1
Q
What are the phases of the pacemaker potential cells?
A
4 - There is a slow leak of Na+ into the cell. This creates an upwards slope. it reaches a point that triggers Ca+ voltage gates channels, but it is just beneath the pacemaker potential ‘all or nothing’ threshold.
0 - Voltage gated Ca+ voltage channels open! There is a an uptick of depolarization.
1 - Not present because the morphology of the cardiac action potential isnt there. So there is no ‘phase 1’ so to speak.
2- Not present because the morphology of the cardiac action potential isnt there. So there is no ‘phase 2’ so to speak.
3 - Peak voltage causes the same Ca+ channels to close! AND for the voltage gated K+ channels to open…Allowing for steep repolarisation (negative deflection in voltage). The cycle begins anew. The slope of phase 4 (the rate of sodium influx which can be modulated) determines the heart rate.
2
Q
How does a pacemaker potential vary in comparison to a myocyte action potential?
A
- A myocyte action potential is sodium driven for depolarisation, where as pacemakers are driven by calcium.
- A mycocyte has automaticity and conductivity. But, it is a contractile cell. Pacemaker cells in the SA node and AV node have no contractility, and a faster automaticity than myocytes.
- Pacemaker potentials, arising from the SA node/AV node ect. never flatline, they just continuously go up and down…ca+ leak channels constantly allowing depolarisation at a steady rate until a voltage gate ca+ channel is triggered. MUST understand different wave-forms between the two. Action potential from cardiac myocyte is more like an ‘elephant under a blanket’.
3
Q
Explain the phases of the myocyte action potential.
A
Phase 4 - Voltage gated K+ channels shut. True isolectric/flat line occurs as voltage maintained by the potassium / sodium leak channels and ATPase pump. The Na+/K+ pump uses ATP to push 3Na+ out and 2K+ in to maintain the resting membrane potential
Phase 0 - Influx of na+ triggers ‘all or nothing’ action potential response. Causing depolarisation -> positive voltage.
Phase 1 - Voltage gated potassium gates are triggered. Rapid Na+ gates are closed -> causes a slight dip in negative voltage as it starts to go down.
Phase 2 - The voltage flat lines up high, as potassium voltage channels are still remaining open which pushes the voltage down, whilst calcium voltage channels are opened in this phase. The calcium wants to make the potential more positive…the balance of potassium and calcium creates the ‘flat line’ of voltage just down from the peak in phase 0.
Phase 3 - Ca+ voltage channels close. Potassium gates K+ channels remain open…steep drop in voltage back down to isoelectric line.
4
Q
What three areas have pacemaker cells?
A
- Bundle of His.
- Av node
- SA Node.
5
Q
You are presented with a patient on his side, snoring, breathing and maintaining an airway. First step?
A
Place him supine and pop in an OPA.
6
Q
ST elevation can occur outside of STEMI when?
A
It can occur in massive cerebral trauma such as in haemorrhagic stroke.
7
Q
What is the difference pathologically between STEMI and N STEMI…how does it show on the ECG?
A
N STEMI - This is partial thickness injury, so necrosis has not dispersed throughout the entire myocardial wall. It is called a ‘sub-endocardial’ MI. Because there is still functional tissue, the delayed conduction that shows in ST elevation is not present. however the general ischemia is still present. So you WILL see potentially…T wave inversion, and ST depression.
STEMI - Transmural or full thickness. Goes through the entire wall and ST elevation evident. T wave inversion at times present as a leading indicator.
8
Q
What are three big causes of MIs?
A
- Toxins - In particular smoking which over time is associated with significant vascular damage.
2) Fats/Cholesterol - Raised LDL in particular - Chronic disease - in particular hypertension and diabetes .
9
Q
Explain the electrical conduction system of the heart?
A
SA Node -> internodal pathways -> AV Node -> bundle of HIS -> splits into left and right bundle branches -> perkinje fibres come off the bundle branches
10
Q
Explain why pain may radiate to the jaw and within the chest cavity during an MI?
A
- Overall the pain mechanisms are not well understood
- Ischemic episodes excite chemo-sensitive and mechanoreceptive receptors in the heart.
- Stimulation of these receptors results in the release of adenosine, bradykinin, and other substances that excite the sensory ends of the sympathetic and vagal afferent fibers.
- Sympathetic Impulses are transmitted via the spinal cord to the thalamus and hence to the neocortex.
- Within the spinal cord, these afferent sympathetic nerve fibre may converge with other somatic thoracic structures. The convergence of these signals may be the basis for referred cardiac pain, for example, to retrosternally within the chest.
- In comparison, cardiac vagal afferent fibers synapse at the medulla, which can cause a descending impulse that excites the upper cervical spino-thalamic tract. This may contribute to the anginal pain experienced in the neck and jaw.
11
Q
Explain why you might experience nausea in an MI?
A
- Ischemic episodes excite chemo-sensitive and mechanoreceptive receptors in the heart.
- Stimulation of these receptors results in the release of adenosine, bradykinin, and other substances that excite the sensory ends of the sympathetic and vagal afferent fibers.
- Vagal stimulation results in nausea
12
Q
Explain how vomiting works in the body, and how anti-emetics exert their effect?
A
- The vomiting centre is located in the central medulla and this co-ordinates the complex events behind vomiting.
