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AMC MCQ - You Can Do It!!!!!❤️❤️ > Cardiology by Dr. Cintia > Flashcards

Cardiology by Dr. Cintia Flashcards

1
Q

Pulmonary Embolism Clinical Features

A

Pleuritic Chest pain: Aggravated by cough and deep inspiration, worse with lying flat, relieved by sitting up.

Shortness Of Breath

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2
Q

Pulmonary Embolism
First Investigations (3)

A

Fist: Chest pain-ECG (S1Q3T3) Diagnostic

Second: SOB-CXR—> Rule out pulmonary pathology

Pregnancy (Doppler USD of legs)

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3
Q

Pulmonary Embolism
Best Investigations

A

Wells Score:

  • Low: D dimer
  • High: CTPA (Gold standard)
    V/Q (Pregnancy or ♀< 45 yo)
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4
Q

Wells Score for PE (7 criteria)

A

Clinical symptoms of DVT (leg swelling, pain with palpation) 3

Another diagnosis less likely than pulmonary embolism 3

Heart rate >100 1.5

Immobilization (≥3 days) or surgery in the previous four weeks 1.5

Previous DVT/PE 1.5

Hemoptysis 1

Malignancy 1

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5
Q

Wells Score Probability for PE

A

Wells criteria
High >6.0
Moderate 2.0 to 6.0
Low <2.0

Modified Wells criteria
PE likely >4.0
PE unlikely ≤4.0

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6
Q

PERC rule (8 criteria)

A
  1. Aged <50 years
  2. Pulse <100 bpm
  3. SaO ≥95%
  4. No haemoptysis
  5. No oestrogen use
  6. No surgery or trauma requiring hospitalisation within 4 weeks
  7. No prior venous thromboembolism
  8. No unilateral leg swelling

RESULT: IF ALL YES RULE OUT PE

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7
Q

Pulmonary Embolism
Management

A

ABCD/Oxygen/Morphine

Stable:
- LMWH.
- Renal disease –> Unfractionated

Unstable: Thrombolysis

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8
Q

Acute Pulmonary Oedema (APO) Clinical Features

A

Sudden-onset of SOB with tachypnea
Diaphoresis and cyanosis
Productive cough: pink or white frothy sputum
Crackles and Wheezes (Kettle boiling)

  • Hypotension: Cardiogenic shock
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9
Q

Acute Pulmonary Oedema (APO) Most common causes

A
  1. Acute Mitral and Aortic Regurgitation
  2. LV Systolic Dysfunction: anterolateral MI
  3. AF with rapid ventricular response
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10
Q

Acute Pulmonary Oedema (APO) Initial investigation

A
  1. CXR
  2. ECG
  3. Troponin
  4. FBE
  5. TTE
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11
Q

Acute Pulmonary Oedema (APO) Best investigation

A

Arterial/Venous Blood Gases to assess the severity of hypoxemia.

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12
Q

Acute Pulmonary Oedema (APO) Treatment

A
  1. O2
  2. IV line
  3. NGT spray or SL / IV is preferred to Morphine (BP > 100)
  4. Furosemide IV
  5. Morphine IV (chest pain)
  6. CPAP

APO + AF = BB
APO + AF + CHF = Digoxin inf

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13
Q

Infective Endocarditis Clinical Features

A

Fever (Most common)

New murmur (AI-most common)
NOT A CRITERIA FOR DIAGNOSE

Osler’s nodes (toes/fingers)

Petechiae including “nail bed
splinter hemorrhages”

Mitral and Aortic valves most frequently affected

Janeway lesions: Irregular painless erythematous macules on palms, soles, thenar and hypothenar eminence —> S. aureus!!!

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14
Q

Order of most common microorganisms that cause infective endocarditis

A
  1. Staphiloccocus Aureus
  2. Streptococci
  3. Enterococci (at least 90% faecalis)
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15
Q

Infective Endocarditis RISK FACTORS

A

 Artificial heart valves.

 Congenital heart defects.

 A history of endocarditis.

 Damaged heart valves: rheumatic fever

 History of intravenous (IV) illegal drug use.

 Immunocompromised patient.

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16
Q

Infective Endocarditis Diagnose

A

Modify Duke’s criteria:

DEFINITIVE Infectious Endocarditis:
2 Major Criteria
OR
1 Major + 3 Minor Criteria
OR
5 Minor Criteria

POSSIBLE Infectious Endocarditis:
1 Major Criteria + 1 Minor criteria
3 Minor Criteria

In POSSIBLE Management: Repeat TTE + TOE

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17
Q

Modify Duke’s Major criteria

A

TWO MAJOR CRITERIA

  1. Positive blood cultures for infective endocarditis:

Typical microorganisms for infective endocarditis: Coxiella burnetii, Viridans streptococci, Streptococcus bovis, and HACEK group

OR

Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus.

NOTE: 2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with the first and last drawn at least one hour apart

OR

  1. Evidence of endocardial involvement:

Positive echocardiogram for infective endocarditis

OR

Cardiac Vegetation

OR

Cardiac Abscess

OR

New partial dehiscence of prosthetic valve

OR

New valvular regurgitation

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18
Q

Modify Duke’s Minor criteria

A

FIVE MINOR CRITERIA

  1. Predisposing heart condition or intravenous drug user
  2. Fever: 38°C
  3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
  4. Immunologic phenomena:
    Glomerulonephritis
    Osler nodes
    Roth spots
    Rheumatoid factor (+)
  5. Microbiologic evidence: positive blood culture but not meeting major criterion as noted previously or
    echocardiography findings consistent with infective endocarditis but not meeting major criteria as noted previously
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19
Q

Infective Endocarditis Initial Investigations

A
  1. Blood culture: Diagnostic
  2. FBE: leucocytosis with neutrophilia and anemia.
  3. ECG: Cardiac monitoring
  4. CXR: Signs suggestive of heart failure.

NOTE: 2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with the first and last drawn at least one hour apart

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20
Q

Infective Endocarditis Best Investigations

A

Transesophageal echo (TOE)

BUT:
- If HACEK: CT angio

  • If arrhythmias: ECG
  • If spread: CT/MRI (brain, thorax, and abdomen)
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21
Q

HACEK group

A

Slow-growing, fastidious gram-negative organisms

  1. Haemophilus species: Aggregatibacter aphrophilus, H. Paraphrophilus.
  2. Aggregatibacter actinomycetemcomitans
  3. Cardiobacterium hominins
  4. Eikenella corrodens
  5. Kingella kingae
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22
Q

COMPLICATED Infective Endocarditis include

A

Large vegetation

Perivalvular abscess

Multiple emboli

Secondary septic events

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23
Q

Infective Endocarditis Empirical Treatment

A

Benzylpenicillin + Gentamicin + Flucloxacillin IV

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24
Q

Infective Endocarditis Staphylococcus Aureus Treatment

A

Methicillin-susceptible:
Flucloxacillin x 6 weeks

Methicillin-resistant (MRSA):
Vancomycin IV x 6 weeks

ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks

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25
Q

Infective Endocarditis Streptococcus ADULTS Treatment

A

UNCOMPLICATED:
Benzylpenicillin + Genta IV x 2 weeks
OR
Benzylpenicillin IV x 4 weeks
OR
Ceftriaxone IV x 4 weeks

