PARA226 Notes: Paramedic Theory Medical 2 PDF

PARA226 LECTURE NOTES PARAMEDICAL THEORY MEDICAL 2 WEEK ONE: 12 LEAD ECG OVERVIEW Why do we do a 12 lead: - Aids in diagnosis of cardiac conditions (AMI, pericarditis), metabolic disturbances (hyperkalemia/hypokalemia, hypercalcaemia/hypocalcaemia) & respiratory conditions (pulmonary embolism) Acute/occlusive myocardial infarction treatment: (needs ECG to confirm) - Thrombolysis: breaks up the clot - Percutaneous coronary interventions: procedure in hospitals that have a catheter lab. Activated by paramedics & bypass emergency ward. Antiplatelet & anticoagulant medications are given when planning for a PCI. a wire is inserted through the artery, expanding a balloon, pushing the clot out of the way & leaving a stent which opens a vessel. Who should get a 12 lead: (serial 12 leads need to be done @10/60) - Anyone who is suspected to be experiencing acute coronary syndrome - Nose to navel pain - Syncope - Altered level of consciousness - Shortness of breath - Abnormality noted in rhythm analysis ECG basics: 1. Isoelectric line 2. P wave / SA node firing / atrial depolarisation & contraction (L&R) 3. PR interval / AV node holds conduction 4. QRS complex / conduction through Bundle of His & bundle branches & purkinje / ventricles depolarisation & contraction (atrial repolarisation & relaxation now as well) (R wave = left ventricular contraction & S wave = right ventricular contraction) 5. T wave / ventricles repolarisation & relaxation) In an ECG, the ‘viewing point’ is from the positive electrode in each lead. The waveform shown on the ECG strip may be positive, if the conduction is moving towards the positive (aVF), and may be negative if the conduction is moving away from the positive (aVR) 12 lead layout: Pre analysis SAFE check: - S: speed @ 25mm/sec (small square = 0.04, big square = 0.2 seconds) - A: amplitude (X1.0, 10mm = 1mV) (at bottom of page OR rectangle/box before leads = 2 big squares - F: frequency = 0.05 - 150 Hz - E: electrode placement (R wave direction: lead 1 does not equal aVR. Lead 1 = V6. Wandering baseline: needs a flat isoelectric line = no arcing. Due to movement from patient or cords, pt breathing, poor electrode contact = need to reprint Artefact/interference: due to patient tremors, electrical equipment, mobile phones = remove source if possible & reprint Limb leads: Einthoven's triangle: Limb leads: RA, LA, LL & RL (grounding lead) & looks from a frontal/coronal plane - Lead 1: - RA → + LA - Lead 2: - RA → + LL (main lead, due to proximity & direction) - Lead 3: - LA → + LL These 3 leads are bipolar = positive & negative electrodes Augmented leads make up the remaining 3 leads (aVR, aVL, aVF). These views are unipolar - aVF: midpoint between RA & LA & is - aVF → + LL (positive electrode @ foot) - aVL: midpoint between RA & LL & is - aVL → + LA (positive electrode @ left) - aVR: midpoint between LA & LL & is - aVR → + RA (positive electrode @ right) (as wave of conduction/depolarisation is moving away from RA, the positive electrode, waveforms are usually seen as negative) These leads form a crossover @ Goldberger's central terminal Inferior views: Lead 2, aVF, Lead 3 Lateral views: Lead 1, aVL - Left ventricle is strongest conduction pathway & most concerning part, therefore each 12 lead is looking at the left ventricle (other leads look at other sections) Einthoven's triangle turns into hexaxial reference system: - Angle of each lead stays the same, but relocate to centre point of heart/conduction system - Lead 2 becomes more left & lead 3 becomes slightly more right side of the heart - Lead 1 is slightly lower (inferior) & aVL is slightly upper (superior) on the heart wall Chest leads: Positive electrodes: - V1: 4th intercostal space, right of sternum - V2: 4th intercostal space, left of sternum - V3: mid point between V2 & V4 - V4: 5th intercostal space, mid clavicular line - V5: midpoint between V4 & V6 - V6: level with V4, mid axillary line These leads are as close to the ventricles electrical pathway as possible. Negative point: Wilson's central terminal - Midpoint averaged between 3 active limb lead electrodes - All 6 chest leads (positive) look into WCT (negative) V1 & V2: septal wall (separates R & L sides) V3 & V4: anterior wall V5 & V6: lateral wall (slightly lower on lateral wall than Lead 1 & aVL Extra leads: Right ventricle lead = V4R - Move V4 from left side to right side @ 5th intercostal space, mid clavicular line - Looks on the right hand side of the heart Posterior - V4 → V7 = moved level with V6, between V6 and V8 (left side) - V5 → V8 = moved level with V6, mid scapular line (left side) - V6 → V9 = moved level with V8, left of spine (left side) WEEK TWO: 12 LEAD ISCHEMIC CHANGES Coronary circulation: first vessels to be fed with oxygenated blood from the aorta - In 4% of population, a posterior right coronary artery comes directly off aortic arch & about 70-90% it comes off right coronary artery & 10% where posterior comes off left circumflex artery - SA node, AV node & proximal third of septum are fed by the right coronary artery. - Coronary arteries are perfused during diastole, due to the aorta squeezing during systole, and therefore no time to perfuse the heart in systole. Right coronary artery feeds the inferior portion (in 80% of people), left posterior wall (in 70% of people) & right ventricle Left coronary artery splits into left anterior descending & feeds the septal (lower 2/3 ) and anterior portions, with the left circumflex artery feeding the lateral portion (mainly around the back) Clinical significance: - Anterior wall shows occlusion of the left anterior descending artery (LAD) & is the worst prognosis of all infarct locations, mostly due to larger infarct size. Acute myocardial infarction: 1. Myocardial ischaemia: lack of blood (reversible with reperfusion) 2. Myocardial injury: tissue injury (reversible with reperfusion) 3. Myocardial infarction: tissue death (not reversible) Always starts with ischemia, therefore we look for ischemic changes on a 12 lead ECG. Ischemic changes: - ST elevation: myocardial injury - ST depression: myocardial injury - T wave: hyper acute/inverted = myocardial ischemia/injury - Q wave: pathological = myocardial infarction (work T wave backwards when analysing = progression) Contiguous means sharing a border, or in sequence: - Anatomically next to each other - Lead 3 is contiguous to aVF, aVF is contiguous to lead 2, but lead 3 is NOT contiguous to lead 2 - Limbs leads in frontal/coronal plane, & chest leads in transverse plane, therefore can't know if they are contiguous ST elevation: - ST elevation can indicate myocardial injury presently occurring - ST elevation can have causes other than ACS - When its ACS it's referred to as: STEMI (ST elevated myocardial infarction), STEACS (ST elevated acute coronary syndrome), OMI with ST (occlusive myocardial infarction with ST elevation) ST segment & J point: - J point: where the S wave turns into the ST segment. A change in direction. Where the straight point of the QRS turns into a curve - Track isoelectric line backwards, from line - T - QRS, & count little squares Pathological definition: - > 1mm STE in two or more contiguous limb leads (lead 2 + aVF & aVF & lead 3) - >2 mm STE in two or more contiguous chest leads Pathological definition: (AV & hospitals) STE in two or more contiguous leads, with ST elevation cut off as follows - All leads other than V2 or V3 = >1mm - V2 or V3: > 1.5 mm in women, >2mm in men >40, >2.5mm in men 0.5mm below baseline & pathological if found in two or more contiguous leads - Elevation in leads 2,3 & aVF + depression in leads 1 & aVL - ST depression is a sign of ischemia in the reciprocal leads. Not all leads have reciprocal views and therefore ST depression can show ischemia/injury in areas of the myocardium we cant view. T wave: hyperacute or inversion Hyperacute: very early sign or ischemia leading into injury - >5mm in limb leads - >10mm in chest leads T wave inversion: - Down facing T wave Biphasic T wave: - Up & down facing T wave Pathological Q wave: - Q wave deeper than ⅓ the height of the R wave - Typically indicates previous cardiac tissue death = Q wave is permanent - If new/caught early, can be a sign of injury & corrected Ischemic changes; ST elevation STE in two or more contiguous leads - >1mm in limb leads - >2mm in chest leads STE in two or more contiguous leads: - All leads other than V2 or V3 = >1mm - V2 or V3: > 1.5 mm in women, >2mm in men >40, >2.5mm in men 0.5 mm below baseline in two or more contiguous leads T wave Hyperacute: - >5mm in limb leads - >10mm in chest leads Inverted Q wave Pathological Q wave is deeper than ⅓ the height of the R wave Types of STEMI/STEAC Anterior STEMI/STEAC Variations: - Septal = V1, V2 - Anterior = V3, V4 - Anteroseptal = V1-V4 - Anterolateral = V3-V6, I & aVL (V3, & V4 + any lateral areas) These affect the LAD artery & is the worst prognosis of all infarct locations mostly due to larger infarct size. Interpretation: - ST elevation is maximal in the anteroseptal leads (V2-V4) - ST depression in lead III & aVF, as well as elevation in aVL & lead I - There are hyperacute T waves in V2-V4 - These features indicate an anteroseptal STEMI with some lateral extension Interpretation: - ST elevation in V1-V5, also present in lead I & aVL - Reciprocal ST depression & T wave inversion in lead III - anteroseptal-lateral STEMI (proximal LCA) Interpretation: - Massive ST elevation with ‘tombstone’ morphology is present throughout chest leads (V1-V6) and high lateral leads (Lead I & aVL) - Reciprocal STD in lead II and aVF & III (inferior) - Proximal LAD occlusion, indicating large territory of infarct & likelihood of cardiogenic shock & death Lateral STEMI/STEACS Variations: - Lateral (I, aVL, V5, V6) - High lateral (I, aVL) - Anterolateral (V3-V6) - Inferolateral (III, aVF, II, V5, V6) These affect the left circumflex (LCx) & left anterior descending (LAD) arteries Infarction of the lateral wall usually occurs as part of a larger territory infarction (eg. anterolateral STEACS). Isolated lateral STEACS are less common but may be produced by occlusion of smaller branch arteries that supply the lateral wall. Interpretation: - ST elevation is present in the high lateral leads (I & aVL), with subtle STE in V5&V6 - Reciprocal ST depression in inferior leads (II, III, aVF) with associated STD in V3 (could be a reciprocal change from the posterior wall, option to check V7-V9 for STE) - A high lateral +- posterior STEACS Inferior STEMI/STEACs Variations: - Inferior (II, III, aVF) - Inferolateral (II, II, aVF, V5, V6) * reciprocal ST depression possible in the inferior leads (I, aVL) Affects right coronary artery & left circumflex artery (less common) Can have a more subtle elevation due to further distance from the heart. They generally have a more favourable prognosis than anterior myocardial infarction. - RCA feeds inferior, but also posterior, right ventricle, SA node & AV node & therefore more likely to affect right side of heart = left side (feeds body) & still functions pretty well. - Up to 40% of patients with inferior STEACS will have a concomitant right ventricular infarction. Up to 20% of patients with inferior STEACS will develop significant bradycardia due to 2nd or 3rd degree AV block, with increased in-hospital mortality. - Inferior STEACS may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk. - If there is not enough blood pre filling (preload) the right ventricle, there won't be enough blood pre filling the left ventricle, meaning there won't be enough stretch, and perfusion & CO will drop. Therefore be very cautious with GTN, as GTN drops preload, dropping filling of right ventricle & so on. - Will want to check V4R & posterior leads. Interpretation: - ST elevation in inferior leads (II, III, aVF) - Pathological Q wave in III & aVF (old AMI or longer current AMI) - Reciprocal ST depression and T wave inversion in aVL - Inferior STEMI, do V4R for right ventricular involvement (will want to lower/withhold GTN) Interpretation: - STE inferior leads (II, III, avF) - Hyperacute T waves in inferior leads more than 5mm (II, III, aVF) - Reciprocal change in high lateral (I, aVL) - STD in V2 - option to do posterior (V7-V9) - Bradycardia & greatest STE in III (lead III most on the right may mean right ventricle involvement), = do V4R, high enough it's affected pacemakers (lack/shortened of P waves/PR interval & bradycardia) - Inferior STEMI +- right ventricular involvement & posterior involvement Right ventricular STEMI/STEACS - None of the standard 12 lead ECGs look at the right ventricle, only V4R (anterior, lateral & inferior are talking about the left ventricle) - Right ventricular infarction is a complication i up to 40% of inferior STEACS due to both being fed by RCA (most commonly) - Isolated RV infarction is extremely uncommon - Caution advised when giving GTN to inferior ACS: patients with RVI are very preload sensitive due to poor RV contractility. They may develop severe hypotension in response to nitrates & other preload reducing agents. Interpretation: - STE (II, III, aVF), greatest in III - STE in septal leads. RCA feeds proximal ⅓ of septum, - Reciprocal STD (1 & avL) - V4R STE consistent with RVI - Inferoseptal STEMI with RV involvement Left main coronary artery occlusion (LMCAO) - ST elevation in aVR >1mm suggests an occlusion in the LMCA or proximal LAD - Often associated with global ST depression - LMCA supplies the entire left ventricle & therefore associated with high mortality - STE in aVR isn't always LMCAO (can be triple vessel disease, systemic poor perfusion/hypoxia) Interpretation: - Sinus tachycardia with widespread ST depression (V3-V6, I, II & aVL) - ST elevation in aVR>V1 (likelihood of LMCAO) - Suspected LMCAO (esp with ACS symptoms) Interpretation: - Deep horizontal STD in multiple leads (V4-V6, I & aVL, II, III & aVF) - ST elevation in aVR - Suspected LMCAO (differential diagnosis = rate related hypoxia) WEEK THREE: STEMI MIMICS & OCCLUSIVE PATTERNS STEMI/STEACS mimics: - 50% of ACS will not have STE on the first ECG - 33% of ACS will never show STE - About 50% of STE is not due to ACS You have to be sure your pt is definitely having a STEMI (rule out mimics) due to risk of STEMI drugs & hospital resources. ST elevation can be seen in: - Left ventricular hypertrophy (very large R wave) - Ventricularly generated rhythms (widen QRS & therefore unable to see accurate ST changes) - Left bundle branch block (LBBB) (widen QRS & therefore unable to see accurate ST changes) - Hyperkalaemia - Early repolarisation - Pericarditis Left ventricular hypertrophy: - Most common mimic & caused by an enlarged left ventricle - Makes QRS too high as the larger muscles make larger voltage, QRS remains narrow - V1 S wave + V5 or V6 R wave (biggest) > 35mm (add V1 S + biggest of V5/V6 R wave) - On an ECG the QRS complexes may run into each other in different leads due to their size & is a hint its LVH rather than a STEMI Ventricular rhythms: Its very difficult to determine AMI in the presence of wide QRS complexes - Third degree block (p waves separate from QRS complex) : as long as QRS is wide, its ventricular block & cannot assess for ischemic changes - Ventricular escape rhythm/idioventricular : ischemic changes cannot be assessed (absence of p waves) - Ventricular tachycardia - Ventricularly paced rhythm (two p waves & wide QRS can indicate a dual paced rhythm & cannot assess ischemic changes, if it's only atrially paced there will be one pace peak & narrow QRS) Bundle branch blocks: - Can be pre existing, or caused by an old AMI. 60-70% associated with pump failure & 40-60% mortality without reperfusion The conduction pathway on one bundle branch is blocked, therefore the electrical impulse must find new pathways around the block, leading to ventricular depolarization taking longer & has a delay = wide QRS. - The conduction in the right ventricle is not strong enough for a RBBB to hide ischemic changes or create enough variation in conduction to mimic a STEMI. A LBBB conduction delay is strong enough to hide & mimic a STEMI. Left bundle branch blocks: - In LBBB the block means the RBB depolarises first, meaning the heart depolarises from right to left. - In V1 this means the last wave of the QRS will be in the left ventricle, moving away from V1. Therefore a negative wave in V1 Right bundle branch block - In RBBB the block means the left depolarises first, meaning the heart depolarises left to right. - In V1 this means the last wave of the QRS will be in the right ventricle, moving towards V1. Therefore a positive wave in V1. Method to determine left or right BBB: - Look at V1 & trace backwards alone isoelectric line, skipping T wave. Does the next wave turn left/down or right/up? Left = LBBB, right = RBBB. Often a new LBBB coupled with ACS symptoms is treated the same as a STEMI (due to most common cause being ischemia & its ability to hide normal ischemic changes) A LBBB is new if: - Compare to an old 12L ECG (potentially at a GP clinic, or kept old ambulance ECG) - Patient has no cardiac history (no reason to believe it's an old BBB) - Patient has cardiac history but isn't aware of having a LBBB - Modified sgarbossa criteria: can double check with MICA/cardiologist Interpretation: - Lead II: QRS = wide - P waves present? Yes = BBB, No = ventricular rhythm - BBB in V1 = left = left, right = right. LBBB = can't analyse for ischemic changes - LBBB common morphology will often have downward deflection/STE in V1-2 & then swaps to look like STD in V5-V6 Hyperkalaemia: Normally: majority of potassium is inside the cells (>95%), maintained by the sodium potassium pump & is excreted by the kidneys: Hyperkalemia is where there are high levels of potassium in the extracellular fluid. Reduced ability to excrete K+: - Kidney failure - Medications (NSAIDs, ACE inhibitors, K sparing diuretics, meds that affect aldosterone) - Adrenal diseases (reduced aldosterone level) Transfer of K+ from intracellular to extracellular: - Rhabdomyolysis (crush, burns, infarct of muscle, prolonged seizures = muscle hypoxic - ischemic - damage - release of intracellular substances) - Medications (beta blockers, digoxin = affect NA/K pump) - Low insulin levels (Na/K pump is stimulated by insulin, therefore pump wont work) - Acidosis (high hydrogen ions = low pH, = want to dilute by going into cell & therefore push K out of cell) - Hyperosmotic state (extreme dehydration = water leaves cell = potassium follows) Hyperkalemia can be fatal Normal pump/potential activity 1. Base action membrane potential of - 90mv 2. Na sodium channels open slowly until they reach threshold of - 70mv 3. At threshold, they open rapidly & depolarise, until they reach +30 mv (phase 0) 4. Sodium channels close, fast potassium channels open, allowing potassium to leave the cell, reducing membrane potential (phase 1) 5. Potassium channels slow down, and calcium channels open (entering the cell) which creates a plateau (phase 2) 6. Calcium channels then close, allowing potassium to continue to leave the cell & repolarise, brining membrane potential below threshold (phase 3) 7. Slow potassium channels remain stable (phase 4), allowing potassium to slowly leave cell to keep potential at -90 Hyperkalaemia: - Extra potassium floating around = potassium channels increase = leads to rapid repolarisation & peaked t waves - Phase 3 of repolarisation happens even faster due to more potassium & more potassium channels - Peaked T waves = rapid repolarisation - Diminished P waves = more excitable membrane potential (goes from -90 → -80 /threshold still at -70, but less potential to travel = heart is more excitable, = smaller conduction & smaller P waves - Wide QRS = higher potassium & lower threshold = less activation of sodium channels, resulting in slower, delayed sodium entry = wide QRS - Can become sinusoidal pattern = wide QRS can merge into T waves (last ECG change before fatality) - ECG happens in limb & chest leads (potassium is systemic) ECG changes: - Early hyperkalemia - Peaked T waves : looks like diamond/kite shape - Late hyperkalemia - No p waves, wide QRS & merging Benign early repolarisation (BER): - Usually found in fit people & generally disappears in middle age & rare in the elderly - Elevated J point, often with notching - Predominantly in anterior chest leads (V3 & V4) - Associated with large symmetrical, concordant (same direction as QRS) t waves - Absence of reciprocal changes or pathological Q waves Pericarditis: Inflammation of the pericardial sac & can be viral, bacterial or metabolic - Can occur post MI & post cardiac surgery, as well as IV drug users - High index of suspicion if the patient has had a recent viral or bacterial infection Clinical presentation: - Sharp chest pain, localised, radiated to base of neck & between shoulder blades, pain affected by movement & respiration (lean & lie test, better when lean forward) ECG changes: - Produces PR depression - Diffuse ST elevation (global & in most leads) - Notching at the end of the QRS Other occlusive myocardial infarction patterns: OMI patterns: - Wellens syndrome - De Winter syndrome - NSTEMI/NSTEACS Wellens syndrome: - An ECG abnormality strongly associated with significant left anterior descending coronary artery stenosis - Call for backup, call ahead for clinical or to hospital There are two types: - Symmetric deeply inverted T waves in V2 & V3 - Biphasic T waves in V2 & V3 (less common) De winter syndrome: - ST depression with peaked T waves in chest leads, as well as elevation in aVR - The De Winter pattern in seen of 2% of acute LAD occlusions & is often missed NSTEMI/NSTEACS - Anyone with ACS symptoms and ischaemic changes that don' me t meet STEMI criteria should be assumed as having an NSTEMI - This can only be confirmed with a positive troponin blood test, can be mistaken for angina & often understated as a result. Suspect occlusive myocardial infarction with no STE. Really push & advocate for your patient based on other ischemic signs - Serial 12 lead ECGs should be a priority for dynamic changes/evolving STEMI patterns Percutaneous Coronary Intervention (PCI): - Refers to the whole strategy of taking a patient who presents with a STEMI