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
Infective Endocarditis Streptococcus ADULTS Treatment
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
26
PROSTHETIC valve Streptococcus endocarditis Treatment
Benzylpenicillin x 6 weeks Complicated: Add gentamicin IV ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks
27
Infective Endocarditis Streptococcus CHILDREN Treatment
Uncomplicated or complicated: Benzylpenicillin x 4 weeks
28
Infective Endocarditis Enterococcal Treatment
Two-drug regimen: Benzylpenicillin IV OR amoxicillin IV OR Ampicillin IV PLUS Gentamacin IV x 4-6 weeks
29
Staphylococcus Aureus Infective Endocarditis in ABORIGINAL Patient Treatment
Benzylpenicillin IV (No ATB resistance)
30
CONSIDER vancomycin treatment in Infective Endocarditis for
MRSA Hospital Acquired infection Prosthetic valve
31
Infective Endocarditis Early Surgery Indications
 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.
32
Infective Endocarditis Profilaxis Indications
 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
33
Procedures that require Infective Endocarditis prophylaxis
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
34
Infective Endocarditis Prophylaxis ATBs
 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
35
Pericarditis Clinical Features
Chest pain+SOB+viral infection Kussmaul sign. S4 Gallop: Cardiac Tamponade
36
Pericarditis Duration: Chronic & Acute
Acute (<6w) Chronic (>6w).
37
Kussmaul sign phisical exam
Paradoxical: ↑ JVP with insp and ↓ JVP with exp) Means: constrictive and/or cardiac tamponade.
38
Pericarditis Causes
- 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
39
Pericarditis Complications
 Constrictive pericarditis.  Cardiac tamponade
40
Pericarditis Initial Investigations
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
41
Pericarditis Best Investigation
Echocardiogram with drainage and culture (Pericardiocentesis)
42
Pericarditis Medical Treatment
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
43
Pericarditis Surgical Treatment
Severe Pericarditis, include admision 1. Cardiac tamponade: Pericardiocentesis 2. Severe, Recurrent or Constrictive: Pericardiectomy
44
Beck's triad = Cardiac Tamponade
Low blood pressure (weak pulse or narrow pulse pressure) Muffled heart sounds Raised jugular venous pressure.
45
Pericarditis Physiopathology
Restrictive Cardiomyopathy Diastolic Dysfunction with impaired filling – relaxation Normal Ejection fraction + S4 gallop
46
Dressler's Syndrome definition
Pericarditis in the context of major heart attack or heart surgery
47
Dressler's Syndrome risk factors
1. Young age 2. B-negative blood type 3. Prior history of pericarditis 4. Prior treatment with prednisone
48
Dressler's Syndrome investigations
Gold Standard: Echocardiogram UNSTABLE patient: bedside ultrasonographic (E-FAST) ECG: Same pattern as pericarditis (global ST segment elevation and T wave inversion)
49
Dressler's Syndrome Treatment
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.
50
Dressler's Syndrome COMPLICATION
Cariac Tamponade
51
Myocarditis Clinical Features
- Chest pain - S3 Gallop (Systolic Disfuntion) - Dyspnoea - Viral infection - Fever - Arrhythmia
52
Myocarditis Infective Causes
- 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
53
Myocarditis Non-Infective Causes
- ALCOHOL!!!! ---> Reversed with abstinence - Collagen vascular diseases - Systemic diseases: Rheumatic Fever, sarcoidosis, giant cell arteritis - Cardiotoxic drugs: Clozapine
54
Myocarditis Investigation
1. Urgent transthoracic echocardiogram (TTE)
55
Myocarditis Physiopathology
Dilated Cardiomyopathy Impaired contractility with thin weak heart muscle - systolic dysfunction Decreased Ejection Fraction + S3 gallop
56
Myocarditis Treatment
1. Correct underlining cause (alcohol, infection) 2. Same tratment that CHF
57
Mediastinitis Clinical Features
Dysphagia Chest pain Fever Respiratory distress
58
Mediastinitis Causes
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
59
Mediastinitis Investigations
First: CXR Mediastinal widening or pneumomediastinum Best: CT Torax, Mediastinal aspiration
60
Mediastinitis Treatment
In community: - Empirical: Amoxi-Clav IV - If septic shock: Cefazolin+Metro IV In hospital: - Piper+Tazo OR Cefepime+Metro
61
Stable Angina Diagnose
Chest pain < 20 min Negative ECG Negative troponin Negative CK MB
62
Cardiac Enzymes Measurement in MI
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
63
Stable Angina other investigations:
- CXR: CHF sings. Exclude other causes (Ao dissection – lung path) - Bloods: FBE (anemia) – LFT (dyslipidemia) – RFT– BSL (DM) - Electrolytes - Echocardiogram
64
Stable Angina BEST Investigation:
