Yello,
This is the Link of the Day (reminiscent of last year's MUSO discussion board, eh?). I daresay, this may even be the Link of the Week! ;)
http://www.blaufuss.org
You need flash player for the tutorials. Relevant to PCL 2 are the heart sounds tutorials and quiz, and relevant to PCL 1 is the ECG thingy.
Have fun.
Showing posts with label pcl 1. Show all posts
Showing posts with label pcl 1. Show all posts
Wednesday, 7 March 2007
Monday, 5 March 2007
Cardiac Arrest Part II
There are 3 causes to the above condition:
Ventricular fibrillation (most common)
Treatment is to defibrillate the heart รจ stop the uncoordinated “quivering” of the ventricles and allow heart to reset its normal rhythm as it pumps again
Asystole
Treatment is to trigger any contraction of the heart for example CPR. Adrenaline or atropine can also be administered.
Dissociation
atrial dissociation
independent beating of the left and right atria, each with normal rhythm or with one or both having an abnormal rhythm.
atrioventricular dissociation
control of the atria by one pacemaker and of the ventricles by another, independent pacemaker.
electromechanical dissociation
continued electrical rhythmicity of the heart in the absence of effective mechanical function.
Ventricular fibrillation (most common)
Treatment is to defibrillate the heart รจ stop the uncoordinated “quivering” of the ventricles and allow heart to reset its normal rhythm as it pumps again
Asystole
Treatment is to trigger any contraction of the heart for example CPR. Adrenaline or atropine can also be administered.
Dissociation
atrial dissociation
independent beating of the left and right atria, each with normal rhythm or with one or both having an abnormal rhythm.
atrioventricular dissociation
control of the atria by one pacemaker and of the ventricles by another, independent pacemaker.
electromechanical dissociation
continued electrical rhythmicity of the heart in the absence of effective mechanical function.
Thursday, 1 March 2007
Echocardiography (ECG)
ECG: a non invasive diagnostic technique that is used in clinical cardiology. It involves the use of ultrasound( either alone or with contrast agent) to asses cardiac structure and function based on the differing ability of various structures within the heart to reflect ultrasound waves. Thus the ECG is able to show the structure of the heart as well as provide a continuous display of the functioning heart throughout its cycle.
There are various types of ECG
1) M-mode
2) 2 dimensional
3) Doppler and colour flow
4) Trans- Oesophageal
5) Stress
Clinical Use of ECG
Valve stenosis
Mitral stenosis
Valve regurgitation
Aortic aneurysms and dissections
Prosthetic heart valves
Cardiac failure: left ventricular function and response to treatment can be assessed. Left and right side cardiac output can also be estimated.
Pericardial effusion: fluid in the pericardial cavity shows as an echo-free region between the myocardium and the intense echo of the parietal pericardium.
Ischaemic disease: coronary arteries cannot be imaged adequately using echo techniques but images maybe useful for diagnosis of complications related to myocardial infarction.
Quantification of left ventricular function: heart failure maybe due to systolic or diastolic ventricular impairment or both. Echo helps by measuring end diastolic volume. If this is large, systolic dysfunction is most likely.
( the above are just brief descriptions of how ECG may be used clinically, for more details please refer to KUMAR AND CLARKE, clinical medicine p749-755)
There are various types of ECG
1) M-mode
2) 2 dimensional
3) Doppler and colour flow
4) Trans- Oesophageal
5) Stress
Clinical Use of ECG
Valve stenosis
Mitral stenosis
Valve regurgitation
Aortic aneurysms and dissections
Prosthetic heart valves
Cardiac failure: left ventricular function and response to treatment can be assessed. Left and right side cardiac output can also be estimated.
Pericardial effusion: fluid in the pericardial cavity shows as an echo-free region between the myocardium and the intense echo of the parietal pericardium.
Ischaemic disease: coronary arteries cannot be imaged adequately using echo techniques but images maybe useful for diagnosis of complications related to myocardial infarction.
Quantification of left ventricular function: heart failure maybe due to systolic or diastolic ventricular impairment or both. Echo helps by measuring end diastolic volume. If this is large, systolic dysfunction is most likely.