COMPLICATED:
Add gentamicin IV x 2 weeks

ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks

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26
Q

PROSTHETIC valve Streptococcus endocarditis Treatment

A

Benzylpenicillin x 6 weeks

Complicated: Add gentamicin IV

ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks

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27
Q

Infective Endocarditis Streptococcus CHILDREN Treatment

A

Uncomplicated or complicated:

Benzylpenicillin x 4 weeks

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28
Q

Infective Endocarditis Enterococcal Treatment

A

Two-drug regimen:

Benzylpenicillin IV
OR
amoxicillin IV
OR
Ampicillin IV

PLUS Gentamacin IV x 4-6 weeks

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29
Q

Staphylococcus Aureus Infective Endocarditis in ABORIGINAL Patient Treatment

A

Benzylpenicillin IV (No ATB resistance)

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30
Q

CONSIDER vancomycin treatment in Infective Endocarditis for

A

MRSA

Hospital Acquired infection

Prosthetic valve

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31
Q

Infective Endocarditis Early Surgery Indications

A

 Prosthetic valve endocarditis (PVE)

 Native valve endocarditis (NVE) with heart failure: severe Ao or mitral insufficiency or stenosis with refractory pulmonary edema.

 Refractory ATB treatment in NVE.

 Management of persistent uncontrolled infections.

 Prevent embolism

 Fungal infection.

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32
Q

Infective Endocarditis Profilaxis Indications

A

 Prosthetic cardiac valve

 Previous infective endocarditis

 Congenital heart disease: Unrepaired Cyanotic - Acyanotic defects (VSD; Ao-Mi defect; TOF; PDA)

 Repaired congenital heart defect with prosthetic material/device <6 months after procedure.

 Cardiac Transplantation recipients who develop cardiac Valvulopathy.

 Rheumatic heart disease in indigenous Australians

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33
Q

Procedures that require Infective Endocarditis prophylaxis

A
  1. Dental procedures
  2. Invasive respiratory procedures with incision or biopsy of respiratory mucosa (including tonsillectomy and adenoidectomy)
  3. Incision and drainage (I&D) of local abscesses
  4. Surgery procedures through infected skin (cellulitis)

NOTE: Antibiotic cover for genito-urinary or gastrointestinal procedures is NOT recommended for prophylaxis of endocarditis

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34
Q

Infective Endocarditis Prophylaxis ATBs

A

 ORAL: Amoxycillin 2 g 1 hour before
OR
 IM: Amoxy/Ampi 2g 30 mins before
OR
 IV: Amoxy/Ampi 2g just before

 If allergic – clindamycin or vancomycin

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35
Q

Pericarditis Clinical Features

A

Chest pain+SOB+viral infection

Kussmaul sign.

S4 Gallop: Cardiac Tamponade

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36
Q

Pericarditis Duration: Chronic & Acute

A

Acute (<6w) Chronic (>6w).

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37
Q

Kussmaul sign phisical exam

A

Paradoxical: ↑ JVP with insp and ↓ JVP with exp)

Means: constrictive and/or cardiac tamponade.

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38
Q

Pericarditis Causes

A
  • Viral infection: Coxsackie B, CMV, influenza, EBV, COVID, HIV
  • After a major heart attack or heart surgery: Dressler syndrome.
  • Systemic inflammatory disorders: Lupus, rheumatoid arthritis.
  • Trauma
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39
Q

Pericarditis Complications

A

 Constrictive pericarditis.

 Cardiac tamponade

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40
Q

Pericarditis Initial Investigations

A
  1. ECG:
    - ST elevation except in AVR & V1
    - Reciprocal PR
  2. CXR:
    - Pericardial fluid
    - Pulmonary congestion
  3. Echocardiogram: Is diagnostic! Chest FAST scan should be done ASAP.
  4. Cardiac CT
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41
Q

Pericarditis Best Investigation

A

Echocardiogram with drainage and culture (Pericardiocentesis)

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42
Q

Pericarditis Medical Treatment

A

Mild to moderate Pericarditis

  1. AAS/Ibuprofen (7 to 10 days)
  2. Colchicine x 3 months. Indication: Recurrent symptoms (Side Effects: Diarrhea, abd pain)
  3. Prednisone

If infection: ATBs and drainage

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43
Q

Pericarditis Surgical Treatment

A

Severe Pericarditis, include admision

  1. Cardiac tamponade: Pericardiocentesis
  2. Severe, Recurrent or Constrictive:
    Pericardiectomy
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44
Q

Beck’s triad = Cardiac Tamponade

A

Low blood pressure (weak pulse or narrow pulse pressure)

Muffled heart sounds

Raised jugular venous pressure.

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45
Q

Pericarditis Physiopathology

A

Restrictive Cardiomyopathy

Diastolic Dysfunction with impaired filling – relaxation

Normal Ejection fraction + S4 gallop

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46
Q

Dressler’s Syndrome definition

A

Pericarditis in the context of major heart attack or heart surgery

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47
Q

Dressler’s Syndrome risk factors

A
  1. Young age
  2. B-negative blood type
  3. Prior history of pericarditis
  4. Prior treatment with prednisone
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48
Q

Dressler’s Syndrome investigations

A

Gold Standard: Echocardiogram

UNSTABLE patient: bedside ultrasonographic (E-FAST)

ECG: Same pattern as pericarditis (global ST segment elevation and T wave inversion)

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49
Q

Dressler’s Syndrome Treatment

A

1st LINE: NSAIDs in high doses (aspirin, ibuprofen, naproxen) tapered over 4 to 6 weeks.

2nd LINE: Corticosteroids (prednisone) tapered over a 4-week period

3rd LINE: Colchicine.

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50
Q

Dressler’s Syndrome COMPLICATION

A

Cariac Tamponade

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51
Q

Myocarditis Clinical Features

A
  • Chest pain
  • S3 Gallop (Systolic Disfuntion)
  • Dyspnoea
  • Viral infection
  • Fever
  • Arrhythmia
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52
Q

Myocarditis Infective Causes

A
  • Virus: Coxsackie, adenovirus, human herpes virus 6, Parvovirus B19, Epstein-Barr virus, COVID-19 HIV, hepatitis B and C.
    [pediatric eruptive and STDs virus]
  • Protozoa: Toxoplasmosis
  • Bacteria: Legionella, staphylococci, Salmonella, Shigella, streptococci, Clostridium, tuberculosis
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53
Q

Myocarditis Non-Infective Causes

A
  • ALCOHOL!!!! —> Reversed with abstinence
  • Collagen vascular diseases
  • Systemic diseases: Rheumatic Fever, sarcoidosis, giant cell arteritis
  • Cardiotoxic drugs: Clozapine
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54
Q

Myocarditis Investigation

A
  1. Urgent transthoracic
    echocardiogram (TTE)
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55
Q

Myocarditis Physiopathology

A

Dilated Cardiomyopathy

Impaired contractility with thin weak heart muscle - systolic dysfunction

Decreased Ejection Fraction + S3 gallop

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56
Q

Myocarditis Treatment

A
  1. Correct underlining cause (alcohol, infection)
  2. Same tratment that CHF
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57
Q

