Degree summary deck (wikis) Flashcards
Why does diabetes lead to vascular changes?
It leads to athersclerosis via:
- Metabolic factors such as dyslipidaemia-> more free fatty acids
- Hyperglycaemia increases oxidative stress -> A byproduct of Increased release of free radicals -> increases lipid per-oxidation and therefore foam cells forming in arterial walls.
- Insulin resistance casuses endothelial dysfunction-> this means less nitric oxide production. This is a key precursor to atherosclerosis.
- Diabetes also promotes a low grade inflammatory state -> changes the balance of hormonal growth factors -> More smooth muscle cells are produced (pro thrombotic) -> platelet aggregation occurs (pro thrombotic). Therefore diabetes is a pro thrombotic state to be living in.
Why do we get free radicals or reactive oxygen species?
- 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.
What causes type 1 diabetes
An autoimmune response where endogenous antibodies attack the islet beta cells in the pancreas which are responsible for insulin production. Once these are destroyed (inevitably they are) insulin loss is absolute.
What causes type 2 diabetes?
No exactly known, many lifestyle related factors. It typically begins with insulin resistance and ‘metabolic syndrome’. This causes
a) downregulation insulin receptors and/or
b) derangement of intracellular signalling (secondary messengers). Collectively this is insulin resistance. As insulin sensitivity decreases, insulin release increases in order to maintain glucosehomeostasis
In DM2, the pancreatic beta cells cannot compensate for this loss of sensitivity and become dysfunctional as a result of persistent stimulation. Hyperglycaemia develops. The degree of resistance also tends to increase over time, progressive beta cell dysfunction.
What is metabolic syndrome?
MS is characterised by insulin resistance (IR), and encompasses a cluster of related metabolic disorders that includes hypertension, abdominal obesity and dyslipidaemia. It identifies those at risk of T2DM.
Why is abdominal fat associated with metabolic syndrome? Why does this lead to T2DM?
Obesity correlates strongly with MS due to accumulation adipose tissue. Both the tissue, and a high fat diet is associated with increased free fatty acids in the body. Experiments in mice show high fat diets lead to hepatic inflammation and release of adipokines.
Therefore FFA’s = inflammation. FFA’s have also been shown both in vivo and in vitro to directly cause insulin resistance in muscle tissue. Therefore FFA = increased insulin resistance. This is also thought to also occur in the liver causing IR and then dyslipidaemia. Abdominal fat causes FFAs to transport via the portal vein. Under normal conditions insulin produced in B cells is transported via the portal vein to receptors in the liver, in direct response to raised concentrations of glucose, setting in motion two key actions. Insulin firstly inhibits glucose release, and secondly initiates de novo lipogenesis (DNL) responsible for the synthesis of triglycerides and their release into plasma as very low density lipoproteins (VLDL).
In persons with hepatic IR, the insulin pathway for inhibition of gluconeogenesis is impaired resulting in excessive glucose release whilst sensitivity in the DNL pathway is more aggressively enhanced (figure 2) The overstimulation of the DNL pathway increases hepatic lipid storage and increases release of VLDL leading to dyslipidaemia. Persons with MS compensate by hyperinsulinemia, it is mainly genetic but once this system fails. T2DM ensues.
An acid is any substance that?
When added to a solution dissossciates and produces H+ ions.
What is a normal range of PH in blood?
Very narrow - 7.35 - 7.45
Any base is a substance that?
Absorbs H+ ions increasing PH.
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:
- It dissolves directly into blood (5-7%)
- It binds directly to haemoglobin without disassociation into bicarbonate (10%)
- 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.
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 Novel Bicarbonate Generation: The kidneys can directly influence the extracellular pH by eliminating ECF hydrogen ions through their urinary excretion.
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.
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.
What type of drug is amiodarone?
Class III anti-arrhythmic and is a K+ channel blocker.
When is amiodarone indicated?
REFACTORY Ventricular Tachycardia or Ventricular Fibrillation in cardiac arrest (ie, if the patient remains in VT/VF post 3 cycles of CPR/shocks or if the patient has a tendency to revert to VT/VF on repeated conversions). In some cases it has also been used in tachyarrythmias such as AF and SVT.
What is the mechanism of action for amiodarone?
Amiodarone blocks some K+ channels resulting in slowed efflux of K+, thereby prolonging phase III of the cardiac action potential. This leads to slowed repolarisation, increased refractory period and increased QT interval, making it more likely that higher pacemaker cells (outside the ventricles) take over through the interruption of re-entrant tachycardia’s and suppressing ectopic activity.it also has a minor action of blocking Na+ channels, Ca2+ channels and beta receptors, thus slowing HR and conduction through the AV node.
Does amiodarone improve survival?
