Cardiology Flashcards

1
Q

No ST elevation
AND
Troponin is normal

A

Unstable angina

Non occlusive thrombus

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2
Q

No ST elevation
AND
Troponin is raised

A

Non ST elevation myiocardial infarction

NSTEMI

Occluding thrombus sufficient to cause tissue damage and mild myocardial necrosis

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3
Q

ST elevation

A

ST elevation myocardial infarction

STEMI

Complete thrombus occlusion

(May present new LBBB)

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4
Q

Classic symptoms of acute coronary syndrome

A

Chest pain
Central/left sided/ substernal/ epigastric

May radiate to the jaw, left arm or shoulder

Described as heavy or constricting “elephant on my chest”

Other symptoms> dyspnoea, sweating, nausea and vomiting, may appear pale and clammy

remember that pxs with DM or elderly may not experience any chest pain! = Silent MI

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5
Q

Unmodifiable Risk factors of Ischemic Heart Disease

A

Increasing age
Male gender
Family history

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6
Q

Modifiable Risk factors of Ischemic Heart Disease

A
Smoking
DM
Hypertension
Hypercholesterolaemia
Obesity
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7
Q

ST elevation on DII, III and aVF

A

Inferior MI

Right coronary

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8
Q

ST elevation on DI, aVL, V5 and V6

A

Lateral MI

Left Circumflex

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9
Q

ST elevation on V1, V2, V3 and V4

A

Anterior (anteroseptal) MI

Left Anterior Descending

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10
Q

ST elevation on DI, aVL, V4, V5, V6

A

Anterolateral MI

Left anterior Descending
OR
Left Circumflex

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11
Q

Wide spread ST depression

ST elevation in aVR

A

Left main coronary artery occlusion

EMERGENCY CORONARY ANGIOGRAPHY

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12
Q

Management of Acute settings in ST elevation

A
MONA
Morphine
O2
Nitrates
Aspirin 300mg
\+
Heparin (unfractionated or LMW --> enoxaparin or fondaparinux)
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13
Q

If the patient with ACS presents within …… of the onset of the symptoms then a …… can be done

A

12 hours

PCI/angioplasty (stent) (percutaneous Coronary Intervention)
GOLD STANDARD

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14
Q

What should be done if PCI is unavailable or the patient presents after 12 hours of the onset of symptoms?

A

Thrombolysis

Alteplase is preferred over Streptokinase

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15
Q

Chronic/Long term Management of MI

A

-Aspirin for life
-Ticagrelor or Prasugrel or Clopidogrel for 12 months
-Beta blockers for 12 months (atenolol, bisoprolol)
-ACE inhibitor for life (captopril, enalapril, ramipril)
If intolerant then ARBs (losartan, valsartan, irbesartan)
-Statins for life Atorvastatin 80mg PO OD

**5 drugs= AABC+S
Aspirin, ACE inhibitors, Beta blockers, Clopidogrel, Statins

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16
Q

Management of NSTEMI & Unstable Angina

A

-Aspirin 300mg
+
-Antithrombin>LMWH (enoxaparin, dalteparin or Fondaparinux)
AS SOON AS POSSIBLE

  • Nitrates or morphine to relieve pain
  • Second antiplatelet (clopidogrel, prasugrel)
  • IV glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban)
  • Coronary angiography should be considered
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17
Q

Who should LMWH be offered to?

A

Pxs with NSTEMI & Unstable Angina who are not at high risk of bleeding and who are not having angiography in the next 24 hours

If angiography is likely or creatinine is >265 umol/l, unfractionated heparin should be given (UH is IV!)

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18
Q

To whom should IV glycoprotein IIb/IIIa receptor antagonists be given?

A

Epifibatide and tirofiban

Pxs with NSTEMI & Unstable Angina who have intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3%) and who are scheduled to undergo angiography within 96 hours of hospital admission

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19
Q

Who should be considered for coronary angiography?

A

Pxs with NSTEMI & Unstable Angina who have predicted 6-month mortality above 3%.
It should be considered within 96 hours of 1st admission to hospital

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

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20
Q

Px with acute chest pain radiating to jaw and shoulder WITHOUT ST elevation, what should be done next?

A

Measure cardiac enzymes (troponin)

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21
Q

Px with acute chest pain radiating to jaw and shoulder WITHOUT ST elevation, and high troponin levels, what should be done next?

A

Give subcutaneous LMWH or Fondaparinux + Aspirin 300mg

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22
Q

60 YO man with Hx of smoking, HTN and DM complaining of 25 minutes of left side dull aching chest pain radiating to the jaw. He was given 300mg of Aspirin. He is no longer in pain and the ECG is NORMAL. The troponin levels are 202 ng/L (Normal < 5ng/L). What is the next step?

A) Alteplase
B) SC fondaparinux
C) IV Glyceryl trinitrate
D) IV Morphine

A

Since the ECG is normal, alteplase is WRONG

ECG normal with high troponin levels = NSTEMI

Correct answer: Anticoagulation (LMWH> Dalteparin, Enoxaparin, Fondaparinux)

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23
Q

62 YO man with Hx of smoking and HTN complaining of 25 minutes of left side constricting chest pain radiating to his left shoulder. He was given 300mg of Aspirin and trinitrates for the pain. The ECG shows ST elevation in V1-V4. What is the most appropriate next step in management?

A

PCI- Percutaneous Coronary Intervention

If not among the choices> Atleplase (thrombolysis)

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24
Q

59 YO with Hx of HTN, complaining of chest pain for around 4 hours. Vitals are stable. He was given IV morphine for his chest pain. ECG shows T wave inversion in DII, DIII and aVF. What is the next step in management?

A

Chest pain+T wave inversion = myocardial ischemia

ASPIRIN 300mg
AND
LMWH or Fondaparinux

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25
Q

59 YO with Hx of HTN, complaining of chest pain for around 4 hours. Vitals are stable. He was given IV morphine for his chest pain. ECG shows wide spread ST depression and ST elevation in aVR. What is the next step in management?