directly to the cardiac catheterisation lab for mechanical revascularization, balloon angioplasty, stents & other interventions. What do stents do: - They hold the artery open in areas where there is narrowing/atherosclerosis & can be done in an emergency, or planned due to narrowing of artery through plaque formation. - Balloon angioplasties stretch open the artery without a stent, however there is a 30% chance of re narrowing, as opposed to 10-15% with a stent. - They are generally around 15-20mm in length, and 2-5mm in diameter. - Process: a long, hollow tube/catheter is inserted at the wrist or groin & guided via x rays to the narrowed artery. The stent, which is made from metal, is left in place & the procedure usually takes under an hour. - A stent is permanent, with a very small (11 mmol/l. Can be made with one of the tests if they are symptomatic at the same time. Glycated haemoglobin (HbA1c) levels can also be used at any time: >6.5% (48 mmol/l). Glycosylation is the attachment of glucose to proteins. Glucose has attached to the red blood cells, & in hyperglycemic states, this happens more & more. Pre diabetics also have elevated levels of HbA1c, however they don't have the insulin resistance yet. Damage to blood endothelium, kidney damage, nerve damage etc. can be attributed to these levels. Diabetes mellitus: - High levels of glucose cause damage to the body, but starvation of cells (fatigue, thirst, nausea, blurred vision etc.) Diabetes Mellitus Type 1: Characterised by autoimmune destruction of the beta cells in the pancreases which causes an absolute insulin deficiency. Involves destruction of the beta cells in their entirety. Often involves a stressor/cause/trigger. - Highest diagnoses occurs in 10-14 year olds. - As they cannot produce any insulin into cells (due to beta cell destruction), they cannot uptake any glucose into cells, and it is insulin dependent. - Initial presentation: increase thirst, increased urination, weight loss, extreme hunger & fatigue. Often present in DKA state (body goes into own pathway of producing energy to try & raise BGL) Diabetes Mellitus Type 2: Characterised by a relative insulin deficiency and insulin resistance leading to dysregulation of blood glucose levels & hyperglycemia. - Often has a more gradual onset & generally occurs later in life. - Usually due to poor lifestyle factors (diet, obesity, smoking, alcohol consumption), more common in men & ATSI. - High levels of adipose tissue mean even at full production of insulin, levels may not be enough to service all of the cells in the body. Constant need for insulin due to the hyperglycemic environment (constant glucose molecules coming in), leads to insulin receptors losing their sensitivity. Beta cells are extremely sensitive to hyperglycemia & in high glucose states, leads to chronic hyperglycemia, leading to decrease in size & number of beta cells. - Can be managed with dietary changes & oral medications, but can progress to needing insulin. Gestational diabetes: Characterised by an insulin response suppression caused by a hormonal change during pregnancy resulting in a relative insulin resistance and hyperglycemia. - Relative insulin resistance that occurs during pregnancy. During pregnancy we need more hormone levels & in high levels, they can cause insulin resistance, due to the constant hyperglycemia environment. - 60% of gestational diabetes lead to diagnosis of T2DM. - Risk factors: certain ethnicities, pre pregnancy BMI >30, previous hyperglycemia, high maternal age >40, family history of DM, PCOS, use of steroids or antipsychotics, previous macrosomia (large birth weight baby). Hypoglycemic events: Occur due to relative or absolute insulin excess & impaired response to a fall in glucose levels in the plasma. - Incorrect insulin administration - Insufficient exogenous carbohydrate - Increased utilisation of carbohydrate/depletion of hepatic stores - Increased insulin sensitivity - Delayed gastric emptying - Decreased insulin clearance - Eating disorders (anorexia) If the hypoglycaemia state continues/pt continues to fast, adrenomedullary system comes in & will secrete cortisol & adrenaline. Patients with poor diabetic medication/repeated events can be at risk of long term complications including cardiac disease & cerebral/ischemic damage. May consider referring to GP or going to hospital for stricter monitoring/management regime. Treatment: Glucose - Oral (15g, repeat once, max 30) or IV dextrose (10% 15g 150ml, repeat 10% 10g 100ml) - IM glucagon (1 IU): requires the liver to breakdown stores of glycogen into glucose. May not be effective due to poor liver stores. Side effects can also be reported more with glucagon, due to release of catecholamines (decreased metabolism, N&V, tachycardia, hypertension) - If it is secondary to alcohol, the body cannot regulate glucose as the liver is processing the alcohol. No conversion of glycogen into glucose & release of glucose. Alcohol can put diabetics at risk of hypoglycemia. Hyperglycaemic events: Acute state: - Dawn phenomenon: Natural response to get us to wake up in the morning. Before we wake up, the body triggers glycogenolysis & triggers release of insulin for us to wake up. In diabetic patients, the insulin absence just results in hyperglycemia. Low before we wake up & then create sugars to give us energy for the day. - Somogyi effect: Happens in response to too much insulin & occurs as a result of poor management. When blood glucose levels drop, it leads to regulation of counterregulatory hormones, leading to activation of gluconeogenesis & results in hyperglycemia in early morning. Exaggerated dawn, goes too low & then rebounds too high. (often seen with massive hypo in the middle of the night, super sweaty & altered GCS, often found by partner) Constant state: - Common in T2DM Diabetic ketoacidosis (DKA): - Relative or absolute insulin deficiency. - The body thinks there is no glucose in cells due to insulin not being produced to allow glucose to be taken up into cells. Essentially it converts whatever stores it has of glucose into usable forms. In skeletal muscles, protein is broken down into amino acids (proteolysis) & is transported to the liver, triglycerides in adipose tissue are converted into glycerol & free fatty acids (lipolysis). Byproduct of lipolysis is inflammatory cytokines. They get transported to the liver & glycogen is broken down into glucose which can then be used. This compounds the hyperglycemia the individual is suffering with. The blood brain barrier does not require insulin for glucose to diffuse across the membrane = the general body is starving & the brain gets an excess supply of glucose (altered mental status changes in hyperglycemia). Leads to the following → Metabolic acidosis: breaking down of proteins & fats into usable forms produces acetoacetate & beta hydory-buturate (ketones). Differentiating factor of DKA. - In normal metabolism we can use ketones as a source of energy in peripheral tissues, but in the starvation state of DKA, ketones cannot be used. As acid is metabolised, byproducts are produced & accumulate at increased rate in the blood. - Increased ketone production & decreased peripheral cell use = signs of metabolic acidosis. - In pts with DKA this is ketoacidosis. In pts blood, there is a decreasing pH value & other body systems begin to fail, due to narrow window = enzyme efficiency decreases & cell