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CFB > WCS05, WCS06 Cardiovascular System 1, 2: History Taking + Physical Examination > Flashcards

WCS05, WCS06 Cardiovascular System 1, 2: History Taking + Physical Examination Flashcards

1
Q

History taking

A
  1. Chief complaint
    - Injury
    - Pain
    - Stiffness (generalised / localised, all direction / one plane, functional deficit)
    - Swelling (bone / soft tissue, painful / painless)
    - Deformity (location, progressiveness)
    - Instability (muscle weakness / ligamentous deficiency)
    - Weakness (generalised / confined)
    - Altered sensibility (compression / ischaemia)
    - Loss of function
    - Disability
  2. History of present illness
    - Onset
    - Precipitating / Provocation / Alleviating factors
    - Quality
    - Region + Radiation (Referred pain)
    - Severity (Grade 1-4)
    - Time / Course
    - Continuous / Intermittent
    - Associated features
  3. Medical history
  4. Drug history + Allergy
  5. Social history
    - smoke, drink
    - occupation
    - hobby
    - home circumstance
    - family / friend support
    - travel
    - drug abuse
  6. Obstetric history
  7. Family history
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2
Q

History for CVS disease

A
  1. Cardiac symptoms
  2. Past history
    - Angina
    - MI
    - Stroke
    - Atrial fibrillation
    - Rheumatic fever
    - Dental work (Infective endocarditis)
    - Prior test / intervention
    - TB (Pericarditis)
    - Thyroid problems
    - Surgical history
    - Acute hospital admissions
  3. Risk factors
    - HT
    - DM
    - Hyperlipidaemia
  4. Drug history
    - CVS medications
    - Contraceptives (↑ thromboembolic risk)
    - OTC e.g. NSAIDs, Aspirin
    - Herbal e.g. St John’s Wort: enzyme inducer (affect Warfarin level)
    - Heroin, Cocaine
    - Allergy
  5. Social history
    - Smoking
    - Drinking
    - Occupation
    - Exercise
  6. Family history
    - Sudden death
    - CAD
  7. Childhood and development
    - Kawasaki disease
  8. OG history
    - Pregnancy
    - Delivery
    - Menopause (higher risk 10 years after menopause)
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3
Q

***Common symptoms of heart diseases

A

***1. Chest pain (SOCRATES)
- MI
- Angina
- Pericarditis
- Aortic dissection

***2. Dyspnea (exertional, postural, paroxysmal nocturnal dyspnea)
- Heart failure
- Valvular disease
- Angina
- Pulmonary embolism
- Pulmonary hypertension

***3. Palpitations
- Tachyarrhythmia
- Ectopic beats

***4. Syncope / dizziness (exertional, postural, random)
- Arrhythmia
- Postural hypotension (SpC Medicine: Definition: SBP↓>=20 mmHg, DBP↓ >=10 mmHg)
- Aortic stenosis
- Hypertrophic cardiomyopathy
- Atrial myxoma

  1. Edema (peripheral, sacral)
    - Heart failure
    - Constrictive pericarditis
    - Venous stasis
    - Lymphedema
  2. Intermittent claudication (leg pain worsened on exertion, improved at rest)
  3. Systemic symptoms (fatigue, fever, weight loss / gain)
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4
Q

Chest pain / discomfort

A

2 families:
1. Ischaemic chest pain / Angina pectorals
- Stable / Unstable / Acute MI
- Imbalance between blood supply and demand:
—> Coronary artery stenosis
—> Coronary spasm
—> Anaemia, Thyrotoxicosis
—> Aortic stenosis, Hypertension

  1. Atypical chest pain

SOCRATES:
Site
Onset
Character
Radiation
Associations
Time course
Exacerbating / Relieving factors
Severity

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5
Q

Angina pectoris

A

Quality: ***Tightness, Pressure, Squeezing, Heaviness, Burning

Location: ***Retrosternal / slightly to left

Radiation (based on dermatome): Neck, Throat, Lower jaw, Left Shoulder / arm, Interscapular, Epigastrium, Back, ***Never below diaphragm

Mode of onset, offset, duration: Gradual increase + Fade away, 2-10 mins (longer if unstable / MI)

