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Shane
Unconsciousness:
"A dramatic alteration of mental state that involves complete or near-complete lack of responsiveness to people and other environmental stimuli"
eg. a coma
Unconsciousness is not an altered state of consciousness (eg. delerium), normal sleep, or hypnosis, as response to stimuli is shown.
Unconsciousness should not be confused with the psycoanalytical unconscious (cognitive processes)
Causes include traumatic brain injury, brain hypoxia, poisoning with CNS depressants, and severe fatigue.
Syncope:
The medical term for fainting.
"Syncope is a sudden (and generally momentary) loss of consciousness, or blacking out due to the Central Ischaemic Response, [due] to a lack of sufficient... oxygen reaching the brain"
Symptoms immediatly before fainting include:
- dizziness
- dimming of vision
- tinnitus
- hot flush
Causes:
- dehydration
- hypotension
- hypoglycaemia
- lack of sleep
- excessive physical exertion
- arrythmia
- other cardiovascular conditions (eg. subclavian steal syndrome, aortic stenosis)
All quoted or paraphrased from Wikipedia (keywords "unconsciousness" and "fainting")
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Cardiac Conduction - Elliot
*Cardiac Action Potential*
Cardiac action potentials are generated spontaneously as a result of an unstable resting membrane potential of the cells in the SA node. There is a constant slow depolarisation/drift towards the action potential threshold due to gradual closure of K+ channels and inward leak of Na+ and Ca2+. The action potential is due to the opening of voltage-activated Ca2+ channels which allow an influx of calcium ions from both the sarcoplasmic reticulum and extracellular fluid. Repolarisation is achieved through outward K+ movement.
Resting heart rate is influenced by continuous parasympathetic stimulation via the vagus nerve. Acetylcholine released from the nerve decreases the rate of closure of K+ channels and the inward leak of Na+ and Ca2+. As a result there is a slower depolarisation and therefore it takes longer for the threshold to be reached and so heart rate decreases. Noradrenaline released during sympathetic stimulation causes the opposite affect and so heart rate increases due to a faster depolarisation.
As opposed to the SA node cardiac cells, the resting membrane potential of the ventricular and atrial cardiac muscle cells is stable and these cells do not normally exhibit spontaneous depolarisation. In the case of these cells, the action potential is due to a fast inward Na+ current which quickly inactivates, followed by a slow inward Ca2+ current that triggers contraction before repolarisation occurs due to an outward K+ current and the closure of Ca2+ channels.
Intercalated discs that link each myocyte contain gap junctions that form channels allowing ions to flow from one cell directly into the next. As a result each myocyte can directly stimulate its neighbouring cells allowing the action potential to be nearly simultaneous distributed to all the cells and causing the entire myocardium to act almost as if it were a single cell. The speed of conduction is aided by specialised “conducting tissue” made up of modified myocytes that conduct action potentials faster at the expense of contractive power. However between the atria and ventricles, the AV node causes a slight delay in the propagation of the action potential ensuring a more efficient pumping mechanism as the atria are emptied before contraction of the ventricles occur.
The cardiac conduction system consists of the following major components:
• Sinoatrial (SA) node – A group of modified myocytes in the right atrium. This is considered the pacemaker that initiates each heart beat and determines the heart rate. The cells in the SA node have the fastest inherent rhythm and therefore determine the speed of the whole heart.
• Atrioventricular (AV) node – Electrical gateway to the ventricles located near the right AV valve that allows for a slight delay between the contraction of the atria and ventricles, giving the ventricles time to fill with blood before they begin to contract.
• Atrioventricular (AV) bundle (Bundle of His) – Pathway by which signals leave the AV node. Splits into to branches in the interventricular septum, one to activate the left ventricle and the other to activate the right ventricle.
• Purkinje fibres – Smaller braches that come off the two bundle branches near the apex that more fully distribute the electrical excitation throughout the ventricular myocardium. The left ventricle contains a more elaborate network of fibres than the right.