( the above are just brief descriptions of how ECG may be used clinically, for more details please refer to KUMAR AND CLARKE, clinical medicine p749-755)
Syncope
Syncope
Definition:
Partial or complete loss of consciousness due to a temporary reduction in blood flow and therefore a shortage of oxygen to the brain.
Non-cardiac causes:
Postural hypotension: Drop in blood pressure due to changing body position to a more vertical position after lying or sitting;
Dehydration causing a decrease in blood volume.
Blood pressure medications leading to low blood pressure.
Diseases of the nerves to the legs in older people (especially with diabetes or Parkinson's disease) when poor tone of the nerves of the legs draws blood into the legs from the brain.
High altitude.
Brain stroke or "near-stroke" (transient ischemic attack).
A migraine attack.
Emotions (e.g. fear, anxiety)
A reflex of the involuntary nervous system (the vasovagal reaction) triggered by certain situations (situational syncope) such as blood drawing, urinating, defecating, swallowing and coughing.
Cardiac causes:
Abnormal heart rhythms (heart beating too fast or too slow).
Abnormalities of the heart valves (aortic stenosis or pulmonic valve stenosis).
High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension).
Tears in the aorta (aortic dissection).
Widespread disease of the heart muscle (cardiomyopathy).
Taken from:
Britannica.com
MedicineNet.com
(For detailed information: http://www.medterms.com/script/main/art.asp?articlekey=5612)
Definition:
Partial or complete loss of consciousness due to a temporary reduction in blood flow and therefore a shortage of oxygen to the brain.
Non-cardiac causes:
Postural hypotension: Drop in blood pressure due to changing body position to a more vertical position after lying or sitting;
Dehydration causing a decrease in blood volume.
Blood pressure medications leading to low blood pressure.
Diseases of the nerves to the legs in older people (especially with diabetes or Parkinson's disease) when poor tone of the nerves of the legs draws blood into the legs from the brain.
High altitude.
Brain stroke or "near-stroke" (transient ischemic attack).
A migraine attack.
Emotions (e.g. fear, anxiety)
A reflex of the involuntary nervous system (the vasovagal reaction) triggered by certain situations (situational syncope) such as blood drawing, urinating, defecating, swallowing and coughing.
Cardiac causes:
Abnormal heart rhythms (heart beating too fast or too slow).
Abnormalities of the heart valves (aortic stenosis or pulmonic valve stenosis).
High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension).
Tears in the aorta (aortic dissection).
Widespread disease of the heart muscle (cardiomyopathy).
Taken from:
Britannica.com
MedicineNet.com
(For detailed information: http://www.medterms.com/script/main/art.asp?articlekey=5612)
Pacemaker
Artificial Cardiac Pacemakers
General:
- device used 2 regulate the beating of the heart by mimicking the actions of the nodes and conducting system
- successfully used to treat sick sinus syndrome (inability of the sinus node to regulate a steady heart rate due damage to the sinus node resulting in atrial rhythm disturbances) and heard heart block (atriaoventricular system, the conducting system of both fail to communicate with the ventricles). Also for patients with prolonged PR intervals, left bundle branch block, severe mitral regurgitation.
Types:
Type of pacemaker used depends on patient’s needs
o For temporary use:
§ external pacemakers for initial stabilization of a patient
- 2 pads placed on chest, one on upper portion of sternum, other along left axilla
- electrical impulse travels between pads and stimulates muscles between them including cardiac muscles and muscles of the chest wall to contract
- muscles twitch at a pre-determined rate the pacemaker is set to
- should not be relied upon for an extended period of time. If patient is conscious, frequent stimulation of chest wall muscles may cause discomfort
- also, stimulation of chest wall muscles does not necessarily indicate cardiac muscles are stimulated as well.
§ internal pacing wire
- wire that is place under sterile condition; distal tip placed into either right atrium or right ventricle, proximal tip attached to pacemaker generator outside of the body
o For permanent use (usually required for most conditions):
- made up of:
o pulse generator/battery pack implanted with a computer chip under the skin just deep to the collarbone
o coiled metal conductor leads insulated with plastic and anchored to appropriate chamber(s). inserted using X-ray control via a vein found in this area
o a bare metal electrode fixed against the heart
- pulse generator sends electical signal down the lead to the electrode and targeted heart chamber is prompted to contract.
