Cardiology by Dr. Cintia Flashcards
Pulmonary Embolism Clinical Features
Pleuritic Chest pain: Aggravated by cough and deep inspiration, worse with lying flat, relieved by sitting up.
Shortness Of Breath
Hypoxemia
Pulmonary Embolism
First Investigations (3)
First: Chest pain-ECG (S1Q3T3) Diagnostic
Second: SOB-CXR—> Rule out pulmonary pathology
Pregnancy (Doppler USD of legs)
Pulmonary Embolism
Best Investigations
Wells Score:
- Low: D dimer
- High: CTPA (Gold standard)
V/Q (Pregnancy or ♀< 45 yo)
Wells Score for PE (7 criteria)
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
Wells Score Probability for PE
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
PERC rule (8 criteria)
for pulmonary embolism
in low risk pat
Aged <50 years
Pulse <100 beats per minute
SaO2 ≥95%
No haemoptysis
No oestrogen use
No surgery or trauma requiring hospitalisation within four weeks
No prior venous thromboembolism
No unilateral leg swelling
RESULT: IF ALL YES no PE
Pulmonary Embolism
Management
ABCD/Oxygen/Morphine
Stable:
- LMWH.
- Renal disease –> Unfractionated
Unstable: Thrombolysis
Acute Pulmonary Oedema (APO) Clinical Features
Sudden-onset of SOB with tachypnea
Diaphoresis and cyanosis
Productive cough: pink or white frothy sputum
Crackles and Wheezes (Kettle boiling)
- Hypotension: Cardiogenic shock
Acute Pulmonary Oedema (APO) Most common causes
- Acute Mitral and Aortic Regurgitation
- LV Systolic Dysfunction: anterolateral MI
- AF with rapid ventricular response
Acute Pulmonary Oedema (APO) Initial investigation
- CXR
- ECG
- Troponin
- FBE
- TTE
Acute Pulmonary Oedema (APO) Best investigation
Arterial/Venous Blood Gases to assess the severity of hypoxemia.
Acute Pulmonary Oedema (APO) Treatment
- O2
- IV line
- NGT spray or SL / IV is preferred to Morphine (BP > 100)
- Furosemide IV
- Morphine IV (chest pain)
- CPAP
APO + AF = BB
APO + AF + CHF = Digoxin inf
Infective Endocarditis Clinical Features
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!!!
Order of most common microorganisms that cause infective endocarditis
- Staphiloccocus Aureus
- Streptococci
- Enterococci (at least 90% faecalis)
Infective Endocarditis RISK FACTORS
Artificial heart valves.
Congenital heart defects.
A history of endocarditis.
Damaged heart valves: rheumatic fever
History of intravenous (IV) illegal drug use.
Immunocompromised patient.
Infective Endocarditis Diagnose
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
Modify Duke’s Major criteria
TWO MAJOR CRITERIA
- 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
- 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
Modify Duke’s Minor criteria
FIVE MINOR CRITERIA
- Predisposing heart condition or intravenous drug user
- Fever: 38°C
- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
- Immunologic phenomena:
Glomerulonephritis
Osler nodes
Roth spots
Rheumatoid factor (+) - 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
Infective Endocarditis Initial Investigations
- Blood culture: Diagnostic
- FBE: leucocytosis with neutrophilia and anemia.
- ECG: Cardiac monitoring
- 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
Infective Endocarditis Best Investigations
- Transesophageal echo (TOE)
BUT:
- If HACEK: CT angio
- If arrhythmias: ECG
- If spread: CT/MRI (brain, thorax, and abdomen)
HACEK group
Slow-growing, fastidious gram-negative organisms
- Haemophilus species: Aggregatibacter aphrophilus, H. Paraphrophilus.
