PCL 1 - Hans at the Football
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Case Summary

Patient – male, 70, tall, full head of grey hair

Location – Football game, in the hot food que

Incident – man falls on ground heavily and silently. As a result he becomes unconscious and does not appear to be breathing. CPR is administered by a person at the game and he becomes conscious. A doctor later appears and asks Han’s if this has happened before, Han’s says that it hasn’t and he hasn’t needed to see a doctor in the past several years. The doctor checks his verbal and motor responses as well as his eye openings. All observations appear to be OK.

He advises Han’s to go to an emergency department for an examination and ECG but Han’s refuses and says he feels fine.



Interruption of awareness of oneself and one’s surroundings. Lack of ability to notice or respond to environmental stimuli. Being in a comatose state, or coma, is an illustration of unconsciousness. Fainting (or syncope) is also an example of a temporary loss of consciousness.

Partial or complete loss of consciousness. When the loss of consciousness is temporary and there is spontaneous recovery it is referred to as syncope (non-medically known as fainting).
It is due to temporary reduction in blood flow, and therefore shortage of oxygen, to the brain. This leads to light-headedness, or a “black out” episode.

Pathophysiology of Loss of Consciousness

[example text]

Pathophysiology of Syncope

**CARDIOVASCULAR RELATED SYNCOPE - Due to inadequate cerebral blood flow.**


•Neurocardiogenic/Vasovagal Syncope: peripheral vasodilation and bradycardia (HR<60bpm) > blood pooling > reduced amount of blood being returned to the heart. The near empty heart responds by contracting vigorously > stimulates mechanoreceptors (stretch receptors) in the wall of the left ventricle > triggers reflexes via the CNS which act to reduce ventricular stretch but this causes a drop in BP > syncope
•Postural (Orthostatic) Hypotension: sudden drop in BP of 20mmHg or more when moving from sitting or lying to standing. Due to blood pooling in the legs
•Postprandial Hypotension: a drop in Systolic BP of 200mmHg or more within 2 hours of a meal or if systolic pressure drops from above 100mmHg to under 90mmHg in the same time frame. Due to blood pooling in the splanchnic vessels (viscera)
•Micturition Syncope: occurs after urination. Due to parasympathetic overactivity > bradycardia and vasodilation.
•Carotid Sinus Syncope: occurs when there is an exaggerated vagal response to carotid sinus stimulation eg. wearing a tight collar, looking upwards, turning the head

Syncope due to restriction of blood flow from the heart into the rest of the circulation or between the different chambers of the heart
•Aortic Stenosis
•Pulmonary Stenosis
•Pulmonary Hypertension/Embolism
•Defective Prosthetic valve
•Many more

Syncope due to restriction of blood flow from the heart into the rest of the circulation or between the different chambers of the heart
•Rapid Tachycardia
•Profound Bradycardia (Stokes-Adams Attacks: patient usually falls to the ground without warning, pale and deeply unconscious. Pulse is very slow or absent. After a few seconds the patient flushes brightly and recovers consciousness as the pulse quickens)
•Significant pauses in rhythm
•Artificial pacemaker failure

Blood supply to the heart

• The tissues of the heart are supplied by the right and left coronary arteries
• The right coronary artery originates from the aorta just distal to the aortic valve
o Branches off into the sinuatrial (SA) nodal, right marginal, posterior descending and antrioventricular (AV) nodal arteries
o Supplies the right ventricle, right atrium, the interatrial septum, the SA and AV nodes and 25-35% of the left ventricle
• The left coronary artery also comes off the base of the aorta
o Branches off into the circumflex, left anterior descending and left marginal arteries
o Supplies both ventricles, the interventricular septum and the left atrium
• There is very little redundant bloody supply, making any blockage to these vessels critical

Effects of cardiac arrest

• Cardiac arrest is defined as the abrupt end of normal circulation of blood throughout the body due to the failure of the heart to contract effectively during systole
• After a brief period of cardiac arrest, the concentration of O2 in the body will fall dramatically as it continues to be consumed
o Within approximately 15 seconds cerebral hypoxia occurs and consciousness is lost
o Further cerebral hypoxia can cause permanent damage to brain tissues leading to possible permanent cognitive dysfunction, coma and death within approximately 6 minutes
o General hypoxia throughout the body can also lead to multiple organ failure
• Acidosis, increased acidity within the blood and organ tissues, will take place due to the accumulation of carbon dioxide, and the increased rate of anaerobic respiration as O2 supplies are exhausted
o This will threaten tissue survival within 5-6 minutes, again leading to multiple organ failure
• Damage to the brain can also occur through cerebral oedema (excess accumulation of fluid in the brain) due to it having very little room to expand
• Survival rates for cardiac arrest vary widely depending on how early treatment (CPR, defibrillation and advanced care) is administered and the cause of the arrest
o For example hypothermia patients have an increase survival rate as the cold protects vital organs from the effects of tissue hypoxia