Stress test will confirm the suspected diagnosis
65
Stable Angina ACUTE Treatment
- 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
66
Nitrates Contraindications
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
67
Stable Angina LONG TERM Treatment
**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.
68
Unstable Angina Clinical Features
Clinical Features: 1. Chest pain that has changed or >20 min 2. ECG: - Low Risk: NORMAL - High Risk: ST Depression 3. Troponin - Low Risk: Negative - High Risk: Positive 4. CK MB: Negative
69
Unstable Angina Management
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)
70
Worsening of Unstable Angina Management
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)
71
Non-STEMI Clinical Features:
1. Chest pain that has changed or >20 min 2. ECG: ST Depression 3. Troponin: Positive 4. CK MB: Positive
72
Non-STEMI Management
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
73
STEMI Clinical Features
Extreme chest pain ECG: ST Elevation Troponin: Very high CK MB: Positive
74
Acute STEMI Management
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)
75
Thrombolysis Side Effects
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
76
Absolute Contraindications for Thrombolytic Treatment (9)
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
77
Relative Contraindications for Thrombolytic Treatment
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
78
POST MI Treatment
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
79
Heart Failure: 3 more important causes
Hypertension Heart valve disease: rheumatic heart disease Cardiac arrhythmias
80
Heart Failure Classification by Left Ventricle Ejection Fraction (LVEF)
LVEF < 40%: Heart failure with REDUCED EF. LVEF = 50%: Heart failure with PRESERVED EF NOTE: The CHF management depends on EF.
81
Heart Failure First Investigations
1. CXR 2. ECG
82
Heart Failure Best Investigation
Echocardiogram
83
Heart Failure Treatment
- 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)
84
Hypertrophic Obstructive Cardiomyopathy (HCOM) or Idiopathic Hypertrophic Subaortic Stenosis DEFINITION
Left ventricular outflow tract obstruction (LVOTO) due to hypertrophied ventricular septum It is the most common genetically transmitted cardiomyopathy (Autosomal Dominant) DIASTOLIC DYSFUNCTION
85
Hypertrophic Obstructive Cardiomyopathy (HCOM) Clinical Features
- 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
86
Hypertrophic Obstructive Cardiomyopathy (HCOM) Differential Diagnosis
Prolong QT syndrome (AD) Dx with ECG – also VT
87
Hypertrophic Obstructive Cardiomyopathy (HCOM) Initial Management
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)
88
Hypertrophic Obstructive Cardiomyopathy (HCOM) Best Investigation
Cardiac MRI (Gold Standard)
89
HCOM Management
1. Referral: - Genetic counseling, then genetic testing - Cardiologist
90
HCOM Screening
IF POSITIVE FAMILY HISTORY: Echocardiogram
91
Hypertrophic Obstructive Cardiomyopathy (HCOM) Medical treatment
Symptomatic: 1st line: BB 2nd line: CCB Contraindicated: Nitrates and ACE inhibitors (↓ preload)
92
Hypertrophic Obstructive Cardiomyopathy (HCOM) surgical treatment
Septal myectomy: Only in young patients very symptomatic even with medical treatment. IF Ventricular Tachy: Implantable cardioverter-defibrillator (ICD)
93
Takotsubo Cardiomyopathy Definition
Transient regional systolic dysfunction of the left ventricle in the absence of angiographically significant coronary artery disease
94
Other names for Takotsubo Cardiomyopathy
- Stress cardiomyopathy - Gebrochenes-Herz syndrome
95
Takotsubo Cardiomyopathy Clinical features
Presentation: similar to acute coronary syndrome.
96
Takotsubo Cardiomyopathy ECG:
STEMI or pericarditis pattern.