- Aggregatibacter actinomycetemcomitans
- Cardiobacterium hominins
- Eikenella corrodens
- Kingella kingae
COMPLICATED Infective Endocarditis include
Large vegetation
Perivalvular abscess
Multiple emboli
Secondary septic events
Infective Endocarditis Empirical Treatment
Benzylpenicillin + Gentamicin + Flucloxacillin IV
Infective Endocarditis Staphylococcus Aureus Treatment
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
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
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
Infective Endocarditis Streptococcus CHILDREN Treatment
Uncomplicated or complicated:
Benzylpenicillin x 4 weeks
Infective Endocarditis Enterococcal Treatment
Two-drug regimen:
Benzylpenicillin IV
OR
amoxicillin IV
OR
Ampicillin IV
PLUS Gentamacin IV x 4-6 weeks
Staphylococcus Aureus Infective Endocarditis in ABORIGINAL Patient Treatment
Benzylpenicillin IV (No ATB resistance)
CONSIDER vancomycin treatment in Infective Endocarditis for
MRSA
Hospital Acquired infection
Prosthetic valve
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.
Infective Endocarditis Prophylaxis 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
Procedures that require Infective Endocarditis prophylaxis
- Dental procedures
- Invasive respiratory procedures with incision or biopsy of respiratory mucosa (including tonsillectomy and adenoidectomy)
- Incision and drainage (I&D) of local abscesses
- Surgery procedures through infected skin (cellulitis)
NOTE: Antibiotic cover for genito-urinary or gastrointestinal procedures is NOT recommended for prophylaxis of endocarditis
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
Pericarditis Clinical Features
Chest pain + SOB+ viral infection
Kussmaul sign.
S4 Gallop: Cardiac Tamponade
Pericarditis Duration: Acute & Chronic
Acute (<6w)
Chronic (>6w).
Kussmaul sign physical exam
Paradoxical: ↑ JVP with insp and ↓ JVP with exp)
Means: constrictive and/or cardiac tamponade.
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
Pericarditis Complications
Constrictive pericarditis.
Cardiac tamponade
Pericarditis Initial Investigations
- ECG:
- ST elevation except in AVR & V1
- Reciprocal PR - CXR:
- Pericardial fluid
- Pulmonary congestion - Echocardiogram: Is diagnostic! Chest FAST scan should be done ASAP.
- Cardiac CT
Pericarditis Best Investigation
Echocardiogram with drainage and culture (Pericardiocentesis)
Pericarditis Medical Treatment
Mild to moderate Pericarditis
- AAS/Ibuprofen (7 to 10 days)
- Colchicine x 3 months. Indication: Recurrent symptoms (Side Effects: Diarrhea, abd pain)
- Prednisone
If infection: ATBs and drainage
Pericarditis Surgical Treatment
Severe Pericarditis, include admision
- Cardiac tamponade: Pericardiocentesis
- Severe, Recurrent or Constrictive:
Pericardiectomy
Beck’s triad = Cardiac Tamponade
Low blood pressure (weak pulse or narrow pulse pressure)
Muffled heart sounds
Raised jugular venous pressure.
Pericarditis Pathophysiology
Restrictive Cardiomyopathy
Diastolic Dysfunction with impaired filling – relaxation
Normal Ejection fraction + S4 gallop
Dressler’s Syndrome definition
Pericarditis in the context of major heart attack or heart surgery
Dressler’s Syndrome risk factors
- Young age
- B-negative blood type
- Prior history of pericarditis
- Prior treatment with prednisone
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)
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.