Aggravating factors (***4Es): Eating (∵ redistribution of blood to stomach (CL Lai)), Exertion, Emotion, Environment (hot / cold) (cold: vasoconstriction causing ↑ afterload of heart (CL Lai))

Relieving factors: Rest, Cessation of activity / stress, NTG

Associated symptoms: SOB, Dizziness, Syncope

Silent ischaemia: Angina may be absent in 25% patients esp. DM, elderly
—> present with SOB, Collapse, Dizziness

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6
Q

***Angina vs MI vs Aortic dissection vs Pericardial pain vs Esophageal pain

A

Angina:
- **Constricting pain
- **Arm, Neck (Never below diaphragm)
- ***Relieved by rest / TNG
- Progressive onset
- SOB

MI:
- **Constricting pain
- **Both Arms, Neck (Never below diaphragm)
- ***NOT relieved by rest
- Rapid onset over a few minutes
- N+V, SOB

Aortic dissection:
- **Tearing pain
- **Back
- Sudden onset
- Signs of limb / mesenteric ischaemia e.g. Abdominal pain

Pericardial pain:
- **Sharp pleuritic pain (pain on deep breathing)
- **Postural change may aggravate (Harrison: aggravated by supine, alleviated by sitting up + leaning forward, web: reduce pressure on parietal pericardium by leaning forward)
- Gradual onset
- Flu-like prodrome, fever
- Relieved by NSAIDs

Esophageal pain:
- ***Burning pain
- Heartburn, acid reflux

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7
Q

Stable angina vs Unstable angina vs Acute MI

A
  1. Stable:
    - Triggered by 4E’s
    - < 2-10 mins

Acute Coronary Syndrome (ACS): Unstable angina + MI (NSTEMI + STEMI)

  1. Unstable:
    - More severe pain
    - Lower tolerance for exertion / at rest
    - < 20 mins
  2. Acute MI:
    - More severe pain
    - Sudden onset
    - > 30 mins
    - Associated with SOB, N+V
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8
Q

Functional classification of stable angina

A

Canadian Cardiovascular Society CCS: Grade 1-4

Grade 1:
- Ordinary physical activity
- Angina with strenuous, rapid / prolonged exertion at work / during recreation

Grade 2:
- Slight limitation of ordinary activity

Grade 3:
- Marked limitation of ordinary physical activity
- Climbing <1 FOS

Grade 4:
- Inability to carry on any physical activity without discomfort
- Angina present at rest

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9
Q

Clinical characteristics of Unstable angina

A
  1. Rest angina (worst)
    - angina occurring at rest + prolonged
    - > 20 mins
  2. New-onset angina
    - no previous angina
    - new-onset angina >= CCS class 3 severity
  3. Increasing / Crescendo angina
    - angina that becomes more frequent, longer in duration, lower in threshold
    - increased by >=1 CCS class to class 3 severity
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10
Q

Clinical characteristics of Acute MI

A

Typical features
- middle age / older men, postmenopausal women
- Severe + Prolonged chest pain
- N+V, SOB, ***Diaphoresis (sweating), anxiety

Atypical features
- Extrathoracic pain
- GI symptoms e.g. heartburn
- Prolonged fatigue, weakness
- Palpitation, dizziness, syncope, stroke, embolism
- Silent: DM, elderly, female, post-op

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11
Q

Atypical chest pain

A

Speak against myocardial ischaemia

  1. ***Pleuritic pain (Pericardial effusion)
  2. Primary location in ***middle / lower abdominal region
  3. Pain ***localised at tip of one finger
  4. Pain reproduced with ***movement / palpation of chest wall / arms
  5. Constant pain that persists for ***hours
  6. Very brief pain that lasts ***a few seconds
  7. Pain that radiates to ***lower limbs
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12
Q

Dyspnea

A

Difficult / Laboured respiration / Unpleasant awareness of one’s breathing

Presentation:
- Acute
- Chronic

Etiology:
1. Cardiovascular disorder (30%)
2. Respiratory disorder (30%)
3. Others e.g. Anaemia, Thyrotoxicosis (40%)