metabolism can’t occur. Body tries to counteract acidosis, occurring in the respiratory system by Kussmaul’s breathing (deep rapid respirations, trying to blow off CO2, byproduct of production of acid), & CO2 gives off fruity breath odour. However Kussmaul's breathing is not isolated to DKA. Osmotic diuresis: when BGL reaches a certain amount, significant amounts of glucose are secreted into urine as an attempt to secrete from the body. However, the glucose molecule creates an osmotic effect drawing water across the semipermeable membrane. When there is excess glucose in the renal tubules, it draws a large amount of water & produces a large amount of urine leading to volume depletion & dehydration. - Polyuria: excessive urination - Polydipsia: excess craving of fluids - Other S&S: N&V (due to dehydration), abdo pain (in kids due to gastric distension), fatigue (cell starvation), weakness, lethargy, confusion, poor skin turgor, dry mucous membranes, tachycardia (to counteract hypotension/dehydration). In worsening cases we see altered mental status. Electrolyte disturbance: - Fatty acids are broken down into Acetyl-CoA, & byproducts of ketones are produced. Ketones collect in large amounts in blood, & as they are such strong organic acids, they need to be buffered. Whilst sodium is typically used as the buffer, where sodium goes, water follows. This draws large amounts of water into renal tubules = excessive urine amount. Large amount of water lost & large amount of electrolytes lost = can present with electrolyte imbalance. - We also get inflammatory cytokine byproducts, which are released into the intestinal lining, causing increased nausea & vomiting, exacerbating dehydration & lethargy. Hyperosmolar hyperglycaemic state (HHS): Essentially the same as DKA without ketogenesis. Same S&S from osmotic diuresis occurs in HHS. Due to hyperglycemia, we get hyperosmolar urine, and water & glucose loss in urine. We also get sodium & potassium following, leading to electrolyte imbalance. Therefore, due to increased thirst & urination, we can see increased dehydration, causing increased HR & BP, and altered mental status. - In HHS insulin is present, effectively there is no lipolysis & no ketoacidosis. - Because pts with HHS still have insulin, just decreased sensitivity, they are still able to suppress lipolysis = smaller increase in counterregulatory hormones & no secondary effects of ketoacidosis. Alcoholic ketoacidosis: Occurs after heavy drinking (1-3 days of ethanol intake & no intake of food/fluids), presenting in a dehydrated state after a lack of volume intake. There are no glycogen stores (due to lack of oral intake, the body has been converting glycogen stores), and it shifts metabolism from carbs to fats, lipids & proteins. Shift to lipolysis increases counterregulatory hormones (adrenaline, cortisol etc.) and increases in digestive enzymes that break down fats. While we break down ethanol, we break it down into Acetyl-CoA which releases ketones. - We have ketone production from lipid metabolism as well as breakdown of ethanol. As keto acids accumulate further, we have worsening dehydration, decreased renal perfusion & removal of keto acids becomes more difficult. - As well, heavy drinkers put themselves at risk of T2DM & therefore could just be a normal presentation of DKA. - S&S: tachycardia, dehydration, tachypnea, abdominal pain (secondary to gastritis or pancreatitis) - Treatment: fluid therapy. They may be at risk of seizures and may require benzodiazepines. Antiemetics can also be given. - Glucose needs to be avoided as they require thiamine prior to glucose administration to avoid Wernicke's encephalopathy. Diabetes Insipidus: - Unrelated to diabetes mellitus, however, does have similar symptoms of dehydration. There is an issue with antidiuretic hormone production, causing issues with fluid retention/depletion. - Central: don't make enough ADH. When you have low fluid volume, hypothalamus releases ADH into the bloodstream, and signals kidneys to conserve fluids. When this does not occur, fluid gets flushed out through urine & leads to dehydration. Can be caused due to damage to hypothalamus, autoimmune disorder or inherited gene mutation. - Nephrogenic: body makes enough ADH, but kidneys are not resulting. Too much fluid flushed = dehydration. Causes can be related to bipolar medications, low levels of potassium, high levels of calcium, blocked urinary tract, gene mutation, rare cases of chronic kidney disease. - Dipsogenic: problem with hypothalamus, causing you to feel thirsty. Intake more fluids & urinate more. Causes can be through damage to the hypothalamus. - Gestational: rare & temporary condition. Occur during pregnancy & mothers placenta makes too much of an enzyme that breaks down ADH. Pregnant with more than 1 baby msy cause more at risk, or individuals with conditions that affect liver function (preeclampsia) Long term complications of diabetes mellitus: - Cardiovascular disease: high glucose levels lead to chronic inflammation = atherosclerosis & fibrous caps/plaques. Excessive sugar can necrotise our tissues, irritation to blood vessels & accompanied with dyslipidemia (high LDLs), causes increase in atherosclerosis (RAAS system involvement, high plaque, = higher risk of strokes, heart attacks & ischemia, conduction abnormalities/arrhythmias) - Nephropathy: mechanisms by which kidney are affected can be multifaceted for acute & long term poor management. Increased proteins & glucose molecules which can damage endothelial lining, as well as continual activation of RAAS system to compensate for fluid loss, and long term implications of hypertension on kidneys. - Retinopathy: inability to metabolise glucose in retinal cells. large blood glucose molecules can damage small vasculature in the body leading to microvascular problems. - Diabetic foot: caused by neuropathy or peripheral artery disease. - Neuropathy: effectively chronic inflammation & stress from cytokines can damage nerves over time, leading to neuropathy. - Also at risk to effects of continual immune system activation. Cells become exhausted & desensitised & effectiveness against invading pathogens are deteriorated. - Free radicals can lead to damage of nerve endings leading to neuropathy & all these problems. Diabetes & hormones: Insulin: - Decreases blood glucose through increased expression of GLUT4, increased expression of glycogen synthase, inactivation of phosphorylase kinase (thus decreasing gluconeogenesis), and decreasing the expression of rate-limiting enzymes involved in gluconeogenesis. Somatostatin: - Decreases blood glucose levels through local suppression of glucagon release and suppression of gastrin and pituitary tropic hormones. This hormone also decreases insulin release; however, its net effect is a decrease in blood glucose levels. Cortisol: - Increases blood glucose levels via the stimulation of gluconeogenesis and through antagonism of insulin. Growth hormone: - Promotes gluconeogenesis, inhibits liver uptake of glucose, stimulates thyroid hormone, inhibits insulin. ACTH: - Stimulates cortisol release from adrenal glands, stimulates the release of fatty acids from adipose tissue, which can then feed into gluconeogenesis. Adrenaline: - Increases blood glucose levels through glycogenolysis (glucose liberation from glycogen) and increased fatty acid release from adipose tissues, which can then be catabolized and