Dressler’s Syndrome COMPLICATION
Cardiac Tamponade
Myocarditis Clinical Features
- Chest pain
- S3 Gallop (Systolic Disfuntion)
- Dyspnoea
- Viral infection
- Fever
- Arrhythmia
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
Myocarditis Non-Infective Causes
- ALCOHOL!!!! —> Reversed with abstinence
- Collagen vascular diseases
- Systemic diseases: Rheumatic Fever, sarcoidosis, giant cell arteritis
- Cardiotoxic drugs: Clozapine
Myocarditis Investigation
- Urgent transthoracic
echocardiogram (TTE)
Myocarditis pathophysiology
Dilated Cardiomyopathy
Impaired contractility with thin weak heart muscle - systolic dysfunction
Decreased Ejection Fraction + S3 gallop
Myocarditis Treatment
- Correct underlining cause (alcohol, infection)
- Same tratment that CHF
Mediastinitis Clinical Features
Dysphagia
Chest pain
Fever
Respiratory distress
Mediastinitis Causes
- Tracheal or esophageal rupture:
- After an endoscopic procedure
- Boerhaave syndrome
- Foreign body aspiration - Postoperative mediastinitis (thoracic surgery)
- Traumatic injury
- Spread of pulmonary infection
- Pancreatitis
NOTE: Descending necrotizing mediastinitis caused by neck abscess, Ludwig angina, or dental infections
Mediastinitis Investigations
First: CXR
Mediastinal widening or pneumomediastinum
Best: CT Torax, Mediastinal aspiration
Mediastinitis Treatment
In community:
- Empirical: Amoxi-Clav IV
- If septic shock: Cefazolin+Metro IV
In hospital:
- Piper+Tazo OR Cefepime+Metro
Stable Angina Diagnose
Chest pain < 20 min
Negative ECG
Negative troponin
Negative CK MB
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
Stable Angina other investigations:
- CXR: CHF sings. Exclude other causes (Ao dissection – lung path)
- Bloods: FBE (anemia) – LFT (dyslipidemia) – RFT– BSL (DM) - Electrolytes
- Echocardiogram
Stable Angina BEST Investigation:
Stress test will confirm the suspected diagnosis
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
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
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.
Unstable Angina Clinical Features
Clinical Features:
1. Chest pain that has changed or >20 min
- ECG:
- Low Risk: NORMAL
- High Risk: ST Depression - Troponin
- Low Risk: Negative
- High Risk: Positive - CK MB: Negative
Unstable Angina Management
- Admission to coronary unit
- Oxygen 4–6 L/min (PaO2>90%)
- IV line
- Aspirin 150 - 300 mg
- Clopidogrel
- Enoxaparin (1 mg/kg) SC
- Glyceryl trinitrate (patch)
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)
Non-STEMI Clinical Features:
- Chest pain that has changed or >20 min
- ECG: ST Depression
- Troponin: Positive
- CK MB: Positive
Non-STEMI Management
- Admission to coronary unit
- Oxygen 4–6 L/min (PaO2>90%)
- IV line
- Glyceryl trinitrate
- Aspirin 150 - 300 mg
- Clopidogrel
- 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
STEMI Clinical Features
Extreme chest pain
ECG: ST Elevation
Troponin: Very high
CK MB: Positive
Acute STEMI Management
- PCI (Gold Standard)
- Optimal: Within 60 minutes of symptom onset.
- Acceptable: 90 min. - 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)
Thrombolysis Side Effects
- Bleeding
- Hypotension
- Reperfusion arrhythmias
- Allergic reactions
- Angioedema
- Anaphylactic shock
NOTE: Streptokinase is most frequently complicated by allergic reactions and hypotension
Absolute Contraindications for Thrombolytic Treatment (9)
- Active Bleeding or bleeding diathesis (excluding menses)
- Suspected aortic dissection
- Significant closed head or facial trauma within 3 months
- Any prior intracranial hemorrhage
- Ischaemic stroke within 3 months
- Known cerebral vascular lesion
- Known malignant intracranial neoplasm
- Recent Intracranial or spinal surgery
NOTE: For streptokinase, previous treatment within six months and ASTI people
Relative Contraindications for Thrombolytic Treatment
- Current anticoagulants (including novel anticoagulant agents)
- Non-compressible vascular puncture
- Recent major surgery (<3 weeks)
- Traumatic or prolonged (>10 minutes) CPR
- Recent internal bleeding (within 4 weeks) / Active Peptic Ulcer
- Suspected Pericarditis
- Advanced Liver Disease / Advanced
- Metastatic Cancer
- History of chronic, severe, poorly controlled hypertension
- Severe uncontrolled hypertension on this presentation (Systolic >180 / Diastolic > 110 mmHg)
- Ischaemic Stroke > 3months ago
- Dementia
- Pregnancy or within 1 week postpartum
POST MI Treatment
- BB (within 12 h)
- ACE inhibitors (within 24 h)
- Dual antiplatelet therapy: Aspirin 75 - 150 mg + Ticagrelor (Clopidogrel or Prasugrel x 12 m)
- Statins
Heart Failure: 3 more important causes
Hypertension
Heart valve disease: rheumatic heart disease
Cardiac arrhythmias
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.