Mediastinitis Clinical Features

A

Dysphagia

Chest pain

Fever

Respiratory distress

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58
Q

Mediastinitis Causes

A
  1. Tracheal or esophageal rupture:
    - After an endoscopic procedure
    - Boerhaave syndrome
    - Foreign body aspiration
  2. Postoperative mediastinitis (thoracic surgery)
  3. Traumatic injury
  4. Spread of pulmonary infection
  5. Pancreatitis

NOTE: Descending necrotizing mediastinitis caused by neck abscess, Ludwig angina, or dental infections

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59
Q

Mediastinitis Investigations

A

First: CXR
Mediastinal widening or pneumomediastinum

Best: CT Torax, Mediastinal aspiration

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60
Q

Mediastinitis Treatment

A

In community:
- Empirical: Amoxi-Clav IV
- If septic shock: Cefazolin+Metro IV

In hospital:
- Piper+Tazo OR Cefepime+Metro

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61
Q

Stable Angina Diagnose

A

Chest pain < 20 min
Negative ECG
Negative troponin
Negative CK MB

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62
Q

Cardiac Enzymes Measurement in MI

A

1st line: Troponin I & T
- On arrival.
- If normal (< 0.02): Repeat in 6 - 8 h
- Return to normal in 5-14 days = No suitable for reinfarction diagnosis

2nd line: Total CK & CK-MB (if not troponins available)
- Raise in 4 h.
- Return to normal in 72 h = Usefull for reinfarction diagnosis

NOTE: Troponins can also be elevated in Chronic Renal Failure. Diferencial: CK-MB will be raised in MI but not in CRF

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63
Q

Stable Angina other investigations:

A
  • CXR: CHF sings. Exclude other causes (Ao dissection – lung path)
  • Bloods: FBE (anemia) – LFT (dyslipidemia) – RFT– BSL (DM) - Electrolytes
  • Echocardiogram
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64
Q

Stable Angina BEST Investigation:

A

Stress test will confirm the suspected diagnosis

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65
Q

Stable Angina ACUTE Treatment

A
  • Nitrates after 5 mins if pain persists (max. 3 doses) or Nifedipine 5 mg capsule (suck or chew)
  • Intolerant or contraindications for nitrates: Aspirin 150 mg oral
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66
Q

Nitrates Contraindications

A

Phosphodiesterase inhibitors (sildenafil, tadalafil) used in the past 1–5 days

Suspected right-sided/inferior myocardial infarction (hypotension, sweating, vomiting, and sinus brady)

Hypertrophic cardiomyopathy

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67
Q

Stable Angina LONG TERM Treatment

A

**Aspirin + statin + antiHT **meds (antianginal: BB – CCB + glyceryl
trinitrate)

1st line: BB
2nd line: CCB (Diltiazem, verapamil)

Glyceryl trinitrate
- Short-acting (spray): before exercise that is likely to induce angina
- Long-acting nitrate (transdermal): Recurrent angina.

 Tolerance to all forms of nitrate therapy develops rapidly, so allow a nitrate-free period.

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68
Q

Unstable Angina Clinical Features

A

Clinical Features:
1. Chest pain that has changed or >20 min

  1. ECG:
    - Low Risk: NORMAL
    - High Risk: ST Depression
  2. Troponin
    - Low Risk: Negative
    - High Risk: Positive
  3. CK MB: Negative
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69
Q

Unstable Angina Management

A
  1. Admission to coronary unit
  2. Oxygen 4–6 L/min (PaO2>90%)
  3. IV line
  4. Aspirin 150 - 300 mg
  5. Clopidogrel
  6. Enoxaparin (1 mg/kg) SC
  7. Glyceryl trinitrate (patch)
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70
Q

Worsening of Unstable Angina Management

A

Maximize dose of BB

Consider nifedipine or amlodipine

Consider IV nitrate infusion

If persistent pain (high risk)
- Abciximab (stronger antiplatelets)
- Transfer patient for Percutaneous coronary intervention (PCI)

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71
Q

Non-STEMI Clinical Features:

A
  1. Chest pain that has changed or >20 min
  2. ECG: ST Depression
  3. Troponin: Positive
  4. CK MB: Positive
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72
Q

Non-STEMI Management

A
  1. Admission to coronary unit
  2. Oxygen 4–6 L/min (PaO2>90%)
  3. IV line
  4. Glyceryl trinitrate
  5. Aspirin 150 - 300 mg
  6. Clopidogrel
  7. Enoxaparin (1 mg/kg) SC or UF Heparin IV 5000 IU bolus followed by infusion 1000 IU/h

Add if necessary: Morphine

Continuous monitoring with ECG and cardiac enzymes

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73
Q

STEMI Clinical Features

A

Extreme chest pain
ECG: ST Elevation
Troponin: Very high
CK MB: Positive

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74
Q

Acute STEMI Management

A
  1. PCI (Gold Standard)
    - Optimal: Within 60 minutes of symptom onset.
    - Acceptable: 90 min.
  2. Thrombolysis: Within 30
    minutes of arrival (most common reteplase, alteplase or tenecteplase)
  • Streptokinase: Inappropriate for use in Indigenous patients and those who have received it on a previous occasion (RESISTANCE due to high levels of anti-streptokinase IgG level)
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75
Q

Thrombolysis Side Effects

A
  1. Bleeding
  2. Hypotension
  3. Reperfusion arrhythmias
  4. Allergic reactions
  5. Angioedema
  6. Anaphylactic shock

NOTE: Streptokinase is most frequently complicated by allergic reactions and hypotension

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76
Q

Absolute Contraindications for Thrombolytic Treatment (9)

A
  1. Active Bleeding or bleeding diathesis (excluding menses)
  2. Suspected aortic dissection
  3. Significant closed head or facial trauma within 3 months
  4. Any prior intracranial hemorrhage
  5. Ischaemic stroke within 3 months
  6. Known cerebral vascular lesion
  7. Known malignant intracranial neoplasm
  8. Recent Intracranial or spinal surgery

NOTE: For streptokinase, previous treatment within six months and ASTI people

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77
Q

Relative Contraindications for Thrombolytic Treatment

A
  1. Current anticoagulants (including novel anticoagulant agents)
  2. Non-compressible vascular puncture
  3. Recent major surgery (<3 weeks)
  4. Traumatic or prolonged (>10 minutes) CPR
  5. Recent internal bleeding (within 4 weeks) / Active Peptic Ulcer
  6. Suspected Pericarditis
  7. Advanced Liver Disease / Advanced
  8. Metastatic Cancer
  9. History of chronic, severe, poorly controlled hypertension
  10. Severe uncontrolled hypertension on this presentation (Systolic >180 / Diastolic > 110 mmHg)
  11. Ischaemic Stroke > 3months ago
  12. Dementia
  13. Pregnancy or within 1 week postpartum
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78
Q

POST MI Treatment

A
  1. BB (within 12 h)
  2. ACE inhibitors (within 24 h)
  3. Dual antiplatelet therapy: Aspirin 75 - 150 mg + Ticagrelor (Clopidogrel or Prasugrel x 12 m)
  4. Statins
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79
Q

Heart Failure: 3 more important causes

A

Hypertension

Heart valve disease: rheumatic heart disease

Cardiac arrhythmias

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80
Q

Heart Failure Classification by Left Ventricle Ejection Fraction (LVEF)

A

LVEF < 40%: Heart failure with REDUCED EF.

