 years Start with an ACE inhibitor Patients ≥ 55 years or Afro-Caribbean origin Start with a calcium channel blocker.
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Escalation Stage 2 Hypertension
If BP remains >140/90 mmHg after initial treatment, move to step 2 treatment as in the following table. Ace inh Ccb Thiazide like diuretic Stepwise
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Classification of Hypertension:
1. Stage 1 Hypertension: o Clinic BP: ≥ 140/90 mmHg. o Confirmed by Ambulatory BP Monitoring (ABPM) or Home BP Monitoring (HBPM): Daytime average BP ≥ 135/85 mmHg. 2. Stage 2 Hypertension: o Clinic BP: ≥ 160/100 mmHg. o Confirmed by ABPM or HBPM: Daytime average BP ≥ 150/95 mmHg. 3. Stage 3 (Severe) Hypertension: o Clinic systolic BP: ≥ 180 mmHg OR o Clinic diastolic BP: ≥ 120 mmHg.
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Long QT Syndrome and Ventricular Tachyarrhythmia
Overview: A 19-year-old male presents with recurrent episodes of syncope, particularly during exercise. His ECG reveals a prolonged QT interval, suggesting long QT syndrome (LQTS), which is associated with a high risk of ventricular tachyarrhythmias, such as torsades de pointes. This condition often presents in childhood and is triggered by physical activity, which can precipitate dangerous arrhythmias, leading to syncope or even sudden cardiac death.
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Long Qtsyndrome features
Key Features: • Prolonged QT Interval: Identified on ECG, which increases the risk of life- threatening arrhythmias. • Syncope with Exercise: Episodes are commonly triggered by physical exertion in patients with LQTS. • Ventricular Tachyarrhythmias: The most likely arrhythmia in this case, associated with the prolonged QT interval and syncope.
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DD s. OF PROLONG QT SYNDROME OR TACHYARRHYTHMIAS
Differential Diagnosis: • Sick Sinus Syndrome: Causes bradyarrhythmias and syncope due to slow heart rates, but not associated with prolonged QT intervals. • Ventricular Ectopics: Extra heartbeats that are common in young individuals and often benign. SThese are not linked to syncope or prolonged QT interval unless very frequent. In summary, this patient's presentation is highly suggestive of long QT syndrome, and the likely arrhythmia responsible for his symptoms is ventricular tachyarrhythmias such as torsades de pointes Early identification and management are crucial to prevent severe complications, including sudden cardiac death.
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and most dangerous complication of congenital long QT syndrome (LQTS).
Important Note: Torsades de pointes is a type of ventricular tachyarrhythmia that is associated with a prolonged QT interval . It is the hallmark
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Ventricular Septal Rupture (VSR) Post-Myocardial Infarction Ventricular septal rupture (VSR) is a rare but serious mechanical complication that occurs following a myocardial infarction (MI). It typically develops 3–5 days after the MI due to necrosis of the interventricular septum, which leads to a communication between the left and right ventricles.
Key Features: √ New Murmur: A characteristic pan-systolic murmur, best heard at the left lower sternal border (LLSB). √ Hemodynamic Instability: VSR often leads to cardiogenic shock, evidenced by hypotension (e.g., blood pressure 90/60 mmHg), diaphoresis, and jugular venous distension. √ Respiratory Symptoms: Pulmonary crackles on auscultation, indicating pulmonary edema due to the acute hemodynamic changes.
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Dds of VSR( ventricular septal rupture) Investigation VSR post-MI is a critical diagnosis characterized by a pan-systolic murmur at the left sternal border and hemodynamic instability.
Diagnosis: → Echocardiography: This is the definitive diagnostic tool. It confirms the presence and severity of the septal rupture and helps in planning further management. Clinical Context: • VSR should be suspected in any patient who develops a new pan-systolic murmur a few days after an MI, especially if accompanied by signs of hemodynamic instability. • The murmur is typically loudest at the left sternal border. • Immediate intervention is crucial as the condition rapidly progresses, often requiring surgical repair. Differential Diagnoses: Acute Pericarditis: Usually presents with pleuritic chest pain and a pericardial rub, not a murmur. Dressler Syndrome: A form of post-MI pericarditis that occurs weeks after the event, presenting with fever and pleuritic chest pain. Left Ventricular Aneurysm: Occurs weeks to months post-MI, presenting with heart failure symptoms rather than a new murmur. Mitral Regurgitation: While it may present with a pan-systolic murmur, the murmur typically radiates to the axilla. In summary, VSR post-MI is a critical diagnosis characterized by a pan-systolic murmur at the left sternal border and hemodynamic instability. Early diagnosis and intervention are essential to prevent fatal outcomes
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Quick Notes to Remember: ◙ If QRISK3 is ≥ 10% → ◙ High doses of can lead to Citalopram, (a SSRI), can cause prolonged QT intervals, which can lead to
Start atorvastatin “regardless of lipid profile level”. Torsade De Pointes.