97
Takotsubo Cardiomyopathy Troponins:
Modest elevation. No correlation with the ECG findings
98
Takotsubo Cardiomyopathy Cause
Sympathetic overdrive with increased catecholamines
99
Takotsubo Cardiomyopathy Risk factors
- Post-menopausal women - Pregnancy - Recent stressful event NOTE: If occur in man, very bad prognosis
100
Takotsubo Cardiomyopathy Initial Investigation (2)
1. ECG 2. TTE is diagnostic w/ confirmation (EF 35-40%)
101
Takotsubo Cardiomyopathy Best Investigation
Cardiac MRI
102
Blood pressure measurement. Sphygmomanometer CUFF'S sizes: Width
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
Blood pressure measurement. Sphygmomanometer CUFF'S sizes: Length
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
Blood Pressure Ambulatory 24-hour monitoring INDICATIONS
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
Phisical Exam in Hypertension to rule out renal stenosis
The low-pitched bruits of kidney artery stenosis are best heard by placing the diaphragm of the stethoscope firmly in the epigastric area.
106
Hypertension Diagnosis
At least 2 follow-up measurements with average: Systolic: >140 mmHg or Diastolic: >90 mmHg
107
Hypertension General Clasification
- 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
Renovascular Hypertension causes
- glomerulonephritis - reflux nephropathy - kidney artery stenosis
109
Secondary Hypertension: Metabolic causes
- Primary aldosteronism (Conn's syndrome) - Cushing syndrome - Phaeochromocytoma
110
Medication associated with Hypertension
 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
Refractory/resistent Hypertension
BP > 140/90 mmHg after maximum doses of 2 drugs for 3-4months
112
Hypertension + Abdominal systolic bruit
Renal artery stenosis
113
Hypertension + Proteinuria, haematuria, casts
Glomerulonephritis
114
Hypertension + Bilateral kidney masses with or without haematuria
Polycystic disease
115
Hypertension + History of claudication and delayed femoral pulse
Coarctation of the aorta
116
Hypertension + Progressive nocturia, weakness
Primary aldosteronism (check serum potassium)
117
Hypertension + Obesity, snoring, daytime sleepiness
Sleep apnoea
118
Hypertension + Paroxysmal hypertension with headache, pallor, sweating, palpitations
Phaeochromocytoma
119
Most common long-term drug use disease
Hypertension
120
Most common complications of Hypertension (5)
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
Main causes of Death associated to Hypertension
Stroke (45%)
122
Hypertension Value Clasification by Murtagh NORMAL
< 130/85 mmHg Follow Up: 2 years
123
Hypertension Value Clasification by Murtagh OPTIMAL
< 120/80 mmHg Follow Up: 2 years
124
Hypertension Value Clasification by Murtagh HIGH NORMAL
< 140/90 mmHg Follow Up: 1year
125
Hypertension Value Clasification by Murtagh G1 MILD
< 160/100 mmHg Follow Up: 2 months
126
Hypertension Value Clasification by Murtagh G2 MODERATE
< 180/110 mmHg Follow Up: 1 month
127
Hypertension Value Clasification by Murtagh G3 SEVERE
> 180/110 mmHg Follow Uo: 1-7 days
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Hypertension Value Clasification by Murtagh ISOLATED SYSTOLIC
>140 / <90 mmHg Follow Up: 1 month
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Absolute Cardiovascular Risk Assessment Variables (7)
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
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Risk of a cardiovascular event over the next 5 years: Low, moderate and High values
Low <10% (green) Follow-Up 6-12 months Moderate 10-15% (blue) Follow Up: 3months High >15% (yellow & red) Indication for medical treatment
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LOW CV Risk (10%) Hypertension Management
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MODERATE CV Risk (10-15%) Hypertension Management
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HIGH CV Risk (>15%) Hypertension Management
Mantain life-style modification Start medical treatment immediately
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Hypertension Non-pharmacological management (7)
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
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Hypertension Referral Criteria (5)
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
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BP Treatment Targets
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Circle of Love (image)
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Ineffective Antihypertensives Combinations
Diuretic and calcium-channel blocker Beta blockers and ACE inhibitors
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1st Line Antihypertensive Drugs by J Murtagh
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Starting Hypertensive Treatment (Murtagh)
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Antihypertensive medication in Old and Young Patients
Older: Diuretics, calcium-channel blockers and ACE inhibitors. Younger: Beta blockers or ACE inhibitors.
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Hypertension Drug Teraphy in the elderly
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.