LVEF = 50%: Heart failure with PRESERVED EF

NOTE: The CHF management depends on EF.

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81
Q

Heart Failure First Investigations

A
  1. CXR
  2. ECG
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82
Q

Heart Failure Best Investigation

A

Echocardiogram

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83
Q

Heart Failure Treatment

A
  • Class II (EF 40-50): Mild Symptoms
    on activity. Ace Inhs/ARB + BB, On/Off Diuretics (Furosemide)
  • Class III (EF<40): Severe symptoms
    on activity but comfortable at rest: Add Spironolactone
  • Class IV (EF<35): Severe symptoms
    on activity and at rest: Add Digoxin or Entresto (stop ACE inh/ARB)
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84
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) or Idiopathic Hypertrophic Subaortic Stenosis DEFINITION

A

Left ventricular outflow tract obstruction (LVOTO) due to hypertrophied ventricular septum

It is the most common genetically transmitted cardiomyopathy (Autosomal Dominant)

DIASTOLIC DYSFUNCTION

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85
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) Clinical Features

A
  • Family history
  • Young athlete with syncope during exercise
  • Midsystolic murmur that increases
    with Valsalva
  • Dyspnea, syncope, angina, palpitations, or dizziness

NOTE: Same findings that Ao stenosis  Murmur differences: no radiation & exacerbation with Valsalva maneuver

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86
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) Differential Diagnosis

A

Prolong QT syndrome (AD)

Dx with ECG – also VT

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87
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) Initial Management

A
  1. Admit to Cardiology
  2. ECG: Dagger Q waves in left leads
  3. CXR: CHF findings
  4. Echocardiogram (THE MOST IMPORTANT BUT NOT THE GOLD STANDARD)
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88
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) Best Investigation

A

Cardiac MRI (Gold Standard)

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89
Q

HCOM Management

A
  1. Referral:
    - Genetic counseling, then genetic testing
    - Cardiologist
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90
Q

HCOM Screening

A

IF POSITIVE FAMILY HISTORY: Echocardiogram

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91
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) Medical treatment

A

Symptomatic:
1st line: BB
2nd line: CCB

Contraindicated: Nitrates and ACE inhibitors (↓ preload)

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92
Q

Hypertrophic Obstructive Cardiomyopathy (HCOM) surgical treatment

A

Septal myectomy: Only in young patients very symptomatic even with medical treatment.

IF Ventricular Tachy: Implantable cardioverter-defibrillator (ICD)

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93
Q

Takotsubo Cardiomyopathy Definition

A

Transient regional systolic dysfunction of the left ventricle in the absence of angiographically significant coronary artery disease

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94
Q

Other names for Takotsubo Cardiomyopathy

A
  • Stress cardiomyopathy
  • Gebrochenes-Herz syndrome
95
Q

Takotsubo Cardiomyopathy Clinical features

A

Presentation: similar to acute coronary syndrome.

96
Q

Takotsubo Cardiomyopathy ECG:

A

STEMI or pericarditis pattern.

97
Q

Takotsubo Cardiomyopathy Troponins:

A

Modest elevation. No correlation with the ECG findings

98
Q

Takotsubo Cardiomyopathy Cause

A

Sympathetic overdrive with increased catecholamines

99
Q

Takotsubo Cardiomyopathy Risk factors

A
  • Post-menopausal women
  • Pregnancy
  • Recent stressful event

NOTE: If occur in man, very bad prognosis

100
Q

Takotsubo Cardiomyopathy Initial Investigation (2)

A
  1. ECG
  2. TTE is diagnostic w/ confirmation (EF 35-40%)
101
Q

Takotsubo Cardiomyopathy Best Investigation

A

Cardiac MRI

102
Q

Blood pressure measurement. Sphygmomanometer CUFF’S sizes: Width

A

At least 40% of the arm circumferencese (Murtagh)

Cover 2/3 of the arm, not more! (AMC)

NOTE: Cuffs that are too wide underestimate the BP (lower), cuffs that are too narrow overestimate it (higher) - AMC

103
Q

Blood pressure measurement. Sphygmomanometer CUFF’S sizes: Length

A

At least double the arm circumference (Murtagh)

Bladder length should not completely encircle the limb, but only 80% (AMC)

Bladder width is half the length of the bladder (AMC)

104
Q

Blood Pressure Ambulatory 24-hour monitoring INDICATIONS

A
  1. Unusual variability of office BP
  2. Marked discrepancy between office and home BP
  3. Resistance to drug treatment
  4. Suspected sleep apnoea
  5. Borderline levels
105
Q

Phisical Exam in Hypertension to rule out renal stenosis

A

The low-pitched bruits of kidney artery stenosis are best heard by placing the diaphragm of the stethoscope firmly in the epigastric area.

106
Q

Hypertension Diagnosis

A

At least 2 follow-up measurements with average:

Systolic: >140 mmHg
or
Diastolic: >90 mmHg

107
Q

Hypertension General Clasification

A
  • Essential (90–95%)
  • Secondary (approx. 5–10%)
    *Renovascular <3%

*Endocrine: 0.3–1%

*Other:
- Coarctation of the aorta
- Immune disorder (polyarteritis nodosa)
- Drugs
- Pregnancy

108
Q

Renovascular Hypertension causes

A
  • glomerulonephritis
  • reflux nephropathy
  • kidney artery stenosis
109
Q

Secondary Hypertension: Metabolic causes

A
  • Primary aldosteronism (Conn’s syndrome)
  • Cushing syndrome
  • Phaeochromocytoma
110
Q

Medication associated with Hypertension

A

 Oral and depot contraceptives

 Hormone replacement therapy (HRT)

 Steroids

 NSAIDs- Cox2 inhibitors

 Cold remedies

 Diet pills: sibutramine

 Amphetamines

 Ergotamine

 Cyclosporine

 St. Jhons Wort’s

111
Q

Refractory/resistent Hypertension

A

BP > 140/90 mmHg after maximum doses of 2 drugs for 3-4months

112
Q

Hypertension + Abdominal systolic bruit

A

Renal artery stenosis

113
Q

Hypertension + Proteinuria, haematuria, casts

A

Glomerulonephritis

114
Q

Hypertension + Bilateral kidney masses with or without haematuria

A

Polycystic disease

115
Q

Hypertension + History of claudication and delayed femoral pulse

A

Coarctation of the aorta

116
Q

Hypertension + Progressive nocturia, weakness

A

Primary aldosteronism (check serum potassium)

117
Q

Hypertension + Obesity, snoring, daytime sleepiness

A

Sleep apnoea

118
Q

Hypertension + Paroxysmal hypertension with headache, pallor, sweating, palpitations

A

Phaeochromocytoma

119
Q

Most common long-term drug use disease

A

Hypertension

120
Q

Most common complications of Hypertension (5)

A
  1. CV disease (stroke)
  2. CHD, LVH, AF.
  3. Renal disease: Focal segmental glomerulosclerosis (FSGE)
  4. HT Retinopathy.
  5. Peripheral vascular disease (Aortic aneurism/dissection)
121
Q