Mx of cardiac arrest including adv life support

Common Rhythms
Firstly there are 4 main cardiac arrest rhythms and depending on which one it is the treatment is different.
1. Asystole
2. Pulseless electric activity
3. Ventricular Fibrillation
4. Pulseless Ventricular Tachycardia

Asystole and Pulseless electric activity are “shockable”, while Ventricular Fibrillation and Pulseless Ventricular Tachycardia are considered “non-shockable”. An ECG (Electrocardiogram) will determine which of the four rhythms a patient belongs to and thus which type of management to use. The following are the graphs for each type of rhythm as seen on an ECG.

Explanation of the Rhythms

Asystole: As can be seen from the above graph, asystole is nearly a straight line (ie death) and occurs predominately in small children due to progressive slowing of heart rate, bradycardia. It is seen sometimes when elderly patients undergo Electroconvulsive therapy.

Pulseless Electric Activity: The graph for Pulseless electric activity looks normal and has P waves at regular intervals. Thus the absence of a pulse is troubling. It is considered a possible leading stage to Asystole and can be caused by, but not limited to, trauma, hypovolaemia (decreased blood plasma volume), tension pneumothorax (build up of air in chest cavity which results in low inflation of lung), pericardial tamponade (build up of blood between the pericardium and the heart muscle which results in heart failure/ low output).

Ventricular Fibrillation: The graph shows an irregular sequence and no clear defined P waves.

Pulseless Ventricular Tachycardia: This graph on the other hand shows a regular sequence but has no clearly defined P waves either.

Ventricular Fibrillation and Pulseless Ventricular Tachycardia are common in the elderly, sudden collapse, hypothermia, excessive use of tricyclic antidepressants and cardiac disease.


PS: haven't worked out how to include the graphs/diagram yet but they can be found in this pdf file. http://www.alsg.org/fileadmin/_temp_/Specific/Ch06_CA.pdf


  • Cardiac arrhythmia: general term referring to abnormality in the electrical rhythm of the heart.(does not necessarily indicate cardiac disease)
  • Ventricular arrhythmias occur in the ventricles. Supraventricular arrhythmias occur in the atria
  • Further characterized by the speed of the heartbeats. Bradycardia- very slow heart rate, less than 60 beats per minute. Tachycardia -very fast heart rate, faster than 100 beats per minute. Fibrillation, the most serious form of arrhythmia, is fast, uncoordinated beats, which do not pump blood.
  • Caused by alterations in impulse formation, impulse conduction or both.
    • Problems of impulse formation:
      • Can originate in any pacemaker cell -cells capable of spontaneous depolarisation in the pacemaking & conduction system
      • Altered automaticity of sinus node
        • The ANS - important modulator of normal sinus node automaticity.
          • Sympathetic stimulation increases probability of pacemaker channels being open, increases heart rate.e.g. of normal effect: exercise/emotional stress
          • PNS main mediator of HR at rest. Cholinergic(parasympathetic) simulation decreases probability of pacemaker channels being open, decreasing heart rate.

* Abnormal automaticity
- Pathological changes in impulse formation due to cardiac tissue injury
- Cells outside the specialised conduction system acquire automaticity and spontaneously depolarise
If rate of depolarisation of these cells exceeds that of the sinus node, they take over the pacemaker function

  • Problems of impulse conduction:

- Conduction block
- Occurs when propagating impulse is blocked when it encounters a region of the heart that is electrically unexcitable.
- May be caused by: ischemia, fibrosis, inflammation, certain drugs
- functional block : propagating impulse encounters cardiac cells that are still refractory
- Reentry
-Impulse recurrently depolarises a region of cardiac tissue
-Fibrillation: When an entire heart chamber is involved in multiple reentry circuits, therefore quivering.