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13
Q

***Mechanisms of Dyspnea

A
  1. Increased work of breathing
    - **Left heart failure —> ↑ Pulmonary capillary wedge pressure (> 18mmHg) —> Edema of alveolar wall —> **↓ Lung compliance —> ↑ work of breathing
  2. ↓ Vital capacity
  3. Hypoxia due to oxygen desaturation from pulmonary edema —> Reflex hyperventilation
  4. Bronchial narrowing
  5. Hypoxaemia and CO2 retention e.g. Cyanotic heart disease
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14
Q

Positional Dyspnea

A
  1. Orthopnea (supine) —> CHF, COAD, Ascites, Obesity, Anterior mediastinal mass, Respiratory muscle weakness
  2. Trepopnea (lateral) —> ***Effusion, Airway obstruction, Unilateral lung disease
  3. Platypnea (upright) —> Intracardiac shunt (∵ **positional right-to-left shunt), Parenchymal lung shunt (∵ **↓ V/Q ratio), Hepatopulmonary syndrome (Intrapulmonary shunt)
    - related condition: Orthodeoxia (i.e. Platypnea-Orthodeoxia syndrome)
  4. ***Paroxysmal nocturnal dyspnea —> CHF
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15
Q

***Paroxysmal Nocturnal Dyspnea (PND)

A

Wake up 1-2 hours after sleep to fight for breath

Mechanisms:
1. Lying flat
—> Reabsorption of fluid from tissues into plasma
—> ↑ Venous return
—> Relatively normal right ventricle pump into lung
—> Weak left ventricle cannot pump out additional volume
—> Pulmonary congestion
—> ***Fluid redistribution into lung (1-2 hours)
—> ↑ Left atrial pressure

  1. Fall in PaO2 during sleep

Symptoms:
- Dyspnea
- Cough
- ***Frothy sputum
- Tachycardia
- Crackles

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16
Q

Dyspnea symptoms

A
  1. Dry, unproductive cough
    - pulmonary congestion associated with HF
  2. Haemoptysis
    - bright red pulmonary venous blood from rupture of submucosal pulmonary venules in **Mitral stenosis, **HF
    - darker blood / clots with ***PE
  3. Pink, frothy sputum
    - acute pulmonary edema
  4. Wheezing
    - dyspnea caused by heart disease (cardiac asthma)
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17
Q

Cardiac vs Respiratory Dyspnea

A

Cardiac:
- short duration
- **characteristic PND
- **characteristic Orthopnea
- Edema often present
- associated with **Angina, Palpitation
- Edema, **↑ JVP, ***Cardiomegaly, Basal crepitation, Tachycardia

Respiratory:
- long duration
- NO PND
- Orthopnea may be present
- Edema in **Cor Pulmonale
- associated with Cough, Sputum, Wheezing
- **Inflated chest, ***Wheezing

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18
Q

Classification of Heart Failure

A

New York Heart Association Class 1 (best) to 4 (worst)

Class 1:
- No limitations
- Ordinary physical activity NOT cause fatigue, dyspnea, palpitation (Asymptomatic LV dysfunction)

Class 2:
- Slight limitation of physical activity
- Comfortable at rest
- Ordinary physical activity results in fatigue, palpitation, dyspnea, angina pectoris (Symptomatically “mild” heart failure)

Class 3:
- Marked limitation of physical activity
- Less than ordinary physical activity will lead to symptoms (Symptomatically “moderate” heart failure)

Class 4:
- Symptoms of congestive heart failure are present, even at rest
- With any physical activity, increased discomfort is experienced (Symptomatically “severe” heart failure)

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19
Q

Palpitation

A

Feeling of heart action more vigorous than usual
Unpleasant feeling in chest: Pounding, Racing

  1. Physiologic (Sinus tachycardia e.g. exercise) vs Pathological
    —> Characters: Missed beat, Irregular, Sustained
    —> Trigger: Coffee, Tea, Exercise, Postural change, Meal, Emotion
  2. Onset and Offset
  3. Haemodynamic effects e.g. SOB
  4. Duration, Frequency, Pattern
  5. Associated symptoms: Syncope, Chest pain
  6. Rate and rhythm: indicate whether tachycardia is regular vs irregular: ask patient to tap out rate + rhythm of episode
20
Q