- It projects to the vagus nerve and spinal motor neurons, which innervate the abdominal muscles.
- The chemoreceptor trigger zone (CTZ) is ALSO located within the medulla oblongata in a different location….BUT…primarily recieves inputs from blood-borne drugs or hormones, and communicates with the vomiting center to initiate vomiting.
Mainly triggered by
- Drugs
- Toxins
- Chemicals
- The vomiting centre contains muscarinic (acH) and histamine receptors. Comparatively, the CTZ is rich in dopamine (D2) and 5-HT3 b (seratonin) receptors. Hence antiemetic drugs such as ondansatron only effect the CTZ, because they are 5-ht-3 receptor antagonists.
The vomiting centre can recieve inputs for vomiting from the limbic system and other areas within the cortex. It also links with the vestibular system (the inner ear responsible for balance/vertigo).
***The limbic system is the part of the brain involved in our behavioural and emotional responses, especially when it comes to behaviours we need for survival: feeding, reproduction and caring for our young, and fight or flight responses.
The vomiting centre is triggered by
- Pain
- Fear
- Olfactory
13
Q
Which leads correspond with which vessels within the heart?
A
II, III and AvF = RCA (Right coronary artery)
V1, V2, V3, V4 = LAD (Left anterior descending)
V5, V6, 1, AvL = LcX (left circumflex) or obtuse marginal.
14
Q
Why might a patient with a heart attack breath quicker?
A
- Not enough oxygen is delivered to tissue -> Change to anaerobic respiration. Increased lactic acid production
- This is buffered in blood, converted to carbonic acid, and then c02 to be blown off at the lungs.
- This increase in pac02 is picked up by the aortic arch receptors and the carotid sinus receptors
- They feed into the MRC - The muddulary respiratory centre to increase breathing and remove the c02.
15
Q
Explain which leads correspond on the ECG, with which areas of the heart?
A
II, III, AvF = Inferior
V1, V2 = Septal
V3, V4 = Anterior
1, AvL, V5, V6 = Lateral
16
Q
Explain the maladaptive haemodynamic responses to MI, and what hormones drive this?
A
The hormones are all the adrenergic hormones, all of them. So Alpha 1, Beta 1, Beta 2 and Alpha 2.
The maladaptive response:
- MAP and CO goes down
- Hormones released. Inotrope increased. Chronotrope increased. SVR increased.
- Afterload increases. Mv02 demand increases.
- More ischemia, less CO. Cycle begins anew.
17
Q
Within the cell, what is the primary regulator of vascular tone…how does it exert its effect?
A
- GTN interacts with other nitrate groups within the body, ultimately forming nitric oxide.
- nitric oxide is a potent activator of cyclic guanosine mono phosphate (cGMP). cGMP is formed via gaunosine triphosphate.
- cGMP is a secondary messenger. It is the primary regulator of vascular tone. Noitric oxide increases the intracellular concentration of cGMP. This cGMP uses kinase dependent processes, to cause de-phosphoralisation of myosin CHAINS. This causes efflux of calcium, thereby decreasing troponin binding with ca+ and therefore muscle relaxation occurs.
- Link this with myosin/actin actions. Lack of calcium means that the tropamyosin cannot be moved out of the way, and muscle contraction cannot occur.
18
Q
How do myosin heads act?
A
- ATP binds to myosin heads (little golf club like proteins) and this ‘releases’ the myosin head from the actin filament.
- ATP is broken down, into ADP and one phosphate group. This ‘cocks the spring’ of the myosin head. Puts it into high energy state.
- Phosphate is released from the myosin head. This chemical energy is converted into physical action as the myosin head crawls along the actin filament.
- ADP is released and the cycle begins anew.
19
Q
Explain actin, myosin, tropamyosin, and tropanin. How does calcium play a role?
A
- Actin is the filament that myosin heads crawl along.
- Myosin are the heads that move along the actin filament. In order to perform their action there needs to be an ‘open’ actin filament.
- At rest the tropamyosin blocks the binding site for myosin heads. It moves out of the way when the toponin ‘bolts’ are activated with calcium.
- Troponin is activated when calcium binds to the troponin. This releases the tropomyosin rope, allowing myosin to engage with the actin filament using ATP to crawl along it.
20
Q
How do PDE-5 inhibitors interact with GTN in a negative way?
A
- Phosphodiesterase-5 is an enzyme that regulates cGMP within the cell.
- It is an enzyme that causes hydrolysis of cGMP. The downsteam effect of cGMP, is to use kinase dependent processes, to dephosphoralise myosin chains, hence increasing ca+ efflux and causing smooth muslce RELAXATION.
- Therefore PDE-5 inhibitors such as viagra, REDUCE the availability of PDE-5 - > increasing cAMP and allowing for vasodilation and therefore erections.
- If you give GTN, this drug INCREASES cGMP via nitric oxide. Therefore the two together can cause a pathological increase in cGMP, massive vasodilation and a code brown.
21
Q
What are some of the signs and symptoms in terms of ECG for pericardial effusion?
A
- Sinus tachycardia
- Low QRS voltages
- Electrical alternans (beat to beat variation in QRS height). This happens because the heart swings side to side within the pericardial cavity.