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few days after MI: • Pansystolic murmur best heard at the left lower sternal border. • Shock (hypotension and tachycardia). • Heart failure/ pulmonary edema (eg, bibasilar crackles).
Think → Ventricular septal defect/ rupture. Why NOT tricuspid regurgitation (TR)? √ Tricuspid regurgitation can occur as a complication of MI, but it develops over weeks to months, not acutely and within a few days after MI. √ Also, hypotension and shock are another sign of ventricular septal defect, not TR.
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Important Note on Primary Prevention of Cardiovascular Events For all people ≤ 84 YO who have QRISK3 Score of ≥ 10
Offer → ( Statin ) for 1ry prevention of CVD).
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Systolic murmur at the left lower sternal border worsened by Valsalva manoeuvre + ECG evidence of left ventricular hypertrophy (LVH)
Think → Hypertrophic cardiomyopathy (HOCM).
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Important Notes on Hyperkalemia calcium Gluconate 10% or calcium A patient presents with both (Hyperkalemia; eg, potassium 6.9 mmol/L) associated with broad QT complexes on ECG AND Bradycardia (HR is < 60 bpm). What to treat first?
→ Treat hyperkalemia first (by giving IV calcium gluconate or calcium carbonate or calcium chloride As initial intervention, treating hyperkalemia with IV calcium -which would stabilize the cardiac membrane and prevent cardiac arrest- is more critical than treating bradycardia with atropine. Notes: normal). • If K+ is ≥ 6.5 mmol/L (ie, severe) → treat with IV calcium (even if ECG is normal) • If K+ is 6 – 6.4 (ie, moderate) → treat with IV calcium (if there is ECG changes)
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Remember (Regarding Hypokalemia): √ Severe vomiting can cause hypokalemia. √ Hypokalemia features include muscle weakness and cramping. √ ECG features of hypokalemia involve: U wave (an additional wave after the “T” wave). Others: Inverted T wave, Depressed ST segment.
Management of hypokalemia 1) Oral or IV (potassium Chloride) based on severity), e.g. 2) Stop/ Treat the cause (e.g. stop furosemide, thiazide like diuretics
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Remember: √ Ischemic stroke Long-term antiplatelet/anticoagulant drugs in:
Ischemic stroke Long-term antiplatelet/anticoagulant drugs in: (or √ Ischemic stroke + AF TIA) → Aspirin for 2 weeks, then clopidogrel for life. → Aspirin for 2 weeks, then warfarin/DOAC for life. If he was already on warfarin (anticoagulant) and develops atrial fibrillation (AF), continue on warfarin and do not shift to DOAC unless his INR is poor. √ MI → Aspirin for life, clopidogrel (or ticagrelor) for 12 months.
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AF + Stable patient
AF + Stable patient → BB (eg, metoprolol) or CCB (if asthmatic) or Digoxin (if with HF
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) AF + Unstable patient (e.g. SBP ≤ 90, HR > 150, Loss of conscious)
→ Cardioversion
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AF + Unstable patient but presents > 48 hours after beginning of symptom
→ Do not cardiovert; but give rate control (e.g. BB) + LMWH → Then: assess for long-term intake of Warfarin or DOAC (e.g. apixaban, rivaroxaban, dabigatran) upon discharge using CHA2Ds2-VASc score.
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A 60 YO asthmatic man presents to A&E complaining of chest discomfort and difficulty in breathing over the past few hours. On chest auscultation, there are widespread fine inspiratory crepitations. His vitals are as follows: HR 100, RR 28, BP 120/80, O2 saturation 90%. Chest X-ray was performed (see the picture below). ECG: normal. Echo showed left ventricular impairment. The patient was given high flow O2, sublingual glyceryl trinitrates, and IV furosemide (Lasix). His breathing improved significantly. What is the most appropriate medication to be added?