***Causes of palpitation

A
  1. Extrasystoles
    - jump, missed beat, flutter
  2. Sinus tachycardia
    - gradual onset
  3. Supraventricular tachycardia
    - **Regular
    - **    Polyuria (∵ Atrial stretch —> release ANP)
    - triggered by bending / postural change (∵ Re-entry circuit)
    - relieved by vagal manoeuvres e.g. deep breathing, cardiac massage
  4. Atrial fibrillation
    - **Irregular beat
    - **    Polyuria (∵ Atrial stretch —> release ANP)
  5. Ventricular tachycardia
    - **Regular
    - **    Syncope (∵ incomplete filling of ventricle)
21
Q

***Syncope

A

Transient loss of consciousness due to inadequate cerebral blood flow with spontaneous recovery

Causes:
1. Neurocardiogenic syncope (60%, relatively benign)

  1. ***Arrhythmia
    - Supraventricular / Ventricular tachycardia
    - Adams-Stokes attack: asystole / ventricular arrhythmia
  2. **Exertional syncope (structural causes)
    - **    Aortic stenosis
    - **Hypertrophic cardiomyopathy
    - **    CAD
  3. Carotid sinus syncope
    - Reflex bradycardia
    - Hypotension
  4. Postural syncope
22
Q

History for syncope

A
  1. Witnesses
    - witnessed the entire event
  2. Situation / Trigger
  3. Age
    - elderly: rule out heart disease
    - young: neurocardiogenic more likely
  4. Underlying heart disease
  5. Family history
  6. Number of episodes
    - <3: more malignant / life-threatening
    - >3: more likely benign
  7. Previous evaluation
  8. Medications
    - hypotension
    - bradycardia
    - pro-arrhythmia (QT prolongation)
23
Q

***Syncope vs Seizure

A
  1. Loss of consciousness by pain, micturition, exercise, pain, defaecation, stress
    Syncope: +
    Seizures: -
  2. Sweating + Nausea
    Syncope: +
    Seizures: -
  3. Aura
    Syncope: -
    Seizures: +
  4. Tongue biting
    Syncope: -
    Seizures: +
  5. Disorientation
    Syncope: -
    Seizures: +
  6. Clinic / Myoclonic jerks / Rhythmic movements
    Syncope: +/-
    Seizures: ++
  7. Slowness in returning to consciousness
    Syncope: -
    Seizures: +
  8. Unconscious > 5 mins
    Syncope: -
    Seizures: +
24
Q

Drug history

A

Angina:
- Thyroxine
- Aspirin / NSAID: drug-induced anaemia

Dyspnea:
- Beta-blocker: in asthmatics
- Beta-blocker: exacerbating heart failure
- Ca-blocker (Verapamil, Diltiazem)
- NSAIDs

Palpitation:
- Thyroxine: tachycardia
- Beta2-agonist
- Digoxin toxicity
- Diuretics: hypokalaemia
- Tricyclic antidepressant

Syncope:
- Vasodilator
- Beta-blocker, Ca-blocker, Digoxin, Amiodarone: bradycardia

Edema:
- Glucocorticoid
- NSAIDs
- Ca-blocker e.g. Nifedipine, Amlodipine

25
Q

Family history

A
  1. CVS disease at a young age
    - MI
    - Hypertension
    - Thrombophilia
  2. Parents still in good health?
    - age + cause if deceased
  3. Unexplained deaths in young relatives?
    - long QT syndrome
    - channelopathies
26
Q

Social history

A
  1. Smoking
  2. Alcohol
  3. Recreational drug
  4. Diet
  5. Exercise
  6. Living situation
  7. ADLs
  8. Occupation
27
Q

Systemic enquiry

A

Symptoms from other systems
1. Respiratory
2. GI
3. Urinary
4. CNS
5. MSS
6. Dermatology