22
Q
What would you expect on an ECG if the patient was hyperkalaemic?
A
- Bradycardia
- Flattening/loss of P waves ( https://lifeinthefastlane.com/wp-content/uploads/2010/01/ECG_Hyperkaemia_L.jpg )
- Peaked T waves (this is the main symptom).
23
Q
What is the acronym that is useful for AMA’s (Against medical advice)?
A
VIRCA
V - Voluntary - Free decision, no coercion or undue influence
I - Informed - The person is informed of the possible risks or consequences of refusal.
R - Relevant - The refusal must be relevant, in that it relates to the treatment that has been recommended.
C - Capacity - The person has capacity, and understands the nature and consequence of the decision to refuse
Advice - The patient has been provided with advice for safety, comfort and follow up given the refusal of service.
24
Q
In what type of MI might you see bradycardia?
A
It can be a sign of inferior infarcts, because they involve the RCA (right coronary artery) which feeds the right ventricle, and right atrium.
Ischemia within the R) atrium can lead to poor electrical conduction and hence effects the SA node. Slower rate—-> Bradycardia is the result.
25
When describing any kind of 'rate related' or 'preload dependent' rhythm in a VIVA, how do you describe and think about the potential consequences?
Always relate it back to cardiac output. CO = HR x SV
26
What are the two primary features of PE pathology, and how does this effect your thoughts on GTN?
The two primary effects:
- Hypoxaemia due to a significant V/Q mismatch (good ventilation and poor perfusion).
- Hypotension - Massive reduction in preload to the left ventricle, due to the 'backed up' blood flow from the RV that is potentially not getting through efficiently.
Therefore PE is a PRELOAD dependent rhythm! You want to be sure someone is not having a PE and poor perfusion before giving GTN!!
27
Explain the oxygen/hameglobin dissassociation curve?
https://www.medicalexamprep.co.uk/understanding-oxygen-dissociation-curve/
The curve has on the y axis, sp02. Or the amount of haemoglobin that is bound to oxygen -> forming oxyhaemoglobin. The X axis, has the pa02. Or the amount of free oxygen floating around.
The lower the p02, the less oxygen floating around, there is a propensity for oxy-haemoglobin to form haemoglobin and release the 02 molecule.
The reason there is a signmoid shape on the graph, is the concept of co-operative binding. Co-operative binding means that haemoglobin has a greater ability to bind oxygen after a subunit has already bound oxygen. Haemoglobin is, therefore, most attracted to oxygen when 3 of the 4 polypeptide chains are bound to oxygen.
If you took the thigh for example -> this area is low in pa02 and so you would expect the sp02 to be lower in this area, as oxyhaemoglobin releases oxygen molecules to form haemoglobin.
- So low pa02 (the o2 dissassociation curve) is one reason for 02 delivery.
- Another reason is the bohr effect -> The Bohr Effect refers to the observation that increases in the carbon dioxide partial pressure of blood or decreases in blood pH result in a lower affinity of hemoglobin for oxygen.
This bohr effect shifts the curve to the RIGHT. High temps and acidity shifts to the right.
A rightwards shift assists in the natural inclination of 02 to bind less aggressively at lower pa02 levels.
A leftward shift would be alkalinity and colder temperatures. This would increase the binding affinity and compromise oxygen delivery.
28
What is the haldane effect
In the presence of oxygen, there is a decrease in the affinity of hameoglobin for c02. And hence, more c02 is released (for example at the lungs -> high 02 environment) and delivered to tissue for expulsion.
29
How heme binding sites are there for oxygen molecules?
4
30
What is KVO rate?
30 ml per hour
Or
10 drops per minute
31
Why do we get free radicals or reactive oxygen species?
1. During cellular respiration, normal oxygen molecules lose an electron, making them hyper reactive. The process in which ATP is produced, called oxidative phosphorylation, involves the transport of protons (hydrogen ions) across the inner mitochondrial membrane by means of the electron transport chain. In the electron transport chain, electrons are passed through a series of proteins via oxidation-reduction reactions, with each acceptor protein along the chain having a greater reduction potential than the previous.
The last destination for an electron along this chain is an oxygen molecule. In normal conditions, the oxygen is reduced to produce water; however, in about 0.1–2% of electrons passing through the chain oxygen is instead prematurely and incompletely reduced to give the superoxide radical. In aerobic organisms the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain.
In addition to energy, reactive oxygen species (ROS) with the potential to cause cellular damage are produced. ROS can damage lipid, DNA, RNA, and proteins, which, in theory, contributes to the physiology of aging.ROS are produced as a normal product of cellular metabolism. In particular, one major contributor to oxidative damage is hydrogen peroxide (H2O2), which is converted from superoxide that leaks from the mitochondria.
32
How is C02 transported in the body?
I thought it relevant to explain the manner in which c02 is predominately transported as bicarbonate ions within plasma. C02 is carried in three ways within the body:
1. It dissolves directly into blood (5-7%)
2. It binds directly to haemoglobin without disassociation into bicarbonate (10%)
3. It dissociates into bicarbonate and a hydrogen ion. It is broken up essentially into two molecules which can combine to recreate c02. This is responsible for transporting 82% of c02). I will deal with the third mechanism:Diffusion is the driving force for c02, which moves from plasma into red blood cells (rbc's), and as this occurs it comes into contact with a water molecule.