Heart Failure First Investigations
- CXR
- ECG
Heart Failure Best Investigation
Echocardiogram
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)
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
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
Hypertrophic Obstructive Cardiomyopathy (HCOM) Differential Diagnosis
Prolong QT syndrome (AD)
Dx with ECG – also VT
Hypertrophic Obstructive Cardiomyopathy (HCOM) Initial Management
- Admit to Cardiology
- ECG: Dagger Q waves in left leads
- CXR: CHF findings
- Echocardiogram (THE MOST IMPORTANT BUT NOT THE GOLD STANDARD)
Hypertrophic Obstructive Cardiomyopathy (HCOM) Best Investigation
Cardiac MRI (Gold Standard)
HCOM Management
- Referral:
- Genetic counseling, then genetic testing
- Cardiologist
HCOM Screening
IF POSITIVE FAMILY HISTORY: Echocardiogram
Hypertrophic Obstructive Cardiomyopathy (HCOM) Medical treatment
Symptomatic:
1st line: BB
2nd line: CCB
Contraindicated: Nitrates and ACE inhibitors (↓ preload)
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)
Takotsubo Cardiomyopathy Definition
Transient regional systolic dysfunction of the left ventricle in the absence of angiographically significant coronary artery disease
Other names for Takotsubo Cardiomyopathy
- Stress cardiomyopathy
- Gebrochenes-Herz syndrome
Takotsubo Cardiomyopathy Clinical features
Presentation: similar to acute coronary syndrome.
Takotsubo Cardiomyopathy ECG:
STEMI or pericarditis pattern.
Takotsubo Cardiomyopathy Troponins:
Modest elevation. No correlation with the ECG findings
Takotsubo Cardiomyopathy Cause
Sympathetic overdrive with increased catecholamines
Takotsubo Cardiomyopathy Risk factors
- Post-menopausal women
- Pregnancy
- Recent stressful event
NOTE: If occur in man, very bad prognosis
Takotsubo Cardiomyopathy Initial Investigation (2)
- ECG
- TTE is diagnostic w/ confirmation (EF 35-40%)
Takotsubo Cardiomyopathy Best Investigation
Cardiac MRI
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
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)
Blood Pressure Ambulatory 24-hour monitoring INDICATIONS
- Unusual variability of office BP
- Marked discrepancy between office and home BP
- Resistance to drug treatment
- Suspected sleep apnoea
- Borderline levels
Physical 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.
Hypertension Diagnosis
At least 2 follow-up measurements with average:
Systolic: >140 mmHg
or
Diastolic: >90 mmHg
Hypertension General Classification
- Essential (90–95%)
- Secondary (approx. 5–10%)
*Renovascular <3%
*Endocrine: 0.3–1%
*Other:
- Coarctation of the aorta
- Immune disorder (polyarteritis nodosa)
- Drugs
- Pregnancy
Renovascular Hypertension causes
- glomerulonephritis
- reflux nephropathy
- kidney artery stenosis
Secondary Hypertension: Metabolic causes
- Primary aldosteronism (Conn’s syndrome)
- Cushing syndrome
- Phaeochromocytoma
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
Refractory/resistent Hypertension
BP > 140/90 mmHg after maximum doses of 2 drugs for 3-4months
Hypertension + Abdominal systolic bruit
Renal artery stenosis
Hypertension + Proteinuria, haematuria, casts
Glomerulonephritis
Hypertension + Bilateral kidney masses with or without haematuria
Polycystic disease
Hypertension + History of claudication and delayed femoral pulse
Coarctation of the aorta
Hypertension + Progressive nocturia, weakness
Primary aldosteronism (check serum potassium)
Hypertension + Obesity, snoring, daytime sleepiness
Sleep apnoea
Hypertension + Paroxysmal hypertension with headache, pallor, sweating, palpitations
Phaeochromocytoma
Most common long-term drug use disease
Hypertension
Most common complications of Hypertension (5)
- CV disease (stroke)
- CHD, LVH, AF.
- Renal disease: Focal segmental glomerulosclerosis (FSGE)
- HT Retinopathy.