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Hypertension Treatment >65yo with CHF
Thiazides
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Hypertension Treatment >65yo with Ischaemia risk
BetaBlockers
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Hypertension Treatment - Young with CHF
ACE inhibitors
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Hypertension Treatment Young with Ischaemia risk
Amlodipine (Never Verapamil or Diltiazem)
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Hypertension Treatment in Asthma
CCB
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Hypertension Treatment in DM
1st Line: ACEi / ARBs 2nd Line: CCB (doesn’t affect insulin + Reno protective effect) NOTE: Diuretics aggravate glucose intolerance so use with care.
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Hypertension Treatment in Psychiatric patients
Diuretics (least central activity)
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Hypertensive Urgency Treatment
>180/110 mmHg ORAL: Nifedipine Captopril Clonidine IV: Hydralazine
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Hypertensive Emergency Treatment (4)
>220/140 mmHg Hydralazine Metoprolol Nitroprusside Esmolol All IV
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HYPERTENSIVE ENCEPHALOPATHY Clinical Features
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)
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HYPERTENSIVE ENCEPHALOPATHY Investigations
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).
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HYPERTENSIVE ENCEPHALOPATHY Management
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
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Antihypertensive Drugs List
1. Diuretics 2. Angiotensin converting enzime (ACE) inhibitors 3. Angiotensine II Receptors Blockers (ARBs) 4. Beta Blockers (BB) 5. Calcium Channel Blockers (CCB)
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ACE inhibitors LIST
1. Captopril: Short half life (emergency use) 2. Enalapril 3. Lisinopril 4. Ramipril The other two longer half life: Daily use
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ARBs LIST
Valsartan (more pontent 1 tablet/day) Losartan Candesartan Rest lest potent 2 tablets/day
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ACE inhibitors MECHANISM OF ACTION (MOA)
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
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ACE inhibitors & ARBs Indications
1. hypertension 2. heart failure 3. peripheral vascular disease 4. diabetes 5. cardioprotective after miocardial infarction NOTE: ACE Inhibitors are always 1st line
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ACE inhibitors & ARBs Contraindications
1.Bilateral kidney artery stenosis (precaution in chronic kidney disease) 2. Hyperkalemia (avoid potassium sparing diuretics combination). Can lead to Metabolic Acidosis 3. Pregnancy
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ACE inhibitors side effects (6)
1. Cough (↑Bradikinins) 2. Angioedema (↑Bradikinins) 2. Disturbance in taste (dysgeusia) 3. Rash (↑Bradikinins) 4. HYPERkalemia (↓ Aldosterone = ↓ K excretion) 5. Hypotension (just the first dose)
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Antihypertensive Drugs: Diuretict types LIST
1. Loop 2. Thiazides & thiazides like 3. Potasium sparing 4. Osmotic 5. Carbonic Anhidrase Inhibitors
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Loop Diuretic Mechanism of Action
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)
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Loop Diuretic LIST
Sulfonamide derivatives: 1. Furosemide 2. Bumetanide 3. Torsemide Non- Sulfonamide derivatives: 4. Ethacrynic acid
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Loop Diuretic INDICATIONS
1. Edematous states: CHF, APO, cirrhosis with ascites, nephrotic syndrome 2. Hypertension 3. Hyperkalemia 4. Hypercalcemia 5. Acute bromide, iodine and fluoride intoxication
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Loop Diuretic CONTRAINDICATIONS
Sulfonamide allergy Alternative: Use Ethacrynic acid
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Loop Diuretic SIDE EFFECTS
HYPOS: Kalemia Natremia Calcemia Mangesemia Cloremia HYPER: Uricemia
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Loop Diuretic COMPLICATIONS
1. Here's a simplified and concise explanation of the points you provided: 1. **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. 2. **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). 3. **Ototoxicity**: Some drugs can cause hearing loss, which is usually reversible if the drug is stopped. Ethacrynic acid is the most common culprit. 4. **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 2. Hypokalemic Meabolic Alcalosis: ↑pH ↑HCO3 ↓K ↓Na ↓Mg 3. Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid. 4. Sulfonamide Allergy: - Acute interstitial nephritis - Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN) 1. Dehydration: This can lead to hyperuricemia/gout 2. Hypokalemic Meabolic Alcalosis: ↑pH ↑HCO3 ↓K ↓Na ↓Mg 3. Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid. 4. Sulfonamide Allergy: - Acute interstitial nephritis - Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN) 1. Dehydration: This can lead to hyperuricemia/gout 2. Hypokalemic Meabolic Alcalosis: ↑pH ↑HCO3 ↓K ↓Na ↓Mg 3. Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid. 4. Sulfonamide Allergy: - Acute interstitial nephritis - Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
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Thiazides & thiazides like Mechanism of Action
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
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Thiazides & thiazides like LIST
Benzothiadazine derivatives: Thiazides 1. Clorothiazide 2. Hydroclorothiazide Sulfonamide derivative: 3. Indapamide 4. Chlortalidone
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Thiazides & thiazides like INDICATIONS
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
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Thiazides & thiazides like SIDE EFFECTS