This sets off a reaction identical to that of the bicarbonate buffer system, however carbonic anhydrase (which sits inside the red blood cell) essentially speeds up the reaction. As C02 combines with water carbonic acid (H2c03) is formed momentarily, in order to produce both Hc03- (bicarbonate) and H+. In order to maintain electrical neutrality within the cell, the bicarbonate is exchanged for Cl- in a mechanism termed the chloride shift, and cl- enters the RBC in this process, whilst the bicarbonate diffuses out of the RBC into plasma. This bicarbonate by-product plays a crucial role in maintaining the high ratio of bicarbonate in blood that serves as our buffer system against acids.
The ratio of bicarbonate to carbonic acid in plasma is approximately 20:1 according to the vast majority of processes within the body that generate acid by-products. The left over H+ ion binds to the haemoglobin for transport to the lungs where the reaction is reversed, bicarbonate is exchanged for chloride and both water and C02 diffuses across the RBC membrane.
This allows for expulsion of c02 and this important mechanism is also central to the maintenance of PH within blood. For example, if enough acid were added to soak up half of the available bicarbonate our PH would drop from 7.4 to 6.0 within plasma. But the ability to convert excess carbonic acid (h2c03) into c02, as well as enhancing respiration rate allows PH to only drop from 7.4 to 7.2.
33
What role does the kidney play in maintaining blood PH?
It reclaims bicarbonate. 80-90% of bicarbonate is filtered through the glomerulus and reabsorbed within the proximal tubule. H+ Secretion and Bicarbonate Generation.
Importantly, excretion of hydrogen ions by the kidneys is molecularly coupled to novel generation of bicarbonate which is subsequently added to the extracellular fluid, thus replenising the ECF bicarbonate buffer. The specific molecular mechanisms and regulation of these processes are covered in Renal Acid Excretion.
Bicarbonate Excretion: The bicarbonate buffer is the principal physiological buffer of the extracellular fluid. As discussed in bicarbonate buffer, the extracellular pH is largely determined by the ratio of the Weak Acid (CO2) to Weak Base (HCO3-) form of this buffer. The kidneys can influence the extracellular pH by regulating urinary excretion of bicarbonate HCO3- as discussed in renal bicarbonate excretion. It should also be pointed out that as mentioned above, the kidneys can also synthesize and add novel bicarbonate to the ECF as part of renal acid excretion.
Fixed Acid Elimination: As discussed in physiological acid production, normal and pathological metabolic processes can generate a number of strong acids which are added to the extracellular fluid. Although these acids immediately release a free hydrogen ion which can be eliminated by other processes, the remaining molecule must also be eliminated to prevent its gradual build up in the extracellular fluid. The only organ which can ultimately eliminate these fixed acids is the kidney which does so through their urinary excretion.
34
How is breathing controlled under normal circumstances?
Breathing is mediated by the medullary respiratory centre (MRC), which controls breathing depth and frequency according to inputs from chemoreceptors Central chemoreceptors in the medulla respond to changes in PH, whilst peripheral receptors in the carotid sinus and aorta are sensitive to changes in plasma that effect the partial pressure of oxygen (Pa02) and carbon dioxide (PaC02). PC02 provides the stimulus for breathing rather than pa02.
35
What are the 4 H's?
1. Hypoxia
2. Hypovolemia
3. Hypo/Hyper kalaemia and h+ hydrogen ions
4. Hhypothermia
36
What are the four T's?
1. Toxins
2. Tamponade
3. Tension Pnemothorax
4. Thrombosis.
37
What changes occur to metabolism in metabolic acidosis?
Without oxygen, the body cannot facilitate aerobic metabolism (oxygen driven metabolism of fats, protein and carbohydrates). Anaerobic metabolism is VASTLY less efficient (way less ATP). It also has H+ ion byproducts predominatley due to lactic acid production associated with this process.
These H+ ions are converted to c02, and as pac02 increases, RR increases accordingly to expel it. Once biarbonate and respiration increases cannot compensate - metabolic acidosis occurs (later stage sign in MI for example).
38
What is the patho of an MI?
MI is commonly precipitated by a ruptured coronary atheroma, exposing a lipid core to platelets that aggregate and initiate a coagulation cascade (Brener 2006, p. 2). As a thrombus forms myocytes become ischemic and switch to anaerobic metabolic production, reducing availability of adenosine triphosphate (ATP) (Aymong, Ramanathan & Buller 2007, p. 705).
Contractile function is impaired and ionic dysregulation results in necrotic or oedematous myocytes (Aymong, Ramanathan & Buller 2007, p. 705). As cardiac output (HR x stroke volume - so only stroke volume is reduced) and mean arterial pressure (MAP) decline, heart rate, inotrope and systemic vascular resistance (SVR) increase, worsening ischemia and potentially expanding the infarct (Lilly 2012, p. 168).
39
Why is a BP potentially narrow in an MI?
Stroke volume and heart rate are the determinants of cardiac output. SV tends to decrease as ventricular contractile function is impaired, which occurs due to cellular deficits of ATP and the presence and propagation of necrotic tissue.
