Hiatus hernia - herniation of part of the stomach into the chest region, usually asymptomatic
Sliding hiatus hernia - gastro-0esophageal junction slides through hiatus and lies above diaphragm. no symptoms unless reflux
Para-oesophageal/rolling hernia - small part of fundus of stomach rolls up through the hernia along the oesophagus.. sphincter reamins below the diaphragm & remains competent. sometimes, however, this will produce severe pain & need surgial treatment.
Gastro-oesophageal reflux - reflux of gastric contents which can occur normally
Gastro-oesophageal reflux disease (GORD) - reflux with persistent symptoms
GORD occurs only when anit-reflux mechanism fail to allow gastric contents to make prolonged contact with lower oesophageal mucosa. (can occur without an hiatus hernia)
Lower oesophageal sphincter (LOS) is formed by distal 4cm of oesophageal smooth muscle. After relaxation to allow bolus to enter stomach, it rapidly regains its normal tone & prevents reflux. It is able to increase tone in response to increased pressures.
Pathogenosis:
- Transient LOS relaxations
- Low resting LOS tone which fails to increase when lying flat
- LOS tone fails to increase when pressure increased eg. pregnancy
- Increase oesophageal mucosal
- Large hiatus hernia impairs the mechanism of crural diaphragm.
- Reduced oesophageal clearance of acid due to poor peristalsis and made worse by trapping of acid in hernial sac due to hiatus hernia.
Clinical Features:
1) Heartburn
2) Regurgitation of food & 'acid'
Why I think I was made to research this.. haha..
The difference between GOR & myocardia ischaemia
Gastro-oesophagal reflux
1) Burning pain produced by bending, stooping or lying down
2) Pain seldom radiates to arms
3) Pain precipitated by drinking hot liquids or alcohol
4) Relieved by antacids
Myocardia ischaemia
1) Gripping/crushing pain
2) Pain radiating into neck, shoulders, both arms
3) Pain by exercise
4) Accompanied by dyspnoea
Source: kumar & clarke
Note: words like oesophageal, diaphragm are really hard to spell..
Friday, March 13, 2009
Thursday, March 12, 2009
ECG- electrocardiogram
ECG- electrocardiogram or electrocardiograph
Introduction
The contraction of any muscle is associated with electrical changes called ‘depolarisation’, and these changes can be detected by electrodes attached to the surface of the body. Since all muscular contractions will be detected, the electrical changes associated with the heart muscle will only be clear if the patient is fully relaxed and no skeletal muscles are contracting.
The ECG can be used to help determine;
- the anatomical orientation of the heart and the relative sizes of its chambers eg- left ventricular hypertrophy
- disturbances of rhythm and conduction eg- arrhythmias
- the extent and location of ischemic damage to the heart muscle
- the effects of abnormal concentrations of various plasma electrolytes
- digital imbalance of medications eg- Digoxin
Path of electrical impulse through the heart
the electrical discharge fro each cardiac cycle normally starts at the sinoatrial node in the right atrium. Depolarization then spreads through the atrial muscle fibres. There is a delay whilst the depolarization spreads through the atrioventricular node, after which it travels through the bundle of his, through the right and left bundle branches and through specialized fibres known as purkinje fibres.
diagram 1 + 2
How to interpret and ECG
The muscle mass of the atria, when in comparison with that of the ventricles is small, and thus the electrical change accompanying the contraction of the atria is small.
Contractions of the atria are associated with the ‘p’ wave.
The ventricular mass is large and the large deflection of the ECG when the ventricles are depolarized is seen by the ‘QRS’ complex.
The ‘T’ wave of the ECG is associated with the return of the ventricular mass to its resting state- repolarisation.
*in some ECGs and extra wave ‘U’ can be seen, the origin of which is uncertain. However if a ‘U’ wave follows a normally shaped ‘T’ wave, it can be assumed normal.
PR interval- the period between the beginning of the p wave and the QRS complex. I.e.- time taken for excitation to spread from sa node, through the atrial muscles to the AV node. Normally takes ~ 0.12-0.20 sec.
QT interval- beginning of Q wave till the end of T wave. varies with heart rate. Its prolonged in patients with some electrolyte abnormalities, and more importantly it is prolonged by some drugs. [ a prolonged QT interval ,greater then 450ms may lead to ventricular tachycardia.]
ST segment- reflects a time when the entire ventricular myocardium is depolarized, and should therefore have the same potential ad that present when the muscle is relaxed. –isoelectric line.
Few Problems that you might encounter-
-abnormalities of the p wave ~ enlargement of one or other atria
-prolonged pr interval ~ disorder of the AV node
-abnormalities of the QRS complex ~ disorders of cardiac conduction, ischeamic damage to heart muscle
-ST segment deviate from resting potential ~ hypoxia [may indicate myocardial ischaemia]
-abnormalities of T wave~ may indicate myocardial damage, electrolyte disturbances or cardiac hypertrophy.
- a higher than normal T wave~ excess ca++
- missed p wave~ sa node malfunction [av node taken over]
How to attach the leads
diagram 3
arms- attach onto medial anterior side towards the ulna, at the feet- on the medial anterior aspect over the tibia.
The unipolar electrodes on the chest;
V1- 4th right intercostal space to the right of the sternum
V2- 4th left intercostal space adjacent to the sternum
V3- between V2 and V4
V4- 5th intercostal space in the mid clavicular line
V5- in the same horizontal plane as V4 in the anterior axillary line
V6- in the same horizontal plane as V5 in the mid axillary line
~ they all look at the heart in a horizontal plane
V1 and v2- right ventricle
V3 and v4- septum between the ventricles and the anterior wall of the left ventricle
V5 and v6- anterior and lateral walls of the left ventricle
Measurements
A typical electrocardiograph runs at a paper speed of 25 mm/s, although faster paper speeds are occasionally used. Each small block of ECG paper is 1 mm². At a paper speed of 25 mm/s, one small block of ECG paper translates into 0.04 s (or 40 ms). Five small blocks make up 1 large block, which translates into 0.20 s (or 200 ms). Hence, there are 5 large blocks per second. A diagnostic quality 12 lead ECG is calibrated at 10 mm/mV, so 1 mm translates into 0.1 mV. A calibration signal should be included with every record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.