*Similarities between cardiac and skeletal muscle*
• Both made up of thick and thin filaments arranged in sarcomeres
• Striated
• Cross-bridge cycling
• Contraction controlled by Ca2+
*Differences between cardiac and skeletal muscle*
• Short branched cells as opposed to long cylindrical fibres in skeletal muscle
• Less developed sarcoplasmic reticulum (SR)
• Nuclei near middle of cell
• Wide T tubules
• Autorhythmicity
• Much longer action potential duration of about 200msec
• Innervation and control by autonomic fibres (involuntary) but nerve input is not on each myocyte and is not required for the firing of action potentials
• Nervous stimulation can be excitatory or inhibitory as opposed to just excitatory in skeletal muscle
• Each myocyte (muscle cell) is linked to several others at the end by intercalated discs rather than connecting to tendons as in skeletal muscle
• Almost exclusively aerobic respiration aided by the larger mitochondria which occupies about 25% of the cell contrasting to about the 2% it occupies in skeletal muscle fibres
*Resources*
Week 1 Lectures
Saladin – Anatomy and Physiology Third Edition
http://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_heart
Causes of Unconsciousness
-Stroke
-Heart attack
-Hypotension
-Drug overdose
-Alcohol abuse
-CO poisoning
-Hypoglycemia, hyperglycemia
-Hypoxic/ischemic brain injury
-Hypertensive encephalopathy
-Severe uremia
-Respiratory failure with CO2 retention
-Hypocalcaemia, hypocalcaemia
-Trauma
-Epilepsy
-Encephalitis
-Subarachnoid haemorrhage
-Cerebral oedema from chronic hypoxia
-Brainstem haemorrhage or infarction
-Brainstem demyelination
-Trauma
-Hemisphere tumour, infarction, haematoma, encephalitis or trauma
From Kumar & Clark pg.1207
Ok, I think I've fixed this up... I'll explain in PCL tomorrow how it will work, it should be easy enough, its just that they've changed how this site works since last year!
Investigations for causes of syncope are
12 lead ECG
24h Holter monitoring
Echocardiography
MRI or CT head
Tilt table test
Blood glucose, HbA1c
Urea & Electrolyes
Cardiac markers
Arterial Blood Gases
Toxicology screen
V/Q Scan
Source: Oxford Handbook of Clinical and Laboratory Investigation 2nd ed (Drew Provan, editor)
The electrocardiogram (ECG) records the potential difference between electrodes for 12 leads.
Lead I
Negative terminal: Right Arm
Positive terminal: Left Arm
Lead II
Negative terminal: Right Arm
Positive terminal: Left Leg
Lead III
Negative terminal: Left Arm
Positive terminal: Left Leg
V1
Negative terminal:
Right Arm, Left Arm & Left Leg
Positive terminal:
V1 (4th intercostal space right of sternum)
V2
Negative terminal:
Right Arm, Left Arm & Left Leg
Positive terminal:
V2 (4th intercostal space left of sternum)
V3
Negative terminal:
Right Arm, Left Arm & Left Leg
Positive terminal:
V3 (directly between V2 & V4)
V4
Negative terminal:
Right Arm, Left Arm & Left Leg
Positive terminal:
V4 (5th intercostal space, midclavicular)
V5
Negative terminal:
Right Arm, Left Arm & Left Leg
Positive terminal:
V5 (directly between V4 & V6)
V6
Negative terminal:
Right Arm, Left Arm & Left Leg
Positive terminal:
V6 (5th intercostal space, midaxillary)
aVR
Negative terminal:
Left Arm & Left Leg
Positive terminal:
Right Arm
aVL
Negative terminal:
Right Arm & Left Leg
Positive terminal:
Left Arm
aVF
Negative terminal:
Right Arm & Left Arm
Positive terminal:
Left Leg
The results are shown on a graph as potential difference in millivolts against time in seconds.
