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Comprehensive Cardiovascular Examination Guide

The document describes examining a patient's cardiovascular system including vital signs, ECG, urine dipstick, and fundoscopy. It then discusses examining the patient's general appearance, peripheral pulses, neck, chest, heart sounds, murmurs, and lab tests relevant to cardiovascular examination.

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202213
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100% found this document useful (1 vote)
10 views6 pages

Comprehensive Cardiovascular Examination Guide

The document describes examining a patient's cardiovascular system including vital signs, ECG, urine dipstick, and fundoscopy. It then discusses examining the patient's general appearance, peripheral pulses, neck, chest, heart sounds, murmurs, and lab tests relevant to cardiovascular examination.

Uploaded by

202213
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

CVS examination

I want to complete my examination by checking his vital signs including blood pressure, performing an ECG
to look for ischemic changes, ordering a urine dipstick for microscopy haematuria, and fundoscopy to look
for Roth’s spots.

I did a cardiovascular examination on patient’s name and age

On general examination, the patient is alert and conscious, able to obey command
He is not in obvious pain or in respiratory distress
- He was in respiratory distress by evidence of increased respiratory rate, use of accessory muscle,
presence of oxygen supply, central/peripheral cyanosis
He appeared pale/jaundiced.
Nutritional status was adequate/cachexic/obese.
There was a branula attached on the left/right dorsum part of the hand connected to the IV drip.
At the bedside, there is the presence of __________ (sputum pot, medication, walking aid)

On peripheral examination, there were no clubbing, peripheral cyanosis, tar staining and stigmata of
infective endocarditis. Capillary refill time was less than 2s. The palm was moist, pink, and warm. Pulse rate
was normal with __ bpm with regular rhythm and good volume. Radio-radial delay was present/absent and
collapsing pulse was present/absence.
- There is the presence of finger clubbing grade (?) by evidence of loss of Lovibond’s angle and
Schamroth’s window
- There is the presence of stigmata of infective endocarditis such as splinter hemorrhage, Osler
nodes, Janeway lesions

On examination of the face and neck, there was no conjunctival pallor, scleral jaundice, corneal arcus and
xanthelasma. There was no central cyanosis and oral hygiene was fair. High arch palate was absent. JVP
was raised measuring about __ cm-water.

On inspection of the chest, there was chest wall deformity possibly pectus carinatum/excavatum, there was
also mid sternotomy scar measuring about __ cm, suggesting of __________. On palpation, apex beat was
palpable at the 5th intercostal space midclavicular line. Parasternal heave and thrills were not palpable/
were palpable. On auscultation, the 1st and 2nd heart sounds present, dual rhythm and no murmur. There
was no carotid bruit. There was also no bibasal crepitation heard in the lungs. There is no pitting sacral or
lower limbs edema.

Scar
- Median sternotomy scar – Open heart surgery (valve replacement, CABG, cardiac transplant)
- Thoracotomy scar at the left infraclavicular area – Pacemaker insertion
- Posterolateral thoracotomy – Pulmonary resection
- Anterolateral thoracotomy – Pneumonectomy, pneumothorax surgery
- Scar within the safety triangle – Chest drainage

Murmur
- Type
- Grade
- Location
- Maneuver
- Radiation
- Heart failure signs

There is pansystolic murmur, grade 3, best heard at the apex area, accentuated by expiration, radiating to
the axilla, suggesting of mitral regurgitation and not in failure.
Lab investigation:
1. FBC (anaemia, leucocytosis)
2. Cardiac enzyme
- Myoglobin start 1-4 hr, peak 6-12 hrs
- Troponin T start 3-4 hr, peak 24 hrs
- Troponin I start 4-6 hr, peak 18 hrs
- CKMB start 4-6 hr, peak 24 hrs
- Creatinine kinase
- Lactate dehydrogenase (48 hr-72 hrs)
3. Blood culture
4. ESR, CRP,
5. Chest x ray, ECG, CT angiogram, Echo,
6. LFT, RP
Finger clubbing
Method
 Loss of Lovibond’s angle
 Loss of Schamroth’s window

Grading
1: Fluctuation and softening of nail bed
2: Increased normal Lovibond’s angle
3: Increased nail bed convexity
4: Clubbed appearance
5: Shiny or glossy change in nail with longitudinal striations

Etiologies
Cardiovascular Respiratory ABCDEF Gastrointestinal Endocrine
- Cyanotic congenital - Pulmonary abscess - Liver cirrhosis - Thyrotoxicosis
heart disease - Bronchiectasis, - Inflammatory bowel - Hyperparathyroidism
- Infective endocarditis bronchogenic disease
- Aortic aneurysm carcinoma - Celiac disease
- Atrial myxoma - Cystic fibrosis
- Don’t say COPD
- Lung empyema
- Lung fibrosis

Dyslipidemia
Clinical manifestations
 Hypercholesterolemia: Corneal arcus, xanthelasma, tendon xanthomata, tuberous xanthoma
 Hypertriglyceridemia: Eruptive xanthoma