To calculate heart rate- 300 divided by the number of large squares between each QRS complex.
Introduction
The contraction of any muscle is associated with electrical changes called ‘depolarisation’, and these changes can be detected by electrodes attached to the surface of the body. Since all muscular contractions will be detected, the electrical changes associated with the heart muscle will only be clear if the patient is fully relaxed and no skeletal muscles are contracting.
The ECG can be used to help determine;
- the anatomical orientation of the heart and the relative sizes of its chambers eg- left ventricular hypertrophy
- disturbances of rhythm and conduction eg- arrhythmias
- the extent and location of ischemic damage to the heart muscle
- the effects of abnormal concentrations of various plasma electrolytes
- digital imbalance of medications eg- Digoxin
Path of electrical impulse through the heart
the electrical discharge fro each cardiac cycle normally starts at the sinoatrial node in the right atrium. Depolarization then spreads through the atrial muscle fibres. There is a delay whilst the depolarization spreads through the atrioventricular node, after which it travels through the bundle of his, through the right and left bundle branches and through specialized fibres known as purkinje fibres.
diagram 1 + 2
How to interpret and ECG
The muscle mass of the atria, when in comparison with that of the ventricles is small, and thus the electrical change accompanying the contraction of the atria is small.
Contractions of the atria are associated with the ‘p’ wave.
The ventricular mass is large and the large deflection of the ECG when the ventricles are depolarized is seen by the ‘QRS’ complex.
The ‘T’ wave of the ECG is associated with the return of the ventricular mass to its resting state- repolarisation.
*in some ECGs and extra wave ‘U’ can be seen, the origin of which is uncertain. However if a ‘U’ wave follows a normally shaped ‘T’ wave, it can be assumed normal.
PR interval- the period between the beginning of the p wave and the QRS complex. I.e.- time taken for excitation to spread from sa node, through the atrial muscles to the AV node. Normally takes ~ 0.12-0.20 sec.
QT interval- beginning of Q wave till the end of T wave. varies with heart rate. Its prolonged in patients with some electrolyte abnormalities, and more importantly it is prolonged by some drugs. [ a prolonged QT interval ,greater then 450ms may lead to ventricular tachycardia.]
ST segment- reflects a time when the entire ventricular myocardium is depolarized, and should therefore have the same potential ad that present when the muscle is relaxed. –isoelectric line.
Few Problems that you might encounter-
-abnormalities of the p wave ~ enlargement of one or other atria
-prolonged pr interval ~ disorder of the AV node
-abnormalities of the QRS complex ~ disorders of cardiac conduction, ischeamic damage to heart muscle
-ST segment deviate from resting potential ~ hypoxia [may indicate myocardial ischaemia]
-abnormalities of T wave~ may indicate myocardial damage, electrolyte disturbances or cardiac hypertrophy.
- a higher than normal T wave~ excess ca++
- missed p wave~ sa node malfunction [av node taken over]
How to attach the leads
diagram 3
arms- attach onto medial anterior side towards the ulna, at the feet- on the medial anterior aspect over the tibia.
The unipolar electrodes on the chest;
V1- 4th right intercostal space to the right of the sternum
V2- 4th left intercostal space adjacent to the sternum
V3- between V2 and V4
V4- 5th intercostal space in the mid clavicular line
V5- in the same horizontal plane as V4 in the anterior axillary line
V6- in the same horizontal plane as V5 in the mid axillary line
~ they all look at the heart in a horizontal plane
V1 and v2- right ventricle
V3 and v4- septum between the ventricles and the anterior wall of the left ventricle
V5 and v6- anterior and lateral walls of the left ventricle
Measurements
A typical electrocardiograph runs at a paper speed of 25 mm/s, although faster paper speeds are occasionally used. Each small block of ECG paper is 1 mm². At a paper speed of 25 mm/s, one small block of ECG paper translates into 0.04 s (or 40 ms). Five small blocks make up 1 large block, which translates into 0.20 s (or 200 ms). Hence, there are 5 large blocks per second. A diagnostic quality 12 lead ECG is calibrated at 10 mm/mV, so 1 mm translates into 0.1 mV. A calibration signal should be included with every record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.
To calculate heart rate- 300 divided by the number of large squares between each QRS complex.
References-
1)Tutorial notes
2)The ECG made easy by John R. Hampton - 7th ed
Pneuomonia
PNEUOMONIA
Pneumonia is defined as an inflammation of the substance of the lungs where it can be caused by both bacteria and virus. Clinically it usually presents as an acute illness with most cases illustrating patients with a cough, purulent sputum and fever.
The various pneuomonias are either localized with the whole of one or more lobes of the lungs or they can often diffuse to the bronchi and bronchioles.
There are many types of pneumonia but the only one which is remotely close to the symptoms illustrated is cryptogenic organizing pneumonia, which is associated with some pleuritic chest pain. However this is still very unlikely.
_ kumar and clarke
Pneumonia is defined as an inflammation of the substance of the lungs where it can be caused by both bacteria and virus. Clinically it usually presents as an acute illness with most cases illustrating patients with a cough, purulent sputum and fever.
The various pneuomonias are either localized with the whole of one or more lobes of the lungs or they can often diffuse to the bronchi and bronchioles.