Amiodarone has been shown to significantly improve the chances of survival to hospital. There is however, no benefit of amiodarone in survival to discharge or neurological outcomes. The ARREST and ALIVE (double blind randomised controlled trials) both concluded that amiodarone had higher rates of survival to hospital admission.
If a patient with chronic AF is on long term amiodarone what does this indicate?
It means they have serious AF, amiodarone is only given long term as a last resort due to serious side effects.
How does amiodarone cause torrsades des pointes?
amiodarone can cause early after depolarisations, which it has been argued can initiate torsades des pointes. An early afterdepolarisation is a situation in which depolarisation occurs a second time within the same action potential cycle. So in a practical sense this means there is depolarisation occuring within phase 2, 3 or 4 within the action potential cycle leading to occillations in the membrane potential
How does amiodarone effect the thyroid with side effects?
14-18% of patients experience amiodarone induced thyrotoxicosis (AIT) or amiodarone induced hypothyroidism (AIH). In AIT type 1 a pre-existing abnormality within the thyroid gland is exacerbated, and the high iodine content of amiodarone results in excessive thyroid hormone synthesis. In the AIT type 2, iodine in excess levels exerts adirect toxic effect on cells within the thyroid, causing them to lyse and release their hormonal contents within the general circulation
Conversely, in AIH there is an autoregulatory response to excessive iodine consumption, in which thyroid hormone production is inhibited in order to prevent thyrotoxicosis. This is called the Wolff-Chaikoffeffect and in some vunerable patients they remain stuck within this cycle unable to reach a homeostatic level of hormone production – resulting inhypothyroidism
What are the 4 H’s?
- Hypoxia
- Hypovolemia
- Hypo/Hyper kalaemia and h+ hydrogen ions
- Hhypothermia
What are the four T’s?
- Toxins
- Tamponade
- Tension Pnemothorax
- Thrombosis.
What changes occur to metabolism during hypoxia?
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).
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).
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
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).
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%.
What are the three classifications of hypothermia?
mild = 35-32°C
Moderate 32°C- 28°C
Severe = <28°C
Hyperkalemia is a serum potassium level above?it causes? How is it detected in ECG?
- 5.5mmol.
Potassium plays a vital role in heart function, particularly in heart rhythm with its involvement in the SA node and influence on diastolic depolarization. In the AV node, the permeability of potassium determines the time required for depolarisation to reach the action potential voltage threshold, once reached the electrical conduction can be transmitted to the ventricles. During the recovery or repolorisation phase, hyperkalaemia can be detected on an ECG through its characteristic ‘peaked T-waves’, often an early sign.
Why does hypokalaemia matter? How is it detected on ECG?
hypokalaemia is a level <3.5mmol/L. It is a less common cause of cardiac arrest; however, decreased extracellular potassium levels can lead to myocardial hyperexcitability potentially leading to the development of re-entrant arrhythmias. The presence of hypokalaemia is noted on an ECG through increased amplitude of the P wave, prolonged PR interval, T wave flattening/inversion and/or ST depression
DRSABCD is now wrong ONLY in traumatic arrest. Explain the new order
DRSCABDED -
D- Danger R - Response S - Send for help C- Circulation (only in traumatic cause - fluid bolus of 20 ml per kilo given because hypovolemia a likely cause) A - Airway B- Breathing D- Disability E - Environment
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.
How does glucose get into cells?
- The insulin binds to a receptor on the membrane
- Signalling cascade within the cell
- GLUT4 glucose transporter penetrates the cell membrane
- Glucose enters the cell.
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.
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.
Why would someone with poorly controlled diabetes have weight loss?
Glucose cant get into cells. So lipolysis occurs (fat burning for ATP) and protein breakdown (muscle tissue). This causes weight loss but paradoxically increased hunger.
Why does polyuria occur?
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)
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 BBB5. 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.
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. 6. Acetone is how ketoacids are broken down. Gives the breath it’s fruity smell.
Insulin resistance in type 2 diabetes is caused by?
Excess adipose tissue, which causes release of adipokines -> then inflammation -> leading to insulin resistance.
Explain how chronic polydipsia and polyuria occur in diabetes 1 and 2. It differs from acute situations.
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)
What is gestational diabetes?
When women have increased BGL during the 3rd trimester. Thought to be related to pregancy hormones effecting insulin receptors.
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.
What happens to the kidneys in diabetes?
Glomerlus damage, and thus glycouria. polyuria, and polydipsia. Nephrotic syndrome can occur resulting in dialysis. Glucose in the urine also provides a suitable environment for bacteria, causing UTIs
What happens to circulation in diabetes?
- Thickening of basement membranes 2. Poor 02 diffusion and therefore tissue hypoxia. 3. Athersclerosis Overall = Poor blood supply and narrowing of vasculature. 4. Poor blood supply + poor nerve function = ULCERS occuring.