28
Q

General inspection

A
  1. Body built
    - Weight
    - Height
    —> Marfan: Mitral valve prolapse, Aortic dissection
  2. Facial features
    - Down’s: Congenital heart diseases: Atrial septal defect, AV canal malformation
    - Acromegaly: Hypertension, LV hypertrophy, CAD
    - ***Malar flush: Mitral stenosis
    - Xanthelasma
  3. Other features
    - Tendon xanthoma (move with tendon vs Tophi)
    - Striae: Cushing disease
    - Gynaecomastia: Digoxin, Spironolactone
    - Hyperthyroidism: Rapid atrial fibrillation, Heart failure
    - Hypothyroidism: Hypertension, Pericardial effusion, Heart failure
29
Q

General examination

A

Eyes:
1. Pallor
2. Jaundice
3. Cyanosis
4. Xanthelasma
(- High arch palate (Marfan))

Hands:
5. Clubbing
- Cyanotic heart disease
- Infective endocarditis
- Differential clubbing in PDA (only when Eisenmenger syndrome) —> ∵ PDA is distal to left subclavian artery —> affects mainly lower limb with oxygen desaturation

  1. Signs of Infective endocarditis
    - Splinter haemorrhage, Osler’s nodes, Janeway lesion, Petechiae in eyelid / oral cavity, Roth’s spot (fundoscope)
  2. Palmar erythema
  3. Tendon xanthoma (move with tendon vs Tophi)
    (- Tar stain)
    (- Arachnodactyly (Marfan))

Legs:
9. Edema
- Ankle edema
- Sacral edema
10. Toe clubbing
11. Ulcer
12. Temperature

Others:
13. Radial Pulse
- Rate
- Rhythm
- Radio-radial / Radio-femoral delay (Coarctation, Subclavian stenosis, **Aortic dissection)
- Collapsing pulse (AR, **PDA, ***Hyperdynamic circulation)

  1. Brachial pulse
    - Volume
    - Character (**Slow rising (AS), **Bounding (AR))
  2. Lymphadenopathy
  3. Temperature
  4. Respiratory rate
  5. BP
30
Q

Arterial system examination

A

ALL arterial pulses + Compare both sides
1. **Radial
2. **Brachial
3. Subclavian
4. ***Carotid
5. Femoral
6. Popliteal
7. Posterior tibial
8. Dorsalis pedis

Check:
1. Atherosclerosis
2. Embolism occlusion
3. Dissection
4. Vascular compression
5. Congenital anomaly
6. Aortic coarctation

31
Q

Arterial Pulse characteristics

A
  1. Rate: 60-100 beats / min
  2. Rhythm: Skipped beats (regularly irregular), ***Atrial fibrillation (irregularly irregular)
  3. Volume:
    - Diminished —> Poor cardiac output, AS (Slow rising, anacrotic), Pericardial effusion
    - Increased —> Pounding pulse (    AR) —> Collapsing pulse
  4. Character / Waveform
    - Normal
  • **Bisferiens (Biphasic: Bouncing pulse + Slow rising pulse)
    —> **    Hypertrophic obstructive cardiomyopathy (HOCM) (1st pulse: ejection of blood —> drop in ventricle volume —> obstruction —> SV decrease —> obstruction relieved —> SV increase again)
    —> AR (bouncing) + AS (slow rising)
  • Corrigan’s sign / Collapsing pulse
    —> **AR
    —> **    Hyperdynamic circulation (e.g. anaemia, AV fistula, thyrotoxicosis)
    —> *** Intracardial shunting (e.g. PDA, other shunting)
    —> Rupture sinus of Valsalva
  • Slow rising
    —> ***AS
  • Pulsus alternans (alternating strong and weak beats)
    —> LV systolic impairment

Volume + Character best felt in Carotid / Brachial arteries
—> ∵ waveform changes when going into peripheral
—> 2nd wave dampen (same as atherosclerosis, aging, hypertension)

  1. BP
    - High BP —> check for Hypertensive retinopathy
32
Q

Pulsus Paradoxus

A

Exaggerated BP drop during inspiration due to ***Cardiac tamponade

Deep breath
—>
1. Expansion of pulmonary vasculature
—> ↑ blood pooled in lungs
—> ↓ venous return to Left heart

  1. ↑ Venous return
    —> ↑ blood in Right heart
    —> Push against Left heart
    —> ↓ BP (<10 mmHg)