There are many types of pneumonia but the only one which is remotely close to the symptoms illustrated is cryptogenic organizing pneumonia, which is associated with some pleuritic chest pain. However this is still very unlikely.
_ kumar and clarke
Blood Testing
PCL 2 TASK – Blood Tests & Relevant components
"Nondetectable TN levels in asymptomatic patients at admission and within the first 6 hours after admission can rule out relevant myocardial injury.”
When a patient presents to Emergency with chest pain, generally the first test ordered is a blood test. This is because it is
- Relatively affordable
- Easy to administer
- Convenient
- Results are readily available
Importantly, treatment should commence before results are available.
Components obtained should include –
- Full blood count
- Serum electrolytes
- Glucose
- Lipid profile
Certain components identified in a blood test can indicate the source of a patients chest pain –
- Cardiac Troponin
o Serum troponin level testing is routine in those presenting with cardiopulmonary complaints
o Results within 24 hours
o A marker of cardiac damage from any cause
o Elevated Troponin levels are typically related to cardiac damge –
defining in the diagnosis of acute myocardial infarction
However, it is not pathognomonic for acute coronary syndrome
o Cardiac Troponin is a regulatory protein and is found in striated (skeletal and cardiac) muscle
o It has 3 subunits
TN-T
TN-I
TN-C
TN-C is found in smooth muscle and as such is the least cardiac-specific. Because of this, it is TN-T and TN-I that are tested for in suspected cardiac episodes.
TN-I is the most cardiac-specific as it has not been found in skeletal muscle
TN-T may be indicative of renal damage
DISEASE TROPONIN LEVELS
ACS TN increase
- Indicative of adverse cardiac events
- Should prompt more aggressive treatment
Congestive Heart Failure TN elevations
- High risk patients with poor short term prognosis
- Also associated with increased risk of ventricular dysrhythmias
Myocarditis and Pericarditis TN elevations
- Useful in identifying myocyte necrosis (myocytisis)
- May also be present in pericarditis
While TN levels do not correlate with patient prognosis, there is some correlation between elevated TN and 1-month duration of heart failure symptoms
Cardiac Trauma - Patients with TN elevations have a higher risk of cardiac dysrhythmias and LV dysfunction
- Interestingly, TN level is not related to a patients prognosis
Cardiotoxins - Snakebite can cause acute MI or vasospasm elevated TN levels
- This is as the venom has a direct myocardial effect
Tachycardia - Severe tachycardia can induce TN elevations
- This is due to increased myocardial oxygen demand and decreased supply
Chronic Obstructive Pulmonary Disease - Severe exacerbations are associated with right ventricular strain thus produce TN (as below)
- Another option is that patients may have concurrent acute MI or PE, and thus have elevated TN
- TN elevations correlate with severity of COPD
Pulmonary embolism - TN elevations predict complications and mortality
- The proposed reason for TN release is large PEs induce acute right ventricular pressure overload causes increased wall tension regional wall ischemia
- CKMB
o Results in 2 hours
o
- Haemoglobin
o Results in 2 hours
http://www.medscape.com/viewarticle/582721
Kumar & Clarke
http://www.sydpath.stvincents.com.au/spec_db/
Gah it looked much prettier in word!
Will try and improve this this afternoon
thanks everyone, and apologies for the lateness!
georgia
"Nondetectable TN levels in asymptomatic patients at admission and within the first 6 hours after admission can rule out relevant myocardial injury.”
When a patient presents to Emergency with chest pain, generally the first test ordered is a blood test. This is because it is
- Relatively affordable
- Easy to administer
- Convenient
- Results are readily available
Importantly, treatment should commence before results are available.
Components obtained should include –
- Full blood count
- Serum electrolytes
- Glucose
- Lipid profile
Certain components identified in a blood test can indicate the source of a patients chest pain –
- Cardiac Troponin
o Serum troponin level testing is routine in those presenting with cardiopulmonary complaints
o Results within 24 hours
o A marker of cardiac damage from any cause
o Elevated Troponin levels are typically related to cardiac damge –
defining in the diagnosis of acute myocardial infarction
However, it is not pathognomonic for acute coronary syndrome
o Cardiac Troponin is a regulatory protein and is found in striated (skeletal and cardiac) muscle
o It has 3 subunits
TN-T
TN-I
TN-C
TN-C is found in smooth muscle and as such is the least cardiac-specific. Because of this, it is TN-T and TN-I that are tested for in suspected cardiac episodes.
TN-I is the most cardiac-specific as it has not been found in skeletal muscle
TN-T may be indicative of renal damage
DISEASE TROPONIN LEVELS
ACS TN increase
- Indicative of adverse cardiac events
- Should prompt more aggressive treatment
Congestive Heart Failure TN elevations
- High risk patients with poor short term prognosis
- Also associated with increased risk of ventricular dysrhythmias
Myocarditis and Pericarditis TN elevations
- Useful in identifying myocyte necrosis (myocytisis)
- May also be present in pericarditis
While TN levels do not correlate with patient prognosis, there is some correlation between elevated TN and 1-month duration of heart failure symptoms
Cardiac Trauma - Patients with TN elevations have a higher risk of cardiac dysrhythmias and LV dysfunction
- Interestingly, TN level is not related to a patients prognosis
Cardiotoxins - Snakebite can cause acute MI or vasospasm elevated TN levels
- This is as the venom has a direct myocardial effect
Tachycardia - Severe tachycardia can induce TN elevations
- This is due to increased myocardial oxygen demand and decreased supply
Chronic Obstructive Pulmonary Disease - Severe exacerbations are associated with right ventricular strain thus produce TN (as below)
- Another option is that patients may have concurrent acute MI or PE, and thus have elevated TN
- TN elevations correlate with severity of COPD
Pulmonary embolism - TN elevations predict complications and mortality
- The proposed reason for TN release is large PEs induce acute right ventricular pressure overload causes increased wall tension regional wall ischemia
- CKMB
o Results in 2 hours
o
- Haemoglobin
o Results in 2 hours
http://www.medscape.com/viewarticle/582721
Kumar & Clarke
http://www.sydpath.stvincents.com.au/spec_db/
Gah it looked much prettier in word!
