CVS Signs AND symptoms And Patho

Question 1

State the toxic effects of oxygen

Answer 1

.
Toxic effects of oxygen
i) Respiratory Distress Syndrome (ARDS) may follow prolonged administration of 100% oxygen.
ii) Neonates develop vasoconstriction of arterioles which in the case of the eye leads to retrotental hyperplasia and blindness.
iii) Patientswithrespiratorydiseasedependingon ‘hypoxic drive’ to maintain respiration develop apnoea if the inspired oxygen is raised. The safe maximum concentration for pro- longed oxygen therapy is 40-50 %.

Question 2

State six ddx for Chest pain—alarming and increasing
over minutes to hours ,presentation of each of them and investigations findings for each of them

Answer 2

Angina (new or unstable):
Suggested by: central pain ± radiating to jaw and either arm (left usually). Intermittent, brought on by exertion, relieved by rest or nitrates, and lasting
<30 minutes. May be associated with transient ST depression or T inversions or, rarely, ST elevation.
Confirmed by: no itroponin after 12 hours (excludes MI). Stress test showing inducible ischemia

ST-elevation myocardial infarction (STEMI):

Suggested by: central chest pain ± radiating to jaw and either arm (left usually). Continuous, usually over
30 minutes, not relieved by rest or nitrates
Confirmed by: ST elevation 1 mm in limb leads or
2 mm in chest leads on serial ECGs (this is regarded as sufficient evidence to treat with thrombolysis). itroponin indicates episode of muscle necrosis up to 2 weeks before. itroponin may not be present in the first 4 hours after the onset of chest pain.

Non-ST- elevation myocardial infarction (NSTEMI): Suggested by: central chest pain ± radiating to jaw and either arm (left usually). Continuous, usually over 30 minutes, not relieved by rest or nitrates
Confirmed by: elevated troponin after 12 hours. T-wave and ST-segment changes but no ST elevation on serial ECGs

Esophagitis and esophageal spasm: Suggested by: past episodes of pain when supine, after food. Relieved by antacids
Confirmed by: no i in troponin after 12 hours and no ST-segment changes on ECG. Improvement with antacids. Esophagitis on endoscopy

Pulmonary embolus
arising from leg DVT, silent pelvic vein thrombosis, right atrial thrombus:
Suggested by: central chest pain, also abrupt shortness of breath, cyanosis, tachycardia, loud second sound in pulmonary area, associated deep vein thrombosis (DVT) or risk factors such as cancer, recent surgery, immobility
Confirmed by: V/Q scan with mismatched ventilation and perfusion, spiral (helical) CT (CT-pulmonary angiogram) showing clot in pulmonary artery

Pneumothorax-Suggested by: abrupt pain in center or side of chest with abrupt breathlessness. HyperResonance to percussion over site
Confirmed by: expiration CXR showing dark field with loss of lung markings outside sharp line containing lung tissue
Dissecting thoracic aortic aneurysm: Suggested by: ‘tearing pain often radiating to back and not responsive to analgesia, abnormal or absent peripheral pulses, early diastolic murmur, low BP, and wide mediastinum on CXR
Confirmed by: loss of single clear lumen on CT scan or MRI

Chest wall pain:
e.g., costochondritis and Tietze’s syndrome, strained muscle or rib injury-

Suggested by: chest pain and localized tenderness of chest wall or chest pain on twisting of neck or thoracic cage
Confirmed by: no i in troponin after 12 hours, and no ST-segment changes or T-wave changes serially on ECG. Response to rest and analgesics

Question 3

State six ddx for Chest pain worsened by breathing or movement ,presentation of each of them and investigations findings for each of them

Answer 3

Pleuritic chest pain due to pneumonia-Suggested by: being worse on inspiration, shallow breaths, pleural rub, evidence of infection (fever, cough, consolidation, etc.)
Confirmed by: opacification in lung periphery on CXR and sputum/blood culture

Pulmonary infarct
due to embolus arising from
DVT in leg,
silent pelvic vein thrombosis, silent right atrial thrombosis:
Suggested by: sudden shortness of breath, pleural rub, cyanosis, tachycardia, loud P2, associated DVT, or risk factors such as recent surgery, cancer, immobility
Confirmed by: V/Q scan mismatch, spiral CT showing clot in pulmonary artery

Pneumothorax-
Suggested by: pain in center or side of chest with abrupt breathlessness. Diminished breath sounds, resonance to percussion over site
Confirmed by: expiratory CXR showing loss of lung markings outside sharp pleural line

Pericarditis
caused by MI, infection, espe- cially viral, malig- nancy, uremia, connective tissue diseases:
Suggested by: sharp pain worse lying flat or with trunk movement, relieved by leaning forward. Pericardial rub
Confirmed by: ECG: diffuse concave ST elevations and PR depressions. CXR: globular heart shadow and relief with pericardial drainage (if hypotensive)

Musculoskeletal
injury or
inflammation (oftenBorholm’s disease,
Cocksackie B infection)
Suggested by: associated focal tenderness. Often history of trauma
Confirmed by: excluding other explanations. Normal troponin

Question 4

Ddx for Severe lower chest or upper abdominal
pain

Answer 4

Gastrooesophageal reflux/gastritis
) Suggested by: central or epigastric burning pain, onset
over hours, dyspepsia, worse lying flat, worsened by food, alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs)
Confirmed by: esophagogastroduodenoscopy (EGD) showing inflamed mucosa

Biliary colic:
Suggested by: postprandial pain, severe and “gripping” or colicky, usually in right upper quadrant (RUQ) and that can radiate to right scapula. Onset over hours
Confirmed by: ultrasound showing gallstones and biliary dilatation or characteristic findings on endo- scopic retrograde cholangiopancreatography (ERCP)

Pancreatitis
(often due to gallstone impacted
in common bile duct):
Suggested by: mid-epigastric pain radiating to back, associated with nausea and vomiting, gallstones. Onset over hours.
Confirmed by: iserum amylase to 5 times normal, iserum lipase

Myocardial infarction (often inferior:
Suggested by: continuous pain, usually over 30 minutes, not relieved by rest or (antianginal) medication. Onset over minutes to hours
Confirmed by: T wave inversion ± ST elevation of
1 mm in limb leads or 2 mm in chest leads on serial ECGs or itroponin

Question 5

State ddx for orthopnea and PND and why orthopnea and PND occur

Answer 5

Orthopnea and paroxysmal nocturnal
dyspnea (PND)
Orthopnea is shortness of breath when lying flat. (Try to confirm by observing what happens when patient lies flat.) It is most often associated with congestive heart failure (CHF) when pulmonary venous pressure and alveolar edema, especially in the upper lung fields, are increased in the recumbent position.
Less frequently it occurs with pulmonary disease such as chronic obstructive pulmonary disease (COPD) associated with abdominal obesity when abdominal contents press up on the diaphragm in the recumbent position. PND can occur when the patient slides down in bed at night or by bronchospasm due to nighttime asthma.