Effect exaggerated when heart confined within ***fixed chamber / low compliance e.g. Cardiac tamponade
1. Compression of Right heart prevent ↑ RV output
—> exaggerate ↓ in venous return to Left heart
—> >10-15 mmHg ↓ in BP

  1. Push against Left heart even more since pressure gradient between LV and RV ↓
    —> >10-15 mmHg ↓ in BP

(NOT commonly seen in Constrictive pericarditis since pressure is not totally equalised)

33
Q

Jugular venous waveform

A

3 Positive waves:
- A wave: **Right atrial contraction, **precede carotid pulse (ventricular contraction)
- C wave: Tricuspid closure, separately visible
- V wave: **Right atrial filling during ventricular systole + Tricuspid closed, **roughly synchronous with carotid pulse

2 Negative waves:
- X descent: **Right atrial relaxation + Passive pulling during right ventricular systole
- Y descent: Negative deflection of Right atrial pressure during tricuspid opening, **Ventricular filling

34
Q

JVP vs Carotid pulse

A

JVP (Internal jugular vein):
- lower, lateral
- **double peak / biphasic
- **not palpable
- **more visible with inspiration but mean pressure **decreases (blood forced back into right ventricle so lower waveform but more forceful contraction so higher amplitude waveform except with Kussmaul’s sign: Constrictive pericarditis / Tamponade)
- **decrease with upright posture
- **obliterated by pressure
- Hepatojugular reflux: **transient increase in pressure when abdominal compression —> **sustained increase in **Constrictive pericarditis, **Pericardial effusion, Heart failure ∵ heart cannot handle ↑ venous return

Carotid artery:
- deeper, medial
- single peak
- forceful, palpable
- no change with inspiration
- no change with posture
- cannot obliterated by pressure
- no effect when abdominal compression

35
Q

JVP characteristics

A
  1. ↑JVP (> 4.5cm)
    - **Right ventricular failure
    - Fluid overload
    - SVC obstruction
    - **    Tricuspid regurgitation
    - ***Constrictive pericarditis
  2. ↓ JVP
    - Hypovolemia
    - Dehydration
  3. Normal
  4. ***Absent A wave
    - Atrial fibrillation
  5. Giant A wave
    - ↓ RV compliance —> forceful RA contraction
    - Pulmonary hypertension, PV / TV stenosis
  6. ***Cannon A wave (Intermittent Giant A wave)
    - AV dissociation
    - Complete heart block, Atrial flutter, Ventricular pacing, Ventricular tachycardia
  7. ***Giant V wave
    - Tricuspid regurgitation
  8. Steep X, Y descent
    - Constrictive pericarditis
  9. Attenuated Y descent
    - Cardiac tamponade (difficult to fill ventricle)
36
Q

***Precordium examination

A

Inspection
1. Chest wall abnormalities —> displace heart and affect palpation, auscultation
- Precordial bulging (cardiomegaly esp. RV dilation)
- Pectus excavatum / carinatum
- Kyphosis / Scoliosis

  1. Visible apex + Hepatic pulsation
    - Volume vs Pressure overload
    - LV (apical pulsation) vs RV (left parasternal pulsation)
  2. Surgical scar
    - Central (sternotomy, thoracotomy)
    - Clavicular (pacemaker, ICD)
    - Lateral (valvuloplasty)
  3. Dilated veins
    - SVC, IVC obstruction
    - Coarctation of aorta

Palpation
1. **Apex: most lateral, inferior pulsation (left lateral / lean forward to make it more obvious)
- Displaced: Cardiac enlargement
- Heaving / Sustained: **LV hypertrophy, **AS (longer duration)
- Thrusting / Hyperdynamic: ↑ LV volume e.g. **AR (forceful but short duration), **MR
- Double: **HOCM (sustained LV impulse + prominent early diastolic filling impulse (2nd apical impulse: forceful LA contraction against stiff LV i.e. palpable S4 due to LV hypertrophy))
- Tapping: Palpable 1st heart sound e.g. ***MS