A

Wide spread ST depression + ST elevation in aVR = Left Main Coronary Artery Occlusion

–> EMERGENCY CORONARY ANGIOGRAPHY

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26
Q

Cardiac tamponade triad

A

Beck’s triad> hypotension, muffled heart sounds, high JVP (distended neck veins)

Other symptoms: dyspnea, pulsus paradoxus, tachycardia

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27
Q

How can a cardiac tamponade develop after a MI?

A

Acute pericarditis
>Pericardial effusion
>Cardiac Tamponade

Trauma is the most important cause of cardiac tamponade

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28
Q

How does a cardiac tamponade looks in a Chest X-ray?

A

Enlarged GLOBULAR heart
(It can also be a pericardial effusion)

Looks like a leather bag filled with water

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29
Q

Dx and Rx of a cardiac tamponade

A

Echocardiogram

Urgent pericardiocentesis

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30
Q

Initial Rx of a patient in hypovolemic shock and cardiac tamponade.

A

1-2 L of IV fluids**
Oxygenation and ventilation
Bedside pericardiocentesis

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31
Q

Atrial Myxoma

A

Benign tumour
75% in the left atrium
Tend to grow on the wall (inter-atrial septum)
10% are inherited–> familiar myxoma

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32
Q

Mitral valve obstruction caused by atrial myxoma

A

Mid-diastolic murmur, dyspnea, syncope and congestive HF

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33
Q

What happens if small pieces of an atrial myxoma break off and travel to the arteries?

A

Ischemia

Lung- Pulmonary embolism

Brain- Stroke

Peripheries- Clubbing and blue fingers

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34
Q

Px with mid-diastolic murmur, dyspnea, syncope, congestive HF, clubbing and blue fingers with Hx of pulmonary embolism and atrial fibrilation.

Dx?

A

Obstruction of mitral valve–> mid-diastolic murmur, dyspnea, syncope and congestive HF

Small pieces may break off and travel to arteries –> PE, Stroke or clubbing and blue fingers

Atrial fibrilation

=Atrial Myxoma

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35
Q

An echocardiogram shows a pedunculated heterogeneous mass typically attached to the region of fossa ovalis (inter-atrial septum)

Dx?

A

Atrial Myxoma

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36
Q

Px with Atrial Myxoma with sudden painful swollen limb with a loss of pulse.

A

Acute limb ischemia

Rx> Urgent catheter Embolectomy

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37
Q

QRS in lead I is up (+) and lead II is down (-)

A

Left axis deviation

-30 to -90

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38
Q

QRS in lead I is down (-) and in lead II is up (+)

A

Right axis deviation

90 to 150

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39
Q

QRS in lead I is down (-) and in lead II is down (-)

A

Right superior axis deviation

150 to 270

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40
Q

QRS positive in lead I and II

A

Normal axis

-30 to 90

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41
Q

Causes of Left Axis deviation

A

Inferior MI
Left ventricular hypertrophy
Left Anterior Fascicular block (or hemiblock)
Obese
Wolff-Parkinson-White syndrome (delta wave)

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42
Q

Causes of right axis deviation

A
Lateral MI
Right ventricular hypertrophy
Left posterior fascicular block (or hemiblock)
Thin, tall, children
Chronic lung disease
Pulmonary embolism
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43
Q

Causes of extreme right axis deviation

A

Congenital heart disease

Left ventricular aneurysm

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44
Q

PR interval >0.2 seconds

PR occupies more than 1 large square or 5 small squares

A

1st degree heart block

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45
Q

2nd degree heart block

Mobitz I

A

Progressive prolongation of the PR interval until a dropped beat occurs

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46
Q

2nd degree heart block

Mobitz II

A

PR is constant but the P wave is often not followed by a QRS complex

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47
Q

Complete (third degree) heart block

A

No association between P waves and QRS complexes

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48
Q

1st degree and Mobitz I heart block management

A

Do not require treatment as long as the patient is asymptomatic

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49
Q

Mobitz II and 3rd degree heartblock management

A

Permanent pacemaker

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50
Q

How long is a small square and a big square in an ECG?

A

small= 0.04 seconds

big= 0.2 seconds

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51
Q

Agents used to control rate in patients with atrial fibrilation

A

Beta blockers (atenolol, bisoprolol, metoprolol) –> 1st line but contraindicated in Asthma

Calcium channel blockers (diltiazem, verapamil) –> in asthmatic patients

Digoxin (less effective controlling rate during exercise, no longer 1st line) Preferred in patients with coexistent HF

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52
Q

Patient with atrial fibrillation hemodynamically unstable

A

Cardioversion

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53
Q

Atrial flutter management

A

Cardioversion

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54
Q

Patient conscious or semiconscious with VT and stable

A

Amiodarone

HE IS STABLE!

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55
Q

What is VT?

A

a broad complex tachycardia originating from a ventricular ectopic focus

It can develop into a FV therefore requires urgent treatment!

P wave might be present or absent

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56
Q

Patient unconscious with VT but with present pulse

A

Cardioversion!

Unstable but HAS A PULSE!

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57
Q

Patient unconscious, collapsed, not breathing and no pulse with VT

A

Defibrillation (asynchronized shock)

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58
Q

Most important cause of ventricular tachycardia

A

Hypokalemia (low K)

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59
Q

Atrial Fibrillation symptoms and treatment

A

Palpitation, tachycardia, dyspnea, fibrillatory waves on the ECG, irregularly irregular rhythm

Beta blockers
If asthmatic give calcium channel blocker

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60
Q

Atrial Flutter symptoms and treatment

A

Fluttering feeling in the chest
Sawtooth waves

Cardioversion

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61
Q

Ventricular tachycardia symptoms and treatment

A

Ongoing lightheadness, palpitations, chest pain

Amiodarone

If unstable–> Cardioversion

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62
Q

Ventricular fibrillation symptoms and treatment

A

Older adult, sudden collapse, not breathing, unconscious, no pulse.

Defibrillation

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63
Q

Sinus bradycardia symptoms and treatment

A

Lightheadness, hypotension, vertigo, syncope, dizziness.

Symptomatic bradycardia–> atropine

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64
Q

The following medications have shown to reduce mortality in pxs with Left Ventricular failure.