Ddx-
Pulmonary edema due to congestive (chronic) left ventricular failure (due to ischemic heart disease, valvular disease)
Suggested by: dyspnea, displaced apex beat, third heart sound, bilateral basal fine crackles
Confirmed by: CXR appearances. Impaired left ventricu- lar (LV) function on echocardiogram. Abnormal ECG reflecting underlying heart disease

COPD-
Suggested by: smoking history, cough and sputum. Pursed lip breathing, use of accessory muscles, reduced breath sounds, wheezes. Chest hyperinflation. Reduced peak flow rate
Confirmed by: CXR: radiolucent lungs. Spirometry: reduced FEV1, reduced FEV1/FVC ratio, <12% reversi- bility, hypoxia ± i arterial PCO2 (rarely, reduced A1-antitrypsin levels)

Asthma-
Suggested by: wheeze or dry cough. Other specific triggers to breathlessness. Other allergies. Past history of similar attacks unless first presentation
Confirmed by: reversibility of spirometric abnormalities with bronchodilator treatment, and symptomatic response to treatment

Question 6

Patho of palpitations and ddx

Answer 6

The sensation of rapid fluttering in the chest is thought to result from a sustained ventricular or supraventricular arrhythmia.[

The vagus nerve is one of the nerves responsible for controlling your heart rate. Due to the position of the vagus nerve in your body, it’s possible that lying on your back or left side can stimulate this nerve, sending an errant signal to the heart resulting in palpitations

Rapid or Irregular Heartbeat The heart may speed up to compensate for its failing ability to adequately pump blood throughout the body. Patients may feel a fluttering in the heart (palpitations) or a heartbeat that seems irregular or out of rhythm.

Hyperthyroidism speeds up the body’s metabolism. That can cause many symptoms, such as weight loss, hand tremors, and rapid or irregular heartbeat.

Ddx-

Runs of supraven- tricular tachycardia (SVT):
Suggested by: abrupt onset, sweats and sustained dizziness.
Confirmed by: baseline ECG or 24-hour ECG show- ing tachycardia with normal QRS complexes with absent or abnormal P waves >140/min. Exercise ECG to see if precipitated by exercise (and due to IHD)

Episodic heart block Second-degree
or third-degree atrioventricular (AV) block:
Suggested by: onset over minutes or hours, slow and forceful beats. Loss of consciousness, pallor if significant loss of cardiac output
Confirmed by: nonconducted P waves associated with conducted P waves with fixed or progressive prolonged PR interval, P–R dissociation, and slow QRS rate on 12-lead or 24-hour ECG

Sinus tachycardia
(anxiety, pain, fever, caffeine,hypovolemia, pulmonary embolism, hyperventilation,etc.):
Suggested by: gradual onset over minutes of regular palpitations and pulse. History of precipitatingcause(usually)
Confirmed by: 12 lead ECG or monitor strip and resolutionbystoppingprecipitatingfactorsor resolution of potential cause

Afib-irregular contractions of heart. This causes blood clots due to increased blood stasis cuz of irregular contractions and extra vascular bleeding.
Suggested by: onset over seconds, irregularly irregular radial and apex pulse, apical–radial pulse deficit, and variable BP
Confirmed by: ECG showing no P waves and irregularly irregular QRS complexes

Menopause:
Suggested by: sweats, mood changes, irregular or no more periods, getting worse over weeks or months
Confirmed by: dserum estrogen, iFSH/LH,
and response to hormone replacement therapy

Thyrotoxicosis:
Suggested by: anxiety, irritability, weight loss, sweating, loose frequent stools, lid retraction and lag, proptosis, brisk reflexes, other signs and symptoms of hyperthyroidism. Onset over weeks or months. 12 lead ECG may show sinus tachy- cardia, atrial fibrillation, or ventricular arrhythmias
Confirmed by: iFT4, and/or iFT3 and dTSH

Pheochromocytoma
(rare):
Suggested by: abrupt episodes of anxiety, fear, chest tightness, sweating, headaches, and marked rises in BP
Confirmed by: catecholamines (VMA, HMMA) or free metanephrine i in urine and blood soon after episode

Question 7

Cough and pink frothy sputum Patho and ddx

Answer 7

Cough and pink frothy sputum
This is due to a combination of frothy sputum of pulmonary edema tinged with blood. fluid and small amounts of blood leak from capillaries into the alveoli of the lungs.

Acute pulmonary edema: mechanisms-increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure. Damage to the alveolar-capillary barrier. Lymphatic obstruction.
Suggested by: onset over minutes or hours of short- ness of breath, orthopnea, displaced apex, loud third heart sound, fine crackles at lung base
Confirmed by: CXR appearance (see Fig. 19.13, though 19.14 is more typical), poor LV function on echocar- diogram

Mitral stenosis causing pulmonary edema:
Suggested by: months or years of orthopnea, tapping, displaced apex, loud first heart sound, diastolic murmur, fine crackles at lung bases. Enlarged left atrial shadow (behind heart) and splayed carina on CXR
Confirmed by: large left atrium and mitral stenosis on echocardiogram

Question 8

Patho and 7 ddx of syncope

Answer 8

Syncope
This is sudden loss of consciousness over seconds. The pathophysiology of syncope is summarized as a reduction in systemic blood pressure that causes a decrease in the global cerebral blood flow, which results in loss of consciousness. A sudden cessation of cerebral blood flow for 6 to 8 seconds has been shown to cause loss of consciousness.

( Think of abnormal cardiac or CNS “electrical” activity or a temporary drop in cardiac out- put and BP that improves as soon as the patient is in a prone position. Seizures can occur from a profound fall in BP, so they are not specific for epilepsy.)

Vasovagal attack—simple faint:
Suggested by: seconds or minutes of preceding emotion, pain, fear, urination, or prolonged standing— with nausea, sweating and darkening of vision. Recovery within minutes. Incontinence is rare.
Confirmed by: history, positive upright tilt test

Postural or orthostatic hypotension often due to antihypertensive drugs, dehydra- tion, anemia, or blood loss:
Suggested by: dizziness or sudden loss of consciousness within minutes after getting up from sitting or lying position
Confirmed by: fall in BP and rise in heart rate (HR) from reclining to standing, confirmation of a causal diagnosis

Stokes–Adams attack
due to a variety of cardiogenic causes, e.g., syncope caused by AV conduc- tion block:
Suggested by: recurrent episodes of sudden loss of consciousness with no warning. Pallor, then recovery within seconds or minutes.
Confirmed by: 24-hour ECG showing episodes of asystole or heart block, SVT, or ventricular tachycardia (VT)

Aortic stenosis:
Suggested by: syncope on exercise. Cool extremities, slowly rising carotid arterial pulse, low BP and pulse pressure and heaving apex. Mid-systolic murmur radiating to carotids. ECG showing left ventricular hypertrophy (LVH)
Confirmed by: Echocardiogram and cardiac catheterization: stenosed aortic valve

Hypertrophic cardiomyopathy:
Suggested by: syncope on exercise. FH of sudden death or hypertrophic cardiomyopathy. Angina, breathless, jerky pulse, high JVP with “a” wave, double apex beat, thrill and murmur best at left sternal edge
Confirmed by: characteristic echocardiogram showing increased left ventricular wall thickness, small, well-contracting left ventricle

Hypoglycemia-Suggested by: preceded by seconds or minutes by hunger, sweating, and darkening of vision. Usually in diabetic on insulin.
Confirmed by: blood sugar <50 mg/dL and exclusion of associated cardiac condition

Epilepsy-
Suggested by: preceding aura for a few minutes then tonic phase with cyanosis, clonic jerks of limbs, incontinence of urine and/or feces
Confirmed by: history from witness. EEG changes, e.g., spike and wave

PE-
Suggested by: sudden shortness of breath, pleural rub, cyanosis, tachycardia, loud P2, associated DVT, or risk factors such as recent surgery, childbirth, immobility, etc.
Confirmed by: V/Q scan mismatch, spiral CT showing arising clot in pulmonary artery