- ‘listens’ to the heart and supplements the heart’s natural heart rate. E.g. During physical exertion, sensors in pulse generator can detect changes in breathing and boost the heart rate to appropriate level
- two types:
o single chamber: only one chamber is regulated, usually ventricles
o dual chamber: 2 leads are used. Information from atria regulates the contraction of the ventricles
Person living with an artificial cardiac pacemaker can live a normal life and still engage in moderate strenuous activity such as sex and preferably non-contact sports. Medication, mobile phones, and household electrical appliances such as microwaves are safe to use. However, MRIs should not be performed
Patients require one or two checks a year. Adjustments can be made non-invasively using a radio frequency programmer
Shanthini
Sinoatrial Node (Natural Pacemaker)
General:
- also known as the sinoatrial node
- modified myocytes
- in the right atrium, under epicardium, near superior vena cava
- self-excitable, sets the rate and timing (sinus rhythm) of other cardiac cells to contract
Physiology
- do not have stable RMP
- MP starts at -60, drifts upwards – depolarization due to slow inflow of Na+ without outflow of K+
- At -40mV, fast calcium channels open – depolarization continues till slightly above 0mv
- K+ channels open. K+ leaves the cell – repolarization.
In Short:
When SA node fires, rhythmically sets off a wave of action potentials which triggers the conduction of heart chambers. Each depolarization of the SA node sets off one heartbeat.
Saladin, Anatomy and Physiology, 4th Ed
General:
- device used 2 regulate the beating of the heart by mimicking the actions of the nodes and conducting system
- successfully used to treat sick sinus syndrome (inability of the sinus node to regulate a steady heart rate due damage to the sinus node resulting in atrial rhythm disturbances) and heard heart block (atriaoventricular system, the conducting system of both fail to communicate with the ventricles). Also for patients with prolonged PR intervals, left bundle branch block, severe mitral regurgitation.
Types:
Type of pacemaker used depends on patient’s needs
o For temporary use:
§ external pacemakers for initial stabilization of a patient
- 2 pads placed on chest, one on upper portion of sternum, other along left axilla
- electrical impulse travels between pads and stimulates muscles between them including cardiac muscles and muscles of the chest wall to contract
- muscles twitch at a pre-determined rate the pacemaker is set to
- should not be relied upon for an extended period of time. If patient is conscious, frequent stimulation of chest wall muscles may cause discomfort
- also, stimulation of chest wall muscles does not necessarily indicate cardiac muscles are stimulated as well.
§ internal pacing wire
- wire that is place under sterile condition; distal tip placed into either right atrium or right ventricle, proximal tip attached to pacemaker generator outside of the body
o For permanent use (usually required for most conditions):
- made up of:
o pulse generator/battery pack implanted with a computer chip under the skin just deep to the collarbone
o coiled metal conductor leads insulated with plastic and anchored to appropriate chamber(s). inserted using X-ray control via a vein found in this area
o a bare metal electrode fixed against the heart
- pulse generator sends electical signal down the lead to the electrode and targeted heart chamber is prompted to contract.
- ‘listens’ to the heart and supplements the heart’s natural heart rate. E.g. During physical exertion, sensors in pulse generator can detect changes in breathing and boost the heart rate to appropriate level
- two types:
o single chamber: only one chamber is regulated, usually ventricles
o dual chamber: 2 leads are used. Information from atria regulates the contraction of the ventricles
Person living with an artificial cardiac pacemaker can live a normal life and still engage in moderate strenuous activity such as sex and preferably non-contact sports. Medication, mobile phones, and household electrical appliances such as microwaves are safe to use. However, MRIs should not be performed
Patients require one or two checks a year. Adjustments can be made non-invasively using a radio frequency programmer
Shanthini
Sinoatrial Node (Natural Pacemaker)
General:
- also known as the sinoatrial node
- modified myocytes
- in the right atrium, under epicardium, near superior vena cava
- self-excitable, sets the rate and timing (sinus rhythm) of other cardiac cells to contract
Physiology
- do not have stable RMP
- MP starts at -60, drifts upwards – depolarization due to slow inflow of Na+ without outflow of K+
- At -40mV, fast calcium channels open – depolarization continues till slightly above 0mv
- K+ channels open. K+ leaves the cell – repolarization.