What is the difference between a catabolic and anabolic process>
Anabolic - Creates molecules and requires energyCatabolic - Breaks down molecules and produces energy
Glycolysis is?
A catabolic process in which glucose is broken down into pyruvate.
The three main components of stroke volume are?
- 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.
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
Explain dynamic hyperinflation in COPD?
- Remember the lungs want to PULL IN during exhalation and the chest wall wants to PULL OUT. These forces are always in opposition During relaxed tidal breathing, the lungs tend to return to a basal level of inflation, which is termed the functional resid
Explain cushings reflex and cushings triad
Cushings reflex: This reflex is normally from poor perfusion due to increased ICP. It entails a hypothalamic response to brain ischemia -> Causing sympathetic nervous system activation.
This increases peripheral vascular resistance -> BP therefore increases.
Baroreceptors pick up the high BP and a paradoxical vagal-bradycardia is initiated. Cushings reflex leads to Cushings triad
- Hypertension
- Bradycardia
- Irregular respirations (Cheyne-Stokes breathing) OR widened pulse pressure. Cushings triad signals impending danger of brain herniation, and thus, the need for decompression.
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: NoneWRS Width: >120 ms - WIDE
What is agonal breathing?
The last breaths before death. resents in many forms including; irregular breathing, occasional breaths or gasps, laboured or noisy breaths, sighing, gurgling, moaning, groaning or snorting. It has an insufficient tidal volume and should not be considered a sign of life.
What causes agonal breathing?
Agonal breathing occurs due to hypoxia and cerebral ischaemia. It originates from lower brainstem neurons as higher centre become increasingly hypoxic.
Is there any benefit to agonal breathing?
While tidal volume is insufficient, agonal breathing has favourable cardiopulmonary effects. These include; improved pulmonary gas exchange, increased venous return and cardiac output, improved cardiac contractility, increased aortic pressure and increased coronary perfusion.
How does kaussmaul breathing present?
Kussmaul’s breathing – refers to a pattern with regular increased frequency and increased tidal volume and can often be seen to be gasping.
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.
What is cheyne stokes respiration?
Cheyne–Stokes respiration /ˈtʃeɪnˈstoʊks/ 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]
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.
What are the 4 T’s?
- Toxins2. Tension pnemothorax 3. Tamponade 4. Thrombosis.
Explain Toxins, as part of the 4 T’s
. Some of the most common medication overdoses which result in cardiac arrest are tricyclic antidepressants, beta blockers, calcium channel blockers, digoxin and cocaine. Physical signs of a toxin ingestion can include bradycardia, an altered pupil response, and other neurological changes. An ECG sign is a prolonged QT interval. There are many toxins that cause cardiac arrest via many mechanisms. Some cause airway or respiratory compromise, such as sedatives, opioids, or cholinergic agents. Others cause circulatory compromise, such as sodium channel blockers, or Na+/K+ ATPase inhibition (digoxin/oleander). Other drugs illicit CNS depression, seizures or cerebral oedema. Some drugs cause significant systemic and metabolic effects, such as coagulopathy (venom), hypoglycaemia, hypo/hyperkalaemia, and temperature dysregulation.
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.
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).
Signs and symptoms of pneumothorax?
- 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 tachponea5. Decreasing GCS6. Hyperresonance on one side and Raised JVD
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.
What signs might show on an ECG showing an MI?
An ECG reading may indicate ST-segment changes, T-wave inversion and/or Q waves.
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.
What is a peptic ulcer?
Peptic ulcers are local ruptures of the gastric or duodenal mucosa with tissue destruction to at least to the depth of the [muscularis mucosa].Peptic ulcers include (mainly) those in the- stomach- duodenum]- Merkel’s diverticulumPAIN is the most common symptom.BLEEDING and PERFORATION are the most serious complications.
What is the most common cause of upper GI bleeding?
[Peptic ulcer disease] (PUD) is the most common cause of upper GI bleeding. Most ulcers are directly caused by infection with [Helicobacter pylori] (H. pylori) or by non-steroidal anti-inflammatory (NSAIDs), including aspirin, which inhibit prostaglandin synthesis and block normal mucosal defence mechanisms. There is a fair bit of debate happening as to whether or not isolated corticosteroid use can cause ulcers, although the ability of corticosteroids to enhance NSAID-associated ulcers is well established. IDIOPATHIC ulcers are RARE and most are due to false negative H. pylori tests or unrecognised NSAIDs use.
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
What is the prehospital adaption of the SIRS criteria?
- Temp above 38.5 2. HR above 90 BPM 3. RR > 20
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.
What two simple factors determine blood pressure?
Systemic vascular resistance (SVR) and Cardiac Output (CO).
What determines cardiac output? Including it’s subparts.