enter gluconeogenesis WEEK SIX: RENAL & ELECTROLYTES The urinary system: Consists of: - Two kidneys located in the retroperitoneal cavity, partly protected by the ribs - Two ureters which drain urine from the kidneys into the urinary bladder - Bladder which stores urine - Urethra drains urine from bladder to the external environment/ it has two sphincter muscles to prevent urine loss Nephrons: - Functional units of the kidneys - Approximately 1.25 million nephrons in each kidney - Nephrons can be up to 3 cm long and they extend from the outer cortex down to the inner medulla - Nephrons are intertwined with the kidneys capillaries to allow for exchange of fluid, electrolytes, wastes etc. between the blood & the nephron, where it eventually becomes urine Function of the nephrons: As blood flows through the kidneys, it enters the glomerulus via the afferent arteriole, where pressure forces fluid from the blood into the Bowman's capsule. The fine blood vessels & capillary beds maintain close contact with the nephron & allow for further exchange of fluid & other substances, before it becomes urine. - Exchange includes: H2O, glucose, amino acids, Na+, Cl-, K+, HCO3 - etc. The journey from blood to urine: 1. Glomerular filtration: - Blood plasma is filtered by the glomerulus. Water & solutes from the plasma moves across from the glomerulus to the Bowman's capsule and then into the renal tubules. Blood cells & proteins are too large to pass through the glomerulus so they remain in the blood. Around 20% of cardiac output flows from through the kidneys. - Glomerular filtration rate (GFR) = 125ml/min (180L/day) - Blood plasma → Glomerulus (filtration occurs) → bowman's capsule → renal tubules 2. Reabsorption: - Filtered fluid moves along renal tubules. Reabsorption of useful solutes & water occurs in the PCT (99%) of the filtrate re-enters the blood), and further down the nephron, a fine tuning will occur. This is to ensure that the water & ion concentration remains stable. Water & solutes are reabsorbed back into the blood via the nearby capillaries. - Filtered fluid → renal tubules → PCT (reabsorption occurs) → reabsorbed by nearby capillaries 3. Secretion: - A further movement of the substances from capillaries back into the renal tubules. Body secretes unwanted material (drugs, toxins, waste, ions, excess water). Empties into collecting duct (along with waste from other nephrons) & is excreted in the form of urine - Waste & other materials in capillaries → renal tubule → urine Kidneys: Main functions of the kidneys: 1. Regulates ion concentrations in the blood: Na+, Cl-, K+, Ca+, hydrogenphosphate / HPO4-2 (ensures blood concentration is constant) 2. Regulated blood pH: excretes hydrogen in urine & retains bicarbonate (HCO3-) to reduce acidosis. Excretes HCO3- and retains H- to reduce alkalosis. Aims to maintain an arterial pH of 7.35-7.45 (& venous pH of 6.32-7.42) 3. Regulates blood volume: Through conserving or eliminating water in the urine 4. Regulates blood pressure: adjusting blood volume by increasing/decreasing water secretion in urine (through aldosterone & antidiuretic hormone/ADH). Releases the enzyme renin to activate the renin-angiotensin-aldosterone system to regulate BP. (increasing sodium reabsorption & potassium excretion, leading to increases water retention/reabsorption, leading to increased blood volume, as well as increasing vascular tone = increased BP) 5. Maintains blood osmolarity; regulates water & solutes in the urine, maintaining a relatively constant blood osmolarity at approximately 290 mOsm/L. 6. Hormone production: Calritrol: an active form of vitamin D which is essential for Ca2+ uptake from the GI tract, kidneys, release of Ca2+ from bone & increases blood Ca2+. Erythropoietin (EPO): stimulates the production of RBCs in the bone marrow. 7. Excretes waste & foreign substances: Removal through urine including ammonia, urea, bilirubin, creatinine, urea acid & toxins/chemicals from the diet or drugs. 8. Regulates blood glucose level: the kidneys remove excess glucose to help maintain normal blood glucose. The urinary system overview: - Main organs involved are the kidneys & major role is in waste excretion. Solid waste from the blood leaves our body as urine, as well as regulating blood volume, blood pressure, blood ph & electrolytes etc. - Kidney produces urine, which is transported through the ureters to the bladder, where it is stored & conducted into the environment via the urethra. - Urine is 95% water, with the rest waste (both organic & inorganic) - Kidney anatomy: renal cortex → renal medulla → renal pelvis (hollow opening where nephrons enter & rid urine). Kidney is filled with blood vessels, with 20% of cardiac output going through the kidneys (comes in via renal artery & out via renal vein). Waste excretion occurs in centre blood vessels. - Blood flows into nephron through afferent arteriole → glomerular capillaries → bowman's capsule (filtration of blood plasma) → peritubular capillaries (secretion & reabsorption) - Nephron anatomy: renal corpuscle (filtration occurs) then filtrate travels to proximal convoluted tubule (PCT, where water & solutes are reabsorbed back into circulatory system) → loop of henle (renal medulla) (descending limb reabsorbs a lot of water, ascending limb reabsorbs sodium & chloride) (increasing salt levels as you move further down into renal medulla making it easier to reabsorbs water) → distal convoluted tubule & collecting duct (secretion & reabsorption of solutes & water, under hormone control/ADH) → into renal pelvis → leaves as urine through ureter to bladder Controls of glomerular filtration: Regulation of glomerular filtration (determined by renal blood flow) is mainly accomplished by increasing or decreasing arteriolar resistance. Processes: Autoregulation: the ability of the blood vessels to modify their own resistance in response to changes in systemic blood pressure - Autoregualtoin of pressure by the kidneys (effective when systemic BP is between 80-180mmHg) - Decreased renal blood pressure is detected in baroreceptors and dilates or constricts the afferent or efferent blood vessels. This prevents fluctuations in systemic arterial pressure from transmitting to the glomerular capillaries & aims to maintain a constant filtration pressure & GFR - When BP increases = constriction of afferent arterioles reduces blood flow to capillaries & glomerulus. Constriction = increased resistance = decreased blood flow - When BP decreases = dilation of afferent arterioles (& constriction of efferent arterioles) increases blood flow to capillary & glomerulus. Dilation = decreased resistance = increased blood flow Hormonal: the renin-angiotensin-aldosterone system (RAAS) and natriuretic peptides - Natriuretic peptides are produced in the heart in response to high pressures being detected in the atria & ventricles. These hormones then act to dilate the afferent arterioles, increase Na+ excretion (as well as water), and cause a reduced blood volume, hence reducing systemic BP. - RAAS: important part in regulating blood volume & blood pressure. It is activated when blood pressure and/or fluid volume decreases. - It is triggered by 3 mechanisms: 1. in response to sympathetic nervous system activation, 2. in response to decreased blood pressure, 3. in response to decreased sodium & chloride. - In response to this trigger, renin is produced & released from cells near