Will try and improve this this afternoon
thanks everyone, and apologies for the lateness!
georgia
Driving after a faint
Information obtained from "Assessing fitness to Drive" handbook published by Austroads, which is an organistional body in charge of relaying current information on Australian road rules from the state authorities.
Following an episode of idiopathic syncope one does not qualify to drive for 2 months privately or 6 months commercially. Except if the patient suffers from unheralded recurrent episodes of blackout/syncope which don't respond to treatment. If the underlying cause of the faint was cardiovascular the minimum non-driving period moves up to three months,
CVD - minimum non-driving periods for non-commercial driving
Acute Myocardial Infarction 2 weeks
Aneurysm repair 4 weeks
Angioplasty 2 days
Cardiac arrest 6 months
Cardiac defibrillator 6 months after cardiac arrest
Cardiac pacemaker insertion 2 weeks
Coronary Artery By-pass Grafts 4 weeks
Deep Vein Thrombosis 2 weeks
Heart/Lung transplant 6 weeks
Pulmonary embolism 6 weeks
Syncope 3 months
Point of interest - according to Vicroads website.
Doctors do have a power to grant exemptions for patients to not wear helmets on pushbikes or seatbelts in cars. No exemption can be granted for a motorcycle helmet.
http://www.austroads.com.au/aftd/downloads/AFTD_2003_FA_WEBREV1.pdf
http://www.vicroads.vic.gov.au/Home/Licensing/MedicalConditions/MedicalExemptionsSeatBeltHelmet.htm
Following an episode of idiopathic syncope one does not qualify to drive for 2 months privately or 6 months commercially. Except if the patient suffers from unheralded recurrent episodes of blackout/syncope which don't respond to treatment. If the underlying cause of the faint was cardiovascular the minimum non-driving period moves up to three months,
CVD - minimum non-driving periods for non-commercial driving
Acute Myocardial Infarction 2 weeks
Aneurysm repair 4 weeks
Angioplasty 2 days
Cardiac arrest 6 months
Cardiac defibrillator 6 months after cardiac arrest
Cardiac pacemaker insertion 2 weeks
Coronary Artery By-pass Grafts 4 weeks
Deep Vein Thrombosis 2 weeks
Heart/Lung transplant 6 weeks
Pulmonary embolism 6 weeks
Syncope 3 months
Point of interest - according to Vicroads website.
Doctors do have a power to grant exemptions for patients to not wear helmets on pushbikes or seatbelts in cars. No exemption can be granted for a motorcycle helmet.
http://www.austroads.com.au/aftd/downloads/AFTD_2003_FA_WEBREV1.pdf
http://www.vicroads.vic.gov.au/Home/Licensing/MedicalConditions/MedicalExemptionsSeatBeltHelmet.htm
Wednesday, March 11, 2009
Aneurysmal Disease
Aneurysm
Definition: Localised abnormal dilatation of a blood vessel or the heart.
True Aneurysm
Definition: An aneurysm which involves all 3 layers of blood vessel wall or heart
Abdominal Aortic Aneurysm (AAA)
Definition: Aneurysm occurring in abdominal portion of aorta (usually infra-renal).
Demographics: More common with increasing age, present in 5% of population above 60 years of age. 5 times more frequent in males. 1 in 4 male children of affected individual will develop it.
Causes: Secondary to atherosclerosis, infection, trauma, genetic diseases (eg. Marfan’s / Ehlers-Danlos syndromes).
Symptoms: Most asymptomatic. Obstruction of proximal organs (eg. ureter, duodenum, vena cava). Rupture: Severe pain (epigastric with radiation to back), hypotension, tachycardia, anaemia, sudden death (90% mortality).
Signs: Pulsatile, expansile abdominal mass. “Trash feet” (ie. forefoot / toe ischaemia) due to emboli.
Investigations: Ultrasound, CT scan.
Management: Lifestyle changes (smoking, diet, hypertension control etc.), medical (lipid-lowering, anti-hypertensive drugs), surgery (necessary in emergency case of rupture, otherwise elective).
Prognosis: Return to normal activities within few months of repair.
Thoraco-Abdominal Aneurysm (TAA)
Definition: Aneurysm occurring in ascending, arch or descending thoracic aorta.
Demographics: Most common in individuals with Marfan’s syndrome and hypertension.
Causes: Secondary to atherosclerosis.
Symptoms: Most asymptomatic. Stridor (high-pitched, turbulent air flow in upper airway) due to compression, haemoptysis (coughing blood) due to aortobronchial fistula, hoarseness due to compression of recurrent laryngeal nerve. Rapid expansion: Chest pain radiating to back. Rupture: Hypotension, tachycardia, death.
Investigations: CT scan, aortography, transoesophageal echocardiography.
Management: Operative repair, stenting.
Syphilitic Aneurysm
Syphilis causes inflammation and narrowing of vasa vasorum in ascending and arch of aorta. This leads to ischaemic damage to media, causing fibrosis and loss of elasticity. Aneurysm results.
Mycotic Aneurysm
Infection of media via vasa vasorum (can occur in root of aorta) weakens arterial wall causing aneurysm. Often underlying bacterial endocarditis.
False Aneurysm (Pseudoaneurysm)
Definition: An aneurysm which breaches the vascular wall but is contained by extra-vascular tissues, forming a haematoma.
Ventricular Rupture
Following myocardial infarction, fibrosis of ventricular walls may cause a rupture, resulting in a haematoma that is contained within the pericardium.