This patient has acute pulmonary edema 2ry to left ventricular failure. Pulmonary edema: Kerley B lines, bat’s wing hilar shadow, crepitations, SOB, low O2 sat. Echo in the stem shows left ventricular impairment (HF). HF can lead to → Pulmonary edema Remember, Management of HF: • Furosemide (for symptomatic relief) “was already given here”. • Start with either Beta-blocker or ACE inhibitor (one medication at a time). • If still? Add the other medication. • If still? Add spironolactone Since this patient is Asthmatic, we would begin with ACE inhibitors (e.g. lisinopril) instead of BB. BB is better to be avoided in asthma as it can cause bronchospasm and thus aggravates asthma. So, the answer is that this patient should be discharged on → ACE inhibitor (e.g. Lisinopril).
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A 50 YO man with Hx of MI six months ago presents with a 3-day history of fever, SOB and chest pain. He looks moderately ill. His temp, is 38.2 and his BP is 140/77. On auscultation, a holosystolic murmur over the apex is heard. His ECG shows Q waves in leads I and aVL. What is the most likely Dx
? √ Do not rush and pick papillary muscle rupture thinking it is mitral regurgitation (evidenced by the holosystolic murmur over the apex)! If MR, why there is fever? √ Note that papillary muscle rupture usually occurs 2-15 days after MI, not 6 months! √ Also, papillary muscle rupture is more common with inferior MI (II, III, aVR). √ Q waves here → permanent markers of necrosis (indicate previous MI), here, likely lateral MI (I, aVL, V5, V6). FEVER + NEW MURMUR → INFECTIVE ENDOCARDITIS!
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An old patient with triple vessel disease presents with sudden onset chest pain of 4 hours, shortness of breath, dizziness and sweating. His ECG shows ST depression “ischemia” in several leads. His blood pressure is 140/80. The patient is anaemic with haemoglobin level of 62 g/L. What is the most appropriate management?
→ Dual antiplatelets (Aspirin + Clopidogrel) + Fondaparinux + Blood transfusion. Notes: √ Triple vessel disease means that 3 big vessels (the left anterior descending, right coronary and circumflex arteries) have blockages from atherosclerotic plaques. √ This patient has ACS “acute coronary syndrome” secondary to anemia and the pre-existing triple vessel disease. √ Aspirin (oral) and fondaparinux (SC LMWH) are given whenever there is heart ischemia. √ Blood Transfusion is indicated if: ♠ Hb < 80 g/L + Symptoms of Anemia. Or: ♠ HB < 70 g/L + With or Without Symptoms of Anemia.
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Elderly + Episodes of Fainting + SOB + Systolic murmur at the right second intercostal space
→ Aortic stenosis. Do → Echocardiogram.
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A patient with a classic presentation of MI ( sudden onset central chest pain radiating to neck and left shoulder, sweating, vomiting) but the ECG is normal.
→ request troponin. If troponin is elevated → Myocardial infarction (Non-ST Elevation MI).
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◙ The most appropriate “initial” test for syncopal attacks that are not due to hypoglycemia ( no Hx of sweating, tachycardia, hunger, shakiness before the syncope), and not due to epilepsy (No Hx of tongue biting, incontinence during the syncope
→ ECG Measuring lying and standing blood pressure should also be done to R/O postural hypertension (Note that ambulatory blood pressure monitoring is used to diagnose hypertension, not postural hypertension. Thus, not useful in syncopal attacks).
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◙ The best initial investigation for chest pain is
→ ECG.
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◙ If QRISK3 is 10%, this means that the patient has 10% chance of developing cardiovascular disease over the next 10 years.
◙ The QRISK3 score is used to determine the risk of a cardiovascular event in the next 10 years. ◙ If QRISK3 is > 10% and the age is < or = 84 → the patient needs to start on statins (atorvastatin) to reduce the risk of cardiovascular disease. ◙ If QRISK3 is 10%, this means that the patient has 10% chance of developing cardiovascular disease over the next 10 years.
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◙ Angina, Syncope, Dyspnea, Systolic murmur over the “right” sternal border
Aortic Stenosis.
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◙ Dyspnea, Orthopnea, Diastolic murmur at the “apex”
→ Mitral stenosis.
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SOB, Diastolic murmur, Chest X-ray showing straightening of the left atrial appendage Complications of this condition?
Think→ Mitral stenosis. (Remember, rheumatic fever is the commonest cause of mitral stenosis. Rheumatic fever is commonly found in developing countries e.g. Syria, Mozambique). ◙ Complications of MS: As the left atrium enlarges → Atrial fibrillation → Venous thromboembolism → Cerebral infarction. “imp √”. √ Note: left ventricular hypertrophy is a common complication of aortic stenosis.