CO = heart rate x stroke volume Stroke volume is determined by 1. Preload/end diastolic volume (starlings law) 2. Afterload (retrograde pressure of the system -> against ventricular ejection). 3. Sympathetic innervation of the ventricles.
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.
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.
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.
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.
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.
Why are siezures self limiting?
- There is normally a limit to synchronous neuronal discharge. 2. They use up the excitatory neurotransmistters and ionic balance begins to favour GABA again.
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.
Status epilepticus is now defined as a a continuous seizure lasting more than:
5 minutes.
When is neuronal injury typically thought to occur in status epilepticus?
Between 30 - 60 minutes.
Do we give benzodiazepines for a partial siezure?
No - only generalised.
how does midazolam stop a siezure? What are two important side effects and considerations?
- 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).
What is the difference between adrenaline and nor-adrenaline in terms of TYPE?
Adrenaline - Endocrine hormone in PLASMA Nor-Adrenaline - Neurotransmitter
WHat is the diffeence between glycolysis and gluconeogenisis?
Glycolysis is when you take glycogen and turn it into pyruvate. Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. From breakdown of proteins, these substrates include glucogenic amino acids (although not ketogenic amino acids); from breakdown of lipids (such as triglycerides), they include glycerol (although not fatty acids); and from other steps in metabolism they include pyruvate and lactate.
Glucagon increases both?
Gluconeogenesis AND glucolysis.
Why is adrenaline and noradrenaline released in hypoglycaemia?
Adrenaline - Released from the adrenal gland, it has an effect similar to glucagon on the liver (upregulation of glucolysis and gluconeogenesis). It also acts as an ANTAGONIST to insulin on cell membranes, causing LESS glucose to be absorbed cellularly.Noradrenaline - Released from sympathetic pos-ganglionic neurons (stimulated by ACH via preganglionic signal). In conjunction with adrenaline, it produces a SNS sympathetic response that reduces the uptake of glucose by peripheral tissues. It also prompts lipolysis and release of FFAs. This provides a potent alternate energy source and is crucial in correcting hypoglycemic.
What are the symptoms of low BGL?
- Hunger - ACH 2. Nervousness/anxiety/tremor - SNS 3. Sweating - ACH 4. Tachy/palpatations - SNS 5. Pallor - SNS 6. Pupil dilation - SNS
What are the neuro symptoms of low BGL> (caused by poor glucose availabliity and irritable neurons?
ANY stroke like symptoms
WHat are the two types of cells in the heart?
The propagation of the cardiac action potential is reliant on two cell types, the cardiac pacemaker cells and myocytes, each with their distinct action potentials. Existing between both types of neighboring cells are gap junctions, which allow a flow of ions, and precipitating depolarisation between pacemaker cells and contractile myocytes.
Explain cardiac pacemaker cells?
Pacemaker cells are the functional cells of the cardiac conduction system, located in the Sino Atrial node (SA), Atrioventricular node (AV), bundle of His, right and left bundle branches and the Purkinje fibres. These cells are responsible for the creation of a self-initiated, recurrent action potential through their intrinsic properties of automaticity
Explain depolarisation of pacemaker cells?
Phase 4Na+ influx through slow Na+ channels depolarises the pacemaker cell from a -60mV membrane potential. Ca2+ T-type channels open from -55mV.Phase 0When the -40mV threshold is reached L-type Ca2+ gated channels open, allowing for a more rapid Ca2+ influx and depolarisation of the cell membrane to +10mV.Phase 3Ca2+ channels close at 10mV and K+ voltage gated channels open, allowing for an influx of K+ and a repolarisation of the pacemaker cell. The K+ channels then close at -60mV.
Explain the phases of the cardiac MYOCYTE action potential?
Phase 0The propagation of the cardiac action potential is triggered by an adjacent pacemaker cell through a gap junction, leading to an increase in membrane potential from -90mV and the opening of the rapid Sodium (Na+) channels. At -40mV slow Calcium (Ca2+) channels open, instigating a steady Ca2+ influx into the myocyte. This phase results in the depolarisation of the myocyte to +20mV and the closing of rapid Na+ channels. Phase 1Potassium (K+) channels open briefly, accommodating a small K+ outflow to lower the membrane potential to 0mV and slightly repolarising the membrane. Phase 2In this phase, known as the plateau period, is triggered by the influx of Ca2+ into the cell through L-type Ca2+ channels. Meanwhile K+ follows its concentration gradient leaking into the cell via delayed K+ rectifier channels, subsequently maintaining relatively stable membrane potential throughout. Phase 3Commences with the cessation of the Ca2+ by closure of Ca2+ channels. The influx of K+ continues, repolarising the myocytes by decreasing the membrane potential to -90mV. Phase 4K+ delayed rectifier channels close, K+ open rectifier channels open and Na+/K+ ATPase and Ca2+ pumps restoring the resting membrane potential of -90mV.