A
  • ACE-inhibitors
  • Beta-blockers
  • ARBs
  • Aldosterone antagonists (eplerenone, spironolactone)
  • Hydralazine with nitrates

Loop diuretics and nitrates are key in the acute decompensated HF, but they have no effect on long-term survival.

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65
Q

Tx for HF with symptoms

What if the px has DM?

A

Diuretics to relieve symptoms and reduce overload

Start with ACEi OR Beta-blocker (ONLY 1)

If symptoms persist add the other one (ACEi, BB or ARB)

If symptoms still persist add Spironolactone

If the px has DM we start with ACEi

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66
Q

Spironolactone is a….

A

Potassium-sparing diuretic
AND
an aldosterone antagonist

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67
Q

What drug should be administered if the patient has HF and AF?

A

Digoxin!

Inhibition of the Na/K ATPase in the myocardium.

Personal note: More recent randomized trials have shown an increase in mortality in HF patients with digoxin.

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68
Q

Why furosemide + ACEi don’t lead to hyperkalemia?

A

Furosemide= loop diuretic leads to hypOkalemia

ACEi and Spironolactone= lead to hypERkalemia

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69
Q

Which is the most accurate investigation to demonstrate a patent foramen ovale

A

Transesophageal echocardiography with bubble contrast

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70
Q

What is a patent foramen ovale?

A

The foramen allows blood to pass from RA to LA.

The opening closes soon after birth. In about 1 out of 4 people it never closes.

It may cause paradoxical embolism (an embolism that travels from the venous side to the arterial side)

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71
Q

Most common cause of death following a MI and treatment

A

Cardiac arrest due to ventricular fibrillation.

Tx= Defibrillation

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72
Q

What may occur 48 hours after a MI

A

Pericarditis

Pleuritic chest pain that worsens on lying flat and during inspiration + fever + pericardial rub (extra heart sound, 2 systolic and 1 diastolic that resembles a squeaky leather, described as grating, scratching or rasping)

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73
Q

ECG that shows

Widespread saddle shaped ST elevation with upward concavity and PR depression

A

Pericarditis

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74
Q

Px with fever + pericardial rub + pleuritic chest pain

The X-ray will show…?

A

Pericardial effusion

An enlarged globular heart can be observed and is confirmed by echocardiography

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75
Q

Px with pleuritic chest pain that shows widespread saddle shaped ST elevation with upward concavity and a PR depression.

Dx and Rx?

A

Pericarditis

Full dose of NSAID
Aspirin 2-4g daily
Ibuprofen 1200-1800mg daily
Indomethacin 75-150mg daily

At least 7-14 days.

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76
Q

Px with Hx of MI 3 weeks prior, complains about pleuritic chest pain + fever + and a pericardial rub with ECG that shows widespread saddle shaped ST elevation with PR depression.

Dx and Rx?

A

Dressler’s syndrome

Thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers

Rx> NSAIDs

It tends to occur 2-6 weeks following a MI

It may show a raised ESR (erythrocyte sedimentation rate)

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77
Q

Px with Hx of MI 4 weeks prior, complaining of shortness of breath.

The ECG shows ST elevation.

Most likely diangosis?

A

Left ventricular aneurysm

The ischaemic damage may weaken the myocardium resulting in a thin muscular layer> aneurysm formation

Usually occurs 4-6 weeks post MI

High risk of stroke due to a thrombus> anticoagulate!

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78
Q

ECG, Chest X-Ray and Echo of a left ventricular aneurysm

A

ECG> persistent ST elevation

CXR> enlarged heart with a bulge at the left heart border

Echo> paradoxical movement of the ventricular wall (instead of moving inward, it moves away from the septum during systole)

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79
Q

Px with Hx of MI 5 days ago, complaining of dyspnea, orthopnea, chest pain and diaphoresis. A pan-systolic murmur can be heard.

Dx and Rx?

A

Ventricular septal defect (VSD)

Presents in the 1st week post MI
Only 1-2%

Presents with acute heart failure with pan-systolic murmur

The echocardiogram is diagnostic and excludes acute mitral regurgitation which is similar.

Rx> Urgent surgical correction

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80
Q

Acute Mitral Regurgitation

Occurs x days after MI
Due to...
Presents with ... on auscultation
Dx is with...
Rx?
A

Occurs 2-15 days after MI

Due to ischemia or rupture of the papillary muscles of the mitral valve

pan-systolic murmur is typically heard

May present with hypothension, tachycardia and pulmonary edema

Dx> echocardiogram

Rx> vasodilator therapy but often requires emergency surgical repair.

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81
Q

A px presents with ST elevation and chest pain.

Management?
What if it’s not available?

A

STEMI

MONA and then

PCI if not obtainable

> Alteplase, if not available

> streptokinase

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82
Q

A px presents with chest pain and NO ST elevation.

Management?

A

oral aspirin 300mg

LMWH or Fondaparinux

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83
Q

1st, 2nd and 3rd choice for symptomatic bradycardia

A

1st- atropine (0.5mg IV push and may be repeated up to 3mg)

2nd- Dopamine

3rd- Epinephrine

If the question says “the next best step” or “the initial line” –> O2!!!

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84
Q

A patient presents with fever, malaise and rigors, and a new murmur can be heard

Dx?
Initial step?

A

Infective endocarditis

> Blood culture and then echo

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85
Q

Risk factors for infective endocarditis?

A

A previous episode of IE (strongest RF)

Rheumatic valve disease

Prosthetic valves

Congenital heart defects

IV drug user (typically causes tricuspid lesion)

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86
Q

Causative organisms of IE?

A

Staph. aureus is the most common in general

Staph epidermis is the most common in prosthetic valve surgery

Strept. viridans is the most common in people with poor dental hygiene or following a dental procedure
(Strept. mitis and sanguinis)

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87
Q

Positive Modified Duke criteria

A

2 major criteria or
1 major and 3 minor
5 minor

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88
Q

Major Duke criteria

A

1) Positive cultures
2 + blood cultures showing typical organisms (Strep viridans and HACEK group)
OR
Persistent bacteraemia from 2 blood cultures taken >12h apart or 3 or more + cultures where pathogen is less specific such as Staph aureus and epidermis

2) Evidence of endocardial involvement (+ Echo for IE)
+ echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves)
OR
New valvular regurgitation

89
Q

Minor Duke criteria

A

1) Predisposing heart condition or IV drug use
2) Microbiological evidence that does not meet the major criteria
3) Fever >38C
4) Vascular phenomena–> Major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, Petechiae or purpura
5) Immunologilcal phenomena–> glomerulonephritis, Osler’s nodes, Roth spots.