Question 9

Leg pain on walking—intermittent
claudication pathophysiology and ddx

Answer 9

ntermittent claudication (IC) typically refers to lower extremity skeletal muscle pain that occurs during exercise. IC presents when there is insufficient oxygen delivery to meet the metabolic requirements of the skeletal muscles

Arterial disease in legs due to atherosclerosis :
Suggested by: predictable leg, calf, thigh, or buttock pain (worse on hills, better downhill) that is better with rest (if also present at rest, this implies incipient gangrene). Patient sleeps with leg hanging down, e.g., over edge of bed or in chair. Abnormal pulses, poor perfusion of skin and toes
Confirmed by: Doppler ultrasound or arteriogram or magnetic resonance angiogram (MRA) showing stenosis and poor flow

Aortoiliac occlusive arterial disease associated with erectile dysfunction = Leriche’s syndrome
Suggested by: predictable buttock, hip, or thigh pain on exertion and male erectile dysfunction (impotence)
Confirmed by: arteriogram or MRA showing stenosis and poor flow in the distal aortic or iliac arteries

Neurogenic claudication:
Suggested by: weakness and pain in leg, calf, thigh, or buttock and pain improving slowly with rest but variable. Worse downhill. No cold toes, normal pulses
Confirmed by: MRI showing neurospinal canal stenosis or disc compression of cord or cauda equina

Sciatica

Question 10

Leg pain on standing—relieved by lying
down Patho and ddx

Answer 10

Leg pain on standing—relieved by lying
down
Think of something relieved by reducing pressure on lying down. Two possibilities are relief of the pressure transmitted down to leg tissues by incompetent venous valves, or relief of pressure by the spinal column on a damaged disc, aggravating its protrusion and pressure on adjacent nerve roots.

Peripheral venous disease-
Suggested by: generalized ache, associated itching, varicose veins, and venous eczema ± ulcers. Cough impulse felt and Trendelenberg test shows filling down along extent of communicating valve leaks.
Confirmed by: clinical findings or Doppler ultrasound probe to confirm whether or not incompetence is present in the saphenofemoral junction or the short saphenous vein

Disc protrusion-
Suggested by: severe referred ache or shooting pains, affected by position. Neurological deficit in root distribution
Confirmed by: MRI of sacral and dorsal spine showing disc impinging on nerve roots (but may be less obvious as patient lies down in scanner)

Varicose veins-Varicose veins – These are gnarled, enlarged veins that usually occur in the legs. Though often mild, varicose veins result in complications for some patients, such as bleeding and blood clots.

Chronic venous insufficiency – This occurs when the walls and/or valves in the veins are not working effectively, making it difficult for blood to return to the heart.

Question 11

Bilateral ankle swelling 6 ddx and pathophysiology of edema
(Think of increased pressure within the veins or lymphatic vessels or low albumin in the vascular space, bilateral damage to veins, lymphatics, or capillaries due to local inflammation.)

Answer 11

Bilateral swelling is usually due to systemic conditions (eg, cardiac failure) and unilateral is often due to local trauma, venous disease or lymphatic disease. Unilateral leg swelling is more often due to local causes .

increased capillary hydrostatic pressures secondary to valvular insufficiency or venous obstruction.

Edema can be divided into 4 types based on the mechanisms causing edema: increased capillary hydrostatic pressure, decreased plasma oncotic pressure, enhanced hydraulic permeability of capillary walls, and lymphatic obstruction.

Right ventricular failure
due to pulmonary vascular disease or CHF-
Suggested by: jugular venous distension, edema, liver
enlargement and pulsation, right ventricular (RV) heave. Onset over months, usually
Confirmed by: elevation of central venous pressure (CVP) using a central venous catheter or elevation of right arterial (RA) and RV pressures during right heart catheterization, dilated RV on echocardiogram

Poor venous return
due to abdominal orpelvicmasses, post-phlebitic or thrombotic venous damage-
Suggested by: onset over months. Worse on prolonged standing or sitting, varicosities, venous eczema, pigmentation or ulceration. Non-pitting edema if chronic
Confirmedby:clinicallywithTrendelenbergtest showing filling along extent of communicating valve leaks or on venous Doppler ultrasound

Low albumin states
caused by liver failure, nephrotic syndrome, malnutrition, etc.-
Suggested by: generalized edema often including face after lying down. Onset usually over months
Confirmed by: low serum albumin

Bilateral cellulitis
often associated with diabetes mellitus:
Suggested by: warm, red, and tender legs, thrombo-
phlebitis and tracking, ulcers, etc. Onset over days
Confirmed by: positive blood cultures (usually streptococcal or staphylococcal) (blood sugar increased in diabetes

Inferior vena cava (IVC) obstruction due to prolonged immobility,carcinoma
, and oral combined con- traceptive use)-Suggested by: bilateral leg-swelling onset over hours, associated risk factors (obesity, smoker, FH). Symptoms of PE.
Confirmed by: CT abdomen, low flow on Doppler immobility,carci- ultrasoundscan,orfillingdefectonvenogram.

Bilateral thrombose
Suggested by: onset over hours, risk factor of obesity, history of immobility, carcinoma, oral contraceptive use. Associated with PE. Leg(s) firm, warm, tender
Confirmed by: no flow on Doppler ultrasound scan

Impaired lymphatic drainage::
Suggested by: firm, non-tender, non-pitting edema of
gradual onset over months to years
Confirmed by: obstruction to flow on lymphangiogram (rarely done)

Question 12

Patho of cyanosis

Answer 12

mechanisms are involved in the development of cyanosis, systemic arterial oxygen desaturation and increased oxygen absorption by tissues. Cyanosis is evident when arterial oxygen desaturation falls below 85% or the concentration of deoxygenated hemoglobin (Hb) exceeds 5 gm/dl.

In peripheral cyanosis, systemic arterial oxygen saturation is normal.
Increased oxygen extraction by tissues causes wide systemic arteriovenous oxygen difference and increased deoxygenated blood on the venous side of the capillary beds.
The increased oxygen extraction by tissues results from the sluggish movement of blood through the capillary circulation.

You can also say it’s due to reduced oxygen rich blood delivery to the peripheral tissues

In peripheral cyanosis, there is normal arterial oxygen saturation but increased oxygen extraction by the peripheral tissue in the capillary bed in the setting of peripheral vasoconstriction and decreased peripheral blood flow.

Central-

Question 13

State the differentials for peripheral cyanosis

Answer 13

Raynaud’s phenomenon due to exposure of hands to cold or
vibration:
Suggested by: normal pulse and BP, history of blue hands after exposure to cold, vibrating tools, etc.; history of scleroderma. Confirmed by: hands and feet assume normal color in warm room

Arterial obstruction due to atheroma or small vessel disease in diabetics :
Suggested by: absent or poor or asymmetric radial or dorsalis pedis pulses. Absent hair and skin atrophy in chronic cases
Confirmed by: Doppler ultrasound measure of low blood flow and angiography

Hemorrhage
due to external or internal
bleeding:
Suggested by: pallor, sweating, low BP, high pulse rate, observable external bleeding or melena or massive trauma expected to cause internal bleeding
Confirmed by: low Hb (although Hb is often normal early after a bleed) and response to blood transfu- sion or volume expansion and control of bleeding

Low cardiac output
e.g., due to large
MI or severe valvular disease:
Suggested by: pallor, cold extremities, sweating, low BP
Confirmed by: poor LV function on echocardiogram, low cardiac output measured by a Swan-Ganz catheter

Reduced cardiac output secondary to heart failure or shock
Local vasoconstriction due to cold exposure, hypothermia, acrocyanosis, and Raynaud phenomenon
Vasomotor instability
Arterial obstruction causing regional ischemia secondary to peripheral vascular disease. Causes include atherosclerosis, Buerger disease, atheroembolism
Venous stasis or obstruction, such as in deep vein thrombosis
Hyperviscosity attributable to multiple myelomas, polycythemia, and macroglobulinemia
All causes of central cyanosis can also cause peripheral cyanosis.