Traumatic Rupture
Often the result of traumatic rupture or perforating injury (eg. during arteriography or angioplasty).
Dissection
Definition: Blood enters the wall of an artery as a haematoma, dissecting its layers.
Aortic Dissection
Definition: Blood enters lamina planes of the media to form blood filled channels within the aortic wall. Type A: aortic arch and valve proximal to origin of left subclavian artery. Type B: descending thoracic aorta distal to origin of left subclavian artery.
Demographics: Either hypertensive men aged 40-60 (90% of cases) or younger individuals with systemic or localised connective tissue abnormalities (eg. Marfan’s syndrome).
Causes: Hypertension, connective tissue disorder (eg. Marfan’s syndrome, Ehlers-Danlos syndrome, vitamin C deficiency, etc.) iatrogenic (eg. diagnostic catheterisation, pulmonary bypass), during or after pregnancy.
Symptoms: Severe central chest pain radiating to back and down arms.
Signs: Shock, neurological symptoms secondary to spinal cord ischaemia, renal failure, acute lower limb ischaemia, visceral ischaemia, absent peripheral pulses.
Investigations: Chest X-ray, CT scan, transoesophageal echocardiography.
Management: Medical (urgent anti-hypertensive drugs). Type A: arch replacement surgery. Type B: medical treatment.
References:
1. Kumar and Clark: Clinical Medicine, 6th ed.
2. Robbins Basic Pathology, 8th ed.
3. Underwood: General and Systemic Pathology, 4th ed.
Definition: Localised abnormal dilatation of a blood vessel or the heart.
True Aneurysm
Definition: An aneurysm which involves all 3 layers of blood vessel wall or heart
Abdominal Aortic Aneurysm (AAA)
Definition: Aneurysm occurring in abdominal portion of aorta (usually infra-renal).
Demographics: More common with increasing age, present in 5% of population above 60 years of age. 5 times more frequent in males. 1 in 4 male children of affected individual will develop it.
Causes: Secondary to atherosclerosis, infection, trauma, genetic diseases (eg. Marfan’s / Ehlers-Danlos syndromes).
Symptoms: Most asymptomatic. Obstruction of proximal organs (eg. ureter, duodenum, vena cava). Rupture: Severe pain (epigastric with radiation to back), hypotension, tachycardia, anaemia, sudden death (90% mortality).
Signs: Pulsatile, expansile abdominal mass. “Trash feet” (ie. forefoot / toe ischaemia) due to emboli.
Investigations: Ultrasound, CT scan.
Management: Lifestyle changes (smoking, diet, hypertension control etc.), medical (lipid-lowering, anti-hypertensive drugs), surgery (necessary in emergency case of rupture, otherwise elective).
Prognosis: Return to normal activities within few months of repair.
Thoraco-Abdominal Aneurysm (TAA)
Definition: Aneurysm occurring in ascending, arch or descending thoracic aorta.
Demographics: Most common in individuals with Marfan’s syndrome and hypertension.
Causes: Secondary to atherosclerosis.
Symptoms: Most asymptomatic. Stridor (high-pitched, turbulent air flow in upper airway) due to compression, haemoptysis (coughing blood) due to aortobronchial fistula, hoarseness due to compression of recurrent laryngeal nerve. Rapid expansion: Chest pain radiating to back. Rupture: Hypotension, tachycardia, death.
Investigations: CT scan, aortography, transoesophageal echocardiography.
Management: Operative repair, stenting.
Syphilitic Aneurysm
Syphilis causes inflammation and narrowing of vasa vasorum in ascending and arch of aorta. This leads to ischaemic damage to media, causing fibrosis and loss of elasticity. Aneurysm results.
Mycotic Aneurysm
Infection of media via vasa vasorum (can occur in root of aorta) weakens arterial wall causing aneurysm. Often underlying bacterial endocarditis.
False Aneurysm (Pseudoaneurysm)
Definition: An aneurysm which breaches the vascular wall but is contained by extra-vascular tissues, forming a haematoma.
Ventricular Rupture
Following myocardial infarction, fibrosis of ventricular walls may cause a rupture, resulting in a haematoma that is contained within the pericardium.
Traumatic Rupture
Often the result of traumatic rupture or perforating injury (eg. during arteriography or angioplasty).
Dissection
Definition: Blood enters the wall of an artery as a haematoma, dissecting its layers.
Aortic Dissection
Definition: Blood enters lamina planes of the media to form blood filled channels within the aortic wall. Type A: aortic arch and valve proximal to origin of left subclavian artery. Type B: descending thoracic aorta distal to origin of left subclavian artery.
Demographics: Either hypertensive men aged 40-60 (90% of cases) or younger individuals with systemic or localised connective tissue abnormalities (eg. Marfan’s syndrome).
Causes: Hypertension, connective tissue disorder (eg. Marfan’s syndrome, Ehlers-Danlos syndrome, vitamin C deficiency, etc.) iatrogenic (eg. diagnostic catheterisation, pulmonary bypass), during or after pregnancy.
Symptoms: Severe central chest pain radiating to back and down arms.
Signs: Shock, neurological symptoms secondary to spinal cord ischaemia, renal failure, acute lower limb ischaemia, visceral ischaemia, absent peripheral pulses.
Investigations: Chest X-ray, CT scan, transoesophageal echocardiography.
Management: Medical (urgent anti-hypertensive drugs). Type A: arch replacement surgery. Type B: medical treatment.
References:
1. Kumar and Clark: Clinical Medicine, 6th ed.
2. Robbins Basic Pathology, 8th ed.
3. Underwood: General and Systemic Pathology, 4th ed.
Pulmonary stenosis
Stenosis (narrowing of a valve) means that that the valve is unable to open fully.