Cardiac Rhythm/Conduction/nodes - pacemakers/ECG's/abnormal ECG's
ok, I'm going to try to make this brief and simple, but I'm sorry if I confuse the topic, Im using Saladin and it has a lot of information.

The heartbeat is 'myogenic', meaning the signal originates in the heart itself, in comparison to some animals where the heartbeat is controlled by nerves. I'll do a quick list of how the conduction goes, then I'll fill in all the gaps in brackets.

  • The SA node is where the initial signal comes from. (The node does not have a stable membrane potential therefore every approx. 0.8 seconds the pacemaker potential builds up. this is due to the slow inflow of Na+ without an outflow of K+. When the pacemaker potential (membrane potential in pacemaker cells) builds up to the threshold of -40mV, the Ca2+ channels open and Ca2+ flows in which depolarises at a peak of just above 0mV. then K+ channels open and K+outflow repolarises the cell, then it starts again)
  • The signal then goes to the atrial myocytes and the two atria contract almost simulaneously
  • The signal reaches the AV node (there is a small delay which allows the ventricles to fill with blood)
  • Then the signal runs from the AV node thru the AV bundle and the purkinje fibres.
  • The ventricular systole (contraction) begins at the apex (at the bottom end of the ventricles) as it is stimulated first, then the contraction continues upward, pushing the blood up with it toward the semilunar valves.
  • The muscle contraction of the heart differs to that of skeletal muscles because it has a much longer refractory period(250msec compared to 1-2msec). It holds the contraction for longer to squeeze all the blood out.
  • Repolarisation occurs in the same order and begins in the atrias as soon as the signal has been passed thru the AV node.

There are some other things I need to add to that bit: automatic nerve fibres can the heart modify the rhythm however the SA node creates the signal. Also you can get ectopic focus, which is when another area other the SA node sets off the heartbeat, the most common is when the AV node sets it off, this gives a heart rate of around 40-50 bpm instead of about 70-80bmp and is called 'nodal rhythm'. Without the AV or SA you can get ectopic foci fire 20-40bpm which is insufficient for the brain and th patient will need and artificial pacemaker.

ECG's: there are 3 main parts to the ECG - the P wave, the QRS complex, and the T wave.

  • The P wave; The signal from the SA node spreads thru the atria and depolarises them, the atrial systole begins about 100msec after the P wave during the P-Q section.
  • The P-Q section; impulse travels from SA node to AV node
  • QRS complex; firing of the AV node and onset of the ventricular depolarisation, atrial repolarisation begins in the QRS interval
  • S-T section; The ventricular systole begins, there is a plateau (held contraction) in myocardial action potential and this shows the time it takes for the ventricles to contract and eject blood.
  • T wave; Generated by ventricular repolarization immediately before diastole, ventricles take longer to repolarise therefore it is a smaller peak on the graph.

(I couldn't manage to put in a picture but I'll show you what i mean on friday)

Abnormal ECG's:

  • Enlarged P Wave = atrial hypertrophy, oftern a result of mitral valve stenosis (narrowing)
  • Missing or inverted P wave = SA node damage; AV node has taken over pacemaker role
  • Two or more P waves per cycle = Extrasystole; heart block
  • Extra, misshapen, sometimes inverted QRS not preceded by P wave = premature ventricular contraction (pvc)
  • Enlarged Q wave = myocardial infarction
  • Enlarged R Wave = Ventricular hypertrophy
  • Abnormal T waves = flattened in hypoxia; elevated in hyperkalemia (K+ excess)
  • Abnormally long P-Q section = Scarring of atrial myocardium, forcing impulses to bypass normal conduction pathways and take slower alternative routes to AV node
  • Abnormal S-T section = Elevated above baseline in myocardial infarction; depressed in mycardial hypoxia.

Thats all i have to do, I'm sorry if anyone tried to access the page while i was doing it, i did take ages!

Sick Sinus Syndrome

Sick sinus syndrome is the name for a group of heart rhythm problems (arrhythmias) in which the sinus node — the heart's natural pacemaker — doesn't work properly. The sinus node is an area of specialized cells in the upper right chamber of the heart that controls the rhythm of your heart. Normally, the sinus node produces a steady pace of regular electrical impulses. In sick sinus syndrome, the sinus node beats abnormally causing slow heart rate (bradycardia), rapid heart rate (tachycardia) or alternating slow and fast rhythms.