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Broad complex tachycardia + Unstable patient (e.g. SBP < 90)
→ Synchronized Cardioversion.
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Long QT syndrome Recurrent fainting episodes + Prolonged QT intervals on ECG + Hx of similar ECG during childhood
• Think → Congenital long QT syndrome (Congenital LQTS). • The most common arrhythmia associated with Congenital LQTS is → Ventricular tachyarrhythmia. There is risk of ventricular fibrillation. Thus, some patients use long-term beta blocker treatment.
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____wave inversion in leads (V1, V2, V3, V4) Indicating →
Myocardial Ischemia. T wave
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A 60 YO man on ramipril for his hypertension has serum potassium of 6.7 mmol/L (Normal: 3.5-5). His ECG shows sinus rhythm without hyperkalemic changes. What is the next step in management?
Although there is no ECG changes of hyperkalemia “tall tented T waves”, this patient has severe hyperkalemia (>6.5) and the initial step is to protect the heart and prevent cardiac arrest by giving a medication that antagonizes the cardiac membrane excitability as a temporary measure such as calcium Gluconate 10% or calcium chloride or calcium carbonate.
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A 50 YO presents with a swollen left arm. It started suddenly a few hours ago and it is painful. He has fever and breathlesness. O/E, loud S1 and mid- diastolic murmur are heard. There is no left radial pulse felt. Echocardigram is done and it reveals left atrial myxoma. What is the most appropriate management?
→ Perform an urgent catheter Embolectomy. • A piece of the atrial myxoma has broken off and caused left acute limb ischemia (sudden swollen painful left arm with a loss of radial pulse). • It has been only a few hours and the limb could be saved if embolectomy is performed urgently. • It is perfomed by a interventional radiologist who uses an angiogram in theatre and introduce a catheter to aspirate the emboli “embolectomy”. • Note that this is not a blood clot, but a piece of the benign tumor. Thus, thrombolysis and anticoagulation would not be suitable.
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Fatigue + Shortness of breath on exertion + Ankle oedema
Next test → N-terminal (NT)-pro hormone BNP (NT-proBNP). If raised → Echocardiogram. • N-terminal (NT)-pro hormone BNP (NT-proBNP) is a non-active prohormone that is released from the same molecule that produces BNP. Both BNP and NT- proBNP are released in response to changes in pressure inside the heart. These changes can be related to heart failure and other cardiac problems. • Note: sometimes in heart failure, ECG may be normal.
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hypertension patient on ramipril. What shoulde be monitored?
→ Kidney function tests.
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Dizziness + bradycardia + 3rd degree heart block
◘ Initial management → Atropine. What if he was given atropine but no response? Next step would be → Temporary transcutaneous pacemaker. ◘ Definitive management → Permanent pacemaker. • Bradycardia is a condition typically defined wherein an individual has a resting heart rate of under 60 beats per minute (BPM) in adults, although some studies use a heart rate of less than 50 BPM. Bradycardia typically does not cause symptoms until the rate drops below 50 BPM. • All symptomatic bradycardia should initially be treated with atropine. If no response → temporary pacemaker (in an emergency setting). • Atropine is given 0.5 mg IV push and may be repeated up to a total dose of 3 mg.
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2nd degree Mobitz 1 2 and complete heart. Block mng
◙ 1st Degree Heart Block and Mobitz type 1 usually → do not require treatment (as long as the patient is Asymptomatic). ◙ Mobitz type 2 and Complete heart block (3rd degree heart block) → require permanent pacemaker. • Initially → Atropine (first choice for all symptomatic bradycardia). • Then → Transcutaneous pacing. (Used to buy time until transvenous pacing is done). • Then → Transvenous pacing. • Then → Permanent pacing (Pacemaker).
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A 50 YO man presents for advice as his father dies of MI. He smokes 6 cigarettes a day, drinks 14 units of alcohol a week with 2 days free. He eats an estimate of a teaspoon of salt a day. He eats fruits and vegetable. His clinic BP is 138/87. What is the best advice to reduce the risk of MI?