In Short:
When SA node fires, rhythmically sets off a wave of action potentials which triggers the conduction of heart chambers. Each depolarization of the SA node sets off one heartbeat.
Saladin, Anatomy and Physiology, 4th Ed
CPR
Cardiopulmonary resuscitation (CPR) is an emergency procedure for cardiacarrest, when the heart literally stops beating.It consists of chest compressions and rescue breaths and is intended tomaintain a flow of oxygenated blood to the brain and the heart, extendingthe chance for a successful resuscitation without permanent brain damage.Basically, it mimics natural blood circulation and breathing.
Here's something that may be of interest about the procedure:
Differences in CPR for Lay Rescuers and Healthcare ProvidersDifferences between lay rescuer and healthcare provider CPR skillsinclude the following:Lay rescuers should immediately begin cycles of chest compressions andventilations after delivering 2 rescue breaths for an unresponsivevictim. Lay rescuers are not taught to assess for pulse or signs ofcirculation for an unresponsive victim.Lay rescuers will not be taught to provide rescue breathing without chestcompressions.The lone healthcare provider should alter the sequence of rescue responsebased on the most likely etiology of the victim’s problem.— For sudden, collapse in victims of all ages, the lone healthcareprovider should telephone the emergency response number and get an AED(when readily available) and then return to the victim to begin CPR anduse the AED.— For unresponsive victims of all ages with likely asphyxial arrest (eg,drowning) the lone healthcare provider should deliver about 5 cycles(about 2 minutes) of CPR before leaving the victim to telephone theemergency response number and get the AED. The rescuer should then returnto the victim, begin the steps of CPR, and use the AED.After delivery of 2 rescue breaths, healthcare providers should attemptto feel a pulse in the unresponsive, nonbreathing victim for no more than10 seconds. If the provider does not definitely feel a pulse within 10seconds, the provider should begin cycles of chest compressions andventilations.Healthcare providers will be taught to deliver rescue breaths withoutchest compressions for the victim with respiratory arrest and a perfusingrhythm (ie, pulses). Rescue breaths without chest compressions should bedelivered at a rate of about 10 to 12 breaths per minute for the adultand a rate of about 12 to 20 breaths per minute for the infant and child.Healthcare providers should deliver cycles of compressions andventilations during CPR when there is no advanced airway (eg,endotracheal tube, laryngeal mask airway [LMA], or esophageal-trachealcombitube [Combitube]) in place. Once an advanced airway is in place forinfant, child, or adult victims, 2 rescuers no longer deliver "cycles" ofcompressions interrupted with pauses for ventilation. Instead, thecompressing rescuer should deliver 100 compressions per minutecontinuously, without pauses for ventilation. The rescuer delivering theventilations should give 8 to 10 breaths per minute and should be carefulto avoid delivering an excessive number of ventilations. The 2 rescuersshould change compressor and ventilator roles approximately every 2minutes to prevent compressor fatigue and deterioration in quality andrate of chest compressions. When multiple rescuers are present, theyshould rotate the compressor role about every 2 minutes. The switchshould be accomplished as quickly as possible (ideally in less than 5seconds) to minimize interruptions in chest compressions.According to the American Heart association, beginners are not expectedto know how to check for the pulse of the victim.