Radial pulse
Characteristics
 Pulsus alternans (alternating strong and weak beats) – Left ventricular failure
 Small volume – Aortic stenosis, pericardial effusion, hypovolemia
 Collapsing pulse – Aortic regurgitation, Patent ductus arteriosus (PDA)

Rhythm
 Regularly irregular – Sinus arrhythmia, ectopic ventricular beats
 Irregularly irregular – Atrial fibrillation

Radio-radial delay
Pathophysiology
 Disturbance in aortic diameter proximal to the right subclavian artery

Etiologies
- Atherosclerotic plaque
- Aneurysm
- Subclavian artery stenosis

Radio-femoral delay
Etiologies
- Coarctation of aorta
- Upper limb hypertension
Cyanosis
Definition: Bluish discoloration of the skin and mucosa due to increased deoxygenated hemoglobin >5 g/dL
Central Peripheral
Etiologies Etiologies
 Ventilation:  Cold temperature (peripheral vasoconstriction)
- Airway obstruction,  Fever/hypothermia
- Respiratory muscle weakness  Sepsis
 Gas exchange:  Shock
- Poor pulmonary perfusion (shock, pulmonary embolism,  Hypoglycemia
right to left shunt)  Raynaud phenomenon
- Inadequate gas exchange (pneuthorax, pleural effusion,
pulmonary edema, lung parenchymal disease)
- ↓ O2 carrying capacity (methemoglobinemia)
 Ventilation control

Jugular venous pressure


Characteristics
 Visible but not palpable
 Prominent inward movement
 Biphasic wave
 It decreases on inspiration
 Occludable

Method
 >3cm above the zero point
 Positive hepatojugular reflux: JVP rises with abdominal palpation

Apex beat
Definition: Most lateral and inferior point palpable heart beat
Anatomical location: Left 5th intercostal space at the mid-clavicular line

Abnormal characteristics
 Heaving (pressure overload): Forceful/sustained impulse at the apex area
- Aortic stenosis, systemic hypertension

 Thrusting (volume overload): Displaced, diffuse and non-sustained impulse


- Mitral regurgitation, dilated cardiomyopathy

 Displaced apex beat


- Left/right ventricular hypertrophy

Parasternal heave
Definition: Impulse that lifts the palpating hand at the left sternal edge
Etiologies: Right ventricular hypertrophy, left atrial hypertrophy

Thrills
Definition: Palpable murmur
 Apex: Left ventricular hypertrophy
 Lower left sternal edge: Ventricular septal defect
 Upper left sternal edge: Pulmonary stenosis
 Suprasternal: Aortic stenosis
Heart sounds
S1 (Closure of atrioventricular valve and end diastole) and S2 (Closure of semilunar valve and end systole)
S1 – Heart sound heard with pulsation of carotid artery

Murmur Type Location Maneuver Radiation


Mitral stenosis Mid diastolic murmur Apex Expiration + turn to the left -
Mitral regurgitation Pansystolic murmur Apex Expiration Axilla
Tricuspid stenosis Mid diastolic murmur Left lower sternal edge Inspiration -
Tricuspid regurgitation Pansystolic murmur Left lower sternal edge Inspiration -
Pulmonary stenosis Ejection systolic murmur Left upper sternal edge Inspiration -
Pulmonary regurgitation Early diastolic murmur Left upper sternal edge Inspiration -
Aortic stenosis Ejection systolic murmur Right upper sternal edge Expiration Carotid artery
Aortic regurgitation Early diastolic murmur Right upper sternal edge Expiration + leaning -
forward

Pansystolic murmur
It begins with S1 and ends at S2 with constant intensity
Murmur Characteristics Other signs Etiologies
Mitral regurgitation Tachypnea/dyspnea, Rheumatic heart disease,
Displaced apex beat, Cardiomyopathy,
Thrusting apex beat, Papillary muscle dysfunction,
Apex thrill Infective endocarditis,
Myocardial infarction
Tricuspid regurgitation Raised JVP, Right ventricular failure,
Parasternal heave, Infective endocarditis,
Pulsatile hepatomegaly, Tricuspid valve prolapse,
Right nipple dancing sign, Papillary muscle infarct,
Ascites, edema, pleural effusion, Ebstein’s anomaly,
Pulmonary hypertension Carcinoid syndrome
Ventricular septal defect Loud, harsh, blowing murmur Thrill at lower sternal edge Congenital
Location: Lower left sternal edge Left precordial prominence
Parasternal heave
Displaced apex beat
Apex thrust

Ejection systolic murmur


It begins after S1 and ends before S2 + Crescendo-decrescendo
Murmur Characteristics Other signs Etiologies
Aortic stenosis Exertional chest pain, dyspnea, Degenerative calcification
syncope Rheumatic heart disease
Anacrotic pulse
Apex/suprasternal thrills