A) Refer to a cardiologist. B) Refer to a smoking cessation clinic. C) Refer to alcohol cessation services. D) Advise to reduce salt. √ His clinic BP is normal (<140/90). √ Smoking is the major risk factor here. √ His alcohol intake is within the recommended limit. (no more than 14 units a week with at least 2 days free). His salt intake is within the recommended limit. (Salt intake recommendation for adults in the UK is no more than 6 g per day which is around 1 teaspoon).
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Fatigue + Shortness of breath on exertion + Ankle oedema
Think → Heart failure. Next test → N-terminal (NT)-pro hormone BNP (NT-proBNP). If raised → Echocardiogram. • N-terminal (NT)-pro hormone BNP (NT-proBNP) is a non-active prohormone that is released from the same molecule that produces BNP. Both BNP and NT- proBNP are released in response to changes in pressure inside the heart. These changes can be related to heart failure and other cardiac problems. • Note: sometimes in heart failure, ECG may be normal.
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hypertension patient on ramipril. What shoulde be monitored?
→ Kidney function tests.
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Dizziness + bradycardia + 3rd degree heart block Initial step Next step Definitive mng?
◘ Initial management → Atropine. ◘ What if he was given atropine but no response? Next step would be → Temporary transcutaneous pacemaker. ◘ Definitive management → Permanent pacemaker.
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A 67-year-old man presented to the GP surgery to check on his blood pressure. It is found to be 155/95 mmHg. He was asked to measure his blood pressure at home several times. On the next appointment, the average of his home blood pressure measurements is 146/93 mmHg. His 10-year risk of developing cardiovascular disease is calculated and is found to be 6%. He does not smoke and otherwise healthy. What is the most appropriate management? A) Start ACE inhibitors. B) Start calcium channel blockers. C) Offer lifestyle advice and modification. D) Start statin. E) Reassure and no intervention is required.
Since his home blood pressure is ≥ 140/90, but < 150/95 mmHg. → He has stage (1) hypertension.
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A 53-year-old man from South Asia presents with headache and blurry vision for sometimes. His blood pressure is found to be 149/ 101 mmHg. He was asked to have blood pressure measurements at home. His average blood pressure of 14 home readings is 153/97 mmHg. What is the most appropriate management? A) lifestyle modification only. B) No management required. C) Ramipril. D) Indapamide. E) Amlodipine.
Answer → C. • He has a stage 2 hypertension. • Since he is < 55 YO → Start with ACE inhibitor (eg, ramipril).
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♠ When to Treat Stage 1 Hypertension
? • Treat if the patient’s age is < 80 years AND + any of the following: Target organ damage, established cardiovascular disease, renal disease, diabetes (DM) or a 10-year cardiovascular risk equivalent to (QRISK2) ≥ 10%.
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Note: If a patient is completely free and has a stage 1 Hypertension
→ Lifestyle and Diet Modification + review (Follow up).
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◙ Example: If a patient a stage 1 Hypertension and his QRISK2 ≥ 10?
Discuss initiating antihypertensive therapy.
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Important notes on the management of Atrial Fibrillation: Hemodynamically Stable Unstable Ist and second step
(Atrial fibrillation = narrow-complex irregularly irregular tachycardia). • First line (if hemodynamic stable) → Beta-blockers (eg, metoprolol). • If hemodynamic unstable (eg, hypotension, chest pain, altered mentation) → Start with electrical cardioversion. If still not improved → IV amiodarone.
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A few days after myocardial infarction (especially inferior MI) Based on location of murmur Apex and lower left sternal border
Pan-systolic murmur over the apex Think → Mitral regurgitation. Pan-systolic murmur over the lower left sternal border Think → TR Or ventricular septal rupture. This is due to a possible dysfunction of papillary muscles of the valve
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Q) Since these 2 conditions have the same type of murmur, how to differentiate? VSR AND TR
Ventricular septal defect occurs acutely (within a few days) after MI, and also presents with hypotension (shock). √ Tricuspid regurgitation tends to develop over weeks to months after MI, and hypotension is not a feature. - In both conditions, do → Echocardiogram.
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A 50-year-old man was found unconscious with a absent pulse and undetectable blood pressure. His ECG reading shows VT. What is the best management?
→ Deliver a shock. (VT in a pulseless patient and VF requires immediate shock delivery).
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A 50-year-old man was found unconscious with a absent pulse and undetectable blood pressure. His ECG reading is flat. What is the best management?
→ Start CPR (Chest Compressions). Important: If CPR is not among the options, what’s to pick? → Give adrenaline (Epinephrine) 1 mg IV. (A flat ECG reading means asystole which is a non-shockable rhythm)
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A 50-year-old man was found unconscious with a absent pulse and undetectable blood pressure. His ECG reading shows VT. What is the best management?