Pulmonary stenosis is narrowing of the pulmonary semi-lunar valve. This is due to the fusion of the valve cusps; the valve forms a dome with a central opening (valvular). It can also be supravalvular or subvalvular ( a membrane or ridge forms, occluding the valve).
Infundibular pulmonary stenosis occurs when the conus arteriosus (the part of the right ventricle leading to the valve) is underdeveloped.
Pulmonary stenosis is usually a congential defect, but it can also result from rheumatic fever (which causes the cusps of the valve to fuse together) or from carcinoid syndrome (which is an array of symptoms occurring secondary to the carcinoid/neruoendorcrine tumour (tumour of the enterochromaffin cells in your small intestine)– causes flushing, diarrhoea, bronchoconstriction. I couldn’t really find anything that said what exactly it did to the valve, but basically, it makes them stick together).
Symptoms and signs
· Restricted right ventricular outflow, can lead to hypertrophy of the right ventricle à this, in turn, leads to right atrial hypertrophy
· Pulmonary obstruction
o Syncope
o Fatigue
o Symptoms of right heart failure
§ fatigue
§ breathlessness
§ anorexia
§ nausea
· Mid-systolic ejection murmur
o Best heard on inspiration
o Left of sternum, 2nd intercostals space
o Is often associated with a thrill
· Pulmonary closure sound – delayed and soft
· Pulmonary ejection sound – if obstruction is valvular
· Right ventricular heave (sustained impulse) can be felt
· Mild pulmonary stenosis – asymptomatic
· Moderately severe stenosis
o Right ventricular fourth sound
o Prominent jugular venous a-wave
Investigations
· Chest x-ray
o Prominent pulmonary artery – post-stenotic dilation
· ECG
o Shows right ventricular and atrial hypertrophy
o Can be normal
· Echocardiogram
o Doppler investigation – utilises echoes from tissue surfaces, and on amplification, can detect the echoes from RBCs
§ If blood is moving in the same direction as the ultrasound beam, the frequency of the returning echoes is changed according to the Doppler effect (Doppler Effect is the shift in frequency and wavelength of waves which results from a source moving with respect to the medium, a receiver moving with respect to the medium, or even a moving medium. If you want to see pretty moving diagrams, go to: http://www.kettering.edu/~drussell/Demos/doppler/doppler.html)
§ Shift in Doppler frequency is directly proportional to blood velocity
· Cardiac catherisation
o Catheter into right heart – level and degree of stenosis can be established by measuring systolic pressure gradient
Treatment
- Pulmonary valvotomy
o Balloon valvotomy
o Direct surgery
Pulmonary Embolism
Pulmonary emboli occur as the result of a thrombus (generally formed in the systemic veins) dislodging and embolising in the pulmonary arterial system.
Thrombi (or “clots”) form are caused due to a combination of three factors. These are often referred to as Virchow’s triad and encompass stasis of blood flow, hypercoagulability of the blood and endothelial damage of the vessel walls. Emboli can also occur from tumour, fat (from long bone fractures) amniotic fluid and foreign material injected during i.v. drug use.
The clinical features of pulmonary embolism are often rather vague, but unexplained dyspnoea is the most common (and often the sole) symptom. Pleuritic chest pain and haemoptysis (coughing blood) are present only when infarction has occurred. Many pulmonary emboli occur silently, but there are three typical clinical presentations.
Small/medium pulmonary embolism – an embolus has impacted in a terminal pulmonary vessel. Symptoms are pleuritic chest pain and dyspnoea. Haemoptyis occurs in 30% of cases, often 3+ days after the event. On examination the patient may be tachypnoeic with a localised pleural rub and an exudative pleural effusion can develop. The patient may have a fever, and cardiovascular examination is normal
Massive pulmonary embolism – much rarer, it involves sudden collapse because of an acute obstruction of the right ventricular outflow tract. The patient has severe central chest pain (cardiac ischaemia due to lack of coronary blood flow) and becomes shocked, pale and sweaty. Syncope may result if the cardiac output is transiently but dramatically reduced, and death may occur. On examination, the patient is tachypnoeic, has a tachycardia with hypotension and peripheral shutdown.
Multiple recurrent pulmonary emboli
This leads to increased breathlessness often over weeks or months. It is accompanied by weakness, syncope on exertion and occasionally angina. The physical signs are due to pulmonary hypertension that has developed from multiple occlusions of the pulmonary vasculature.
Diagnosis
The symptoms and signs of small and medium-sized pulmonary emboli are often subtle and non-specific, so the diagnosis is often delayed or even completely missed. Pulmonary embolism should be considered if patients present with symptoms of unexplained cough, chest pain, haemoptysis, new-onset atrial fibrillation (or other tachycardia), or signs of pulmonary hypertension
Investigations – include chest x-ray, plasma D-dimer, ECG, full bloods and radionuclide ventilation/perfusion scanning (V/Q scan)
Treatment
Oxygen, bed rest, heparin and analgesia
References - Kumar and Clarke, emedicine, wikipedia
By Steph
Pulmonary emboli occur as the result of a thrombus (generally formed in the systemic veins) dislodging and embolising in the pulmonary arterial system.
Thrombi (or “clots”) form are caused due to a combination of three factors. These are often referred to as Virchow’s triad and encompass stasis of blood flow, hypercoagulability of the blood and endothelial damage of the vessel walls. Emboli can also occur from tumour, fat (from long bone fractures) amniotic fluid and foreign material injected during i.v. drug use.
The clinical features of pulmonary embolism are often rather vague, but unexplained dyspnoea is the most common (and often the sole) symptom. Pleuritic chest pain and haemoptysis (coughing blood) are present only when infarction has occurred. Many pulmonary emboli occur silently, but there are three typical clinical presentations.