  1. ***Parasternal heave: RV volume / pressure overload
  2. ***Thrills

Auscultation (Mitral, Tricuspid, Pulmonary, Aortic area)
1. Apex: Bell —> **MS (Left lateral) —> compare with Carotid pulse as reference to time cardiac cycle
2. Apex: **Bell —> S3, S4
3. Apex: Diaphragm —> **MR (Radiate to axilla)
4. Tricuspid
5. Pulmonary: PS, PR
6. Aortic: AS
7. Carotid: **Bell —> **AS (Radiate to both carotid) / Carotid stenosis (only one side)
8. Left sternal border: **Diaphragm —> ***AR —> sit up, radiation to carotid + axilla
9. Extra heart sound (e.g. pericardial friction rub)
10. Bi-basal crackles

37
Q

Auscultation

A
  1. Apex
    S1 (Mitral valve closure)
    - Strong: **MS, Tachycardia, High CO
    - Weak: **    MR, Impaired LV contraction, 1st degree AV block
    - Varying: AF, Complete heart block

S3 (low-pitch)
- Rapid LV filling
- Physiological in young person
- Heart failure (***LV volume overload)

S4 (low-pitch)
- Forceful Atrial contraction to fill ***stiff Ventricle (Diastolic dysfunction)
- Always pathological

Gallop rhythm (3 heart sounds heard): Heart failure

  1. Aortic, Pulmonary area
    S2
    - Strong: **Pulmonary hypertension, **ASD, Dilated pulmonary artery
    - Weak: AR, **AS, **PS, Aging
    - Splitting (high pitch heard by diaphragm)
    —> normal in inspiration
    —> **exaggerated in PS, RV overload, Pulmonary hypertension (Delay in closure of pulmonary valve)
    —> exaggerated in RBBB (electrical delay)
    —> **    fixed splitting in ASD
  2. Extra heart sound
    - **Opening snap: MS
    - **    Ejection click: AS
    - **Midsystolic click: MVP
    - Pericardial rub (Friction rub): **    3 phases (Atrial systolic, Ventricular systolic, Ventricular diastolic) (High pitch squeaky)
    - Pleuro-pericardial rub
    - Mechanical heart sound: Prosthetic valve sound
  3. Murmur (Grade 1-6)
38
Q

Mechanism of murmur

A
  1. High velocity flow
  2. Local obstruction
  3. Abrupt increase in caliber
  4. Abrupt increase in caliber + local obstruction
39
Q

Murmur

A
  1. Grading: 1-6
  2. Timing: Systolic / Diastolic (feel the carotid pulse)
  3. Character:
    - Pitch (low, medium, high)
    - Quality (blowing, harsh, musical, rumbling)
  4. ***Site of maximum Propagation + Radiation (Axilla, Neck)
  5. ***Effect of posture (left lateral + sitting)
  6. ***Effect of respiration
    - inspiration: louder right heart sound (e.g. PS, TR, ASD)
    - expiration: louder left heart sound (e.g. AS, HOCM, AR, VSD)
  7. ***Effect of manoeuvre (if needed)
40
Q

Types of murmurs

A

Systolic
1. Ejection Systolic murmur
- AS: **Slow upstroke, Low volume pulse, Merged / **Reverse splitting of S2 if severe (∵ slow closure of aortic valve + LV volume overload), **soft S2
- PS (heard at pulmonary area)
- ASD: **Fixed splitting, ***loud S2

  1. Pansystolic murmur
    - MR: **Radiate to axilla, loudest at axilla, **soft S1
    - TR: ***giant V wave, ↑ with inspiration
    - VSD: all over the place, loudest at left sternal area, thrill
  2. Late Systolic murmur
    - MVP

Diastolic
1. Early Diastolic murmur
- AR: **high pitch blowing, loudest at left sternal border (can be heard at apex like MS if severe: Austin Flint murmur), associated with ejection systolic murmur, **exhale + lean forward
- PR

  1. Mid-Late Diastolic murmur
    - MS: **low pitch, rumbling, **loudest at apex (left lateral), ↑ with exercise, associated with MR, ***loud S1
    - PR (Graham steel), AR (Austin flint)

Continuous murmur
1. **PDA: **differential clubbing, cyanosis, left parasternal heave, ***collapsing pulse, best heard in 2nd left ICS, may radiate to back interscapular space