90
Q

Osler’s Nodes

A

painful, red nodules on the hands or feet that can persist for hours to days

91
Q

Janeway lesions

A

Non-tender, small, erythematous or hemorrhagic macular or nodular lesions on the soles or palms. (they occur due to septic microemboli that deposit the bacteria under skin)

92
Q

IE empirical therapy

A

Amoxicilin + low dose Gentamicin
OR
Vancomycin+ low dose Gentamicin (if apenicillin allergic or MRSA Staph Aureus is suspected or severe sepsis)

If Hx of prosthetic valve endocarditis–>
Vancomycin+low-dose Gentamicin+ Rifampicin

93
Q

A man had dental extraction a few days ago that presents with petechia. His vitals are stable except for his temperature which is 38.9C. On examination he has petechiae, painful nodules on his palms, and a cardiac murmur.

Most likely Dx?
Next investigating step?
Initial management?

A

IE (fever+new murmur)

Blood culture (followed by echo)

Amoxicilin+low dose Gentamicin

94
Q

What score should we use in in atrial fibrilation

A

CHA2DS2-VASc Score

95
Q

What does CHA2DS2-VASc Score determines and what does it measure?

A

The need to anticoagulants in a patient who has atrial fibrillation

C- congestive heart failure - 1pt
H- Hypertension (BP>140/90) - 1pt
A2- Age >75 years - 2pt
D- DM - 1pt
S2- Prior stroke or TIA or Thromboembolism  - 2pts
V- vascular disease (MI, PVD, Aortic plaque) 1pt
A- Age 65-74 years - 1pt
Sc- Sex category (female = 1 pt)
96
Q

A patient with CHA2DS2-VASc Score of 2 pts or more should be given…

A

Warfarin or DOAC (direct-acting oral anticoagulants) like Apixaban, rivaroxaban, edoxaban, dabigatran

Consider warfarin or DOAC to men who score >1 or more

97
Q

What are some advantages and disadvantages of DOAC?

A

Advantages
No need of INR monitoring
Faster Onset of action (2-4 hours)
Reduces the risk of intracranial hemorrhage

Disadvantages
No antidote
Requires strict compliance by the patients

98
Q

ABCD2 score

A

Is used to identify the risk of future stroke in pxs who have had a suspected TIA in the following 7 days. (Not advised to use according to recent 2019 CKS guidelines)

99
Q

HAS-BLED score

A

estimates the risk of major bleeding for patients on anticoagulation for atrial fibrillation

100
Q

DRAGON score

A

predicts the 3 month outcome in ischaemic stroke patients receiving tissue plasminogen activator (tPA like alteplase)

101
Q

QRISK2 score

A

determine the risk of a cardiovascular event in the next 10 years.

102
Q

What is the mechanism of a pulmonary edema?

A

Often caused by congestive heart failure. When the heart is not able to pump efficiently–> the blood may return into the veins –> then the lungs.

As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.

103
Q

Features of a pulmonary edema

A
Desaturation
Dyspnea
Orthopnea
Crepitations (crackles-rales)
Tachycardia
104
Q

Investigation of pulmonary edema

A

Chest X-ray is the single most appropriate investigation
BUT
the underlying cause requires echocardiogram (HF, complication of MI, ventricular aneurysm)

“The most appropriate investigation” = Chest X-ray

“The investigation needed to identify the underlying cause” = Echocardiogram

105
Q

Management of pulmonary edema

A

MONF (MONA but the A is replaced by Furosemide)

Morphine
O2
Nitrates
Furosemide

Sit the px up and give O2 (>95% or >90% in COPD)

Spray 2 puffs of sublingual GTN (Glyceryl TriNitrates)

Give furosemide 40mg IV (SLOWLY)

Diamorphine (2.5-5mg IV slowly) or Morphine (5-10mg IV SLOWLY) to relieve pain, anxiety and distress

106
Q

Difference in the diagnosis between Pulmonary Edema and Pulmonary Embolism

A

Pulmonary edema can be diagnosed by chest x ray (Kerley Lines> expansion of the interstitial space by fluid; + Bat’s wings hilar shadow)

Pulmonary embolism needs CTPA (CT pulmonary angiogram)

107
Q

Dissecting Aneurysm or aortic dissection may present as a MI

However, name some clinchers that could direct us towards a DA and not a MI

A

Unequal pulses in upper limbs

Hx of Marfan Syndrome

Hx of Ehlers-Danlos syndrome or Turner syndrome

Severe tearing chest pain that radiates to the back

HTN is the most important risk factor

The pxs present with hypotension, dyspnea, tachycardia, and sweating.

Symptoms caused by low blood supply to organs like a stroke or mesenteric ischemia

108
Q

Aortic dissection pathophysiology

A

Tear in the tunica intima of the wall of the aorta.

The injury allows blood to flow between the layers of the aortic wall, forcing the layers apart.

109
Q

What is the best diagnostic test for aortic dissection?

A
Transoesophageal echocardiogram (TEE) 
Sens 98% and Spec 97%

CT scan with contrast is also good or MRI

In emergency use US or CT scan

110
Q

Stanford classification of aortic dissection

A

Type A> ascending aorta, 2/3 of cases

Type B> descending aorta, distal or left subclavian origin. 1/3 of cases

111
Q

Management of Type A Standford classification

A

Ascending aorta dissection.

Surgical management, but blood pressure should be controlled to a target systolic of 100-120mmHg whilst awaiting intervention

112
Q

Management of type B Stanford classification

A

Descending aortic dissection

Conservative management, bed rest, reduce blood pressure.
IV labetalol to prevent progression

113
Q

Left Brundle Branch Block (LBBB) features on ECG

A

Notched (M shaped) broad complex QRS usually in lead I, aVL and V6 but not always.