the glomerulus, which results in the conversion of angiotensinogen to angiotensin 1. Angiotensin 1 is then converted to angiotensin 2 by ACE, which is primarily found in the lungs. - Angiotensin 2 then acts to: - Increase BP by stimulating vascular smooth muscle cells, causing vasoconstriction - Stimulates secretion of aldosterone from adrenal gland, which is responsible for stimulating Na+ reabsorption & water retention (increase blood volume) - Increased antidiuretic hormone (vasopressin) which further increases fluid retention & vasoconstriction RAAS: hypotension = release of renin = conversion of angiotensinogen to angiotensin 1 = angiotensin 1 converted to angiotensin 2 by ACE = vasoconstriction + release of aldosterone & AHD = sodium reabsorption, water retention & vasoconstriction = increase in BP Autonomic: sympathetic nervous system control - Increase or decrease in the release of adrenaline causes changes in the lumen of arterioles in response to fluctuations in systemic BP affecting GFR ? RAAS summary: - Decreased BP → changes receptive by kidneys → activation of RAAS - Kidneys are supplied by renal arteries, with blood reaching glomerulus through afferent arterioles & leaving through efferent arterioles (juxtaglomerular cells) - Secrete prorenin. Hypotension is the main stimulator for converting prorenin to renin. Renin acts on angiotensinogen (plasma protein which is synthesis in the liver), and converts it to angiotensin 1. In the lungs, ACE converts angiotensin 1 into angiotensin 2. - Angiotensin 2 is a powerful vasoconstrictor & mediated effects of RAAS. - Angiotensin 2 effects on blood vessels (very rapid changes/in minutes): Vasoconstriction of arteries (increase in total peripheral resistance) & veins (increased venous return), which increase blood pressure. - Angiotensin 2 effects on the kidneys (slower changes/few days): Direct mechanism (GFR is relevant to blood flow to the kidneys). Angiotensin 2 constricts afferent arterioles, reducing blood flow to the kidneys, resulting in decreased GFR, decreasing urine output. Indirect effect: angiotensin 2 acts on adrenal gland, releasing aldosterone, increased sodium & water reabsorption. Overall, decreased urine output, with increased sodium & water reabsorption = increased extracellular fluid volume, and increased capillary & arterial pressure GFR & Tmax: Glomerular filtration rate is an indication of renal function. It is referred to the volume of plasma filtered per minute in the glomeruli of the kidneys (the amount of filtrate two kidneys produce each minute) Adult human GFR is approximately 120-125ml/min, filtering approximately 180 L/day of plasma. GFR depends on 3 factors: - Net filtration pressure - Total surface area available for filtration - Filtration membrane permeability Two common tests are used to assess GFR - Creatinine clearance in 24 hour urine collection (complex formula based on body surface areas) - Creatinine levels in blood (male 60-100 Ummol/L, female 45-90 Ummol/L) Creatinine is produced by the muscles at a constant rate & cleared at a constant rate. This rate of excretion by the kidneys, is a good indicator of GFR. It can also be used to monitor the progression of chronic kidney disease (CKD), the response to treatment or to help decide when to start dialysis in patients with declining renal function. Transport maximum (Tmax): - The among of solute (eg. glucose) which can be reabsorbed from the filtrate into the blood. When the Tmax is exceeded, the solute appears in urine (eg. glycosuria) Renal threshold: - It is the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine. TUTORIAL WORK: THIAZIDE DIURETICS: MOA: - inhibits sodium transport in distal convoluted tubule, with secondary effects as well, working to inhibit reabsorption, increasing amount excreted - Have less of an effect than loop diuretics, as distal convoluted tubule is responsible for a smaller amount of reabsorption Adverse effects: - Hypokalemia: due to aldosterone mediated actions of sodium potassium pump & K excretion - Hyponatremia: decreased sodium reabsorption & fluid reabsorption = decreases circulating levels of sodium - Metabolic alkalosis: hypokalemia metabolic alkalosis due to increase in K & H ions excreted - Hyperglycemia: hypokalemia causes hyperpolarization of beta cells which decreases insulin secretion. Potassium depletion is responsible for decreased insulin secretion or sensitivity (potassium dependent insulin release) - Hypercalcaemia: increasing calcium reabsorption from membrane, thiazides reduce urine calcium levels & increase blood calcium. Can be beneficial for reducing kidney stones & increasing bone health Indications: - Hypertension: Treat hypertension through lowering arterial pressure, reducing cardiac output by reducing extracellular fluid and plasma volume (due to sodium depletion), as well as vasodilation. They have more antihypertensive effects that loop diuretics & are recommended as one of the first line treatments alongside ACE inhibitors, and angiotensin 2 receptor blockers. - Occasionally in fluid overload pts. Brand names: - Diuril, Esidrex, Oretic, Dithiazide, Apo-hydro, LOOP DIURETICS: MOA: - Reduced sodium chloride absorption in ascending loop of henle by inhibiting sodium potassium chloride transporter = no reabsorption of these = water follows Common names: - Lasix & furosemide, POTASSIUM SPARING: MOA: - Blocks sodium potassium exchange pumps, allowing more sodium into filtrate, but also removes potassium & puts it back in the blood. It is an aldosterone antagonist Common names: - Sprinolactone Renal & electrolytes pathophysiology: Renal stones/calculi: - Nephrolithiasis / renal calculi - Common age: 20-55 years - Location: anywhere in the urinary tract. Formed in the nephrons & then travel anywhere distally. - Crystals are formed in presence of organic/inorganic solutes. When they become saturated in solute, they form crystals & become bigger, eventually getting stuck on skin cells, or travel through the urinary system & become physically obstructed due to size. - Most common is the calcium stone (75%). Risk factors: - Warm climates, decreased fluid intake (less fluid = greater concentration of solutes) - Calcium supplements - High protein diets (protein shakes/supplements. Breakdown of protein leads to uric acid & can lead to uric acid stones) - UTI (change pH in filtrate & urine) - Gout (condition which leads to excess uric acid in bloodstream) - Hyperparathyroidism (more calcium in urine & filtrate) - Family history Impact on glomerular filtration: - Stone may cause an obstruction, resulting in increased pressure above the obstruction. Pressure opposes glomerular filtration pressure (increases pressure in glomerulus & changes dynamic between glomerulus & Bowman's capsule, changing how fluid moves from the blood to the kidneys) & prolonged obstruction can result in permanent damage to the urinary system. Signs & symptoms: - Depends on size & location - Renal colic: intermittent unbearable pain associated with stone movement. Pain goes & goes, as it is associated with spasms of the ureter. - Unable to stay still - Haematuria - Pain is accompanied by nausea, vomiting, diaphoresis, haematuria, tachycardia & tachypnoea - May fine relief while passing urine. - Obstruction of the urethra often presents with urinary symptoms such as dysuria, frequency & urgency. May present similarly to a UTI. Treatment: - Most stones