Main causes of Death associated to Hypertension

A

Stroke (45%)

122
Q

Hypertension Value Clasification by Murtagh NORMAL

A

< 130/85 mmHg

Follow Up: 2 years

123
Q

Hypertension Value Clasification by Murtagh OPTIMAL

A

< 120/80 mmHg
Follow Up: 2 years

124
Q

Hypertension Value Clasification by Murtagh HIGH NORMAL

A

< 140/90 mmHg

Follow Up: 1year

125
Q

Hypertension Value Clasification by Murtagh G1 MILD

A

< 160/100 mmHg

Follow Up: 2 months

126
Q

Hypertension Value Clasification by Murtagh G2 MODERATE

A

< 180/110 mmHg

Follow Up: 1 month

127
Q

Hypertension Value Clasification by Murtagh G3 SEVERE

A

> 180/110 mmHg

Follow Uo: 1-7 days

128
Q

Hypertension Value Clasification by Murtagh ISOLATED SYSTOLIC

A

> 140 / <90 mmHg

Follow Up: 1 month

129
Q

Absolute Cardiovascular Risk Assessment Variables (7)

A

Performed every 2 yrs from 45 yrs and 30 yrs for ATSI people.

Assess:
1. Age
2. Sex
3. Smoking status
4. Total and HDL cholesterol
5. Systolic Blood Pressure
6. DM
7. Left ventricular hypertrophy

130
Q

Risk of a cardiovascular event over the next 5 years: Low, moderate and High values

A

Low <10% (green)
Follow-Up 6-12 months

Moderate 10-15% (blue)
Follow Up: 3months

High >15% (yellow & red) Indication for medical treatment

131
Q

LOW CV Risk (10%) Hypertension Management

A
132
Q

MODERATE CV Risk (10-15%) Hypertension Management

A
133
Q

HIGH CV Risk (>15%) Hypertension Management

A

Mantain life-style modification

Start medical treatment immediately

134
Q

Hypertension Non-pharmacological
management (7)

A
  1. Weight reduction
  2. Reduction of excessive alcohol intake
  3. Reduction of sodium intake to ≤4 g/day
  4. Increased exercise and regular physical activity
  5. Reduction of psycologic stress
  6. Smoking sesation
  7. Management of sleep apnoea
135
Q

Hypertension Referral Criteria (5)

A
  1. Refractory HT
  2. HT emergency - urgency
  3. Ongoing target organ impairment
  4. Kidney failure= GFR< 60ml/min
  5. If a secondary treatable cause is found
136
Q

BP Treatment Targets

A
137
Q

Circle of Love (image)

A
138
Q

Ineffective Antihypertensives Combinations

A

Diuretic and calcium-channel blocker

Beta blockers and ACE inhibitors

139
Q

1st Line Antihypertensive Drugs by J Murtagh

A
140
Q

Starting Hypertensive Treatment (Murtagh)

A
141
Q

Antihypertensive medication in Old and Young Patients

A

Older: Diuretics, calcium-channel blockers and ACE inhibitors.

Younger: Beta blockers or ACE inhibitors.

142
Q

Hypertension Drug Teraphy in the elderly

A

First-line: Indapamide (preferred) or thiazide diuretic (low dose)

  • Check electrolytes in 2–4 weeks: if hypokalaemia develops, add a K-sparing diuretic rather than K supplements.

Second-line choice: ACE inhibitors (or ARB) especially with heart failure.

143
Q

Hypertension Treatment
>65yo with CHF

A

Thiazides

144
Q

Hypertension Treatment
>65yo with Ischaemia risk

A

BetaBlockers

145
Q

Hypertension Treatment - Young with CHF

A

ACE inhibitors

146
Q

Hypertension Treatment Young with Ischaemia risk

A

Amlodipine
(Never Verapamil or Diltiazem)

147
Q

Hypertension Treatment
in Asthma

A

CCB

148
Q

Hypertension Treatment in DM

A

1st Line: ACEi / ARBs

2nd Line: CCB

(doesn’t affect insulin + Reno protective effect)

NOTE: Diuretics aggravate glucose intolerance so use with care.

149
Q

Hypertension Treatment in Psychiatric patients

A

Diuretics (least central activity)

150
Q

Hypertensive Urgency Treatment

A

> 180/110 mmHg

ORAL:
Nifedipine
Captopril
Clonidine

IV: Hydralazine

151
Q

Hypertensive Emergency Treatment (4)

A

> 220/140 mmHg
Hydralazine
Metoprolol
Nitroprusside
Esmolol

All IV

152
Q

HYPERTENSIVE ENCEPHALOPATHY Clinical Features

A

Acute and malignant hypertensive crisis.
BP > 200/140 mmHg

Severe headache
Confusion
Vomiting
Blurred vision

May develop later:
- Focal neurological signs
- Seizures
- Coma

Fundoscopy: retinal haemorrhages, exudates and papilloedema. (grade IV changes)

153
Q

HYPERTENSIVE ENCEPHALOPATHY Investigations

A
  1. ECG
  2. CXR
  3. Midstream specimen of urine (MSU/dipstick) and urinalysis. Evidence of renal disease: Casts, abnormal urinary red blood cells (greater than 70% dysmorphic).
154
Q

HYPERTENSIVE ENCEPHALOPATHY Management

A

Aim for oxygen of 94%.

Initially reduce arterial pressure gradually by 25% in the 1st hour or aim for a diastolic BP of 100 -110 within the first 24 hours.

Same drugs as Hypertensive emergency:

1st line: Hydralazine
2nd line: Nitroprusside
Also: Metoprolol, Esmolol

REVIEW THIS FLASH CARD INFO

155
Q

Antihypertensive Drugs List

A
  1. Diuretics
  2. Angiotensin converting enzime (ACE) inhibitors
  3. Angiotensine II Receptors Blockers (ARBs)
  4. Beta Blockers (BB)
  5. Calcium Channel Blockers (CCB)
156
Q

ACE inhibitors LIST

A
  1. Captopril: Short half life (emergency use)
  2. Enalapril
  3. Lisinopril
  4. Ramipril

The other two longer half life: Daily use

157
Q

ARBs LIST

A

Valsartan (more pontent 1 tablet/day)
Losartan
Candesartan

Rest lest potent 2 tablets/day

158
Q

ACE inhibitors MECHANISM OF ACTION (MOA)

A

ACE Inh: Prevent the conversion of angiotensin I to angiotensin II

↓ ANGIOTENSIN II =

  1. ↓ Vasoconstriction =
    - ↓Periferal Resistance
    - EFFERENT renal
    artery vasodilation

2↓Aldosterone = Natriuresis

ARBs Blocks the angiotensin II receptors so same MOA

159
Q

ACE inhibitors & ARBs Indications

A
  1. hypertension
  2. heart failure
  3. peripheral vascular disease
  4. diabetes
  5. cardioprotective after miocardial infarction

NOTE: ACE Inhibitors are always 1st line

160
Q

ACE inhibitors & ARBs Contraindications

A

1.Bilateral kidney artery stenosis (precaution in chronic kidney disease)