- Peripheral vascular disease (Aortic aneurism/dissection)
Main causes of Death associated to Hypertension
Stroke (45%)
Hypertension Value Clasification by Murtagh NORMAL
< 130/85 mmHg
Follow Up: 2 years
Hypertension Value Clasification by Murtagh OPTIMAL
< 120/80 mmHg
Follow Up: 2 years
Hypertension Value Clasification by Murtagh HIGH NORMAL
< 140/90 mmHg
Follow Up: 1year
Hypertension Value Clasification by Murtagh G1 MILD
< 160/100 mmHg
Follow Up: 2 months
Hypertension Value Clasification by Murtagh G2 MODERATE
< 180/110 mmHg
Follow Up: 1 month
Hypertension Value Clasification by Murtagh G3 SEVERE
> 180/110 mmHg
Follow Uo: 1-7 days
Hypertension Value Clasification by Murtagh ISOLATED SYSTOLIC
> 140 / <90 mmHg
Follow Up: 1 month
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
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
LOW CV Risk (10%) Hypertension Management
MODERATE CV Risk (10-15%) Hypertension Management
HIGH CV Risk (>15%) Hypertension Management
Mantain life-style modification
Start medical treatment immediately
Hypertension Non-pharmacological
management (7)
- Weight reduction
- Reduction of excessive alcohol intake
- Reduction of sodium intake to ≤4 g/day
- Increased exercise and regular physical activity
- Reduction of psycologic stress
- Smoking sesation
- Management of sleep apnoea
Hypertension Referral Criteria (5)
- Refractory HT
- HT emergency - urgency
- Ongoing target organ impairment
- Kidney failure= GFR< 60ml/min
- If a secondary treatable cause is found
BP Treatment Targets
Circle of Love (image)
Ineffective Antihypertensives Combinations
Diuretic and calcium-channel blocker
Beta blockers and ACE inhibitors
1st Line Antihypertensive Drugs by J Murtagh
Starting Hypertensive Treatment (Murtagh)
Antihypertensive medication in Old and Young Patients
Older: Diuretics, calcium-channel blockers and ACE inhibitors.
Younger: Beta blockers or ACE inhibitors.
Hypertension Drug Therapy 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.
Hypertension Treatment
>65yo with CHF
Thiazides
Hypertension Treatment
>65yo with Ischaemia risk
BetaBlockers
Hypertension Treatment - Young with CHF
ACE inhibitors
Hypertension Treatment Young with Ischaemia risk
Amlodipine
(Never Verapamil or Diltiazem)
Hypertension Treatment
in Asthma
CCB
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.
Hypertension Treatment in Psychiatric patients
Diuretics (least central activity)
Hypertensive Urgency Treatment
> 180/110 mmHg
ORAL:
Nifedipine
Captopril
Clonidine
IV: Hydralazine
Hypertensive Emergency Treatment (4)
> 220/140 mmHg
Hydralazine
Metoprolol
Nitroprusside
Esmolol
All IV
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)
HYPERTENSIVE ENCEPHALOPATHY Investigations
- ECG
- CXR
- Midstream specimen of urine (MSU/dipstick) and urinalysis. Evidence of renal disease: Casts, abnormal urinary red blood cells (greater than 70% dysmorphic).