Question 14

State ten differentials for central cyanosis
How they present and how they can be diagnosed ( investigations)

Answer 14

Causes of central cyanosis include:[4][5]

Hypoventilation due to conditions affecting the central nervous system, such as intracranial hemorrhage, tonic-clonic seizures, and heroin overdose.
Pulmonary causes leading to ventilation-perfusion mismatch and impaired alveolar-arterial diffusion, for instance, bronchospasm (asthma), pulmonary embolism, pneumonia, bronchiolitis, pulmonary hypertension, hypoventilation, and COPD[6][7][8]
Cardiovascular causes include heart failure, congenital heart diseases (right to left shunting), and valvular heart diseases.
Hemoglobinopathies including methemoglobinemia, sulfhemoglobinemia
Polycythemia
High altitude
Hypothermia
Obstructive sleep apnea

Right-to-left cardiac shunt
due to congenital heart disease, e.g., tetralogy of Fallot, Eisenmenger’s syndrome, tricuspid atresia, Ebstein’s anomaly, pulmonary AV fistula, transposition of the great vessels:

Suggested by: breathlessness, clubbing, systolic or continuous murmur, right ventricular heave
Confirmed by: echocardiogram and cardiac catheterization

Right-to-left pulmonary shunt due to decreased perfusion of lung tissue from extensive collapse or consolidation or alveolar filling:
Suggested by: breathlessness, poor chest movement, dullness to percussion and absent breath sounds over a large area of the chest
Confirmed by: chest X-ray and bronchoscopy

Hemoglobin abnormalities
due to congenital NADH diaphorase, Hb M disease, or acquired methemo- globinemia or sulfhemoglobinemia:
Suggested by: no clubbing, no murmurs, normal chest movement, no chest signs. History from childhood or exposure to toxic drugs, e.g., aniline dyes
Confirmed by: Hb electrophoresis

Question 15

State six differentials for tachycardia and the presentation and investigations for each

Answer 15

Tachycardia (pulse rate >100bpm)

Fever:
Suggested by: warm skin, erythema, sweats, temperature >38*C
Confirmed by: elevated temperature, fever pattern

Hemorrhage:
Suggested by: signs of blood loss, pallor, sweats,
low BP, poor peripheral perfusion
Confirmed by: low Hb (can be normal in initial stages), low central venous pressure

Hypoxia:
Suggested by: cyanosis, respiratory distress
Confirmed by: pulse oximetry or dPaO2

Thyrotoxicosis:
Suggested by: sweating, fine tremor, weight loss, lid lag, frequent bowel movements, sweats, weight loss
Confirmed by: iFT4, ± iFT3 and dTSH

Severe anemia:
Suggested by: subconjunctival and nail-bed pallor,
tiredness, poor exercise tolerance Confirmed by: dHb (and indices)

Heartfailure(LVF, RHF, CHF) associated
with ischemic
heart disease, myocarditis, etc.:
Suggestedby:thirdheartsound,finecracklesat bases, raised JVP
Confirmed by: CXR showing large heart, pulmonary congestion; poor LV function on echocardiogram, low cardiac output measured by a Swan-Ganz catheter

Pulmonary embolus (PE):
Suggested by: history of sudden breathlessness, cyano- sis, raised JVP, loud P2. ECG: right axis deviation
Confirmed by: V/Q scan showing mismatched de- fects, pulmonary angiography of spinal CT showing filling defect in pulmonary artery

Drugs
e.g., amphetamines, B-agonists, anticholinergic agents, cocaine;
Suggested by: drug history
Confirmed by: normal pulse rate if drug stopped

Question 16

State five differentials for bradycardia and how they present plus investigations for each

Answer 16

Drugs:
Suggested by: history e.g., beta blockers
Confirmed by: improvement when drug withdrawn

Sinoatrial disease:
Suggested by: elderly, ischemic heart disease
Confirmed by: ECG: Slow atrial rate with sinus P waves or abnormal P waves

Ventricular or supraventricular ectopy or bigeminy:
Suggested by: known ischemic heart disease
Confirmed by: comparison of pulse rate to ECG: premature ectopic beats may not generate a pulse if early enough to not allow sufficient ventricular filling

Myocardial infarction (MI):
Suggested by: central, crushing chest pain (can be atypical pain)
Confirmed by: ECG: Q waves, raised ST segments, and inverted T waves. iCPK-MB or troponin. Bradycardia is most frequently seen with inferior MI

Hypothyroidism:
Suggested by: constipation, weight gain, dry skin, dry hair, slow-relaxing reflexes, other symptoms and signs of hypothyroidism
Confirmed by: iTSH, dT4

Hypothermia:
Suggested by: history of exposure to cold
temperature and immobility
Confirmed by: Core temperature <35*C

Question 17

State five ddx for irregularly irregular pulse and their presentations and investigations
What is an anacrotic pulse

Answer 17

Atrial fibrillation
caused by ischemic
heart disease, thyrotoxicosis, etc. :
Suggested by: irregularly irregular pulse Confirmed by: ECG showing no P waves, and
irregularly irregular normal QRS complexes

Atrial flutter with variable heart block caused by ischemic
heart disease, etc. :
Suggested by: irregularly irregular pulse
Confirmed by: ECG showing “saw tooth” F waves, and irregularly irregular normal QRS complexes

Atrial or ventricular ectopics
caused by ischemic
heart disease, etc. :
Suggested by: pulse with early or dropped beats, compensatory pause with ventricular ectopy
Confirmed by: ECG showing underlying sinus rhythm with early QRS complexes. Atrial ectopic beats have a narrow or wide QRS and are preceded by an early P wave. Ventricular ectopic beats have a wide QRS, are not preceded by an early P wave, and usually are followed by a compensatory pause.

Wenkebach heart block caused by ischemic heart disease, etc. :
Suggested by: regular rate with periodic slightly longer pauses
Confirmed by: ECG showing AV conduction with progressive prolongation of P-R interval with normal QRS complex followed by a P wave not followed by a QRS complex. The next P-R interval is abruptly shorter.

Anacrotic pulse is a low volume pulse with slow upstroke, sustained peak and a slow downstroke, also a palpable notch in the ascending limb of pulse. Cause of anacrotic pulse. Aortic stenosis - here the percussion wave is delayed beyond the tidal wave.