  1. Hyperkalemia (avoid potassium sparing diuretics combination). Can lead to Metabolic Acidosis
  2. Pregnancy
161
Q

ACE inhibitors side effects (6)

A
  1. Cough (↑Bradikinins)
  2. Angioedema (↑Bradikinins)
  3. Disturbance in taste (dysgeusia)
  4. Rash (↑Bradikinins)
  5. HYPERkalemia (↓ Aldosterone = ↓ K excretion)
  6. Hypotension (just the first dose)
162
Q

Antihypertensive Drugs: Diuretict types LIST

A
  1. Loop
  2. Thiazides & thiazides like
  3. Potasium sparing
  4. Osmotic
  5. Carbonic Anhidrase Inhibitors
163
Q

Loop Diuretic Mechanism of Action

A
  1. Inhibition of sodium and chloride reabsorption in the
    thick ascending limb of the loop of Henle by blocking the Na+-K+-2Cl- symporter (cotransporter)
  2. Stimulates the release of protaglandins = Vasodilatation of the AFFETENT artery = ↑ GFR

NOTE: NSAIDs Inihbit prostaglandins synthesis = ↓ GFR (AFFERENT artery vasoconstriction)

164
Q

Loop Diuretic LIST

A

Sulfonamide derivatives:
1. Furosemide
2. Bumetanide
3. Torsemide

Non- Sulfonamide derivatives:
4. Ethacrynic acid

165
Q

Loop Diuretic INDICATIONS

A
  1. Edematous states: CHF, APO, cirrhosis with ascites, nephrotic syndrome
  2. Hypertension
  3. Hyperkalemia
  4. Hypercalcemia
  5. Acute bromide, iodine and fluoride intoxication
166
Q

Loop Diuretic CONTRAINDICATIONS

A

Sulfonamide allergy

Alternative: Use Ethacrynic acid

167
Q

Loop Diuretic SIDE EFFECTS

A

HYPOS:
Kalemia
Natremia
Calcemia
Mangesemia
Cloremia

HYPER: Uricemia

168
Q

Loop Diuretic COMPLICATIONS

A
  1. Here’s a simplified and concise explanation of the points you provided:
  2. Dehydration and Gout: Dehydration can increase uric acid levels in the blood, leading to gout, a type of arthritis characterized by sudden, severe joint pain.
  3. Hypokalemic Metabolic Alkalosis: This condition involves an increase in blood pH and bicarbonate (HCO3), along with low levels of potassium (K), sodium (Na), and magnesium (Mg).
  4. Ototoxicity: Some drugs can cause hearing loss, which is usually reversible if the drug is stopped. Ethacrynic acid is the most common culprit.
  5. Sulfonamide Allergy:
    • Acute Interstitial Nephritis: An allergic reaction in the kidneys.
    • Stevens-Johnson Syndrome (SJS) or Toxic Epidermal Necrolysis (TEN): Severe skin reactions that can be life-threatening.

These points summarize the key side effects and complications in a straightforward manner.

Dehydration: This can lead to hyperuricemia/gout

  1. Hypokalemic Meabolic Alcalosis:
    ↑pH ↑HCO3 ↓K ↓Na ↓Mg
  2. Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid.
  3. Sulfonamide Allergy:
    - Acute interstitial nephritis
    - Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
  4. Dehydration: This can lead to hyperuricemia/gout
  5. Hypokalemic Meabolic Alcalosis:
    ↑pH ↑HCO3 ↓K ↓Na ↓Mg
  6. Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid.
  7. Sulfonamide Allergy:
    - Acute interstitial nephritis
    - Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
  8. Dehydration: This can lead to hyperuricemia/gout
  9. Hypokalemic Meabolic Alcalosis:
    ↑pH ↑HCO3 ↓K ↓Na ↓Mg
  10. Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid.
  11. Sulfonamide Allergy:
    - Acute interstitial nephritis
    - Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
169
Q

Thiazides & thiazides like Mechanism of Action

A
  1. lnhibition of sodium (Na+) and chloride (CI-) reabsorption from the distal convoluted tubules by blocking the thiazide-sensitive Na+-Cl- symporter (cotransporter)
    * ↑ the Na+, CI-, K+ elimination
    * ↑ Ca+ reabsortion
  2. It is secreted in the proximal tubule where it competes with the excretion of uric acid.
    * ↑ the serum uric acid

NOTE: Less pontent than loops diuretics but longer lasting

170
Q

Thiazides & thiazides like LIST

A

Benzothiadazine derivatives: Thiazides

  1. Clorothiazide
  2. Hydroclorothiazide

Sulfonamide derivative:

  1. Indapamide
  2. Chlortalidone
171
Q

Thiazides & thiazides like INDICATIONS

A
  1. Hypertension (1st LINE Diuretic)
  2. Heart failure
  3. Older patients (>55 yo)
  4. Hypercalciuria: Prevent Ca neprholithiasis and ostheoporosis
  5. Nephrogenic Diabetes Insipidus: Paradoxical effect given by mild hypovolemia caused by the thiazide stimulates the kidney to reabsorb Na and water
172
Q

Thiazides & thiazides like SIDE EFFECTS

A

HYPERS:
Uricemia
Glycaemia
Lipidaemia (increase cholesterol and triglycerides)

HIPOS
Kalemia
Natraemia
Magnesemia

  • Impotence
173
Q

Thiazides & thiazides like CONTRAINDICATIONS

A
  1. Type 2 diabetes
  2. Hyperuricaemia
  3. Kidney failure
  4. Dyslipidaemia
  5. Pregnancy
  6. Sulfonamide allergy: Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
174
Q

Potassium-sparing Diuretic
MECHANISM OF ACTION

A

Direct and indirect ANTAGONIST OF ALDOSTERONE

Indirect: Epithelial sodium channel blockers in the distal tubule and collecting duct

↑ Na+ and water extretion
↓ H+ and K+ excretion

175
Q

Potassium-sparing Diuretics LIST

A

Direct antagonist:
1. Spironolactone

Indirect atagonist:
2. Amiloride
3. Triamterene

176
Q

Potassium-sparing Diuretics INDICATIONS

A
  1. Hypertension
  2. Edemaous states: CHF, APO, cirrhosis with ascites, nephrotic syndrome
  3. After Mopcardial infraction: (↓ mortality rate)
  4. Hyperaldosteronism
  5. PCOS: Bunts effects of testosterone
  6. Liddle’s Syndrome (Na retention and K wasting)
177
Q

Potassium-sparing Diuretics SIDE EFFECTS

A
  1. HYPERkalemia
    AVOID: Combination with ACE Inh/ARBs/K suplements. Risk of Metabolic Acidosis
  2. Spironolactone: Antiandrogenic effect
    - Gynecomastia
    - Impotence
  3. Triamterene:
    - Nephrolithiasis
    - Combination con Indapamide (NSAID) = AKI
178
Q

Osmothic Diuretic: Manitol
Features

A

Aquaretic Diuretic: Mainly excretion of water without electrolites

Only presentation IV

179
Q

Osmothic Diuretic: Manitol
INDICATIONS

A
  1. Head trauma: ↓ ICP
  2. Rabdomyolisis: Kidney flush out (prevent AKI)
  3. Hemolysis: Kidney flush out (prevent AKI)
  4. Glaucoma or Ophtamologic surgery: ↓ Ocular pressure
180
Q