Deep inverted QRS usually in V1

Left axis deviation

114
Q

Patient complaining of chest pain and dyspnea. The ECG shows a notched broad complex QRS in DI and aVL and deep negative QRS in V1. He has no cardiac Hx.

Management?

A

New onset of LBBB!

Myocardial infarction!

Thrombolysis or PCI

(and MONA)

115
Q

A px presents with sudden severe abdominal pain, hypotension and sweating, and has no lower limb pulse.

Dx?

A

Ruptured abdominal aortic aneurysm (AAA)

Triad> pain, hypotension, pulsatile tender abdominal mass.

Sudden onset of severe abdominal pain ± lower back ± flank pain.

Shock (hypotension, sweating and fainting)

Absent lower limb pulse and mottled skin.

116
Q

A px presents with sudden severe abdominal pain, signs of shock and has no pulse on lower limbs.

Management?

A

Surgical emergency!

The initial investigation is an ultrasound

If not available then CT scan.

117
Q

Screening for abdominal aortic aneurysm in the UK

A

Men only

Once only

In 65th year

by ultrasound.

118
Q

A px with Hx of 5 years with dyspnea, orthopnea, lower limb edema that has DM

Management?

A

Symptomatic relief–> furosemide (loop diuretics)

Start with ACEi instead of BB (DM patients)

If the symptoms persist add BB

If still symptomatic add spironolactone (potassium sparing diuretics)

119
Q

Coronary artery dominance

A

The artery that supplies the posterior descending artery (PDA) determines the coronary dominance

In 85% of the population, the right coronary artery (RCA) gives off the PDA (right dominant)

In 15% of the population, the left circumflex gives off the PDA (left dominant)

Hence, the artery dominance is the RCA, as it gives off the PDA in 85% of people.

120
Q

Px with furosemide that presents with muscle weakness and cramps and the ECG shows a U-wave.

Dx and management?

A

U-wave and muscle weakness and cramps = hypOkalemia

Thiazide like diuretics and loop diuretics are the main cause

NOT potassium sparing diuretics like Spironolactone (hypERkalemia)

Rx> oral or IV Potassium chloride (based on severity> K <2.5 = IV)

Stop/treat the cause (thinking about diuretics, vomiting and diarrhea, Cushing syndrome and Conn’s disease)

121
Q

Causes of hypokalemia

A

Loop diuretics
Thiazide like diuretics (bendroflumethiazide, indapamide)
Vomiting and diarrhea
Villous adenoma
Renal tubular failure
Cushing syndrome
Primary hyperaldosteronism (Conn’s disease)

122
Q

Causes of hyperkalemia

A

ACEi
ARBs
Potassium sparing diuretics (spironolactone or eplerenone)
CKD/acute renal failure
Addison’s (primary adrenal insufficiency)
Congenital adrenal hyperplasia (CAH)

123
Q

20 YO px complaining of palpitations and light headedness. Hx of asthma. Presents with 130 HR, rest of vitals stable. The ECG shows narrow-complex ventricular Tachycardia.

Dx and management?

A

Paroxysmal supraventricular tachycardia

Rx
Valsalva manouver or carotid massage

IN ASTHMATIC> Verapamil! (CCB)
(adenosine is contraindicated)

Adenosine 6mg IV

Adenosine 12mg IV

Adenosine 12mg IV

Cardioversion

To prevent future episodes> B blockers or radio frequency ablation.

124
Q

Broad QRS
Prolongued QT
Fainting episodes
May be young px who is an athlete

A

Polymorphic Ventricular Tachycardia (Torsades De Pointes)

Tx if pulse!
IV Magnesium Sulphate. (Verapamil SHOULD NOT BE USED in VT)

125
Q

Stage 1 Hypertension

A

Clinic BP>140/90mmHg and subsequent ABPM daytime average or HBPM average BP≥135/85mmHg

126
Q

Stage 2 hypertension

A

Clinic BP ≥ 160/100mmHg and subsequent ABPM daytime or HBPM average BP ≥ 150/95mmHg

127
Q

Stage 3 hypertension

“Severe hypertension”

A

Clinic systolic BP ≥ 180mmHg or clinic diastolic BP ≥ 110mmHg

128
Q

Lifestyle management of hypertension

A
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
129
Q

When to treat stage 1 hypertension?

A
<80 years old
AND any of the following
Target organ damage
Established CV disease
Renal disease
DM
A 10-year CV risk equivalent of >20%

If not = Lifestyle modification and follow up

130
Q

What should be done in stage 2 hypertension patients before drug management?

A

Record either ABPM or HBPM

131
Q

What should be done in px <40 years old with stage 2 or 3 hypertension?

A

Consider specialist referral to exclude secondary causes of HTN.

132
Q

When should we ALWAYS treat HTN patients?

A

If ABPM or HBPM ≥ 150/95mmHg (confirmed stage 2 or higher)

133
Q

White + <55 YO

with HTN, Rx?

A

Start with ACEi/ARBs

134
Q

White + >55YO with HTN, Rx?

A

Start with CCB

Calcium channel blocker

135
Q

Afro-caribbean + any age with HTN, Rx?

A

start with CCB

Calcium channel blocker

136
Q

Step 2 in HTN management in a px who is still hypertensive after the 1st step and lifestyle changes.

A

Add ACEi/ARBs
Add CCB

A+C (ACEi + CCB)

137
Q

Step 3 in a HTN management who is still hypertensive

A

Add D (Thiazide Diuretic)

ACEi+CCB+Thiazide like Diuretic (A+C+D)

Examples of Thiazide like Diuretics
Chlorthalidone 12.5-25mg OD
Indapamide 1.5mg modified release OD
or 2.5mg OD

Bendroflumethiazide is NO LONGER recommended by NICE as an hypertensive.

138
Q

Step 4 in HTN management in pxs who are still hypertensive?

A

A+C+D
consider further diuretic treatment

If K<4.5mmol/l add spironolactone 25mg OD (K sparing)

If K>4.5 mmol/l add higher dose thiazide like diuretic

If diuretic therapy is not tolerated or is contraindicated or ineffective consider an alpha or beta-blocker

139
Q

HTN patients who fail to respond to step 4 of HTN management

A

A+C+D + further diuretic or alpha/beta blocker

If optimal tolerated doses of four drugs is not enough
–> seek expert advice!