Question 18

State six ddx for a bounding pulse
State six causes of collapsing pulse and explain the Patho of collapsing pulse

Answer 18

Aortic insufficiency
Suggested by: striking “water hammer” quality. Systolic BP high (e.g., >160 mmHg) and diastolic BP very low (e.g., <50 mmHg) early diastolic murmur, forceful, displaced apex impulse
Confirmed by: echocardiogram and cardiac catheterization showing diastolic leaking of the aortic valve

Atherosclerosis:
Suggested by: older age. Systolic BP high (e.g., >160 mmHg) and diastolic BP not low (e.g., >80 mmHg)
Confirmed by: echocardiogram to exclude aortic incompetence

Severe anemia:
Suggested by: pallor. Systolic BP high (e.g., >160 mmHg) and diastolic BP normal (e.g., <85 mmHg)
Confirmed by: Hbd (e.g., <10 grm/dL)

Bradycardia of any cause with normal myocardium
Suggested by: slow heart rate (e.g., <50 bpm)
Confirmed by: ECG showing slow rate and type of rhythm

Hyperkinetic circulation e.g., due to hypercapnia, thyrotoxicosis, fever, Paget’s disease, AV fistula:
Suggested by: warm peripheries and features of cause, e.g., cyanosis, tremor, lid lag, fever, skull deformity, etc.
Confirmedby:highpCO2 (ifhypercapnia)oriFT4, ± iFT3 and dTSH (if thyrotoxic) or fever or
i hydroxyproline (if Paget’s disease)

Patho of collapsing or water hammer pulse or corrigan pulse:
The rapid downstroke is partly due to two causes. The first cause is the sudden fall in diastolic pressure in the aorta, which is due to regurgitation of blood from the aorta, or “aortic run-off,” into the left ventricle through the leaky valve. The second cause is the rapid emptying of the arterial system

In physiological and hyperdynamic circulatory states, the fall in systemic vascular resistance and increased cardiac output causes the water hammer pulse.

Physiological etiologies include:

Exercise
Fever
Pregnancy
Hyperdynamic circulatory states include:

Thyrotoxicosis
Anemia
Paget disease
Liver cirrhosis
Thiamine deficiency or beriberi
Systolic hypertension
Arteriovenous fistula
Cor pulmonale
Cardiac lesions include:

Atrial septal defect Ventricular septal defect Arterio-venous malformation Aneurysm
Aortic regurgitation
Fever
Pregnancy

Aortic regurgitation
Patent ductus arteriosus
Aortopulmonary window
Sinus of Valsalva rupture
Leaking aortic valve prosthesis
A ventricular septal defect with aortic regurgitation
Truncus arteriosus
Mitral regurgitation
Complete heart block
Epidemiology

Aortic regurgitation is the most common condition associated with the water hammer pulse.

Question 19

State three ddx of thready pulse

Answer 19

Poor cardiac
contractility
due to ischemic
heart disease,
cardiomyopathy,
cardiac tampo-
nade, constrictive
pericarditis:
Suggested by: quiet heart sounds, iJVP, peripheral edema, basal lung crackles
Confirmed by: poor LV function on echocardiogram

Hypovolemia due to blood loss and dehydration:
Suggested by: cold peripheries, thirst, dry skin and mucous membranes, low urine output
Confirmedby:bloodureanitrogen(BUN)i,Hb (in blood loss) or i (if hemo-concentrated)

Poor vascular tone, hypotension e.g., due to septic shock : Suggested by: warm peripheries, thirst, dry skin, decreased urine output
Confirmed by: hypotension, other evidence of sepsis (positive blood cultures, azotemia)

Aortic stenosis:
Suggested by: slowly rising carotid pulse, characteristic systolic murmur
Confirmed by: echocardiogram and cardiac catheterization

Question 20

State six ddx for hypertension

Answer 20

Temporary hypertension with no risk factors
Suggested by: normal blood pressure <140 mmHg systolic and <90 mmHg diastolic when repeated
Confirmed boy: 24-hour ambulatory blood pressure monitoring

Essential hypertension:
Suggested by: sustained hypertension
Confirmed by: 24-hour ambulatory blood pressure moni- toring. No symptoms or signs of specific cause, normal BUN and electrolytes, and prompt control on treatment

Hypertension in pregnancy:
Suggested by: only occurring during pregnancy. Very high BP and seizures in eclampsia
Confirmed by: resolution or improvement when pregnancy over or terminated

Renovascular hypertension due to renal artery stenosis or primary renal disease
Suggested by: established renal impairment too soon to be caused by hypertension. Confirmed by: BUN and creatinine raised, reduced Hb (in established renal failure), hyper-reninemia. Ultrasound or isotope scan of kidneys and ureters. Arteriogram or MR angiogram of the renal arteries

Endocrine hypertension due to hyperaldosteronism , Cushing’s disease, phaeochromocytoma:

Suggested by: proximal muscle weakness in Cushing’s syndrome or severe aldosteronism. Paroxysms of vascular symptoms in pheochromocytoma
Confirmed by: i aldosterone and d renin, i 24-hour urinary free cortisol, etc., in Cushing’s syndrome. metanephrines i in pheochromocytoma

Vascular hypertension due to coarctation of aorta , subclavian artery stenosis
Suggested by: upper extremity hypertension (right arm), normal in legs (and left arm in subclavian artery stenosis).Delayedarterialpulsebetweenupperand lower extremities suggests coarctation of the aorta.
Confirmed by: MRA/angiography

Drug induced due to NSAIDS, estrogen, steroids, alcohol, erythropoietin Suggested by: drug history
Confirmed by: resolution or improvement when drug stopped

Question 21

Ddx of low blood pressure and of orthostatic hypertension

Answer 21

Cardiogenic— low output
due to poor myocardial contraction, valvular stenosis or regurgitation, etc. :
Suggested by: very low BP, fast or slow heart rate, peripheral and central cyanosis, quiet heart sound
± abnormal murmur, cool extremities. High or normal JVP, abnormal heart rhythms, enlarged heart, echocar- diogram findings of systolic or diastolic dysfunction, valve stenosis, or regurgitation
Confirmed by: echocardiogram with findings indicating low cardiac output, right heart catheterization showing low cardiac output

Low circulating blood volume due to hemorrhage (GI etc.) dehydration, etc. ;
Suggested by: very low BP, fast heart rate, peripheral cyanosis, JVP low, cool extremities. Background evidence of cause
Confirmed by: low CVP, ECG, normal heart on CXR. Improvement with blood, plasma expander, intrave- nous (IV) fluids with CVP monitoring

Loss of
vascular tone (“distributive” shock)
due to septicemia, adrenal failure, etc.:
Suggested by: very low BP, fast heart rate, peripheral cyanosis, JVP low or normal, warm extremities. Background evidence of cause
Confirmed by: low CVP, normal heart on CXR. Improvement in BP and CVP with blood transfusion, volume expansion (IV fluids), glucocorticoids, and antibiotics

Orthostatic:
Drug induced
due to excessive doseofhypoten- sive agent (opiates, benzo- diazepines, other sedatives, antidepressants):
Suggested by: drug history
Confirmed by: by resolution or improvement after stopping or reducing drug

Autonomic neuropathy
due to diabetes mellitus or tabes dorsalis (rarely):
Suggested by: history of long-standing diabetes (common) or tabes dorsalis (rare). Also, diarrhea, abdominal distension, and vomiting (gastroparesis), impotence, urine frequency
Confirmed by: ECG monitor of beat-to-beat
variation: <10 beats per minute (bpm) change in heart rate on deep breathing at 6 breaths/minute or getting up from lying

Idiopathic orthostatic hypotension:
Suggested by: no other features except elderly Confirmed by: isolated phenomenon

Volume depletion due to mild or early
dehydration or hemorrhage:
Suggested by: history of vomiting or diarrhea or poor po intake or melena or hematochezia; poor skin tur- gor, dry axillae; labs showing azotemia with BUN rise disproportionate to creatinine rise
Confirmed by: low urine Na or FENa; anemia; evidence of hemorrhage; response to fluids or blood transfusion