Something to thinkabout X(
Here's something that may be of interest about the procedure:
Differences in CPR for Lay Rescuers and Healthcare ProvidersDifferences between lay rescuer and healthcare provider CPR skillsinclude the following:Lay rescuers should immediately begin cycles of chest compressions andventilations after delivering 2 rescue breaths for an unresponsivevictim. Lay rescuers are not taught to assess for pulse or signs ofcirculation for an unresponsive victim.Lay rescuers will not be taught to provide rescue breathing without chestcompressions.The lone healthcare provider should alter the sequence of rescue responsebased on the most likely etiology of the victim’s problem.— For sudden, collapse in victims of all ages, the lone healthcareprovider should telephone the emergency response number and get an AED(when readily available) and then return to the victim to begin CPR anduse the AED.— For unresponsive victims of all ages with likely asphyxial arrest (eg,drowning) the lone healthcare provider should deliver about 5 cycles(about 2 minutes) of CPR before leaving the victim to telephone theemergency response number and get the AED. The rescuer should then returnto the victim, begin the steps of CPR, and use the AED.After delivery of 2 rescue breaths, healthcare providers should attemptto feel a pulse in the unresponsive, nonbreathing victim for no more than10 seconds. If the provider does not definitely feel a pulse within 10seconds, the provider should begin cycles of chest compressions andventilations.Healthcare providers will be taught to deliver rescue breaths withoutchest compressions for the victim with respiratory arrest and a perfusingrhythm (ie, pulses). Rescue breaths without chest compressions should bedelivered at a rate of about 10 to 12 breaths per minute for the adultand a rate of about 12 to 20 breaths per minute for the infant and child.Healthcare providers should deliver cycles of compressions andventilations during CPR when there is no advanced airway (eg,endotracheal tube, laryngeal mask airway [LMA], or esophageal-trachealcombitube [Combitube]) in place. Once an advanced airway is in place forinfant, child, or adult victims, 2 rescuers no longer deliver "cycles" ofcompressions interrupted with pauses for ventilation. Instead, thecompressing rescuer should deliver 100 compressions per minutecontinuously, without pauses for ventilation. The rescuer delivering theventilations should give 8 to 10 breaths per minute and should be carefulto avoid delivering an excessive number of ventilations. The 2 rescuersshould change compressor and ventilator roles approximately every 2minutes to prevent compressor fatigue and deterioration in quality andrate of chest compressions. When multiple rescuers are present, theyshould rotate the compressor role about every 2 minutes. The switchshould be accomplished as quickly as possible (ideally in less than 5seconds) to minimize interruptions in chest compressions.According to the American Heart association, beginners are not expectedto know how to check for the pulse of the victim.
Something to thinkabout X(
Cardiac Arrest
Cardiac Arrest
(Source: http://www.sjm.com/conditions/condition.aspx?name=Sudden+Cardiac+Arrest )
Sudden cardiac arrest occurs when the lower chambers of the heart (the ventricles) suddenly stop beating normally and develop what is called ventricular defibrillation. VF is very fast, chaotic heart rate in the lower chambers of the heart, When the ventricles defribillate, they do not contract normally , so they cannot effectively pump blood, The instant VF begins, effective blood pumping stops. VF quickly becomes more erratic, resulting in sudden cardiac arrest.
Risk Factors
(Source: http://www.mayoclinic.com/health/sudden-cardiac-arrest/DS00764/DSECTION=4 )
Because sudden cardiac arrest is so often intertwined with coronary artery disease, the same factors that put you at risk of coronary artery disease may also put you at risk of sudden cardiac arrest. These include:
§ A family history of heart disease
§ Smoking
§ High blood pressure
§ High blood cholesterol
§ Obesity
§ Diabetes
§ A sedentary lifestyle
In addition to a personal or family history of heart disease — including heart rhythm disorders, congenital heart defects, congestive heart failure and cardiomyopathy — other factors that may increase your risk of sudden cardiac arrest include:
§ Low output of blood from you heart (ejection fraction)
§ Previous episode of cardiac arrest
§ Previous heart attack
§ Low output of blood from your heart (ejection fraction)
§ Previous episode of cardiac arrest
§ Markedly changes blood vessels of potassium, and magnesium – minerals called electrolytes that need to be properly balanced in order to maintain vital organ functions, including that of the heart
§ Hyperthyroidism, a condition in which your thyroid gland produces too much of the hhormone thyroxine, speeding up your metabolism and potentially causing arrhythmia
§ Pulmonary hypertension, a type of high blood pressure that affects the arteries of your lungs
§ Taking drigs that affect your heart rhythm, such as prescription anti-arrhythmic or pro-arrhythmic drugs, or over the counter medications, such ass pseudoephedrine-containing cold medicines
§ Using illicit drugs, such as cocaine or amphetamines
(Source: http://www.sjm.com/conditions/condition.aspx?name=Sudden+Cardiac+Arrest )
Sudden cardiac arrest occurs when the lower chambers of the heart (the ventricles) suddenly stop beating normally and develop what is called ventricular defibrillation. VF is very fast, chaotic heart rate in the lower chambers of the heart, When the ventricles defribillate, they do not contract normally , so they cannot effectively pump blood, The instant VF begins, effective blood pumping stops. VF quickly becomes more erratic, resulting in sudden cardiac arrest.