Pulmonary stenosis Raised JVP, Congenital


Pulmonary thrills Carcinoid syndrome
Atrial septal defect Location: Left middle/upper Congenital
sternal edge

Late systolic murmur


It begins in late systole and ends at S2 + Decrescendo
Murmur Characteristics Other signs Etiologies
Mitral valve prolapse Blowing murmur preceded by a Myxomatous degeneration of
mid-systolic click mitral valve tissue
Atrial septal defect
Hypertrophic cardiomyopathy
Marfan syndrome
Early diastolic murmur
It begins with S2 and ends before S1 + Decrescendo
Murmur Characteristics Other signs Etiologies
Aortic regurgitation Collapsing pulse Rheumatic heart disease,
Widen pulse pressure Aortic root dilatation
Peripheral signs Infective endocarditis,
Dissecting aneurysm
Pulmonary regurgitation Pulmonary hypertension
Infective endocarditis
Congenital

Mid diastolic murmur


It begins after S2 and ends before S1 + Decrescendo
Murmur Characteristics Other signs Etiologies
Mitral stenosis Dyspnea, orthopnea and Rheumatic heart disease,
hemoptysis Congenital
Mitral flush
Atrial fibrillation
Tapping apex beat
Tricuspid stenosis Raised JVP Rheumatic heart disease
Liver pulsation

Peripheral signs of aortic regurgitation


 Corrigan’s: Prominent carotid pulsation
 De Musset’s: Head nodding with heartbeat
 Duroziez’s: Femoral artery murmur on palpation
 Muller’s: Uvula pulsation
 Quincke’s: Nail bed pulsation

Common questions

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Ischemic changes on an ECG, such as ST-segment depression or elevation, T-wave inversion, or pathological Q waves, suggest myocardial ischemia or infarction . These findings prompt further investigations like cardiac enzyme studies (e.g., troponin, CKMB) to confirm myocardial injury, and imaging such as echocardiography or coronary angiography to detect structural or vascular changes .

Peripheral cyanosis is primarily due to conditions that cause increased oxygen extraction by tissues, such as peripheral vasoconstriction from cold temperatures, shock, or Raynaud phenomenon, leading to a blue discoloration in extremities . Central cyanosis, on the other hand, results from systemic issues affecting the oxygenation of blood, such as airway obstruction, ventilation-perfusion mismatch, or right-to-left cardiac shunts, which lead to a bluish discoloration observable in both the skin and mucous membranes .

Heart murmurs indicate different pathologies based on their timing, location, and characteristics. Systolic murmurs like ejection systolic and pansystolic can indicate aortic stenosis or mitral regurgitation, respectively, based on their location and radiation . Diastolic murmurs such as mid-diastolic may point to mitral stenosis, while continuous murmurs suggest patent ductus arteriosus . Distinguishing features include radiation patterns, changes with maneuvers, and accompanying symptoms .

A suspicion of left ventricular hypertrophy arises from findings such as a displaced and heaving apex beat, which indicates pressure overload often seen in aortic stenosis or systemic hypertension . These findings suggest that the left ventricle is working against increased resistance, leading to muscle hypertrophy .

Capillary refill time is a quick assessment tool to evaluate peripheral perfusion; normally it should be less than 2 seconds . A prolonged capillary refill time suggests inadequate blood circulation, which may be due to shock, hypovolemia, or peripheral vascular disease, indicating potential cardiovascular or systemic issues .

An ejection systolic murmur due to aortic stenosis is typically heard at the right upper sternal edge and radiates to the carotids, potentially accompanied by exertional chest pain, syncope, and a delayed carotid pulse . In contrast, pulmonary stenosis produces a murmur best heard at the left upper sternal edge, often without carotid radiation, and may cause signs of right heart strain, such as a raised JVP and right-sided thrills .

A pansystolic murmur at the apex, accentuated by expiration and radiating to the axilla, is characteristic of mitral regurgitation . The murmur results from the backward flow of blood from the left ventricle to the left atrium during systole, and the specific location and radiation pattern help differentiate it from other cardiac murmurs .

When assessing finger clubbing, cardiovascular etiologies to consider include cyanotic congenital heart disease, infective endocarditis, aortic aneurysm, and atrial myxoma . These conditions involve either chronic hypoxemia or vascular changes that contribute to the development of clubbing .

A raised JVP, which is visible but not palpable and decomposes upon inspiration, suggests elevated right atrial pressure often seen in right-sided heart failure or constrictive pericarditis . The positive hepatojugular reflux, where JVP rises with abdominal palpation, further supports right-sided heart dysfunction as it indicates an inability of the right heart to accommodate increased venous return .

Hypercholesterolemia is associated with clinical manifestations such as corneal arcus, xanthelasma, tendon xanthomata, and tuberous xanthoma . These manifestations are related to elevated levels of cholesterol in the blood, leading to cholesterol deposition in various tissues such as eyelids, tendons, and joints .

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