Small/medium pulmonary embolism – an embolus has impacted in a terminal pulmonary vessel. Symptoms are pleuritic chest pain and dyspnoea. Haemoptyis occurs in 30% of cases, often 3+ days after the event. On examination the patient may be tachypnoeic with a localised pleural rub and an exudative pleural effusion can develop. The patient may have a fever, and cardiovascular examination is normal
Massive pulmonary embolism – much rarer, it involves sudden collapse because of an acute obstruction of the right ventricular outflow tract. The patient has severe central chest pain (cardiac ischaemia due to lack of coronary blood flow) and becomes shocked, pale and sweaty. Syncope may result if the cardiac output is transiently but dramatically reduced, and death may occur. On examination, the patient is tachypnoeic, has a tachycardia with hypotension and peripheral shutdown.
Multiple recurrent pulmonary emboli
This leads to increased breathlessness often over weeks or months. It is accompanied by weakness, syncope on exertion and occasionally angina. The physical signs are due to pulmonary hypertension that has developed from multiple occlusions of the pulmonary vasculature.
Diagnosis
The symptoms and signs of small and medium-sized pulmonary emboli are often subtle and non-specific, so the diagnosis is often delayed or even completely missed. Pulmonary embolism should be considered if patients present with symptoms of unexplained cough, chest pain, haemoptysis, new-onset atrial fibrillation (or other tachycardia), or signs of pulmonary hypertension
Investigations – include chest x-ray, plasma D-dimer, ECG, full bloods and radionuclide ventilation/perfusion scanning (V/Q scan)
Treatment
Oxygen, bed rest, heparin and analgesia
References - Kumar and Clarke, emedicine, wikipedia
By Steph
Valve Pathology
All of the valve related issues have to do with a change in the capacityfor movement of the leaflets of the valve. The principle is that the leaflets of a valve undergo a pathological change to its composition (making it harder, thicker, etc) which in turn compromises its ability to perform its function as a valve. There are congenital conditions whichcan affect the cardiac valves, but they general present in childhood, soI’ve left them out.
Some of the key, relatively common conditions that came up were valve stenosis and insufficiency. Valve stenosis describes the abnormal narrowing of a blood vessel. The cusps of the valve become fused to form a dome with a smaller, central opening, thus throwing the pressure balance of the chambers out of that of the normal. As a result, it typically results in hypertrophy of the chamber concerned and leads the patient to demonstrate such symptoms as dyspnoea, angina and syncope on exertion.
Valve insufficiency is the inability of a cardiac valve to completely close during systole. As a result, the pressure gradient of the chambers of the heart propel blood in reverse, creating a regurgitation, or a backflow. This produces a characteristic murmur. This regurgitation can generate some chest pain and fatigue.
There are other conditions I found that might lead to similar failings of the heart valves and may be found in association to one of the conditions I’ve already mentioned. One such condition is Cardiac Fibrosis, which is an abnormal thickening of the valves due to high proliferation of cardiac fibroblasts. This thickening and hardening can lead to valvular dysfunction.
Endocarditis is the inflammation of the inner layer of the heart, the endocardium, and often involves the valves. It is characterised by a mass of platelets, fibrin, inflammatory cells and microorganisms. Since the valves of the heart do not receive any real blood supply, white blood cells have limited access to them, and if bacteria attach to them, there is decreased availability for immune response. Normally blood flows smoothly through the valves, but if they are in a damaged state, such as caused by rheumatic fever, then the likelihood of bacterial attachment is increased.
Another, perhaps more unlikely condition I found that might affect cardiac valve function was systemic lupus erythematosus. It’s a connective tissue, auto immune disease which (as the name implies) affects any part of the body. It involves the attacking of cells and tissue by the body’s immune system, resulting in inflammation. When affecting the heart, it can cause inflammation of any of the heart layers, such as endocarditis, as mentioned above.
Netters clinical
e medicine
moores
Sam
Some of the key, relatively common conditions that came up were valve stenosis and insufficiency. Valve stenosis describes the abnormal narrowing of a blood vessel. The cusps of the valve become fused to form a dome with a smaller, central opening, thus throwing the pressure balance of the chambers out of that of the normal. As a result, it typically results in hypertrophy of the chamber concerned and leads the patient to demonstrate such symptoms as dyspnoea, angina and syncope on exertion.
Valve insufficiency is the inability of a cardiac valve to completely close during systole. As a result, the pressure gradient of the chambers of the heart propel blood in reverse, creating a regurgitation, or a backflow. This produces a characteristic murmur. This regurgitation can generate some chest pain and fatigue.
There are other conditions I found that might lead to similar failings of the heart valves and may be found in association to one of the conditions I’ve already mentioned. One such condition is Cardiac Fibrosis, which is an abnormal thickening of the valves due to high proliferation of cardiac fibroblasts. This thickening and hardening can lead to valvular dysfunction.
Endocarditis is the inflammation of the inner layer of the heart, the endocardium, and often involves the valves. It is characterised by a mass of platelets, fibrin, inflammatory cells and microorganisms. Since the valves of the heart do not receive any real blood supply, white blood cells have limited access to them, and if bacteria attach to them, there is decreased availability for immune response. Normally blood flows smoothly through the valves, but if they are in a damaged state, such as caused by rheumatic fever, then the likelihood of bacterial attachment is increased.
Another, perhaps more unlikely condition I found that might affect cardiac valve function was systemic lupus erythematosus. It’s a connective tissue, auto immune disease which (as the name implies) affects any part of the body. It involves the attacking of cells and tissue by the body’s immune system, resulting in inflammation. When affecting the heart, it can cause inflammation of any of the heart layers, such as endocarditis, as mentioned above.