Question 22

Ddx for pulse difference in both arms and both arms and legs
Ddx for Prominent leg veins ± unilateral leg swelling

Answer 22

Aortic dissection
Supravalvular aortic stenosis
Aortic abdominal aneurysm

Ddx for pulse difference in arms and legs
Coarctation of aorta

Varicose veins plus incompetent communicating valves:
Suggested by: veins distended and tortuous made worse when standing. Cough impulse felt and Trendelenberg test shows filling down along extent of communicating valve leaks
Confirmed by: clinical findings usually, but if doubt,
use Doppler ultrasound probe to confirm whether or not incompetence is present in the saphenofemoral junction or short saphenous vein behind the knee

Thrombophlebitis
Suggested by: tender, hot veins with redness of surrounding skin
Confirmed by: resolution on antibiotics

Deep vein thrombosis (DVT)
Suggested by: immobility, prominent dilated veins;
warm, tender, swollen calf; other risk factors for DVT
Confirmed by: reduced flow on compression Doppler ultrasound, blockage seen on venography

Question 23

Ddx for unilateral ankle swelling plus presentations and investigations

Answer 23

DVT
Suggested by: immobility, prominent dilated veins, warm, tender, swollen calf and positive Homan’s sign
Confirmed by: reduced flow on compression Doppler, blockage seen on venography

Ruptured bakers cyst:
Suggested by: sudden onset while straightening knee, warm, tender, swollen calf
Confirmed by: D-dimer titers not raised, normal flow on compression Doppler, no blockage seen on venography. Leaking from joint capsule on arthrography

Cellulitis from infection or insect bites or infections due to insect bites
Suggested by: tender, hot, red leg and fever Confirmed by: resolution on antibiotics

Unilateral varicose veins
Suggested by: distended and tortuous veins made worse when standing
Confirmed by: Doppler ultrasound probe to confirm where incompetence is present

Chronic venous insufficiency from old dvt:
Suggested by: past history, veins distended and made worse on standing
Confirmed by: Doppler ultrasound probe to where incompetence is present

Venous insufficiency from obstruction by tumor or lymph node:
Suggested by: onset over weeks, veins distended
Confirmed by: Doppler ultrasound and venography to explorewhereobstructionispresent by tumor or
lymph node

Lymphedema
from lymphatic obstruction due to primary lymphatic hypoplasia
Suggested by: unilateral swelling that is worse premen- strually, in warm weather, and with immobility.
No venous dilatation
Confirmed by: Doppler ultrasound to show normal venous flow. MRI or CT or lymphangiogram (rarely) to show hypoplastic lymphatics

Acutelymphatic obstruction
due to streptococcal lymphangitis Suggestedby:suddenunilateralswellingdeveloping
over hours. No venous dilatation but lymphangitic streaks
Confirmed by: clinical features and response to penicillin. Doppler ultrasound to show normal venous flow

Question 24

Ddx for bilateral leg swelling plus how they present and investigations

Answer 24

Bilateral varicose veins
Suggested by: veins distended and tortuous made varicose veins or worse when standing
Confirmed by: Doppler ultrasound probe to confirm where incompetence is present

Low albumin
due to poor nutrition, mal- absorption, liver failure, nephrotic syndrome, protein-losing enteropathy:
Suggested by: history of facial puffiness in morning and evidence of possible cause of low albumin
Confirmed by: low serum albumin (<3.0 g/dL to be significant)

Congestive cardiac failure (i.e., right heart failure due to left heart failure) caused by ischemic heart disease, mitral stenosis, cardio- myopathy, etc.:
Suggested by: raised JVP, large liver, fine rales at lung bases or higher, third heart sound. Echocardiogram showing systolic or diastolic dysfunction or valve dysfunction
Confirmed by: CXR: large heart, distension of veins in upper lobes of lung, and fluffy lung infiltrates. Echocardiogram: ventricular dysfunction

Cor pulmonale (right heart failure)
from pulmonary hypertension due to long-standing lung disease, old pulmonary emboli, etc.):
Suggested by: raised JVP, large liver, third heart sound, loud pulmonary second sound, and RV heave
Confirmed by: CXR showing pulmonary disease, ECG showing right axis deviation. Echocardiogram: right ventricular dysfunction

Lymphedema
due to primary lymphatic hypoplasia:
Suggested by: bilateral swelling that is worse premenstru- ally, in warm weather, and with immobility. No venous dilatation.
Confirmed by: Doppler ultrasound to show normal venous flow. Occasional lymphangiography to show hypoplastic lymphatics

Question 25

State six ddx for raised jvp, their presentations and investigations

Answer 25

This is measured with the patient lying at 45*. It is undetectably low if the external jugular empties when the compressing finger is released. An elevated JVP with a and v waves that is accurately assessed means that right atrial pressure is abnormally high.

Fluid overload due to excessive IV or oral fluids:
Suggested by: elevated double pulsations JVP with a and v waves. History of high input of IV or oral fluids. Renal insufficiency or failure. Echocardiogram showing normal or hyperdynamic systolic function
Confirmed by: response to reduced fluid intake and spontaneous diuresis (or diuretics) or fluid removal

Congestive cardiac failure (i.e., right-sided failure due to left-sided failure):
Suggested by: elevated JVP with a and v waves. Dysp- nea, rales on pulmonary exam. CXR consistent with pulmonary edema. Echocardiogram showing LV systolic or diastolic dysfunction or valve dysfunction
Confirmed by: echocardiogram showing ventricular dysfunction, right heart catheterization showing elevated RA and pulmonary capillary wedge pressure, decreased cardiac output

Cor pulmonale
Right heart failure due to pulmonary vascular disease:
Suggested by: elevated JVP; large a waves may be present. Pulmonary exam with hyperresonance and low diaphragms. Sometimes wheezing or rhonchi, but not rales. ECG showing tall P wave in lead 2
Confirmed by: echocardiogram showing dilated RV with reduced systolic function, flattened intraventricular septum indicating elevation of RV pressure, no LV systolic or diastolic dysfunction or valve dysfunction. Right heart catheterization showing elevation of RA, RV, and PA systolic pressure, elevation of pulmonary vascular resistance, but normal pulmonary capillary wedge pressure

Right-sided congestiveheart failure with atrial fibrillation:
Suggested by: elevated JVP with a single pulsation, awavesabsent,irregularlyirregularpulse
Confirmed by: ECG showing no P waves and normal QRS complexes. Other findings of congestive heart failure mentioned above

Complete heart block:
Suggested by: intermittent elevations of JVP when the atria contract when AV valves are closed. Bradycardia
Confirmed by: ECG showing no association between P waves and QRS complexes

Tricuspid regurgitation:
Suggested by: elevated JVP with single pulsation, large v waves in mid-systole. Holosystolic murmur present in the low sternal area
Confirmed by: echocardiogram showing large right atrium and tricuspid incompetence

Pericardial effusion sufficient to compromise heart function
Suggested by: pulsatile JVP with a wave and rapid descent. Very breathless. Quiet heart sounds. Globular heart shadow on CXR. Low-voltage QRS complexes on ECG
Confirmed by: Echocardiogram showing moderate or large pericardial effusion, excessive respiratory variation of the inflow velocity of mitral and tricuspid valves, diastolic collapse of the RA or RV

Constructive pericarditis:
Suggested by: JVP rising with inspiration (Kussmaul sign), a waves have rapid descent. Quiet heart sounds. Large liver and ascites.
Confirmed by: small heart shadow on CXR. Echocardiogram shows small cavity and little contraction

Jugular vein obstruction:
Suggested by: no JVP pulsation, external jugular vein also distended
Confirmed by: ultrasound scan to explore site of obstruction

Question 26

What is the normal JVP?
Why is the internal jugular vein preferred to the external one?
What kind of waveform does the JVP have and what are the causes of large A wave form and canon a wave , absent A wave causes , causes of combine CV wave , SLOW Y DESCENT, causes of venous and arterial paradox

Answer 26

JUGULAR VENOUS PRSSURE
Normal value is two to three mm of water

WHY THE INTERNAL JUGULAR IS PREFERRED TO THE EXTERNAL
JUGULAR
1. Internal jugular vein is in direct communication with the right atrium and the external goes off at a tangent

2. The external jugular vein is very tortuous in its course as it passes through the fascia planes and therefore is subject to kinking
3. There are valves in the external jugular vein which may give false reading. But there are no valves in the internal jugular vein.