140
Q

BP targets in HTN+DM

A

If end organ damage <130/80mmHg

If not <140/80mmHg

141
Q

BP targets for >80 YO pxs with HTN without DM

A

Clinic BP <150/90mmHg

ABPM/HBPM 145/85mmHg

142
Q

BP targets for <80 YO pxs with HTN without DM

A

Clinic BP < 140/90mmHg

ABPM/HBPM 135/85mmHg

143
Q

Why are ACEi used for DM and HTN pxs?

A

It is reno-protective (unless eGFR is low <30= advanced CKD)

It has protection against diabetic retinopathy

It has positive effect on glucose metabolism

144
Q

Management of HTN

52 YO px with Hx of DM and who is African-British

A

ACEi+CCB!

If he was only diabetic start with ACEi regardless of age as it is reno-protective (unless eGFR < 30)

as he is Afro-Caribbean start with both ACEi and CCB!

145
Q
Postural hypotensiob
(Orthostatic Hypotension) definition and dx?
A

A drop in systolic BP of at least 20mmHg within 3 minutes of standing
OR
drop of diastolic BP of at least 10mmHg within 3 minutes of standing

Dx> monitor BP

146
Q

Postural hypotension is most common in which people?

A

Elderly people
especially those who take multiple drugs (polypharmacy)

Pxs with HTN due to drugs.

Remember that baroreflex mechanisms that control HR and Vascular resistance decline with age, specially in pxs with HTN

147
Q

An elderly man complains of difficult mobilization. He often feels dizzy upon trying to stand ± he has Hx of recurrent falls. Management?

A

BP monitoring and assess and review the pxs medications.

148
Q

Px presents with palpitations. His ECG shows absent P wave and irregularly irregular rythm. Dx and Management?

A

Atrial Fibrillation

1st line> beta-blockers
If asthmatic> avoid B-blockers and give CCB
If associated HF> digoxin

Calculate CHAD2S2-VASc-Score and give Warfarin, DOAC or nothing

149
Q

Px with a sense of a skipped beat, unsustained palpitation, dyspnea and dizziness. What will the ECG most likely show?

A

An early and broad QRS complex = Ventricular ectopic

If it has 3-beat patterns= Ventricular trigeminy

50% of all the population has silent/asymptomatic ventricular ectopics which are discovered incidentally on a routine ECG

150
Q

Causes of ventricular ectopics

A
Ischemic heart disease (MI)
Cardiomyopathy
Stress
Alcohol
Caffeine
Cocaine
Medications
or-------> naturally

If these Ventricular ectopics are due to ischemic heart disease or cardiomyopathy > may precipitate life-threatening arrhythmias like VF

151
Q

A px with chronic HF developed gout. A medication for his gout is prescribed. A few days later the patient comes back complaining of worsening of his heart failure symptoms (shortness of breath and orthopnea).

What is the cause of this worsening?

A

Gout> NSAIDs.

Never give NSAIDs nor selective COX-2 inhibitors to CKD, CHD, IHD.
NSAIDs inhibit synthesis of prostaglandins–> decrease the eGFR, retain more salt and water (worsening HF)

Thiazide like diuretics and loop diuretics decrease the clearance of uric acid –> leading to gout (hyperuricemia)

NSAIDs are used to treat gout.

152
Q

In-hospital Cardiac Arrest algorithm

A
  1. Collapsed patient
    > SHOUT for help and assess the patient
  2. No signs of life (no pulse and not breathing) > ring bell/code blue
  3. Start CPR 30 compressions and 2 ventilations
    ASK FOR THE DEFRIBILLATOR
  4. Use defibrillator
    Advanced Life Support Team arrives.
153
Q

Why do DM patients may die suddenly and silently without feeling any chest pain when having a MI?

A

Autonomic neuropathy

>painless MI or silent MI

154
Q

UK guidelines on alcohol

A person should drink…

A

No more than 14 units a week
(1 unit= 10mL or 8g= amount of alcohol that can be processed in an hour by an adult)

No more than 3 units a day

at least 2 alcohol-free days a week

(a pint of strong lager is 3 units; a low strength lager has just over 2 units)

155
Q

A px drinks 7 units of alcohol a week and smokes 20 cigarettes a day. We should refer him to an Alcohol Cessation Clinic or a Smoking Cessation Clinic or both?

A

Smoking Cessation Clinic

No more than 14 units of alcohol a week

His alcohol intake is insignificant as per NICE guidelines.

156
Q

Pre-hospital analgesia (while in ambulance) for MI

A

GTN> Glyceryl Trinitrate sublingual or spray

±opioids IV> 2.5-5mg Diamorphine or 5-10mg morphine

Remember 1/3 of pxs have nitrate resistant chest pain, therefore, morphine is given additionally to relieve chest pain.

157
Q

Why should we give IV analgesia and not IM in the ambulance in the case of a MI?

A

IM absorption is unreliable

If the px receives thrombolysis later on, the site of injection IM might bleed.

158
Q

An ECG showing broad complex tachycardia in a still conscious patient ± atrial activity

A

Ventricular tachycardia

GIVE IV AMIODARONE

159
Q

Most important cause of ventricular tachycardia clinically

A

Hypokalemia

160
Q

Tall tented T wave in ECG is…

A

hyperkalemia

161
Q

U wave in ECG is…

A

hypokalemia

162
Q

Causes of hyperkalemia

A
ACEi
Spironolactone
NSAIDs
Renal Failure
Acidosis
Adrenal insufficiency
Addison's disease
163
Q

Rx of hyperkalemia

A

First protect the cardiac membrane by giving IV calcium gluconate (or calcium chloride)

Then reduce the serum potassium by giving Insulin with dextrose or Salbutamol

164
Q

M shaped QRS in leads I, aVL, V6
AND
Negative inverted QRS in V1

A

LBBB
Left Bundle Branch Block

Associated with acute MI!!!

165
Q

A px with an ejection systolic murmur heard on the right ICS just lateral to the sternum that radiates to the carotid artery.

A

Aortic Stenosis

Symptoms> dyspnea on activity, anginal chest pain, syncope.

