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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
Family history
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
Social history
1. Smoking 2. Alcohol 3. Recreational drug 4. Diet 5. Exercise 6. Living situation 7. ADLs 8. Occupation
27
Systemic enquiry
Symptoms from other systems 1. Respiratory 2. GI 3. Urinary 4. CNS 5. MSS 6. Dermatology
28
General inspection
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
General examination
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 6. Signs of Infective endocarditis - Splinter haemorrhage, Osler’s nodes, Janeway lesion, Petechiae in eyelid / oral cavity, Roth’s spot (fundoscope) 7. Palmar erythema 8. 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) 14. Brachial pulse - Volume - Character (***Slow rising (AS), ***Bounding (AR)) 15. Lymphadenopathy 16. Temperature 17. Respiratory rate 18. BP
30
Arterial system examination
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
Arterial Pulse characteristics
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) 6. BP - High BP —> check for Hypertensive retinopathy
32
Pulsus Paradoxus
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 2. ↑ 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 2. 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
Jugular venous waveform
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
JVP vs Carotid pulse
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
JVP characteristics
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
***Precordium examination
Inspection 1. Chest wall abnormalities —> displace heart and affect palpation, auscultation - Precordial bulging (cardiomegaly esp. RV dilation) - Pectus excavatum / carinatum - Kyphosis / Scoliosis 2. Visible apex + Hepatic pulsation - Volume vs Pressure overload - LV (apical pulsation) vs RV (left parasternal pulsation) 3. Surgical scar - Central (sternotomy, thoracotomy) - Clavicular (pacemaker, ICD) - Lateral (valvuloplasty) 4. 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 2. ***Parasternal heave: RV volume / pressure overload 3. ***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
Auscultation
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 2. 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 3. 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 4. Murmur (Grade 1-6)
38
Mechanism of murmur
1. High velocity flow 2. Local obstruction 3. Abrupt increase in caliber 4. Abrupt increase in caliber + local obstruction
39
Murmur
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)
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Types of murmurs
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 2. 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 3. 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 2. 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 2. AS + AR
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***Manoeuvres for auscultation
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
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Other examinations
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
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Hyperdynamic circulation
- 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
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Collapsing pulse
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 2. Hyperdynamic circulation - Anaemia - Thyrotoxicosis - Cirrhosis - Systolic hypertension with wide pulse pressure 3. Leak in arterial circulation (∵ ↑ LV volume) - AR - PDA - Aorto-pulmonary window - Rupture sinus of Valsalva - Large VSD 4. Complete heart block (∵ ↑ LV volume)
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Continuous murmur
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)
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Pitting vs Non-pitting edema
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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