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
Antihypertensive Drugs List
- Diuretics
- Angiotensin converting enzime (ACE) inhibitors
- Angiotensine II Receptors Blockers (ARBs)
- Beta Blockers (BB)
- Calcium Channel Blockers (CCB)
ACE inhibitors LIST
- Captopril: Short half life (emergency use)
- Enalapril
- Lisinopril
- Ramipril
The other two longer half life: Daily use
ARBs LIST
Valsartan (more pontent 1 tablet/day)
Losartan
Candesartan
Rest lest potent 2 tablets/day
ACE inhibitors MECHANISM OF ACTION (MOA)
ACE Inh: Prevent the conversion of angiotensin I to angiotensin II
↓ ANGIOTENSIN II =
- ↓ Vasoconstriction =
- ↓Periferal Resistance
- EFFERENT renal
artery vasodilation
2↓Aldosterone = Natriuresis
ARBs Blocks the angiotensin II receptors so same MOA
ACE inhibitors & ARBs Indications
- hypertension
- heart failure
- peripheral vascular disease
- diabetes
- cardioprotective after miocardial infarction
NOTE: ACE Inhibitors are always 1st line
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
ACE inhibitors side effects (6)
- Cough (↑Bradikinins)
- Angioedema (↑Bradikinins)
- Disturbance in taste (dysgeusia)
- Rash (↑Bradikinins)
- HYPERkalemia (↓ Aldosterone = ↓ K excretion)
- Hypotension (just the first dose)
Antihypertensive Drugs: Diuretict types LIST
- Loop
- Thiazides & thiazides like
- Potasium sparing
- Osmotic
- Carbonic Anhidrase Inhibitors
Loop Diuretic Mechanism of Action
- Inhibition of sodium and chloride reabsorption in the
thick ascending limb of the loop of Henle by blocking the Na+-K+-2Cl- symporter (cotransporter) - Stimulates the release of protaglandins = Vasodilatation of the AFFETENT artery = ↑ GFR
NOTE: NSAIDs Inihbit prostaglandins synthesis = ↓ GFR (AFFERENT artery vasoconstriction)
Loop Diuretic LIST
Sulfonamide derivatives:
1. Furosemide
2. Bumetanide
3. Torsemide
Non- Sulfonamide derivatives:
4. Ethacrynic acid
Loop Diuretic INDICATIONS
- Edematous states: CHF, APO, cirrhosis with ascites, nephrotic syndrome
- Hypertension
- Hyperkalemia
- Hypercalcemia
- Acute bromide, iodine and fluoride intoxication
Loop Diuretic CONTRAINDICATIONS
Sulfonamide allergy
Alternative: Use Ethacrynic acid
Loop Diuretic SIDE EFFECTS
HYPOS:
Kalemia
Natremia
Calcemia
Mangesemia
Cloremia
HYPER: Uricemia
Loop Diuretic COMPLICATIONS
- Dehydration: This can lead to hyperuricemia/gout
- Hypokalemic Metabolic Alkalosis:
↑pH ↑HCO3 ↓K ↓Na ↓Mg - Ototoxiciti: Hearing loss (stop the drug reverse de effect). Most common with Ethacrynic acid.
- Sulfonamide Allergy:
- Acute interstitial nephritis
- Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
Thiazides & thiazides like Mechanism of Action
- 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 - 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
Thiazides & thiazides like LIST
Benzothiadazine derivatives: Thiazides
- Clorothiazide
- Hydroclorothiazide
Sulfonamide derivative:
- Indapamide
- Chlortalidone
Thiazides & thiazides like INDICATIONS
- Hypertension (1st LINE Diuretic)
- Heart failure
- Older patients (>55 yo)
- Hypercalciuria: Prevent Ca neprholithiasis and ostheoporosis
- Nephrogenic Diabetes Insipidus: Paradoxical effect given by mild hypovolemia caused by the thiazide stimulates the kidney to reabsorb Na and water
Thiazides & thiazides like SIDE EFFECTS
HYPERS:
Uricemia
Glycaemia
Lipidaemia (increase cholesterol and triglycerides)
HIPOS
Kalemia
Natraemia
Magnesemia
- Impotence
Thiazides & thiazides like CONTRAINDICATIONS
- Type 2 diabetes
- Hyperuricaemia
- Kidney failure
- Dyslipidaemia
- Pregnancy
- Sulfonamide allergy: Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
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
Potassium-sparing Diuretics LIST
Direct antagonist:
1. Spironolactone
Indirect atagonist:
2. Amiloride
3. Triamterene
Potassium-sparing Diuretics INDICATIONS
- Hypertension
- Edemaous states: CHF, APO, cirrhosis with ascites, nephrotic syndrome