166
Q

Px with early diastolic murmur heard on the right ICS just lateral to the sternum and symptoms of HF

A

Aortic regurgitation

167
Q

Px with ejection systolic murmur on the left 2nd ICS just lateral to the sternum that radiates to the left shoulder of infraclavicular area.

A

Pulmonary stenosis

Symptoms of systemic cyanosis

168
Q

Px with early-diastolic murmur heard on the left 2nd ICS just lateral t the sternum

A

Pulmonary regurgitation

Symptoms of right sided heart failure

169
Q

Px with mid-late diastolic murmur, with opening click on the apex.

A

Mitral stenosis

Symptoms of heart failure

170
Q

Px with pan-systolic murmur on the apex that radiates to the axilla.

A

Mitral regurgitation

Symptoms of Congestive HF (edema and ascites)

171
Q

Px with diastolic rumble murmur on the 4-5th ICS over the left sternal border and discomfort on the neck.

A

Tricuspid stenosis

Fluttering and discomfort on the neck

172
Q

Px with pan-systolic murmur heard on the 4th-5th ICS over the left sternal border.

A

Tricuspid regurgitation

Symptoms of right-sided heart failure.

173
Q

Pathogenesis of mitral stenosis

A

Stenosis impedes left ventricular filling –> increased left atrial pressure which leads to left atrial hypertrophy (CXR shows straight left side heart border) –> blood returns back to lungs –> pulmonary congestion –> right ventricular failure (hepatomegaly, ascites, oedema)

174
Q

Features of Mitral stenosis

A

Mid-late diastolic murmur (best heard on expiration) “low-pitched”
Loud S1, opening snap
Atrial fibrillation

Low volume pulse
Malar flush

175
Q

Left heart murmurs are better heard on…

Right heart murmur are better heard on…

A

LEft on Expiration (mitral and aortic)

rIght on Inspiration
tricuspid and pulmonary

176
Q

How does dilated cardiomiopathy affects ejection fraction and wall thickness?

A

↓ ejection fraction

↓ septal wall thickness

177
Q

How does hypertrophic cardiomiopathy affects ejection fraction and wall thickness?

A

↑ Ejection fraction

↑ Septal Wall Thickness

178
Q

Causes of dilated cardiomyiopathy

A

Alcohol (improves with tiamine)
Postpartum
Hypertension
Inherited (1/3 of pxs; autosomal dominant)
Previous MI
Infections (Coxsackie B, HIV, diphtheria, parasitic)
Endocrine (hyperthyroidism)
Infiltrative (haemochromatosis, sarcoidosis)
Neuromuscular (Duchenne muscular dystrophy)
Nutritional (Kwashiorkor, pellagra, thiamine/selenium deficiency)
Drugs (doxorubicin)

179
Q

Patient with SOB, severe dizziness, chest pain and HR > 150 with tachycardia

A

UNSTABLE!

Any unstable tachycardia = Cardioversion

180
Q

Stokes Adam attack

A

Intermittent complete heart block that causes a slow or absent pulse resulting in syncope.

181
Q

Preterm baby with continuous or machinery murmur

A

PDA

Patent Ductus Arteriosus

182
Q

Cyanotic baby with ejection systolic murmur

A

TOF
Tetralogy of Fallot

The systolic murmur is due to pulmonary stenosis which is one of the 4 major features of TOF

183
Q

The four major defects in Tetralogy of Fallot

A

VSD (ventricular septal deffect)

Pulmonary stenosis

Right ventricular hypertrophy

Overrriding aorta

184
Q

Progressive (severe) cyanosis + poor feeding + holosystolic (pansystolic) murmur along the left sternal border

A

Tricuspid Atresia

185
Q

Acyanotic with pan-systolic murmur

A

VSD (ventricular septal deffect)

May present poor feeding and poorly gaining weight.

186
Q

Cyanotic Congenital Heart Disease (R→L)

A

5 Ts, 1 to 5
Truncus arteriosus, vessels join to make 1

Transposition of great vessels, 2 major vessels switched

Tricuspid atresia, 3=tricuspid

Tetralogy of Fallot, 4 defects

Total anomalous pulmonary vascular return, 5 letters TAPVR

187
Q

Acyanotic Congenital Heart Disease (L→R)

A

Atrial septal defect (ASD)

Ventricular septal defect (VSD)

Patent ductus arteriosus (PDA)

Coarctation of aorta (CoA)

188
Q

Causes of falls (4)

A

Cardiac cause (arrythmia) > Stokes Adam attack, hot and flushed after recovery = 12 lead ECG

Postural (Orthostatic) hypotension > follow a standing position from a sitting position, dizziness before the fall

Hypoglycemia> sweaty and dizzy before the fall, does not recover until glucose is administered

Seizure> post ictal features like confusion and drowsiness, a witness describes the episode, recovers completely.

189
Q

Preterm baby with continuous or machinery murmur

A

PDA (persistent ductus arteriosus)

190
Q

Cyanotic baby with ejection systolic murmur

A

TOF (tetralogy of fallot)

The ejection systolic murmur is due to pulmonary stenosis

191
Q

Progressive (severe) cyanosis + poor feeding + holosystolic “pansystolic” murmur along the left sternal border

A

Tricuspid atresia

192
Q

Acyanotic + pansystolic murmur

A

VSD (ventricular septal defect)

or poor feeding and poorly gaining weight

193
Q

Patent ductus arteriosus (PDA)

A

Congenital heart defect

Acyanotic

Connection between pulmonary trunk and descendeing aorta

Common in premature babies

May close spontaneously

194
Q

Features of PDA (patent ductus arteriosus) and dx

A

Left subclavicular thrill (sometimes rough systolic murmur along the left sternal border)

Continuous machinery murmur

Large volume, bounding, collapsing pulse

Wide pulse pressure

Dx> echocardiogram

195
Q

Management of PDA (permanent ductus arteriosus)

A

Indomethacin/ibuprofen (NSAIDs) inhibits prostaglandin synthesis, closes the connection in the majority of cases

Remember ind/end= closes the duct

If associated with another congenital heart defect amendable to surgery then prostaglandin E1 is useful to keep the duct open until surgery.

196
Q

Tetralogy of Fallot presents typically at around…… months

A

1-2 months
The most common cause of cyanotic congenital heart disease.