JVP WAVE FORM
Know a c and v
Also x and y
CAUSES OF A LARGE A WAVE
1. Tricuspid stenosis
2. Pulmonary hypertention
3. Pulmonary artery stenosis
CAUSES OF CANON A WAVE
1. Due to contraction of the right atrium and ventricle simultaneously
2. Complete heart block
3. Atrial flutter
4. Single chamber ventricular pacing
5. Nodal rhythm
6. Ventricular extrasystole
7. Ventricular tachycardia

ABSENT A WAVE
Atrial fibrillation

COMBINED CV WAVE (GIANT V WAVE)
Tricuspid regurgitation

SLOW Y DESCENT
Tricuspid stenosis

VENOUS AND ARTERIAL PARADOX (PROMINENT X AND Y DESCENT)
Jugular venous pressure rises on inspiration and systolic BP falls. This occurs in some chronic disesases like tuberculosis or collagen diseases where the pericardium becomes thickened and stiffened and is pulled down by the diaphragm during inspiration
Pericardial effusion
Constrictive pericarditis

Question 27

State five causes of pulsus paradoxes
What is the CLINICAL DIFFERENTIATION OF ATRIAL FIBRILLATION & MULTIPLE ECTOPIC BEAT

Answer 27

Pulsus paradoxus is a phenomenon when your blood pressure decreases with inhalation (breathing in). It’s a sign that you have a condition that affects your heart or lungs

CAUSES OF PULSUS PARADOXUS
1. Constrictive pericarditis
2. Massive pericardial effusion 3. Bronchial Asthma
4. LVF

CLINICAL DIFFERENTIATION OF ATRIAL FIBRILLATION & MULTIPLE ECTOPIC BEAT

1. There is pulse deficit in atrial fibrillation
2. Atrial fibrillation worsens with exercise whiles multiple ectopic beats may even disappear

Question 28

State the difference etween arterial and venous pulsations in the neck
Delayed diminished femoral pulse is seen in what disease?

State four causes of displaced apex best

Answer 28

DIFFERENCES BETWEEN ARTERIAL AND VENOUS PULSE
1. Arterial pulse is palpable
2. Gentle pressure applied above the clavicle will obliterate a venous pulse and the vein will fill above the point of pressure
3. The position of the venous pulse in the neck is affected by the patient’s posture
4. The position of the venous pulse in the neck goes down in inspiration because of the reduction in intrathoracic pressure.
5. Hepatojugular reflux is positive in the internal jugular vein because there are no valves between the hepatic veins, inferior vena cava, right atrium and superior vena cava.
6. The pulse wave form in the carotid artery is simple up and down while that of the internal jugular vein is more complex rapid oscillation at the top of the venous column

Coarctation of aorta

DISPLACED APEX BEAT
1. Massive pleural effusion
2. Massive pneumothorax
3. Lung fibrosis
4. Left ventricular hypertrophy 5. Mediastinal mass or neoplasm 6. Dextrocardia

Question 29

What is the cause or causes of a tapping apex beat, a thrusting apex beat , a heaving apex beat, impalpable or abnormal apex beat

Answer 29

TAPPING APEX BEAT
(Palpable first heart sound) Mitral stenosis
THRUSTING APEX BEAT
(Caused by volume overload)
1. Aortic regurgitation
2. Mitral regurgitation
3. Left to right shunt

HEAVING (SUSTAINED) APEX BEAT
(Due to pressure overload)
1. Aortic stenosis
2. Systemic hypertension

IMPALPABLE APEX BEAT
1. Obesity
2. Under the rib
3. Very muscular chest wall 4. Pericardial effusion
5. Constrictive pericarditis 6. Pleural effusion
7. Emphysema
Mitral stenosis
Right ventricular hypertrophy

Question 30

What do the different heart sounds mean

Answer 30

1. 1st heart sound; closure of mitral and tricuspid valves
2. 2nd heart sound; closure of aortic and pulmonary valves
3. 3rd heart sound; ventricular filling
4. 4th heart sound’ atrial contraction
   Splitting of the 2nd heart sound occur in the young during inspiration because the chest acts as a sucker during inspiration and increasing venous return and therefore the right ventricular output. Thus, the pulmonary component of the 2nd heart sound is delayed. Third heart sound comes after the second heart sound. When heard in the young, could be benign but always pathological in the adults
   Fourth heart sound precedes the first heart sound. When audible, it is always pathological and means heart failure.
   Both 3rd and 4th heart sounds are low pitched they and they are localized in the cardiac apex.
   SPLI

Question 31

What is the location of the four auscultation places on the heart

Answer 31

THE FOUR AUSCULTATORY AREAS
Mitral area: left 5th intercostal space, mid-clavicular line Tricuspid are: 4th intercostal space; left parasternal line Pulmonary area: 2nd intercostal space, left parasternal line Aortic area; 2nd intercostals space: right parasternal line

Question 32

What does splitting of heart sounds signify

Answer 32

SPLITTING SECOND HEART SOUNDS
Physiological splitting; a component precedes P in inspiration Fixed splitting; a split of that does not vary with respiration 1. Atrial septal defect
2. Right ventricular failure
Persistent splitting’ refers to split that is heard during both inspiration and expiration. Though it is persistent, it will vary unlike a fixed split.
1. pulmonary stenosis
Paradoxical splitting; a split during expiration rather than inspiration is due to Delayed closure of aortic valve. Precedes A (reverse splitting)
1. Left bundle branch block.

Question 33

What eight things do you look out for with murmurs and state and explain the grading system of murmurs

Answer 33

Note these about heart murmurs:
Timing
Duration
Character
Pitch
Intensity
Location
Extent and direction of transmission Influence of respiration and position

Grading of murmurs:
Grade 1: the murmur is heard quietly in an ordinary room
Grade 2: the murmur is moderately loud
Grade 3: the murmur is loud and accompanied by a thrill
Grade 4: the murmur is audible without a stethoscope.

Question 34

What cause of murmur causes a Pansystolic murmur, is Heard best at mitral area, Radiates to the axilla (left)
And Convention behooves us to listen to this murmur with the diaphragm as well, although low- pitched sounds are listened to with the bell of the stethoscope.

Answer 34

Murmur of mitral regurgitation

Question 35

What cause of murmur has:
1. Opening snap
2. Mid-diastolic murmur
3. Loud 1st heart sound
4. Heard best at the apex
5. No radiation
6. Possible pre-systolic accentuation when pt is in sinus rhythm
7. If murmur is not heard easily, turn pt to his left side to approximate heart to chest wall.