- After Mopcardial infraction: (↓ mortality rate)
- Hyperaldosteronism
- PCOS: Bunts effects of testosterone
- Liddle’s Syndrome (Na retention and K wasting)
Potassium-sparing Diuretics SIDE EFFECTS
- HYPERkalemia
AVOID: Combination with ACE Inh/ARBs/K suplements. Risk of Metabolic Acidosis - Spironolactone: Antiandrogenic effect
- Gynecomastia
- Impotence - Triamterene:
- Nephrolithiasis
- Combination con Indapamide (NSAID) = AKI
Osmothic Diuretic: Manitol
Features
Aquaretic Diuretic: Mainly excretion of water without electrolites
Only presentation IV
Osmothic Diuretic: Manitol
INDICATIONS
- Head trauma: ↓ ICP
- Rabdomyolisis: Kidney flush out (prevent AKI)
- Hemolysis: Kidney flush out (prevent AKI)
- Glaucoma or Ophtamologic surgery: ↓ Ocular pressure
Osmothic Diuretic: Manitol
SIDE EFFECTS
Rebound effect
1. Worsen edamtous states (pulmonary edema)
- In CHF and Renal Faillure: HYPOnatremia
NOTE: If inadequate water replacement = Dehydration with HYPERnatremia and HYPERkalemia
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
Carbonic Anhidrase Inhibitors (Zolamides) LIST
ORAL
Methazolamide
ORAL & IV
Acetazolamide
TOPICAL (eye drops)
Dorsolamide
Brinzolamide
Carbonic Anhidrase Inhibitors (Zolamides) INDICATIONS
- Elevated intraocular pressure (angle-closure and open-angle glaucoma)
- Brain Pseudotumor
- Edema due to congestive heart failure (with alkalosis)
- Altitude sickness prophylaxis
Carbonic Anhidrase Inhibitors (Zolamides) COTRAINDICATIONS
Sulfonamide allergy
Hepatic disease
Adrenal insufficiency
Renal Faillure
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
Antihypertensive drugs: BETA BLOCKERS - Mechanism of action
ADRENEGIC ANTAGONISTS
- Chronotropic and inotropic heart effects
- Reduction in renin release.
- 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.
BETA BLOCKERS - General Indications
- Hypertension
- > 55yo + Coronary artery disease (CAD)
- Cardiac arrhythmia
- Tachycardia secondary to thyroid storm and anxiety episodes
- Essential tremor
- Glaucoma
BETA BLOCKERS - General Side effects
ALL BB:
- Orthostatic hypotension (take care of the elderly and differentiate from hypoglycemia)
- Bradycardia (AVOID concomitant use with Verapamil / Diltiazem)
- Sudden STOP can cause:
- Arrhythmias
- Rest angina
1st generation BETA BLOCKERS - Side effects
B2 Block (1st generation)
- Bronchoconstriction
- Hypertrigliceridemia
- Hypoglycemia
- Muscular fatigue, insomnia
3rd generation BETA BLOCKERS - Side effects
α1 Block (3rd generation)
- Headache
- Nasal congestion
- Delay ejaculation
BETA BLOCKERS - General Contraindications
ALL:
- Bradycardia, heart block
- Orthostatic hypotension
BETA BLOCKERS - 1st Generation - Contraindications
- Asthma, COPD
- Dyslipidaemia
- DM
- Heart failure
- Peripheral vascular disease
- Pregnancy
BETA BLOCKERS - 2nd Generation -Contraindications
- Heart failure
- Peripheral vascular disease
- Pregnancy
BETA BLOCKERS - 3rd Generation - Contraindications
- Migraine
- Chronic rhinitis
- Delay ejaculation
BETA BLOCKERS - 1st Generation
NON-SELECTIVES
β1 - β2 BLOCKERS
- Propanolol:
- Cross the blood brain barrier → Treatment of MIGRAINE (vasocontriction in the brain) & Essential tremmor - Timolol: ↓ Ocular pressure → Treatment of glaucoma
- Sotalol
BETA BLOCKERS - 2nd Generation
CARDIOSELECTIVE
Only β1 block
- Atenolol
- Metoprolol
- Bisoprolol
- Pindolol
- Esmolol
No side effect of B2 Block: So, safe in asthma, COPD, dyslipidemia and DM
BETA BLOCKERS - 3rd Generation
β1 - α1 BLOCKERS
- Labetalol: Pregnancy and hypertensive emergency
- 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
Antihypertensive drugs: Calcium Channel Blockers - Mechanism of Action
- Negative inotropic and chronotropic heart effect
- Vasodilation
- Relaxation of smooth muscle in the bronchi
Calcium Channel Blockers - Dihydropirimidines Main effect