Risk Factors
(Source: http://www.mayoclinic.com/health/sudden-cardiac-arrest/DS00764/DSECTION=4 )
Because sudden cardiac arrest is so often intertwined with coronary artery disease, the same factors that put you at risk of coronary artery disease may also put you at risk of sudden cardiac arrest. These include:
§ A family history of heart disease
§ Smoking
§ High blood pressure
§ High blood cholesterol
§ Obesity
§ Diabetes
§ A sedentary lifestyle
In addition to a personal or family history of heart disease — including heart rhythm disorders, congenital heart defects, congestive heart failure and cardiomyopathy — other factors that may increase your risk of sudden cardiac arrest include:
§ Low output of blood from you heart (ejection fraction)
§ Previous episode of cardiac arrest
§ Previous heart attack
§ Low output of blood from your heart (ejection fraction)
§ Previous episode of cardiac arrest
§ Markedly changes blood vessels of potassium, and magnesium – minerals called electrolytes that need to be properly balanced in order to maintain vital organ functions, including that of the heart
§ Hyperthyroidism, a condition in which your thyroid gland produces too much of the hhormone thyroxine, speeding up your metabolism and potentially causing arrhythmia
§ Pulmonary hypertension, a type of high blood pressure that affects the arteries of your lungs
§ Taking drigs that affect your heart rhythm, such as prescription anti-arrhythmic or pro-arrhythmic drugs, or over the counter medications, such ass pseudoephedrine-containing cold medicines
§ Using illicit drugs, such as cocaine or amphetamines
Conducting system of the heart
CONDUCTION PATHWAY
1) 1% of the cardiac cells = conducting cells
2) Functions of conducting cells - generate AP/impulses - conduct AP
3) SA node acts as the pacemaker of the heart, determining the rhythm ofthe heart beat.
3)Pathway : SA node - AV node - bundle of His - bundle branches -Purkinjefibers.
4)Conduction pathway ensures the heart pumps in a synchronised,coordinated way. This co-ordination ensures that the atria beat as oneunit, as well as the ventricles.
5)Different parts will conduct at a different speed. - Purkinje fibers and bundle of His (4m/sec) -fastest - SA node (1m/sec) - Ventricular myocardium (0.3-0.5m/sec) - AV node (0.05m/sec)-slowestThis is to ensure that the AP is received at the same time in every partof the heart. This will then allows the heart to contract at the sametime.
Clinical relevance:
1) ventricular fibrillation - the heart beats in a non-coordinatedfashion
2) defibrillation - a method in which a shock is performed to a patientwith an irregular rhythm in hoping that the heart will stop for a whileand start to beat again in a more coordinated fashion.
1) 1% of the cardiac cells = conducting cells
2) Functions of conducting cells - generate AP/impulses - conduct AP
3) SA node acts as the pacemaker of the heart, determining the rhythm ofthe heart beat.
3)Pathway : SA node - AV node - bundle of His - bundle branches -Purkinjefibers.
4)Conduction pathway ensures the heart pumps in a synchronised,coordinated way. This co-ordination ensures that the atria beat as oneunit, as well as the ventricles.
5)Different parts will conduct at a different speed. - Purkinje fibers and bundle of His (4m/sec) -fastest - SA node (1m/sec) - Ventricular myocardium (0.3-0.5m/sec) - AV node (0.05m/sec)-slowestThis is to ensure that the AP is received at the same time in every partof the heart. This will then allows the heart to contract at the sametime.
Clinical relevance:
1) ventricular fibrillation - the heart beats in a non-coordinatedfashion
2) defibrillation - a method in which a shock is performed to a patientwith an irregular rhythm in hoping that the heart will stop for a whileand start to beat again in a more coordinated fashion.
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