Osmothic Diuretic: Manitol
SIDE EFFECTS

A

Rebound effect
1. Worsen edamtous states (pulmonary edema)

  1. In CHF and Renal Faillure: HYPOnatremia

NOTE: If inadequate water replacement = Dehydration with HYPERnatremia and HYPERkalemia

181
Q

Diuretic: Carbonic Anhidrase Inhibitors (Zolamides) MECHANHISM OF ACTION

A

Inhibition of the resorption of HCO3 by the proximal tubular cells = ↑ N+ and Water excresion for differentiation of pH gradients between blood (>acid) and urine (> alkaline)

Sulfonamide derivative

NOTE: Weaker than other diuretics

182
Q

Carbonic Anhidrase Inhibitors (Zolamides) LIST

A

ORAL
Methazolamide

ORAL & IV
Acetazolamide

TOPICAL (eye drops)
Dorsolamide
Brinzolamide

183
Q

Carbonic Anhidrase Inhibitors (Zolamides) INDICATIONS

A
  1. Elevated intraocular pressure (angle-closure and open-angle glaucoma)
  2. Brain Pseudotumor
  3. Edema due to congestive heart failure (with alkalosis)
  4. Altitude sickness prophylaxis
184
Q

Carbonic Anhidrase Inhibitors (Zolamides) COTRAINDICATIONS

A

Sulfonamide allergy

Hepatic disease

Adrenal insufficiency

Renal Faillure

185
Q

Carbonic Anhidrase Inhibitors (Zolamides) SIDE EFFECTS

A

Metabolic acidosis with HYPERcloremia

HYPOkalemia

Calcium oxalate kidney stones

Risk of Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)

Aplastic anemia

Agranulocytosis

Fulminan hepatic Necrosis

Carbonic anhydrase inhibitors like acetazolamide (a type of “zolamide”) can cause several side effects. Here’s a simplified list:

  1. Tingling sensations: You might feel tingling in your fingers, toes, or face.
  2. Taste changes: Foods and drinks might taste different, often with a metallic taste.
  3. Increased urination: You’ll likely need to urinate more often, which can lead to dehydration if you’re not careful.
  4. Fatigue: You might feel unusually tired or weak.
  5. Stomach upset: Nausea or stomach pain can occur.
  6. Electrolyte imbalances: You could lose important salts (like potassium) in your body, leading to muscle cramps or irregular heartbeats.
  7. Kidney stones: There’s a risk of developing kidney stones, especially if you’re not drinking enough water.

These side effects vary in intensity from person to person, but they are generally manageable.

186
Q

Antihypertensive drugs: BETA BLOCKERS - Mechanism of action

A

ADRENEGIC ANTAGONISTS

  1. Chronotropic and inotropic heart effects
  2. Reduction in renin release.
  3. Reduce sympathetic activity

Receptors main locations:
- β1 Adrenergic: Heart

  • β2 Adrenergic: Lungs, gastrointestinal tract, liver, vascular smooth muscle (vasodilatation), and skeletal muscle
  • α1: vascular smooth muscle (vasoconstriction)

NOTE: NSAIDs may interfere with the hypotensive effect of beta blockers.

187
Q

BETA BLOCKERS - General Indications

A
  1. Hypertension
  2. > 55yo + Coronary artery disease (CAD)
  3. Cardiac arrhythmia
  4. Tachycardia secondary to thyroid storm and anxiety episodes
  5. Essential tremor
  6. Glaucoma
188
Q

BETA BLOCKERS - General Side effects

A

ALL BB:

  1. Orthostatic hypotension (take care of the elderly and differentiate from hypoglycemia)
  2. Bradycardia (AVOID concomitant use with Verapamil / Diltiazem)
  3. Sudden STOP can cause:
    - Arrhythmias
    - Rest angina
189
Q

1st generation BETA BLOCKERS - Side effects

A

B2 Block (1st generation)

  1. Bronchoconstriction
  2. Hypertrigliceridemia
  3. Hypoglycemia
  4. Muscular fatigue, insomnia
190
Q

3rd generation BETA BLOCKERS - Side effects

A

α1 Block (3rd generation)

  1. Headache
  2. Nasal congestion
  3. Delay ejaculation
191
Q

BETA BLOCKERS - General Contraindications

A

ALL:
- Bradycardia, heart block
- Orthostatic hypotension

192
Q

BETA BLOCKERS - 1st Generation - Contraindications

A
  • Asthma, COPD
  • Dyslipidaemia
  • DM
  • Heart failure
  • Peripheral vascular disease
  • Pregnancy
193
Q

BETA BLOCKERS - 2nd Generation -Contraindications

A
  • Heart failure
  • Peripheral vascular disease
  • Pregnancy
194
Q

BETA BLOCKERS - 3rd Generation - Contraindications

A
  • Migraine
  • Chronic rhinitis
  • Delay ejaculation
195
Q

BETA BLOCKERS - 1st Generation

A

NON-SELECTIVES

β1 - β2 BLOCKERS

  1. Propanolol:
    - Cross the blood brain barrier → Treatment of MIGRAINE (vasocontriction in the brain) & Essential tremmor
  2. Timolol: ↓ Ocular pressure → Treatment of glaucoma
  3. Sotalol
196
Q

BETA BLOCKERS - 2nd Generation

A

CARDIOSELECTIVE

Only β1 block

  1. Atenolol
  2. Metoprolol
  3. Bisoprolol
  4. Pindolol
  5. Esmolol

No side effect of B2 Block: So, safe in asthma, COPD, dyslipidemia and DM

197
Q

BETA BLOCKERS - 3rd Generation

A

β1 - α1 BLOCKERS

  1. Labetalol: Pregnancy and hypertensive emergency
  2. Carvedilol: Only BB that can be used with CHF

Only BBs that can be used for periferal vascular disease and precoz eyaculation

No side effect of B2 Block: So, safe in asthma, COPD, dyslipidemia and DM

198
Q

Antihypertensive drugs: Calcium Channel Blockers - Mechanism of Action

A
  1. Negative inotropic and chronotropic heart effect
  2. Vasodilation
  3. Relaxation of smooth muscle in the bronchi
199
Q

Calcium Channel Blockers - Dihydropirimidines Main effect

A

Vasodilator (including coronary arteries)

200
Q

Calcium Channel Blockers - Dihydropirimidines LIST

A
  • Nifedipine
  • Amlodipine
  • Nicardipine
201
Q

Calcium Channel Blockers - Dihydropirimidines INDICATIONS

A
  • Hypertension
  • Asthma
  • Stable Angina
  • Peripheral vascular disease
  • Reynaud’s Phenomenon
202
Q

Calcium Channel Blockers - Dihydropirimidines SIDE EFFECTS

A

Reflex tachycardia (↑doses)

Flushing

Dizziness

Peripheral edema

Gingival hyperplasia

203
Q

Calcium Channel Blockers - NON-Dihydropirimidines Features, Indication, Side effect

A

Features: Main effect in the heart < vasodilator

204
Q

Calcium Channel Blockers - NON-Dihydropirimidines Indications

A
  • Verapamil: Cardioselective / Class 4 Antiarrhythmic
  • Diltiazem: Hypertension
205
Q

Calcium Channel Blockers - NON-Dihydropirimidines Side Effects

A
  • Hyperprolactinemia
  • Verapamil: Constipation
206
Q

Calcium Channel Blockers - CONTRAINDICATIONS

A
  1. Heart block 2nd and 3rd degree
  2. Heart failure (verapamil, diltiazem)
207
Q

CCB: Caution using with

A

Beta blockers

Digoxin

Cardiac Faillure

208
Q

Innocent Murmurs Characteristics

A
  • Murmur, varies with posture & inspiration.
  • Soft, SYSTOLIC murmur with:

◦ Normal 2nd heart sound.