→ Deliver a shock. (VT in a pulseless patient and VF requires immediate shock delivery).
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A patient with DM type 1 who presents with abdominal pain, vomiting, lethargy, increased thirst and urination, and fruity smelling breaths is likely suffering from a complication called diabetic ketoacidosis (DKA). Tall tented waves in ecg
• One of the manifestations that would be seen in DKA is: → Hyperkalemia (ECG might show tall tented t waves)
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Consuming alcohol (and also tobacco) excessively can lead to transient palpitations several times a day
(holiday heart syndrome). • The ECG in this case would be unremarkable. The best action is to → and decrease smoking would resolve palpitations completely). Advise on lifestyle modifications (decreasing alcohol)
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In rhabdomyolysis, acute kidney injury and hyperkalemia can develop. • A patient might be found on the floor after a fall for several hours. • A patient can be found stuck under a heavy object for several hours. • Hyperkalemia can develop and ECG may show tall tented T waves. Investigation abn?
Important: the investigation that would likely be abnormal in this case is → Urea and electrolytes. Urea and electrolyte panel includes: → Urea, creatinine, sodium, potassium, eGFR.
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A 61 YO man presents for medication review. He has a history of ischemic stroke a few months ago . His medical background includes hypertension and type 2 diabetes mellitus. His ECG now shows arterial fibrillation. He is on clopidogrel, amlodipine, atorvastatin, and metformin. What is the most appropriate action? A) Switch amlodipine to ramipril. B) Continue clopidogrel and add apixaban. C) Stop clopidogrel and start edoxaban. D) Continue amlodipine and add ramipril. E) Continue amlodipine and add bendroflumethiazide.
The right answer is ©: Stop clopidogrel and start a DOAC eg, edoxaban. • He did not have atrial fibrillation before, that’s why he was on clopidogrel (and not warfarin or DOAC). • Since he is now having atrial fibrillation, switch clopidogrel to an anticoagulant such as warfarin or DOAC (eg, edoxaban, apixaban). DOAC is preferred over warfarin. • His blood pressure is not mentioned so we assume it is controlled and therefore no need to add an additional antihypertensive (even if he is diabetic, he is already on amlodipine and controlled).
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Scenario (1) that tests the above notes (important). A 65 YO man presents for medication review. He has a history of ischemic stroke a few months ago. His medical background includes atrial fibrillation, hypertension and type 2 diabetes mellitus. His ECG still shows arterial fibrillation. He is on warfarin, lercanidipine (CCB), atorvastatin, and metformin. His current blood pressure is 160/100. What is the most appropriate action? A) Switch warfarin to Edoxaban (DOAC). B) Continue warfarin and add clopidogrel. C) Stop lercanidipine and start ramipril. D) Continue lercanidipine and add ramipril. E) Continue lercanidipine and add bendroflumethiazide.
The right answer is (D): continue lercanidipine (CCB) and add ramipril (ACEi). • Since he is diabetic, ACEi is of choice to control HTN. • Since he is already on an antihypertensive (which is lercanidipine; a calcium channel blocker) and his hypertension is still uncontrolled, go to step 2 and add a second antihypertensive (ACE inhibitor eg, ramipril). • We do not shift from warfarin to DOAC unless his INR is not normal. Here, no mention of INR. Thus, continue on warfarin (option A is wrong). • Since he has AF, an anticoagulant (eg, warfarin, DOAC) is given; Not an antiplatelet (eg, clopidogrel).
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Important Points to Remember on Ischemic Stroke • The antihypertensive of choice in patients with diabetes mellitus is → ACE inhibitors (eg, ramipril
• In patients with a history of ischemic stroke, the long-term management to prevent further stroke (2ry prevention of ischemic stroke) is as follows: √ Control Blood Pressure. Remember, if he has diabetes, pick or add ACEi eg, ramipril. √ Statins (for All patients regardless of their cholesterol baseline level). √ Ani-platelets (or) Anti-coagulation: (Based on presence or absence of AF): • If there is Atrial Fibrillation → Anticoagulants: Warfarin [or] DOAC (Dabigatran/ Apixaban/ Rivaroxaban/ Edoxaban). DOAC is now preferred. (Warfarin is almost obsolete nowadays. DOAC is recommended instead). • If No Atrial Fibrillation → Antiplatelets: Clopidogrel 75 mg OD. Important: What if a patient with a history of stroke is already on warfarin and presents with a new onset atrial fibrillation? Since he is already on an anticoagulant, he should continue on warfarin and should not be switched to DOAC (eg, Edoxaban) unless his INR is abnormal
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Remember that the initial treatment for symptomatic bradycardia (lightheadness, syncope -fainting-, dizziness)
is → IV atropine. (Given 0.5 mg IV push and may be repeated every 3-5 minutes up to a total dose of 3 mg). Rx is required if the patient is symptomatic even if the ECG shows first- degree heart block. As long as he has symptoms and bradycardic, start with atropine. • After initial stabilisation of the patient by atropine, he should then be prepared for temporary pacemaker and assessed for whether or not he needs a long-term permanent pacemaker.