Vasodilator (including coronary arteries)
Calcium Channel Blockers - Dihydropirimidines LIST
- Nifedipine
- Amlodipine
- Nicardipine
Calcium Channel Blockers - Dihydropirimidines INDICATIONS
- Hypertension
- Asthma
- Stable Angina
- Peripheral vascular disease
- Reynaud’s Phenomenon
Calcium Channel Blockers - Dihydropirimidines SIDE EFFECTS
Reflex tachycardia (↑doses)
Flushing
Dizziness
Peripheral edema
Gingival hyperplasia
Calcium Channel Blockers - NON-Dihydropirimidines Features, Indication, Side effect
Features: Main effect in the heart < vasodilator
Calcium Channel Blockers - NON-Dihydropirimidines Indications
- Verapamil: Cardioselective / Class 4 Antiarrhythmic
- Diltiazem: Hypertension
Calcium Channel Blockers - NON-Dihydropirimidines Side Effects
- Hyperprolactinemia
- Verapamil: Constipation
Calcium Channel Blockers - CONTRAINDICATIONS
- Heart block 2nd and 3rd degree
- Heart failure (verapamil, diltiazem)
CCB: Caution using with
Beta blockers
Digoxin
Cardiac Faillure
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.
Pathological Murmurs History
◦ Family Hx of cardio-myopathy or sudden unexplained death.
◦ Congenital malformations
◦ Exertional syncope
◦ Symptoms of cardiac failure.
Pathological Murmurs Clinical Features
◦ Cyanosis - Breathlessness.
◦ Failure to thrive, not clearly due to other causes.
◦ Thrill with murmur.
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.
Holosystolic Murmurs List
◦ Mitral valve regurgitation
◦ Tricuspid valve regurgitation
◦ Ventricular septal defec
Early Systolic Murmurs List
◦ Mitral regurgitation
◦ Tricuspid Regurgitation
IMMEDIATE REFERRAL IS REQUIRED!!
Diastolic Murmurs List
Always indicate heart disease!!
- Aortic Regurgitation
- Mitral Stenosis
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
Aortic Stenosis Causes
Degenerative calcific aortic stenosis
Rheumatic heart disease
Systemic lupus erythematosus (SLE)
Paget disease
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.
Aortic Insufficiency Acute Causes
- Infective endocarditis
- Aortic dissection
Aortic Insufficiency Chronic Causes
- Hypertension
- Rheumatic heart disease
- Congenital (bicuspid aortic valve)
- Marfan Syndrome
- Aortitis (tertiary syphilis, spondyloarthritis: ankylosing spondylitis, Reiter’s)
Aortic Insufficiency Murmur Characteristics
High-frequency, decrescendo
DIASTOLIC
Best heard at the 3rd or 4th intercostal space at the rigth sternal border (RSB)
Mitral Stenosis Causes
Rheumatic heart disease
Congenital mitral stenosis
Mitral Stenosis Murmur Characteristics
Low pitch
Decrescendo-crescendo (Long duration)
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
Mitral Insufficiency Acute Causes
Infective endocarditis
Rheumatic fever
Papillary muscle rupture due to myocardial infarction
Mitral Insufficiency Chronic Causes
Mitral valve prolapse
Infective endocarditis
Rheumatic heart disease
Ischaemic heart disease
Left ventricular systolic dysfunction
Hypertrophic cardiomyopathy
Mitral Insufficiency Murmur Characteristics
High-pitched, “blowing”
HOLOSYSTOLIC
Best heard at the apex.
Radiates to the axilla and infrascapular area.
Pulmonary Stenosis Causes
Congenital heart disease: T. Fallot
Rheumatic heart disease
Chronic pulmonary hypertension
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)
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.
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
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
Tricuspid Stenosis Causes
Rheumatic fever
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.
Tricuspid Insufficiency Causes
SAME AS PULMONARY INSUFFICIENCY
- Atrial septal defects
- Infective endocarditis
- Rheumatic fever
- Pulmonary hypertension resulting from left-sided heart disease
- Cor pulmonale due to chronic lung disease
- Pulmonary artery hypertension
- Dilated cardiomyopathy
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.