HYPERS: Uricemia Glycaemia Lipidaemia (increase cholesterol and triglycerides) HIPOS Kalemia Natraemia Magnesemia * Impotence
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Thiazides & thiazides like CONTRAINDICATIONS
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)
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Potassium-sparing Diuretic MECHANISM OF ACTION
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
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Potassium-sparing Diuretics LIST
Direct antagonist: 1. Spironolactone Indirect atagonist: 2. Amiloride 3. Triamterene
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Potassium-sparing Diuretics INDICATIONS
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)
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Potassium-sparing Diuretics SIDE EFFECTS
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
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Osmothic Diuretic: Manitol Features
Aquaretic Diuretic: Mainly excretion of water without electrolites Only presentation IV
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Osmothic Diuretic: Manitol INDICATIONS
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
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Osmothic Diuretic: Manitol SIDE EFFECTS
Rebound effect 1. Worsen edamtous states (pulmonary edema) 2. In CHF and Renal Faillure: HYPOnatremia NOTE: If inadequate water replacement = Dehydration with HYPERnatremia and HYPERkalemia
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Diuretic: Carbonic Anhidrase Inhibitors (Zolamides) MECHANHISM OF ACTION
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
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Carbonic Anhidrase Inhibitors (Zolamides) LIST
ORAL Methazolamide ORAL & IV Acetazolamide TOPICAL (eye drops) Dorsolamide Brinzolamide
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Carbonic Anhidrase Inhibitors (Zolamides) INDICATIONS
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
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Carbonic Anhidrase Inhibitors (Zolamides) COTRAINDICATIONS
Sulfonamide allergy Hepatic disease Adrenal insufficiency Renal Faillure
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Carbonic Anhidrase Inhibitors (Zolamides) SIDE EFFECTS
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.
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Antihypertensive drugs: BETA BLOCKERS - Mechanism of action
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.
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BETA BLOCKERS - General Indications
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
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BETA BLOCKERS - General Side effects
**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
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1st generation BETA BLOCKERS - Side effects
**B2 Block (1st generation)** 4. Bronchoconstriction 5. Hypertrigliceridemia 6. Hypoglycemia 7. Muscular fatigue, insomnia
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3rd generation BETA BLOCKERS - Side effects
**α1 Block (3rd generation)** 8. Headache 9. Nasal congestion 10. Delay ejaculation
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BETA BLOCKERS - General Contraindications
ALL: - Bradycardia, heart block - Orthostatic hypotension
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BETA BLOCKERS - 1st Generation - Contraindications
- Asthma, COPD - Dyslipidaemia - DM - Heart failure - Peripheral vascular disease - Pregnancy
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BETA BLOCKERS - 2nd Generation -Contraindications
- Heart failure - Peripheral vascular disease - Pregnancy
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BETA BLOCKERS - 3rd Generation - Contraindications
- Migraine - Chronic rhinitis - Delay ejaculation
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BETA BLOCKERS - 1st Generation
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
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BETA BLOCKERS - 2nd Generation
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
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BETA BLOCKERS - 3rd Generation
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
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Antihypertensive drugs: Calcium Channel Blockers - Mechanism of Action
1. Negative inotropic and chronotropic heart effect 2. Vasodilation 3. Relaxation of smooth muscle in the bronchi
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Calcium Channel Blockers - Dihydropirimidines Main effect
Vasodilator (including coronary arteries)
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Calcium Channel Blockers - Dihydropirimidines LIST
- Nifedipine - Amlodipine - Nicardipine
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Calcium Channel Blockers - Dihydropirimidines INDICATIONS
- Hypertension - Asthma - Stable Angina - Peripheral vascular disease - Reynaud's Phenomenon
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Calcium Channel Blockers - Dihydropirimidines SIDE EFFECTS
Reflex tachycardia (↑doses) Flushing Dizziness Peripheral edema Gingival hyperplasia
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Calcium Channel Blockers - NON-Dihydropirimidines Features, Indication, Side effect
Features: Main effect in the heart < vasodilator
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Calcium Channel Blockers - NON-Dihydropirimidines Indications
- Verapamil: Cardioselective / Class 4 Antiarrhythmic - Diltiazem: Hypertension
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Calcium Channel Blockers - NON-Dihydropirimidines Side Effects
- Hyperprolactinemia - Verapamil: Constipation
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Calcium Channel Blockers - CONTRAINDICATIONS
1. Heart block 2nd and 3rd degree 2. Heart failure (verapamil, diltiazem)
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CCB: Caution using with
Beta blockers Digoxin Cardiac Faillure
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Innocent Murmurs Characteristics
- 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.