These processes cause a decrease in left ventricular ejection fraction and when paired with increases in systemic vascular resistance (SVR), they lead to a narrowed pulse pressure which may signal the onset of cardiogenic shock
40
What hormonal response occurs in MI, how does this effect the heart?
Increases in SVR occur in response to drops in MAP, which prompt sympathetic release of adrenaline and nor adrenaline causing systemic vasoconstriction, increased inotrope and increased chronotrope (Lilly 2012, p. 168). This response is maladaptive and increases afterload and the inotropic force necessary to eject blood from the left ventricle (Gowda, Fox & Khan 2008, p. 223).
Inotrope rises in accordance with this demand and widespread vasoconstriction enhances preload (Gowda, Fox & Khan 2008, p. 223). Subsequently there is a marked increase in ventricular wall tension and myocyte stretch in accordance with Starlings law, resulting in greater myocardial oxygen demand (MVO2) and exacerbation of ischemia (Gowda, Fox & Khan 2008, p. 223).
An increased HR also enhances MVO2, according to its inverse relationship with diastolic filling time (Gowda, Fox & Khan 2008, p. 223). As ischemia is worsened the function of myocytes tend to decline, promoting further maladaptive responses – which may lead to greater infarct size and cardiogenic shock (Gowda, Fox & Khan 2008, p. 224).
41
What are the three classifications of hypovolemia?
In a 70kg adult male:
Mild = 750ml or 15% of total blood volume
Moderate = 750-1500ml or
15-30%Severe = Above 2 litres of blood or >40%.
42
What are the three classifications of hypothermia?
mild = 35-32°C
Moderate 32°C- 28°C
Severe = <28°C
43
There are alpha cells and beta cells in the pancreas, what function does each one have? These cells are only found in the islets of langerhans and involve the ENDOCRINE function of the pancreas.
Alpha - Glucagon
Beta - Insulin.
44
How does glucose get into cells?
1. The insulin binds to a receptor on the membrane
2. Signalling cascade within the cell
3. GLUT4 glucose transporter penetrates the cell membrane
4. Glucose enters the cell.
45
What condition in particular are type 2 diabetics prone to?
Hyperosmolar hyperglycemic state (HHS). The high levels of glucose in plasma increase the osmolarity of blood. Therefore, fluid is drawn from cells (cellular dehydration) increasing blood volume. As blood volume increases, more urine is produced (polu uria) and more drinking occurs for cell shrivelling due to dehydration (polydipsia). The brain gets dehydrated so they have MENTAL STATUS changes.
46
Explain glycosylation.
Persistent high levels of glucose in the blood stream leads to glycosylation. This is when glucose binds to proteins in the blood. In particular it binds to haemoglobin - they measure this to check how controlled your diabetes is. The product of this reaction is known as advanced glycosylation end (AGE) products, and an accumulation of these in tissues and blood vessels walls causes damage, leading to macrovascular diseases such as atherosclerosis.
47
Why does polyuria occur in T2DM?
As glucose enters the degraded glomerulus, more glucose gets into the filtrate (glycosuria). A higher solute concentration causes osmosis to draw more water. Therefore more urine is produced. They therefore become dehydrated and need to drink more also. (polydipsia + polyuria)
48
Explain DKA (diabetic ketoacidosis).
Mainly occurs in type 1 diabetes. Because type 2 have some insulin mostly.
1. Hyperglycemia occurs.
2. Cells starved of oxygen so lipolysis intiated to produce free fatty acids (FFAs). Glucagon also upregulated worsening the situation.
3. After that the LIVER turns these FFAs into ketone bodies.
4. Ketone bodies can be used by the body for ENERGY. BUT they also increase blood acidity. The ketones are needed primarily becasue the BRAIN needs energy. FFAS cant cross the BBB
5. Blood becomes acidic and PH declines. Kussmaul breathing can occur (deep/laboured breathing).
6. A loss of insulin also means that the ATPase pump is DOWN regulated. Therefore the ionic gradients are changed, more potassium is in the ECF, and then makes it way into plasma.
7. Hyperkalaemia then occurs. Potassium is excreted. Therefore blood K+ is high over time, and intracellular K+ stores are low over time.
8. DKA is broken down into acetone...this is the sweet fruity smell you may get on a persons breath.
9. Complications can include changes in mental status and cerebral oedema.
49
Why might an infection result in DKA for a type ONE diabetic (remembering it is mostly type 1s that suffer DKAs).
NORMALLY associated with type ONE diabetes because type 2 have SOME circulating insulin.
1. It increases body stress.
2. Adrenaline is released
3. This prompts release of glucagon. Increases hyperglycaemia even more@
4. Not enough insulin around-> hyperglycemia -> glucose in urine -> loss of water -> dehydration.
5. Also, the cellular starvation calls for ketone bodies to be released from liver after lipolysis. This can lead to DKA.
50
Explain how nerves become damaged in diabetes
excess glucose causes increased intracellular pressure which damages nerve cells. This is because a higher solute concentration = increased osmotic pressure. This occurs in cells of peripheral nerves, leading to peripheral myelin sheath degradation and disrupted nerve impulse transmission, which can cause altered sensation.
51
The three main components of stroke volume are?
1. End-diastolic volume (pre-load) - The frank starling mechanism tells us this increases inotrope. 2. Afterload ( the pressure against which the heart must work to eject blood during systole) 3. Sympathetic inputs to the ventricles.