The normal ECG will have a P wave, PR interval, QRS complex, ST segment and T wave. There are different types of QRS complexes, see here for more info.
Source: Textbook of Medical Physiology 11th ed (Guyton & Hall), Wikipedia.org
Note: The RR interval can be used to calculate the heart rate since it is the time between beats.
The Heart
Normal Function:
The heart is comprised of three layers:
- The endocardium made up of endothelial tissue
- The myocardium made up of cardiac muscle cells
- The epicardium made up of mainly connective tissue containing the nerves and blood vessels for the heart.
The heart is responsible for circulating blood around the body, thereby providing oxygen and nutrients to the organs of the body while taking away carbon dioxide and other waste materials. A normal heart is essentially made up of two pump, the left and the right sides. Each side is in turn comprised of an atrium and a ventricle. The atrium receives the blood coming into the heart, while the ventricle pumps blood out of the heart, and a one-way valve separates the two. The right side of the heart receives de-oxygenated blood from the body through the vena cava, which the right ventricle then pumps to the lungs through the pulmonary artery to exchange CO2 for O2. The blood then returns to the left side of the heart through the pulmonary vein into the left atrium, the blood then enters the left ventricle where it is pumped out to the rest of the body. The blood pumped to the rest of the body must be pumped at a much higher pressure then that pumped to the lungs. In this way each beat of the heart comprises of two contractions, first that of the atria to push blood into the ventricles, then that of the ventricles to pump the blood to the lungs and body.
The hearts contractive ability springs from the myo-cardiocytes in the myocardium, which are able to contract under stimulation by an electrical signal.
If the heart stops beating then blood can no longer circulate throughout the body, resulting in cell hypoxia, starvation of essential nutrients, a build up of waste material, and ultimately death. The heart also receives oxygen from circulating blood, and in particular cardiac muscle cells become depolarised when hypoxic, which can lead to altered impulse formation or altered impulse conduction. The former is the abnormal generation of pacemaker signals from either the sinoatrial node or other conductive cells. The latter refers to partial or complete block of electrical conduction in the heart. This can become a positive feedback loop, producing further heart failure.
In the case of heart failure the blood will back up and cause problems, particularly in the lungs. This raises the volume and pressure of the lungs, forcing the water from the blood into the air spaces of the lungs, resulting in a pulmonary oedema.
Sorry...
References: MED 2031 Lecture 3, the Heart
Cardiovascular Physiology Concepts;http://www.cvphysiology.com
PCL Week 1: Hans at the Football.
Research Question: Three types of Cardiac Arrhythmias
and illustrations of their ECG’s.
1) Asystole: It is the absolute standstill of the heart muscle with no ventricular depolarisation and hence no cardiac output. This lack of electrical activity in the heart muscle shows as a flat line on the ECG and is a cause of cardiac arrest. It can also be caused by Ventricular Fibrillation.
Inhibition of ventricular depolarisation may result from ischaemia or from degeneration of the SA node or AV conducting system. Primary asystole is preceded by a bradydisarrhythmia (abnormally low heart rate) due to sinus node block (bunch of pacemaker cells in the atrium), complete heart block or both. In secondary asystole, factors outside the heart’s electrical conduction system results in a failure to generate any electrical depolarisation, eg. Tissue hypoxia with metabolic acidosis.
Light-headedness and syncope may precede asystole and it may be reversed with CPR.
2) Ventricular Fibrillation: It occurs when the heart ceases to beat effectively and fibrillates very rapidly. In most cases it is caused by a heart attack. It can be caused by arrhythmias and a defibrillator is required to restart the heart rhythm. Patients can either have a wearable or implantable defibrillator that automatically shocks the heart when necessary or take antiarrhythmic medications. Those who experience VF and it is not related to a heart attack usually have a history of fainting. The most common cause of VF is inadequate flow to the heart muscle as a result of coronary artery disease, but it could also be a result of low blood pressure.