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Pathological Murmurs History
◦ Family Hx of cardio-myopathy or sudden unexplained death. ◦ Congenital malformations ◦ Exertional syncope ◦ Symptoms of cardiac failure.
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Pathological Murmurs Clinical Features
◦ Cyanosis - Breathlessness. ◦ Failure to thrive, not clearly due to other causes. ◦ Thrill with murmur.
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Pathological Murmurs Characteristics
◦ 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.
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Holosystolic Murmurs List
◦ Mitral valve regurgitation ◦ Tricuspid valve regurgitation ◦ Ventricular septal defec
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Early Systolic Murmurs List
◦ Mitral regurgitation ◦ Tricuspid Regurgitation IMMEDIATE REFERRAL IS REQUIRED!!
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Diastolic Murmurs List
Always indicate heart disease!! - Aortic Regurgitation - Mitral Stenosis
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Continuous Murmurs List
◦ 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
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Aortic Stenosis Causes
Degenerative calcific aortic stenosis Rheumatic heart disease Systemic lupus erythematosus (SLE) Paget disease
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Aortic Stenosis Murmur Characteristics
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.
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Aortic Insufficiency Acute Causes
- Infective endocarditis - Aortic dissection
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Aortic Insufficiency Chronic Causes
- Hypertension - Rheumatic heart disease - Congenital (bicuspid aortic valve) - Marfan Syndrome - Aortitis (tertiary syphilis, spondyloarthritis: ankylosing spondylitis, Reiter’s)
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Aortic Insufficiency Murmur Characteristics
High-frequency, decrescendo DIASTOLIC Best heard at the 3rd or 4th intercostal space at the rigth sternal border (RSB)
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Mitral Stenosis Causes
Rheumatic heart disease Congenital mitral stenosis
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Mitral Stenosis Murmur Characteristics
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
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Mitral Insufficiency Acute Causes
Infective endocarditis Rheumatic fever Papillary muscle rupture due to myocardial infarction
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Mitral Insufficiency Chronic Causes
Mitral valve prolapse Infective endocarditis Rheumatic heart disease Ischaemic heart disease Left ventricular systolic dysfunction Hypertrophic cardiomyopathy
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Mitral Insufficiency Murmur Characteristics
High-pitched, “blowing” HOLOSYSTOLIC Best heard at the apex. Radiates to the axilla and infrascapular area.
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Pulmonary Stenosis Causes
Congenital heart disease: T. Fallot Rheumatic heart disease Chronic pulmonary hypertension
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Pulmonary Stenosis Murmur Characteristics
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)
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Pulmonary Stenosis with Obstruction Associated Clinical Features
- Thrill in the suprasternal notch and the left upper sternal border - 4th heart sound in the LSB - Prominent α wave in the jugular pulse.
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Pulmonary Insufficiency Causes
SAME AS TRICUSPID INSUFFICIENCY Atrial septal defects Infective endocarditis Rheumatic heart disease Cor pulmonale due to chronic lung disease Pulmonary artery hypertension Dilated cardiomyopathy
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Pulmonary Insufficiency Murmur Characteristics
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
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Tricuspid Stenosis Causes
Rheumatic fever
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Tricuspid Stenosis Murmur Characteristics
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.
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Tricuspid Insufficiency Causes
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
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Tricuspid Insufficiency Murmur Characteristics
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.