  1. AS + AR
41
Q

***Manoeuvres for auscultation

A

Mitral valve prolapse (Systolic murmur)
1. Squatting: ↑ Peripheral resistance + Ventricular volume —> ↓ Mitral prolapse —> ↓ duration of murmur
2. Standing: ↓ Ventricular volume —> ↑ Mitral prolapse —> ↑ duration of murmur
3. Valsalva’s: ↓ Venous return —> ↑ Mitral prolapse —> ↑ duration of murmur
4. Isometric exercise e.g. handgrip: ↑ Peripheral resistance —> ↓ Mitral prolapse —> ↓ duration of murmur
—> ***記: ↓ Ventricular filling —> ↑ Laxity of Chordae tendinae —> ↑ Mitral prolapse

Obstructive Hypertrophic Cardiomyopathy
- **Ejection systolic murmur but no radiation (vs AS: radiate to carotid)
- Squatting to Standing / Valsalva’s: ↓ Venous return —> ↓ Ventricular volume —> ↑ Obstruction of outflow tract —> ↑ intensity of murmur
- **Jerky pulse (rapid upstroke then suddenly stop due to LVOT)
- **Double apex beat
- S4
—> **記: ↓ Ventricular filling —> ↑ Obstruction of outflow tract —> ↑ intensity of murmur

Aortic stenosis:
- Squatting: ↑ Peripheral resistance + Ventricular volume —> ↑ blood volume ejected into Aorta —> ↑ intensity of murmur
- Standing / Valsalva’s: ↓ Venous return —> ↓ blood volume ejected into Aorta —> ↓ intensity of murmur
—> ***記: ↓ Ventricular filling —> ↓ blood volume ejected into Aorta —> ↓ intensity of murmur

42
Q

Other examinations

A
  1. Lung
    - ***Heart failure —> bilateral basal crackles
  2. Arterial blood pressure
    - ***Orthostatic hypotension (BP↓ >= 10mmHg, HR↑ >= 20 beats/min)
  3. Abdomen
    - ***Tricuspid regurgitation —> Pulsatile + Enlarged liver
  4. Fundal examination
    - ***Hypertension
43
Q

Hyperdynamic circulation

A
  • Abnormally ↑ circulatory volume

Causes:
- Systemic vasodilation + ↓ Peripheral vascular resistance (e.g. septic shock, preeclampsia, AV fistula and other physiological and psychiatric conditions)
—> ↓ pulmonary capillary wedge pressure (i.e. LA pressure) + ↓ BP
—> collapsing pulse / bounding pulse

  • To compensate the heart will increase CO and HR
    —> ↑ pulse pressure + sinus tachycardia
44
Q

Collapsing pulse

A

Indicate ***low filling resistance (i.e. empty artery) in blood vessels from LV
- Rapid upstroke: Rapid filling of empty artery (∵ ↑ amount of blood pumped from LV)
- Collapsing / Downstroke: Sudden fall in diastolic BP (∵ regurgitation / rapid emptying of artery ∵ ↑ blood velocity)

Causes:
1. Physiological states
- Exercise
- Alcohol
- Pregnancy

  1. Hyperdynamic circulation
    - Anaemia
    - Thyrotoxicosis
    - Cirrhosis
    - Systolic hypertension with wide pulse pressure
  2. Leak in arterial circulation (∵ ↑ LV volume)
    - AR
    - PDA
    - Aorto-pulmonary window
    - Rupture sinus of Valsalva
    - Large VSD
  3. Complete heart block (∵ ↑ LV volume)
45
Q

Continuous murmur

A

Patent ductus arteriorsus:
—> ∵ Flow in aorta is continuous (vs other L-to-R shunt e.g. VSD, ASD)
—> Continuous shunt from aorta to pulmonary artery
—> Continuous murmur (accentuation in systolic phase)

46
Q

Pitting vs Non-pitting edema

A

Pitting:
- Purely water in interstitial space
—> ∵ Transudative cause (↑ Hydrostatic pressure / ↓ Oncotic pressure)

Non-pitting:
- Water + Protein in interstitial space (protein is non-pitting)
—> ∵ Exudative cause (↑ Capillary permeability / ↓ Lymphatic drainage)

CFB (43 decks)

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