3) Ventricular Tachycardia: It is a rapid heart rate originating from the ventricles and can lead to VF and /or sudden cardiac death. It may be caused by electrical signals that do not follow the normal conduction system. Additional signals arise from ventricles or are caused by a defect in the heart’s conduction system. As it can lead to VF, defibrillation may be required to avoid death by cardiac arrest. Some symptoms may include the heartbeat feeling like a strong pulse in the neck, fluttering or racing beat in the chest, feelings of discomfort and weakness, shortness of breath, feeling faint, sweaty and dizzy.
Ventricular tachycardia: note fast rate and wide bizarre QRS.
sorry, I didnt realise you couldnt cut and paste the pictures..some useful references are:
1) www.emedicine.com/emerg/topic44.htm
2)www.merck.com/mmhe/sec03/ch027h.html
3)www.heart.health.ivillage.com/arrhythmia
Bradycardia is a constant resting heart rate below 60 beats/minute.
(Brady: slow, cardia: heart)
A slow heart rate is common during sleep (approximately 40 beats/minute) and among athletes (whose enlarged heart can pump more blood with each contraction). Hypothermia also slows the heart as the body attempts to conserve energy and this state is often induced in preparation for heart surgery.
The etiology of pathological bradycardia can be divided up into two categories: non-cardiac and cardiac causes. Non-cardiac causes include illicit drugs, hypertensive drugs (such as beta-blockers and calcium channel blockers), metabolic and endocrine disorders (especially hypothyroidism) and neurological factors. Cardiac factors (probably more relevant to this case) can be detected using an ECG. There are generally two types of problems that result in bradycardias: disorders of the sinus node (SA node), and disorders of the atrioventricular node (AV node). With sinus node dysfunction (sometimes called sick sinus syndrome), there may be a disordered intrinsic firing rate or impaired conduction of the impulse from the sinus node into the surrounding atrial tissue (an "exit block"). Atrioventricular conduction disturbances (AV block) may result from impaired conduction in the AV node, or anywhere below it, such as in the His bundle. Bradycardia is more common in elderly patients and more likely acquired than congenital.
Treatment for patients with asymptomatic bradycardia is not usually necessary. When the heart rate falls below 50 beats/minute symptoms such as dizziness, fainting, fatigue, and shortness of breath usually occur and treatment is warranted.
Drug treatment using atropine (muscarinic antagonist) can be used to treat bradycardia. It works on the vagus nerve (CNXI) supplies the parasympathetic innervation to the heart and reduces its sinus rhythm from 100 beats/minute to approximately 70 beats/minute. Therefore over activity can cause an excessively slow heart rate. When the heart rate falls below 30 beats/minute it is considered a medical emergency as the brain becomes oxygen deprived and convulsions occur. Emergency treatment with dopamine and adrenaline can work to speed up the heart rate via the sympathetic nervous system although side effects allow it to only to be used as a temporary measure.
Long term bradycardia can be corrected using an artificial pacemaker. The artificial pacemaker is a small battery operated computer called a pulse generator which is connected to the heart via one or more pacing leads. It is inserted under local anesthetic and requires a 1-2 day hospital stay. The pulse generator is placed below the collar bone and the leads inserted with x-ray control into a vein (subclavian) and then to the appropriate chamber. The pacemaker works by sending an electric signal down the lead to an electrode which targets a heart chamber to contract. The system relies on feedback and recognizes when the heart rate is insufficient and increases it. After recovery the patient can lead a normal life with check ups twice a year and battery replacement when needed (this depends on how frequently the device is needed to speed up heart rate). MRI scans are contraindicated for patients with pacemakers as they interfere with function.
• Anatomy and Physiology
Saladin
Chapter 19
• Clinical Examination
Tally and O’Connor
(Pg. 37, Causes of bradycardia and tachycardia)
• Clinical Examination
Epstein et al.
(Cardiac arrhythmias)
• http://www.betterhealth.vic.gov.au
(search cardiac pacemakers)
• http://en.wikipedia.org.wiki/bradycardia
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