52
Beta 1, 2 and 3 - primary locations?
Beta 1. Heart and kidney Beta 2. Lungs, GI tract, uterus, vascular smooth muscle Beta 3. Fat cells only
53
Explain a ventricular escape rhythm?
Another word for this is an IDIOVENTRICULAR rhythm. Normally it means the rate is roughly the intrinsic ventricular rate. It is when pacemaking is occuring in the ventricles. Apparently the condition is largely benign...not 100% sure.
Rate: 20-40
Rhythm: Regular
P wave: None
WRS Width: >120 ms - WIDE
54
When does kaussmaul breathing normally happen?
Kussmaul breathing occurs as respiratory compensation for severe metabolic acidosis via expiration of carbon dioxide. Therefore, it is often seen secondary to diabetic ketoacidosis (DKA). It may also arise due to increased intracranial pressure (ICP) and renal failure. Kussmaul breathing results in arterial blood gas analysis showing hypocapnia in normally functioning lungs
.Implications:While Kussmaul breathing is typically associated with DKA other differential diagnoses should be thoroughly explored. This is because treatment for DKA involved fluid therapy which could be detrimental to a patient presenting with Kussmaul breathing secondary to increased ICP or renal failure.
55
What is cheyne stokes respiration?
Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease (shallower and sometimes slower) that results in a temporary stop in breathing called an apnea.
The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes.[1] It is an oscillation of ventilation between apnea and hyperpnea with a crescendo-diminuendo pattern, and is associated with changing serum partial pressures of oxygen and carbon dioxide.[2]
56
What causes cheyne stokes respiration? What conditions cause it?
The mechanisms of Cheyne-Stokes breathing are not well understood. Possible theories include; altered brainstem function, poor cerebral circulation, alterations in respiratory control centre and cortical dysfunction.
Anything that effects the brain can cause it.
BUT Cheyne-Stokes breathing is particularly associated with end of life and congestive heart failure (CHF) while sleeping
.In patients with CHF, Cheyne-Stokes breathing increases risk of adverse cardiac events. This is because diastolic dysfunction and dysrhythmias worsen due to hypoxaemia caused by excessive sympathetic stimulation in response to apnoea.
Therefore, paramedics should thoroughly investigate the cardiovascular system of patients with CHF and Cheyne-Stokes breathing.
57
Quick summary of tension pneumo? Plus treatment?
A pneumothorax (of any kind) is defined as air between the parietal and visceral plura. A tension pneumothorax develops when air enters the plural space and is prevented from escaping.
This build-up of air causes a shift in the mediastinum which obstructs venous return and may result in cardiac arrest. Physical signs include a decreasing level of consciousness, difficulty with ventilation, unequal, decreased or absent breath sounds upon auscultation, hyper-resonance to percussion on the affected side, jugular vein distension, tracheal displacement towards the normal side, and a weak or absent radial pulse.
An ECG may indicate narrow QRS complexes and a slow heart rate. Treatment involves a chest needle decompression in the 2nd intercostal space at the mid-clavicular line on the affected side above the 3rd rib which releases the pressure in the pleural cavity.
58
What makes a tension pneumothorax different to a standard one?What patho?
In a standard pneumothorax the volume of air in the plueral space is constant. In a tension, it is continually increasing due to a 'one-way valve' in which air enters but does not escape. Enters on inspiration, does not exit on expiration. It becomes a tension when the intraplueral pressure exceeds atmospheric pressure. There is a mediastinal shift (the membrane between the lung cavities of each side). There is vena cava compression, reduced venous return and reduced caardiac output. As it continues, the lung continues to be compressed more rapidly leading to quick patient deterioration in respiratory function (in addition to the cardiac issues).
59
Signs and symptoms of pneumothorax?
1. Hypoperfusion (pale, hypotensive)
2. tachy with pulsus paradoxus (BP lowers by 10 mmHg on inspiration).
3. decrease in breath sounds (can be both fields or just one).
4. Dysponea and tachponea
5. Decreasing GCS
6. Hyperresonance on one side and Raised JVD
60
Summary of tamponade - what it is + signs and symptoms?
Cardiac tamponade occurs when blood or other fluids accumulate in the pericardium and compress the heart preventing the ventricles from filling properly and results in ineffective cardiac output.
A cardiac tamponade may be caused by trauma to the chest or inflammation of the pericardium. Physical signs include tachycardia, a narrowing pulse pressure, an absent pulse, muffled heart sounds upon auscultation, and jugular vein distension. An ECG reading may indicate narrow QRS complexes.
61
What is the most significant indicator if you suspect an hypovolemic shock?
Severe hypotension on postural change. Similarly, postural changes in HR >30 are significant.
62
Explain sepsis?
Sepsis is a maladaptive response to infection. Infective sources release bacteria and this prompts an IMMUNE response and therefore INFLAMMATION and release o CYTOKINES. Initially the cytokines are antiinflammatory, but if bacteria continues to accumulate a paradoxical pro-infllamatory cytokine response occurs. Nitric oxide is upregulated. Inflammation also causes endothelium disruption and enhanced capillary permeability. Once the endothelium is involved it interfers with fibrinolysis. Therefore DIC (disseminated intravascular coagulopathy) can occur leading to widespread use of fibrinogen (no clotting).