Sick sinus syndrome is relatively uncommon. When it does occur, it usually affects people who are at least 60 years old. Some people with sick sinus syndrome need a pacemaker to keep the heart in a regular rhythm.

Dizziness or lightheadedness
Fainting or near-fainting
Shortness of breath
Chest pains
Trouble sleeping
Confusion or difficulty remembering things
A sensation of rapid, fluttering heartbeats (palpitations)

Many of these symptoms are a result of reduced blood flow to the brain when the heart beats too fast or too slowly.

What makes the sinus node misfire?
Diseases and conditions that cause scarring or damage to your heart's electrical system can be the reason. Scar tissue from a previous heart surgery also may be the cause, particularly in children. Sick sinus syndrome may also be set off by medications such as calcium channel blockers or beta blockers used to treat high blood pressure, heart disease or other conditions,. However, in most cases, the sinus node doesn't work properly because of age-related wear and tear to the heart muscle.

When your heart's natural pacemaker isn't working properly, your heart can't perform as efficiently as it should. This can lead to a very low heart rate, which may cause fainting. In rare cases, long periods of slow heart rate or fast heart rate can keep your heart from pumping enough blood to meet your body's needs — a condition called heart failure.

If you have bradycardia-tachycardia syndrome, you may also be at a higher risk of developing a blood clot in your heart that may lead to a stroke. That's because the fast heart rhythms that occur in bradycardia-tachycardia syndrome are often atrial fibrillation — a chaotic rhythm of the upper chambers of the heart that can promote blood pooling in the heart. Blood clots are more likely to form when blood flow through the heart is altered in any way. A blood clot can break loose and travel to the brain, causing a stroke.

Treatments and drugs
Treatment for sick sinus syndrome focuses on eliminating or reducing unpleasant symptoms. If you aren't bothered by symptoms, you may only need regular checkups to monitor your condition. For people who are bothered by symptoms, the treatment of choice is usually an implanted electronic pacemaker.

Medication changes
Your doctor may start by looking at your current medications to see if any of them could be interfering with the function of your sinus node. Medications used to treat high blood pressure or heart disease — such as beta blockers or calcium channel blockers — can worsen abnormal heart rhythms. In some cases, adjusting these medications can relieve symptoms.

Pacing the heart
Most people with sick sinus syndrome need a permanent artificial pacemaker to maintain a regular heartbeat. This small, battery-powered electronic device is implanted under the skin near your collarbone during a minor surgical procedure. The pacemaker is programmed to stimulate or "pace" your heart as needed to keep it beating normally.

The type of pacemaker you need depends on the type of irregular heart rhythm you're experiencing. Some rhythms can be treated with a single-chamber pacemaker, which uses only one wire (lead) to pace one chamber of the heart — in this case, the atrium. However, most people with sick sinus syndrome benefit from dual-chamber pacemakers, in which one lead paces the atrium and one lead paces the ventricle.

Additional treatments for fast heart rate
If you have rapid heart rate as part of your sick sinus syndrome, you may need additional treatments to control these rhythms:

Medications. If you have a pacemaker and your heart rate is still too fast, you doctor may prescribe anti-arrhythmia medications to prevent fast rhythms. If you have atrial fibrillation or other abnormal heart rhythms that increase your risk of stroke, you may need a blood-thinning medicine, such as warfarin (Coumadin).
AV node ablation. This procedure can also control fast heart rhythms in people with pacemakers. It involves applying radiofrequency energy through a long, thin tube (catheter) to destroy (ablate) the tissue around the atrioventricular node between the atria and the ventricles. This stops fast heart rates from reaching the ventricles and causing problems.
Radiofrequency ablation of atrial fibrillation. This procedure is similar to AV node ablation. However, in this case, ablation targets the tissue in the atria that triggers atrial fibrillation. This actually eliminates atrial fibrillation itself, rather than just preventing it from reaching the ventricles.


Management of Syncope

Ongoing treatment of patients with syncope focuses on the underlying cause of the symptom, however, in emergency situations the first response is usually the same irrespective of the origin of the attack.

Immediate Management:
- lay patient down
- lift legs
- loosen tight clothing
- record pulse and maintain stable BP (in hospital this can mean administration of fluids etc)
- follow DR ABC to maintain an open airway and making certain that the person is breathing and has a pulse It is important to avoid dehydration and postural hypotension.