◦ Separate, audible heart sounds.

NOTE: At least 50% of school-age children.

209
Q

Pathological Murmurs History

A

◦ Family Hx of cardio-myopathy or sudden unexplained death.

◦ Congenital malformations

◦ Exertional syncope

◦ Symptoms of cardiac failure.

210
Q

Pathological Murmurs Clinical Features

A

◦ Cyanosis - Breathlessness.

◦ Failure to thrive, not clearly due to other causes.

◦ Thrill with murmur.

211
Q

Pathological Murmurs Characteristics

A

◦ Continuous murmur, no postural variation.

◦ Diastolic murmur or Pan-systolic murmur.

◦ Loud & harsh murmur

◦ Heard best at Left Sternal Border (LSB)

◦ Can have early or mid-systolic click.

212
Q

Holosystolic Murmurs List

A

◦ Mitral valve regurgitation

◦ Tricuspid valve regurgitation

◦ Ventricular septal defec

213
Q

Early Systolic Murmurs List

A

◦ Mitral regurgitation

◦ Tricuspid Regurgitation

IMMEDIATE REFERRAL IS REQUIRED!!

214
Q

Diastolic Murmurs List

A

Always indicate heart disease!!

  • Aortic Regurgitation
  • Mitral Stenosis
215
Q

Continuous Murmurs List

A

◦ Patent Ductus Arteriosus – Paeds
Has a harsh, machinery-like quality (Gibson murmur)

◦ Pericardial friction rub: Pericarditis or pericardial effusion. Not a real murmur. Has scratchy, scraping quality

216
Q

Aortic Stenosis Causes

A

Degenerative calcific aortic stenosis
Rheumatic heart disease

Systemic lupus erythematosus (SLE)
Paget disease

217
Q

Aortic Stenosis Murmur Characteristics

A

High-pitched

“Diamond-shaped” crescendo-decrescendo

Mid-SYSTOLIC ejection murmur

Best heard at the right upper sternal border

Radiating to the neck and carotid arteries

Harsh, rasping, grunting, or rough.

218
Q

Aortic Insufficiency Acute Causes

A
  • Infective endocarditis
  • Aortic dissection
219
Q

Aortic Insufficiency Chronic Causes

A
  • Hypertension
  • Rheumatic heart disease
  • Congenital (bicuspid aortic valve)
  • Marfan Syndrome
  • Aortitis (tertiary syphilis, spondyloarthritis: ankylosing spondylitis, Reiter’s)
220
Q

Aortic Insufficiency Murmur Characteristics

A

High-frequency, decrescendo

DIASTOLIC

Best heard at the 3rd or 4th intercostal space at the rigth sternal border (RSB)

221
Q

Mitral Stenosis Causes

A

Rheumatic heart disease

Congenital mitral stenosis

222
Q

Mitral Stenosis Murmur Characteristics

A

Low pitch

Decrescendo-crescendo (Long duration)

Mnemonic to Remember: “SLOW, RUMBLING, SNAP”

•	S - Snap (opening snap after S2)
•	L - Low-pitched, Left side (apex)
•	O - Occurs during Opposite of systole (diastole)
•	W - Without radiation

DIASTOLIC

Rumbling in character

Loud 1st heart sound

Best heard at the apex at end-expiration with the patient in the left lateral position.

Increases with exercise or after a Valsalva maneuver

223
Q

Mitral Insufficiency Acute Causes

A

Infective endocarditis

Rheumatic fever

Papillary muscle rupture due to myocardial infarction

224
Q

Mitral Insufficiency Chronic Causes

A

Mitral valve prolapse

Infective endocarditis

Rheumatic heart disease

Ischaemic heart disease

Left ventricular systolic dysfunction

Hypertrophic cardiomyopathy

225
Q

Mitral Insufficiency Murmur Characteristics

A

High-pitched, “blowing”

HOLOSYSTOLIC

Best heard at the apex.

Radiates to the axilla and infrascapular area.

226
Q

Pulmonary Stenosis Causes

A

Congenital heart disease: T. Fallot

Rheumatic heart disease

Chronic pulmonary hypertension

227
Q

Pulmonary Stenosis Murmur Characteristics

A

Harsh crescendo-decrescendo

SYSTOLIC

Best heard at the left parasternal 2nd or 4th intercostal space when the patient leans forward.

Ejection systolic click that decreases or disappears during inspiration

Increase in intensity with inspiration (Difference with ASD)

228
Q

Pulmonary Stenosis with Obstruction Associated Clinical Features

A
  • Thrill in the suprasternal notch and the left upper sternal border
  • 4th heart sound in the LSB
  • Prominent α wave in the jugular pulse.
229
Q

Pulmonary Insufficiency Causes

A

SAME AS TRICUSPID INSUFFICIENCY

Atrial septal defects

Infective endocarditis

Rheumatic heart disease

Cor pulmonale due to chronic lung disease

Pulmonary artery hypertension

Dilated cardiomyopathy

230
Q

Pulmonary Insufficiency Murmur Characteristics

A

High-pitched “blowing”

Early DIASTOLIC or HOLODIASTOLIC

Decrescendo

Radiates toward the mid-right sternal edge (Graham Steell murmur)

Best heard at the left upper sternal border while the patient holds the breath at end-expiration and sits upright.

Accentuated 2nd heart sound

3rd Heart sound

231
Q

Tricuspid Stenosis Causes

A

Rheumatic fever

232
Q

Tricuspid Stenosis Murmur Characteristics

A

DIASTOLIC murmur

Scratchy character

Short duration

Best heard at the left sternal edge in the fourth intercostal space

Increased: during inspiration, leg raise, inhalation of amyl nitrate, squatting, or exercise.

233
Q

Tricuspid Insufficiency Causes

A

SAME AS PULMONARY INSUFFICIENCY

  1. Atrial septal defects
  2. Infective endocarditis
  3. Rheumatic fever
  4. Pulmonary hypertension resulting from left-sided heart disease
  5. Cor pulmonale due to chronic lung disease
  6. Pulmonary artery hypertension
  7. Dilated cardiomyopathy
234
Q

Tricuspid Insufficiency Murmur Characteristics

A

Frequently not heard.

HOLOSYSTOLIC

Best heard at the left middle or lower sternal border or at the epigastrium when the patient is sitting upright or standing.

Louder with inspiration (Carvallo sign).

When the murmur is not present at all, the diagnosis is best made by the appearance of the jugular venous wave pattern and the presence of hepatic systolic pulsations.

AMC MCQ - You Can Do It!!!!!❤️❤️ (50 decks)

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