Netters clinical
e medicine
moores
Sam
Costochondritis
Costochondritis
Definition: Costochondritis is the inflammation of the costochondral cartilages that joint the ribs to the sternum. It leads to sharp pain in the costosternal joint.
The pain can mimic the one caused by heart attack or other heart conditions.
The inflammation may also be referred as:
- chest wall pain
- costosternal syndrome
- costosternal chondrodynia
- Tietze syndrome – when accompanied by swelling
Symptoms:
- Oftenly sharp pain. Sometimes dull.
- Pain when taking deep breaths.
- Pain when coughing.
- Difficulty breathing.
Causes:
- Injury is among the common cause of costochondritis. A direct blow to the chest would lead to the inflammation.
- Infection can develop in the costosternal joint, causing pain.
- The inflammation may be a symptom of fibromyalgia onset. People with the disease can have several tender spots, commonly on the upper part of sternum.
Tests for costochodritis:
- Physical exam. Feel along the sternum for any sign of tenderness or swelling area.
- History taking from ptx. Costochondritis pain is very similar to pain associated with heart disease, lung disease and GI problems.
- Usually, the disease can’t be seen on chest X-rays. But doctors may do the test to remove other possible conditions.
Treatments:
- Usually it goes away by itself through self healing process. It may take one or two weeks to resolve.
- Doctors may recommend these drugs to ease the pain cause by the inflammation:
- NSAIDs : ibuprofen and naproxen
- Anti depressants if the pain disrupts sleeping at night.
- Muscle relaxants that can ease the pain.
Cardiac tamponade
Cardiac tamponade is a condition where the heart is compressed when blood or fluid builds up in the space between the myocardium & the pericardium, thus preventing the ventricles from expanding fully. The blood or fluid build can occur due to pericardial effusion, dissecting aortic aneurysm, pericarditis, myocardial infarction, wounds to the heart, recent heart surgery etc.
Patient experiences
- Fainting
- Dyspnoea
- Anxiety
- Sharp, stabbing chest pain worsened by deep breathing or coughing
- Palpitations
- Swelling of abdomen or other areas
Signs noticed upon examination
- Low blood pressure
- Faint heart sounds
- Peripheral pulses may be weak or absent
Diagnosis can be established via echocardiogram, ECG, chest x-ray, CT, or MRI.
Patient experiences
- Fainting
- Dyspnoea
- Anxiety
- Sharp, stabbing chest pain worsened by deep breathing or coughing
- Palpitations
- Swelling of abdomen or other areas
Signs noticed upon examination
- Low blood pressure
- Faint heart sounds
- Peripheral pulses may be weak or absent
Diagnosis can be established via echocardiogram, ECG, chest x-ray, CT, or MRI.
Monday, March 9, 2009
Aortic Stenosis for Dummies
Aortic Stenosis at a Glance
- Aortic stenosis is narrowing of the aortic valve, impeding delivery of blood from the heart to the body.
- Aortic stenosis can be caused by congenital bicuspid aortic valve, scarred aortic valve of rheumatic fever, and wearing of aortic valve in the elderly.
Aortic stenosis can cause chest pain, fainting, and heart failure leading to shortness of breath. - Echocardiogram and cardiac catheterization are important tests in diagnosing and evaluating severity of aortic stenosis.
- Patients with aortic stenosis are usually given antibiotics prior to any procedures which might introduce bacteria into the bloodstream, such as dental procedures and surgeries.
Patients with aortic stenosis who have symptoms may require surgical heart valve replacement.
- What causes aortic stenosis?
In adults, three conditions are known to cause aortic stenosis.
Progressive wear and tear of a bicuspid valve present since birth (congenital).
Wear and tear of the aortic valve in the elderly.
Scarring of the aortic valve due to rheumatic fever as a child or young adult.
Bicuspid aortic valve is the most common cause of aortic stenosis in patients under age 65. Normal aortic valves have three thin leaflets called cusps. About 2% of people are born with aortic valves that have only two cusps (bicuspid valves). Although bicuspid valves usually do not impede blood flow when the patients are young, they do not open as widely as normal valves with three cusps. Therefore, blood flow across the bicuspid valves is more turbulent, causing increased wear and tear on the valve leaflets. Over time, excessive wear and tear leads to calcification, scarring, and reduced mobility of the valve leaflets. About 10% of bicuspid valves become significantly narrowed, resulting in the symptoms and heart problems of aortic stenosis.
The narrowing from rheumatic fever occurs from the fusion (melting together) of the edges (commissures) of the valve leaflets.
Patients with mild aortic valve narrowing may experience no symptoms. When the narrowing becomes significant (usually greater that 50% reduction in valve area), the pressure in the left ventricle increases and a pressure difference can be measured between the left ventricle and the aorta. To compensate for the increasing resistance at the aortic valve, the muscles of the left ventricle thicken to maintain pump function and cardiac output. This muscle thickening causes a stiffer heart muscle which requires higher pressures in the left atrium and the blood vessels of the lungs to fill the left ventricle. Even though these patients may be able to maintain adequate and normal cardiac output at rest, the ability of the heart to increase output with exercise is limited by these high pressures. As the disease progresses the increasing pressure eventually causes the left ventricle to dilate, leading to a decrease in cardiac output and heart failure.
- The major symptoms of aortic stenosis are:
chest pain (angina),
fainting (syncope), and
shortness of breath (due to heart failure).
In 4% of the patients with aortic stenosis, the first symptom is sudden death, usually during strenuous exertion. - Fainting (syncope) related to aortic stenosis is usually associated with exertion or excitement. These conditions cause relaxation of the body's blood vessels (vasodilation), lowering blood pressure. In aortic stenosis, the heart is unable to increase output to compensate for the drop in blood pressure. Therefore, blood flow to the brain is decreased, causing fainting.
Subscribe to:
Posts (Atom)