For neurally mediated (vasovagal) syncope, treatment can include;
- patient education ie. Knowing to avoid triggers such as prolonged standing, heat, large meals, fasting, lack of sleep, alcohol, and dehydration, sudden movements, awareness of prodrome
- Tilt training (ie, repeated frequent tilting until the patient’s positive response becomes negative),
- pharmacological agents; beta blockers, serotonin uptake inhibitors, Florinef (a drug that prevents dehydration by retaining sodium), and Midodrine (a drug that tends to limit the dilation of blood vessels).
- dual chamber pacing- usually uses two electrodes, one
in the atrial appendage and one in the right ventricular apex. The atrium is stimulated to contract first, then ventricle is stimulated.
- Vasodilators should be discontinued because they may increase susceptibility to vasovagal syncope

Cardiac syncope management requires thorough examinations and tests to determine the cause, for which a more specific treatment can be formulated. However, treatments for the 2 principal causes of cardiac syncope (obstructions and arrhythmias) are listed below;
Obstructive (due to valvular heart disease, obstructed blood vessels, or cardiac tumors for instance):
- surgical removal of blockage

- bradycardia-inducing: pacemaker implantation
- tachycardia- inducing:
1. antiarrhythmic drugs
2. ablation. Ablation consists of carefully mapping the electrical system of the heart (either in the electrophysiology laboratory or in the operating room), locating the part of the electrical system that is causing the arrhythmia, and ablating the offending area (by freezing it, burning it, or surgically excising it).
3. Implantable defibrillator (stops lethal tachycardias, most effective treatment)

Cardiac Pacemakers

An artificial pacemaker is a medical device which regulates the beating of the heart by delivering electrical impulses through electrodes that contract the heart muscles. The primary purpose of this is to maintain an adequate and constant heart rate. It may be used when there is a problem in the normal electrical conduction of the heart or when a patient has bradycardia. Artificial cardiac pacing can be temporary or permanent.


Prophylactic cardiac pacing is sometimes used in asymptomatic patients with bradycardia or conduction abnormalities who are at risk of progression to symptomatic.
There are two methods of temporary cardiac pacing- transvenous and transcutaneous. Transvenous pacing is used mostly in symptomatic bradycardias. It is set to work ‘on demand’, so it only fires when a beat does not occur. The rate of pacing is usually 60-80bpm.
Transcutaneous pacing is the preferred method for asymptomatic bradycardias. It is more uncomfortable for the patient but is usually tolerable until a transvenous pacemaker is inserted.


Permanent pacemakers are fully implanted into the body and connected to the heart by one or two electrode leads. The pacemaker is powered by solid-state lithium batteries, which last between 5 and 10 years.
Pacemakers are designed to pace and sense either the ventricles or the atria, or both. Pacemakers that are connected to both the right atrium and ventricle (‘dual chamber’ pacemakers) are used to simulate the natural pacemaker. It paces both chambers, senses both chambers and reacts. There are also single chamber ventricular pacemakers and single chamber atrial pacemakers.
Pacemakers may also be rate responsive, that is they detect motion and respiration levels and change their rate of pacing to suit the level of exertion.
The choice of pacemaker depends on the condition of the patient.
Permanent pacemakers are inserted under local anaesthetic using fluoroscopy to guide the insertion of the electrode leads via the cephalic or subclavian veins. The pacemaker is usually positioned subcutaneously over the pectoral muscle. Perioperative prophylactic antibiotics are prescribed.



- 12 lead ECG (may show some ischaemic changes)
- Full blood count ( to exclude anaemia)
- Renal function and electrolytes
- Fasting blood glucose (to exclude diabetes)
- Blood cholesterol and triglycerides
- Liver function tests
- Thyroid function tests (thyrotoxicosis will increase work rate of heart, hypothyroidism is linked to increased cholesterol levels)
- Cardiac enzymes

When patient is stable:
- Exercise ECG testing

Note: If patient is unable to undergo exercise ECG testing they can have myocardial perfusion scintigraphy (MPS). Uses photon emission.

Further, more specific tests
- Coronary angiography (Catheter is inserted into a blood vessel in the upper arm or groin, with the tip positioned either in the heart or at the beginning of vessels supplying the heart. Die is injected that is visible by x-ray.)

- Echocardiography (uses sound waves much like a ultrasound to create pictures of the heart. Can identify size and shape of the heart, pumping capacity, and location/extent of damage)



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