In Summary:
1. Widespread peripheral vasodilation. 2.Increased capillary permeabliity
3. Complex coagulopathy
4. Depressed myocardial function
63
What does cold sepsis mean?
Normally, in SIRS the temperature is elevated because cytokines stimulate the hypothalamus, this upregulates prostaglandin secretion. This changes the temperature setpoint to be higher, in order to kill bacteria. In cold sepsis, they are likely further progressed. Cytokines and nitric oxide have at this point caused widespread peripheral vasodilation and capillary permeabliity. Sympathetic systems are engaged intially, but may be barely coping or failing to maintain organ perfusion. The compensatory sympathetic response is adrenaline and noradrenaline release. This causes peripheral vasoconstriction leading to cool extremities. Furthermore, loss of fluid into the interstitium means less blood volume, heat loss and thus cold sepsis. These patients will be critically unwell.
64
What happens to HR in sepsis?
BP is dropping because nitric oxide (dilation) and capillary permeability (loss of fluid into interstitium). Remember: BP is CO + SVR. A sympathetic response tries to maintain both of these factors. Baroreceptors pick up the drop in BP. Prompting ADRENAL release of adrenaline and noradrenaline. This causes: - Vasoconstriction (increased SVR) - Increased preload and thus stroke volume via contractile enhancement - Increased HR.
65
Why do persons with Sepsis have a raised respiratory rate?
Poor perfusion= widespread lactic acidosis. Therefore the excess H+ and thus C02 needs to be expelled via respiration. Peripheral and central chemoreceptors detect this change in plasma and prompt the MRC (medulla respiratory centre) to increase respiration. Secondarily, increased temperature increases metabolic rate and oxygen demand.
66
Explain DIC in sepsis?
Deseminated intravascular coagulopathy is seen in SEVERE, REFRACTORY SEPSIS. Most commonly in MENNINGICOCCAL SEPTICEMIA. It is a complicated process but is essentially a poor balance between clotting and fibrinolysis.
Endothelial growth factors are released due to cytokine inflammation within the endothelium. This promotes microclotting. The response of the body is to LYSE the clots using endogenous fibrinolytics. These factors are not innumerable. Therefore in DIC either too much clotting, or thin blood will predominate. Eventually, all the factors including fibrin and fibriongen are used up and diffuse microvascular bleeding occurs as blood is not viscus enough. These patients bleed from the eyes, mucusa, genitals ect. This is why meningococcal has the puperic rash which is a subcutaneous microvascular haemorhage.
67
What is occuring in neurons that causes siezures.
People who experience siezures will typically have an inbalance between excitatory and inhibitory neurotransmitters. Most notably glutamate (excite) and GABA (inhibit). Glutamate allows for NA+ to enter neurons, making them more positive.
GABA, allows for CL- to enter neurons making them more negative. This effects the resting membrane potential and how close it is the threshold.
Persons with epilepsy may infact have a HIGHER resting membrane potential and more easily excitable neurons. Therefore surrounding neurons may be susceptible to depolarisation when an aberent firing occurs.
68
What is the primary difference between focal and generalised siezures?
Focal effects a limited and specific neuronal area typically within one hemisphere. Generalised effects both hemispheres. When subcortical structures become involved such as brainstem, medulla, thalamus ect. conciousness is lost.
69
What are normal signs of siezures and why? What should you be concerned about?
Because a seizure uses a vast amount of ATP, cerebral blood flow is aggressively increased. In line with increased demand there is universal increased supply 1. Hyperglycemia
2. Hypertension
3. Tachycardia
4. Tachypnoea Concern: If muscle coordination is impaired in a tonic-clonic...so will respiratory muscles and diaphragmn. Therefore hypercarbia and/or respiratory acidosis may develop. Therefore maintaining airway and assisted PPV breathing is essential in these patients.
70
When is neuronal injury typically thought to occur in status epilepticus?
Between 30 - 60 minutes.
71
how does midazolam stop a siezure? What are two important side effects and considerations?
1. It binds to GABA1 receptors and increases their affinity for GABA. Therefore more CL- enters and the neurons are hyperpolarised, reducing frequency of firing rate and hopefully siezure termination. Side effects: Severe hypotension and respiratory depression. Both of these exacerbated if drugs or alchohol on board. Considerations: Drugs/alchohol, AGE (much more potent), liver compromise (much more potent).
72
What is the difference between adrenaline and nor-adrenaline in terms of TYPE?
Adrenaline - Endocrine hormone in PLASMA
Nor-Adrenaline - Neurotransmitter
73
What are the symptoms of low BGL?
1. Hunger - ACH
2. Nervousness/anxiety/tremor - SNS
3. Sweating - ACH
4. Tachy/palpatations - SNS
5. Pallor - SNS
6. Pupil dilation - SNS
74
What does the alpha 1 adrenoreceptor do? What endogenous neurotransmitter or hormone triggers it?
1. Smooth muscle contraction (vasocontriction - a little a over the finger cutting it off to remember)
2. GI tract and visceral contraction Triggered: Noradrenaline primarily, secondarily adrenaline does have SOME a1 crossover but it primarily a beta agonist.