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60-year-old has just finished his appendectomy surgery and developed dizziness, palpitations, tachycardia and hypotension (BP: 80/50). His ECG: What is the most appropriate diagnosis and management? atrial fibrillation. Cardioversion. √ • The ECG + (palpitations, tachycardia. Dizziness) suggest
Since the AF has just started and the patient is hypotensive (ie, haemodynamically unstable) → cardioversion • If cardioversion is not in the option → IV amiodarone • Another possible answer is IV Flecainide (IV, not Oral). (Careful: beta-blockers are first line in STABLE patients with AF)!
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• Remember that the initial treatment for symptomatic bradycardia (lightheadness, syncope -fainting-, dizziness) is
→ IV atropine. (Given 0.5 mg IV push and may be repeated every 3-5 minutes up to a total dose of 3 mg).
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A 72-year-old man presents to a GP clinic to complain of repetitive dizziness and palpitations over the past few weeks. They mostly occur while walking long distances and they resolve after a few minutes. He has a background history of diabetes mellitus types 2 and hypertension. He is vitally stable. His current ECG shows normal sinus rhythm. He denies any chest pain, fainting or shortness of breath. What is the most appropriate investigation? A) Echocardiogram. B) Ambulatory 24-hour ECG (Holter monitor). C) Exercise ECG (Stress test). D) Random blood glucose. E) Blood pressure monitoring.
• Exercise ECG (stress test) is preferred for stable angina. Here, no chest pain! • Echo: could be requested if the current ECG is abnormal. Here, it is normal. • Also, if you think this might be aortic stenosis (AS) that requires Echo to be diagnosed, then you are mistaken. AS presents with ejection systolic murmur over the right second intercostal space + Fainting episodes (syncope) ± Dyspnea ± Angina (chest pain). None of these features are present! • This patient has dizziness and PALPITATIONS mostly during walking, which may indicate hidden arrhythmia which develops while walking. • The arrhythmia can be detected by ECG. However, the current ECG is normal. Thus, ambulatory 24-hour (Holter) ECG is needed.
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In diabetic patients who have heart failure “HF” with reduced ejection volume SGLT2 inhibitors such as Dapagliflozin, Empagliflozin Give
Give → (When SGLT2 inhibitors are added to the medications of HF which are B-blockers, ACE inhibitors, Aldosterone antagonist → they reduce cardiovascular death). So, in DM with heart failure, use metformin and flozin family. SGLT2 inhibitors such as Dapagliflozin, Empagliflozin
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After Myocardial Infarction, Mitral regurgitation may occur as a complication (pansystolic murmur at the apex +Bi-basal crackles + Shortness of breath Investigation?
). The most appropriate investigation to determine this mitral regurg is → Echocardiogram
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Patients with aortic stenosis (systolic murmur at the right second ICS) are liable to fainting episodes that are called
→ Other features → syncope Dyspnea, Angina.
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58-year-old man had clinic blood pressure of 162/95 mmHg. He was asked to record blood pressure at home (ABPM). He returns to the clinic next week with an average ambulatory blood pressure reading of 155/92 mmHg. He does not have a significant medical history. What is the most appropriate action? A) Repeat ABPM for another week. B) Prescribe enalapril. C) Prescribe felodipine. D) Prescribe indapamide. E) No treatment is required, only encourage lifestyle modifications.
• Since his ambulatory BP is ≥ 150/95 ( His SBP is the high portion in this case) → he needs treatment. (Confirmed stage 2 HTN). (f ABPM or HBPM ≥ 150/95 mmHg (i.e., confirmed stage 2 or higher hypertension) → Always treat.) → Felodipine • Since he is ≥ 55 YO → the first step is Calcium channel blocker (CCB). (Felodipine is a CCB).