What causes of murmur causes:
1. Early diastolic murmur
2. Decrescendo
3. Heard best at the left parasternal border
4. Heard best at peak of expiration
5. Heard best at pt leaning forward in the sitting position 6. Has no radiation

Answer 35

MURMUR OF MITRAL STENOSIS

MURMUR OF AORTIC REGURGITATION

Question 36

What are the characteristics of MURMUR OF AORTIC STENOSIS
What are the characteristics of murmurs of VSD
What are the characteristics of continuous murmurs
What are the characteristics of Austin flint murmurs and innnocent murmurs

Answer 36

1. Ejection systolic (mid-systolic) murmur
2. Diamond shaped (crescendo-decrescendo) 3. Heard best at aortic area
3. radiates to the neck (right side)

MURMUR OF VSD
1. Pan systolic murmur
2. Best heard to the left of the sternum
3. Accompanied by a thrill
4. Sometimes best heard at left 3rd or 4th intercostals space with diaphragm of the stethoscope.

CONTINUOUS MURMUR
1. Heard during systole and diastole and is uninterrupted by valve closure
2. Heard in PATENT DUCTUS ARTERIOSUS
3. Because flow from high-pressure aorta t low pressure pulmonary artery continues throughout the cardiac cycle.
4. Ruptured sinus of Valsava aneurysm also produces continuous murmur.

AUSTIN FLINT MURMUR
1. A murmur heard in SEVERE AORTIC REGURGITATION
2. A MID-DIASTOLIC murmur
3. Caused by the preclosure of the anterior leaflet of the mitral valve by regurgitant jet of blood from the incompetent aortic valve.

INNOCENT MURMURS
a. unrelated to heart disease
b. Always mid-systolic in timing
c. Caused by turbulent flow in the left (sometimes right) ventricular outflow tract
d. Causes are hyperkinetic circulatory state

Question 37

What are the phases of korotkoff sounds
What are the stages of clubbing
State three CVS causes of hepatomegaly

Answer 37

KOROTKOFFF SOUND-1905
Phase I. sounds of clear tapping quality, cuff pressure equals arterial peak

Systolic pressure
Phase II: Sounds become drawn into a murmur
Phase III: sound become clear and increase in intensity
Phase V: complete disappearance of sound.
THE CHOICE OF THE 5TH KOROTKOFF AS THE DIASTOLIC PRESSURE
1. The complete disappearance is closer to the true diastolic pressure than the 4th. 2. The 5th korotkoff sound is more reproducible than the 4th.

STAGES OF CLUBBING
Stage I: increased sponginess of the nail fold
Stage II: obliteration of the angle between the nail bed and the nail fold Stage III: increased convexity of the nail both transversely and longitudinally Stage IV: bulbous swelling of the distal phanlanges
Stage V: swelling and tenderness in the wrist (respiratory- bronchial carcinoma)
Cardiovascular causes of hepatomegaly
1. Congestive heart failure 2. Constrictive pericarditis 3. Budd Chiari syndrome

Question 38

Explain the Patho of clubbing and state some causes of clubbing

Answer 38

Finger clubbing is the swelling and widening of the fingers and nails, which results from changes in the tissues beneath the nails. While the exact mechanism behind finger clubbing is not yet fully understood, several theories have been proposed.

In summary, finger clubbing is a complex process that involves changes in the tissues beneath the nails, which can occur due to reduced oxygen levels in the blood, an increase in prostaglandin E levels, or various underlying medical conditions.

One of the most widely accepted theories suggests that finger clubbing occurs due to reduced oxygen levels in the blood. When there is a lack of oxygen in the blood, the body’s tissues may release chemicals that promote the growth of blood vessels in the fingers and nails. These new blood vessels can cause the tissues beneath the nails to expand, leading to the characteristic appearance of clubbed fingers.

Another theory suggests that finger clubbing is caused by an increase in the levels of a hormone-like substance called prostaglandin E. Prostaglandin E is involved in inflammation and is produced in response to tissue damage or infections. It may also promote the growth of blood vessels and contribute to the development of finger clubbing.

Various medical conditions can cause finger clubbing. These conditions include lung diseases such as cystic fibrosis, lung cancer, and bronchiectasis. Heart disorders, such as congenital heart disease and endocarditis, can also cause finger clubbing. Additionally, gastrointestinal conditions such as inflammatory bowel disease and liver cirrhosis have been linked to finger clubbing.

Question 39

State the ddx of extra heart sounds , presentation and investigations

Answer 39

Extra heart sounds
The third and fourth heart sounds (S3 and S4), respectively, are early and late diastolic ventricular filling sounds. S3 can be heard in healthy chil- dren, but S4 is abnormal even in children.

LVH
due to hypertension, aortic stenosis, or hypertrophic cardiomyopathy
Suggested by: fourth heart sound. Increased LV voltage on ECG
Confirmed by: LV hypertrophy on echocardiogram

Decompensated
heart failure in
cardiomyopathy, findings of CHF constrictive
pericarditis:
Suggestedby:thirdheartsound
Confirmed by: Elevated JVP, pulmonary rales, CXR

Severe heart failure:
Suggested by: third and fourth heart sound giving gallop
Confirmed by: raised JVP, crackles at lung bases, pulmonary edema on CXR and systolic or diastolic dysfunction or valve dysfunction on echocardiogram

S3-Constrictive
pericarditis Left ventricular failure Pericardial effusion
Mitral regurgitation

S4-Heart failure Hypertension
Aortic stenosis Hypertrophic cardiomyopathy

Question 40

State six ddx of a systolic murmur and four diastolic murmurs
And two ddx of continuous murmurs presentations and investigations

Answer 40

Diastolic:
Mitral stenosis
Mitral stenosis with pliable valve
Aortic insufficency

Systolic:
Aortic stenosis
Hypertrophic
cardiomyopathy
Aortic sclerosis
Pulmonary high flow
Atrial septal defect (rare) causing high pulmonary flow
Pulmonary stenosis

Mitral incompetence due to rheumatic heart disease, valvedysfunction after myocardial infarction Tricuspid incompetence (rare alone) sometimes
alone in severe cor pulmonale or after pulmonary embolus
Mitral and tricuspid incompetence due to rheumatic heart disease or dilated ventricles in severe heart failure
Ventricular septal defect (VSD) usually congenital, sometimes rupture of septum after infarction

Continuous murmurs:

Patent ductus arteriosus-Suggested by: newborn infant, high pulse volume, diastolic and systolic murmurs to give continuous, “mechanical” murmur: “shee-shoo, shee-shoo”
Confirmed by: echocardiogram and cardiac catheterization

Pericarditis with pericardial friction rub (not true murmur):
Suggested by: “scratching murmur” heard in systole ± diastole. Chest pain worse when lying back and relieved by lying forward. Raised ST segments or T-wave inversion on ECG
Confirmed by: echocardiographic findings of pericardial effusion

Question 41

Ddx of thrills and ddx of pericardial friction rub and ddx of clubbing

Answer 41

Aortic stenosis
Ventricular septal defect
Patent ductus arteriosus

Rub:
Trauma

TB
Viral infection
Myocardial infarction Rheumatic fever Connective tissue disease
Pericarditis

:

Clubbing
Cyanotic congenital heart disease
Mitral stenosis Infective endocarditis Cardiac myxoema Endomyocardial fibrosis