75
What does the beta 1 adrenoreceptor do? What endogenous neurotransmitter or hormone triggers it?
Trigger: Adrenaline, noradrenaline to a lesser extent. Positive Chronotropic, Dromotropic (conduction speed) and inotropic effects, increased amylase secretion
76
What does the beta 3 adrenoreceptor do? What endogenous neurotransmitter or hormone triggers it?
Trigger - noradrenaline Enhances lipolysis
77
How does magnesium help people in asthma?
Magnesium can induce bronchial smooth muscle relaxation in a dose-dependent manner [1]It inhibits: -Calcium influx into the cytosol (contraction/bronchocontriction) -histamine release from mast cells - inhibit acetylcholine release from cholinergic nerve endings - It also may increase the bronchodilator effect of β2-agonist by increasing the receptor affinity
78
What is an anticholinergic?
An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system. Anticholinergics inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells.
79
QLD ambulance defines cardiogenic shock as what?
Sustained hypotension. <90 mmHg for >30 minutes.
80
In what way are BBBs unique
They are the only rythmn where you see a normal P wave, a wide QRS with M waves (Wolf parkinson the only other wide QRS but with no M wave).And so you know normal conduction from atria so cant be a ventricular rythmn - explained delayed conduction by the bundle branches in ventricles being blocked. Explains wide QRS with notching.
81
Right heart failure what is it?
•Backpressure into the venous system causing: - Hepatosplenomegaly = Liver and spleen hypertrophy- Oedema- Acites - JVD
82
What are complications of left sided heart failure
1. Poor cardiac output causes poor perfusion to the kidney/reduced GFR. A maladaptive response means that the RAS is activated for more Blood volume + ADH. This is BAD, you need to be on dieuretics to counteract
2. pulmonary system- cheyne stokes respiration - The pathophysiology of Cheyne–Stokes breathing can be summarized as apnea leading to increased CO2 which causes excessive compensatory hyperventilation, in turn causing decreased CO2 which causes apnea, restarting the cycle. In heart failure, the mechanism of the oscillation is unstable feedback in the respiratory control system
83
What are four types of PE and their consequences?
1. Massive occlusion: Major artery occlusion causing acute onset respiratory and circulatory compromise
2. Embolus with infarction: Infarction of lung tissue - may or may not cause respiratory distress or circulatory symptomology. May develop over days. eg. symptoms of fever or pain
3. Embolus without infarction: may be no symptoms.
4. Multiple small emoboli- Symptoms may not be present - or may have arisen over a period of time
84
What are three key systemic consequences of a PE?These cause what serious signs and symptoms?
Consequences:
1. May cause hypoxaemia via V/Q mismatch
2. It may reduce left ventricular preload due to compromised blood flow. Thereby reducing cardiac output.
3. Necrosis of lung tissue
Symptoms:
1. Hypoxaemia
2. Hypotension
3. Respiratory distress
4. Pain - particularly on inspiration (necrosis)
85
What are three cardinal features of pericarditis?
1. Decreased pain on leaning forward. Worsened pain on lying supine
2. Fever
3. Pain on inspiration
86
ECG changes associated with pericarditis
1. Acute phase: PR segment depression, ST elevation
2. Later phases: T wave flattening or T wave inversion
3. Changing QRS heights because the heart is bouncing arounda
87
In patients with chronic pericarditis, what changes would you see physiologically?
They get poor myocardial stretch/preload and therefore REDUCED stroke volume. This occurs because they get pericardial thickening so a tamponade -like effect that contrains the heart. to compensate for this they have increased HR. Therefore changes are MORE HR, LESS Stroke volume
88
Name the effects of hypothermia pathologically?
Cardiovascular effects:
- Initial tachycardia and peripheral vasoconstriction.
- Subsequent progressive bradycardia – This is due to decreased spontaneous depolarisation of cardiac pacemaker cells.
- Noted hypotension and reduced cardiac output, with vascular tone lost at <24°C.
- ECG Changes – Osborn wave - Atrial fibrillation is commonly followed by Ventricular Fibrillation then Asystole at temperatures <25°C
Central Nervous System effects:
- Loss of fine motor skills and coordination, progressing to loss of gross motor skills.
- Decline in consciousness
- Cerebrovascular autoregulation lost at <24°C
- Rigidity, pupillary dilation, and areflexia appear at temps <28°C.
Respiratory effects:
- Resp rate initially increased, progresses to bradypnoea as metabolism slows.
- CO2 retention and respiratory acidosis indicate disturbances to normal respiratory responses. (Severe Hypothermia)
- Initial left shift of HbO2 dissociation curve in response to reduced CBT. Therefore impaired O2 delivery and tissue hypoxia.
- Severe hypothermia causes a right shift of HbO2 as there is a decline in O2 demand in the tissues at lower temps.Renal effects:
- GFR falls in moderate hypothermia as CO and renal blood flow fall. Increases in severe due to cold dieresis.Metabolic effects:
- Rapid onset hypothermia -> hyperglycaemia - Slow onset hypothermia -> hypoglycaemia i.e. glycogen stores depleted from shivering. Haematological effects:
- Increase in blood viscosity and fibrinogen - Haemoconcentration with the hypovolaemia compounded by a cold-diuresis - Haematocrit increased by 2% for every 1°C drop.
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