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A 50 YO man is to be started on Modafinil (to counter his extreme sleepiness). A baseline ECG was requested and it shows: What is the most appropriate management? A) Atropine B) Permanent pacing C) Temporary pacing D) Reassurance.
• The ECG shows PR prolongations followed by a dropped beat. • This is a second-degree heart block (Mobitz type 1). Also called (Wenckebach). • Asymptomatic patients with this type of heart block do not need specific Rx
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Pericarditis Sharp chest pain + Age 20-55 YO + ECG shows Widespread ST elevation + Recent Hx of upper viral respiratory tract infection
Think → Rx → Acute pericarditis. NSAIDS (eg, Ibuprofen) + Colchicine. ◙ Other Criteria of Acute Pericarditis → Central sharp stabbing chest pain relieved by sitting up and leaning forward and worsened by lying down + Pericardial rub. ◙ Management of Pericarditis (imp): √ A full-dose NSAID should be used ( eg, aspirin, 2-4 g/d; ibuprofen 1200-1800 mg/d; indomethacin 75-150 mg/d); √ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence). treatment should last at least 7-14 days.
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A 66 YO diabetic and hypertensive patient developed chest pain radiating to the left arm 1 hour ago. His ECG is normal and his Troponin level is normal (below 12). He was given aspirin. What is the next step?
→ Admit and repeat troponin level after 3 hours of the symptom’s onset. • The patient has arrived to the hospital after one hour of the beginning of the chest pain. So, the troponin level was taken only one hour after the chest pain. • Elevated troponin can be detected within 3 to 4 hours after the onset of myocardial injury. Serum levels can remain increased for 7 to 10 days for troponin I and 10 to 14 days for troponin T. • Therefore, a second troponin level is needed after 3 hours of the onset of the chest pain. Taking into consideration that he is Old + DM + HTN (All RFs for MI
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Rules: If arrived < 3 hours of the chest pain onset: √ troponin is < 12 → repeat after 3 hours of chest pain onset. √ troponin is > 30 → correlate with ECG and Hx → treat as ACS.
If arrived > 3 hours of the chest pain onset: √ troponin is < 12 → ACS is unlikely → suspect stable angina and refer to cardiology outpatient or rapid access chest pain clinic. √ troponin is > 30 → correlate with ECG and Hx → treat as ACS.
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Arrhythmia causing dizziness and palpitations sometimes but the ECG is normal
Ambulatory 24-hour ECG. This is because the arrhythmia occurs in some Do → ambulatory 24 hour ecg periods of the day and so the ordinary ECG may be normal. We need ambulatory 24-hour ECG to try to detect the arrhythmia. Also known as an ambulatory ECG or EKG monitor, a Holter monitor records your heart’s activity over 24 to 48 hours or up to 2 weeks while you maintain a diary of your activity to help your doctor identify the cause of your symptom
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√ If Stable angina (chest pain on exercise) is suspected
→ Exercise ECG “stress test”.
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A 67 YO man with hypertension for 7 years. He is on ramipril “ACEI”. However, his BP now is not controlled. Knowing that he had used amlodipine “CCB” in the past but stopped it because of ankle edema, what medication can be added? • Choices are ( Valsartan, Indapamide, Bisoprolol, Furosemide).
The right option is → Indapamide (which is a thiazide like diuretic0 He has started with CCB (step 1) and cannot use it because of ankle edema S/E. Then stopped it and went for ACEi ramipril (step 2) Now, (step 3) is a thiazide like diuretic e.g., indapamide. Note that valsartan is ARBs. It is used instead of ACEi in some cases like those who develop dry cough as a side effect of ACEi.
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the patient of congestive heart failure is already on FUROSEMIDE, Beta blocker, and ACEi and still has lower limb edema → This means that the diuretic is not efficient (the furosemide) → Therefore, one of the following is needed:
• Increase the dose of the furosemide . • Switch the furosemide to either bumetanide or torsemide. • Consider admission for IV loop diuretics.
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Dx → Anterior MI (note ST elevation in V1-V4).
The likely occluded artery → LAD “left anterior descending artery”.
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a patient has either systolic BP ≥ 140 and/or diastolic BP ≥ 90 in a clinic
→ Ambulatory blood pressure monitoring (ABPM) is needed before starting lifestyle modifications and antihypertensive medications.
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