However at birth, transposition of the great arteries is more common lesion as patients with TOF present symptoms later.

Can be picked up until the baby is 6 months old.

TOF is a result of anterior malalignment of the aorticopulmonary septum.

197
Q

Features of TOF (tetralogy of Fallot)

A

Cyanosis (the severity is determined by the right ventricular outflow tract obstruction)

Causes right to left shunt

Ejection systolic murmur due to pulmonary stenosis (VSD doesn’t usually cause a murmur)

A right sided aortic arch is seen in 25% of pxs

Chest X ray shows a boot-shaped heart

ECG shows right ventricular hypertrophy.

198
Q

Management of TOF

A

Surgical repair is often undertaken in 2 parts (shunt then surgical repair)

Cyanotic episodes may be helped by beta blockers to reduce infundibular spasm

199
Q

Familiar hypercholesterolemia genetics

A

Autosomal dominant

200
Q

When to suspect familiar hypercholesterolemia?

A

Cholesterol > 7.5 (normal <5mmol)

Family history of MI in 1st degree relative before the age of 60 or 2nd degree below 50

1st degree parents and siblings

2nd degree grandparents aunts and uncles

201
Q

While in a hospital, an elderly patient was found unresponsive, no pulse and no breathing. Management?

A

IN THIS ORDER!

Ring the emergency bell and call the resuscitation team

Start CPR 30:2

Get defibrillator

Commence ALS when resuscitation team arrives.

202
Q

Acute treatment of congestive heart failure with pulmonary oedema (desaturation, dyspnea, orthopnea, crepitations)

A
MONF
Morphine
Oxygen
Nitrates
Furosemide
203
Q

History of Rheumatic fever and pansystolic murmur at the apex

A

Mitral regurgitation

Secondary to rupture of papillary muscles or rheumatic fever

It leads to right sided heart failure (ascites, pulmonary oedema)

204
Q

Difference between mitral stenosis and mitral regurgitation?

A

Stenosis- Mid late dyastolic murmur, with opening click
At the apex (5th ICS MCL)
Symptoms of HF

Regurgitation- pansystolic murmur
At the apex (5th ICS MCL) radiates to the axilla

Symptoms of congestive HF (oedema, ascites)

205
Q

An elderly px presented a syncope, he is transferred to A&E and is now fully conscious. ECG shows irregular rhythm. What is the next BEST investigation?

A

Echocardiogram
Holter ECG is not beneficial as the ECG already shows irregular rhythm (no point in using it again)

Echo will identify the underlying cause of the irregular rhythm.

Aortic stenosis is the most common valvular heart disease that causes syncopal attacks.

If the syncope was during or shortly after exertion then Exercise ECG

This px likely has AF causing TIA (syncope+ irregular rhythm)

206
Q

Causes of AF

A

Endocardium- endocarditis, mitral valve disease

Myocardium- cardiomyopathy

Pericardium- Constrictive pericarditis

HF, HTN and MI

Hyperthyrroidism, excessive alcohol intake, chronic lung disease.

207
Q

What should be done prior prescribing amiodarone?

A

Request serum electrolytes and urea

It is a class III antiarrhythmic agent used in the tx of atrial, nodal and ventricular tachycardias. It blocks potassium channels which inhibit repolarisation and prolongs the action potential.

Thyroid and liver functions prior and every 6 months

ECG every 12 months

208
Q

Adverse effects of amiodarone

A

Thyroid disfunction (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 (usually given via central veins)

Bradycardia

Prolonged QT interval

209
Q

A px with history of alcholism presents with a racing heart. Management?

A

Reassurance

It is not serious or harmful and it is a common phenomenon in alcoholics.

210
Q

A px with history of TOF who underwent surgery in his childhood will present with what murmur decades later and why?

A

The corrected pulmonary stenosis can be complicated into PULMONARY REGURGITATION (diastolic murmur at the left upper sternal border)

211
Q

Young adult with history of asthma presents recurrent palpitations, light headedness and tachycardia and paroxysmal supraventricular tachycardia in the ECG. Management?

A

ADENOSINE IS CONTRAINDICATED IN ASTHMATICS!

Valsalva manoeuvre and carotid massage
Verapamil (CCB)
Cardioversion

212
Q

Digoxin toxicity features

A

GIT (most common)- nausea, vomiting and anorexia

Neurological- Hallucinations and confusion

Visual- Yellow green vision (yellow haloes) and blurred vision

Arrhythmias- bradycardia, V tach, premature contractions.

213
Q

Digoxin toxicity management

A

Order digoxin level

Digibind (DigiFab) = digoxin immune FAB

Correct arrhythmia

monitor K

214
Q

Aspirin toxicity features

A

Earliest symptoms include ringing ears (tinnitus) and impaired hearing

More clinically significant signs and symptoms include hyperventilation, vomiting, fever, dehydration, double vision and feeling faint.

215
Q

Common adverse effects of Thiazide like diuretics?

A

Postural hypotension

Hypokalemia and Hyponatremia

Gout (hyperuricemia)

Dehydration

impaired glucose tolerance

Impotence

Thiazide diuretics can cause hypercalcaemia and hypocalciuria

216
Q

Side effects of calcium channel blockers (CCB)

A

Ankle swelling
and
Gingival hyperplasia

Diltiazem, amlodipine, verapamil, nifedipine.

217
Q

Heart disease in alcoholics?

A

Ankle swelling and orthopnea

Alcoholic cardiomiopathy (enlarged on x ray) which causes AF

may cause flutter but AF is more common. (holiday heart syndrome= irregular heartbeat after bouts of acute bringe drinking)

Palpitations, dyspnea, dizziness, syncope, chest discomfort or pain, stroke or TIC, irregularly irregular pulse.

218
Q

Blood transfusion is indicated if…

A

Hb <80g/L + symptoms of anemia
OR
Hb < 70g/L + with or without symptoms of anemia

219
Q
Recurrent fainting episodes
\+
Prolonged QT intervals on ECG
\+
History of similar ECG during childhood
A

Congenital long QT syndrome

The most common arrhythmia associated is V tach

Risk of VF so some use long term beta blocker treatment