are passed unaided - Increased size = decreased likelihood of passing - Some stones are too large (>5mm) to pass & require intervention: Lithotripsy (shock wave therapy, waves break up stones & small parts can pass normally), percutaneous nephrolithotomy (endoscopic instrument to remove stone), surgery Urinary tract infection: Risk factors: - Age (more vulnerable: more suppressed immune system, can't completely enter bladder on urination = greater risk of bacteria entering) - Female (length of the urethra) - Congenital abnormalities - History of UTIs (increase recurrence rate) - Diabetes (at risk of neuropathy, causing stasis or inadequate emptying of bladder = increased risk of bacteria entering) - Obesity (greater risk of bacteria, due to inability to or lack of cleaning) - Poor hygiene (greater risk of bacteria, due to inability to or lack of cleaning - Recent sexual intercourse Signs & symptoms: - Fever, chills, dysuria, burning, abdominal pain, increased frequency & urgency, haematuria. Can lead to pyelonephritis & sepsis. - Pyelenepthrits (kidney infection): above symptoms, plus fever, nausea & vomiting. Can lead to permanent renal damage, scarring & repeat infection. Usually travels up to only one kidney. - Diagnosis: history, presenting symptoms, urinalysis, blood cultures, FBC & urine cultures - Beware of urosepsis. Acute urinary retention: - Most common urological emergency Three key, often overlapping pathophysiological mechanisms: - Obstruction in outflow - Neurologic impairment (problems with nerves innervating urinary system = inadequate emptying) - Over distension (causes retention & can't release spontaneously) Causes may include: - Benign prostatic hyperplasia, constipation, prostate cancer, urethral stricture, postoperative, neurological disorder, medications, urolithiasis etc. - Most commonly seen in older males. Treatment: - Urinary catheter, urine specimen analysis, determine & manage the underlying cause, may require suprapubic catheter (increases risk of developing urinary infection), surgery Acute kidney injury (AKI): Abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume & electrolytes - An abrupt reduction in renal function, generally sudden onset. - In increase in serum creatinine - Decrease in GFR resulting in increased creatinine - Potentially reversible if diagnosed and treated early - Associated with oliguria (decreased output) Causes may include: - Tubular necrosis, autoimmune disease, blood clots, decreased blood flow to kidneys or decrease in blood pressure (haemorrhage, shock, sepsis, burns, etc.) Acute kidney/renal failure (AKF/ARF): - Failure implies death unless there is an intervention Renal function is inadequate to clear the waste product of metabolism despite the absence or correction of haemodynamic or mechanical causes. Usually requires renal replacement therapy. (patient requires dialysis) RIFLE: - Risk: increased creatinine X1.5 & urine output (UO) decreased for 6 hours - Injury: increased creatinine x 2, UO decreased x12 hours - Failure: increased creatinine X3, UO decreased X24 hours, or anuria x12 hours - Loss: persistent acute renal failure = complete loss of renal function >4 weeks - ESRD: end stage renal disease. Loss of kidney function >3 months, irreversible. Glomerular filtration rate: - The calculation of the rate at which the kidneys filter the blood, removing excess wastes & fluids. - Direct representation of how well the kidneys are functioning & whether they are filtrating st an appropriate rate (balance of pressure, balance of ions are all right) - Calculating creatinine clearance to determine estimate GFR - Creatinine is developed in the metabolism of cells (usually muscle cells), and is normally excreted freely in the urine. It is excreted at an expected & predictable rate. If GFR slows, creatinine levels in blood start to build up. - At 120 ml/min GFR, creatinine should be close to 0. GFR has to be reduced to around 30 ml/min to see a sharp increase in creatinine levels. Incidence: - AKI 5-20% of all hospital admissions - 35-65% of all ICU admissions - 2-5 times higher risk of death if you have AKI Risk factors for ARF: - Older age (more nephrons worn out, more susceptible to kidney problems) - Diabetes mellitus (higher levels of glucose in blood, directly damaging nephrons) - Heart failure (reduced blood flow & decreased perfusion of kidneys) - Hypertension (too much pressure can cause injury) - Liver failure (50% present with kidney failure, impaired production of urea, change in intrathoracic pressures, changes in blood supply & volume to kidneys) - Nephrotoxic drugs (directly cause injury) - Rhabdomyolysis (condition in which proteins/muscle cells breakdown, generate myoglobin which is damaging to the kidneys) - Long term anticoagulant use (change interaction between kidneys & filtration) - Intrabdominal hypertension (greater pressure going into kidneys & changed balance - Radiocontrast dyes & some antibiotics (nephrotoxic) Risk populations: - Older adults, critically ill patients, ICU patients, Indigenous Australians, pts with chronic illnesses Aetiology: Pre-renal: - Sudden or severe reduction of blood flow (mass haemorrhage, sepsis, dehydration etc), decrease in pressure causes injury. Comes from a site before the kidney. - Most common, 70% of causes. - Hypotension, hypovolemia, renovascular disease, hepatorenal syndrome, vasoactive toxins, rhabdomyolysis. Intra-renal: - Cause injury within the kidneys. Medications or nephrotoxic drugs, acute tubular necrosis, prolonged ischemia Loss of nephrons is irreversible. - Glomerular disease (diabetes, hypertension, drugs/toxins). Tubular disease (rhabdomyolysis, trauma, infection, drugs, toxins). Trauma. - Common nephrotoxins: Allopurinol, aminoglycosides, amphotericin, furosemide, herbal medicines, heavy metals, NSAIDs, organic solvents, paraquat, pentamine, IV contrast, sulfonamides, thiazides - nephrotoxic agents cause vasoconstriction, direct damage to tubular cells & intratubular obstructions. Post-renal: - Obstruction after kidneys in ureter or bladder. Kidney stones, prostate problems, urine retention, UTI. obstruction to outflow of urine & pressure balance becomes off, causing injury. - Uretic, bladder or urethral obstruction, trauma, infection, tumour, abdominal compartment syndrome. Acute tubular necrosis: Most common cause of AKI - A sudden decline in GFR. inability of the kidney to regulate the balance of sodium, electrolytes, acid & water. Accumulation of nitrogenous wastes in blood (rhabdomyolysis). - Urinalysis can show granular casts (dead tubule cells) - Oliguria is most common sign Causes: - Myoglobin: travelled into urine & damaging due to size & shape, as well as byproducts - Haemoglobin: travelled into urine & damaging due to size & shape, as well as byproducts - Heavy metals: directly nephrotic - Nephrotoxic drugs: nephrotoxic agents cause vasoconstriction, direct damage to tubular cells & intratubular obstructions. Chronic kidney disease: Chronic kidney disease (CKD/CRD) - Stage 1, 2, 3, 4, End stage kidney disease (ESKD/ESRD) - Stage 5 disease Chronic kidney disease is the presence of damage or decreased kidney function for three or more months irrespective of cause. - Time differentiates from acute & chronic - Acute injury can lead to chronic disease - Failure means that chronic intervention is required (dialysis) CKD defined as estimated GFR (eGFR) 24 hours apart, OR one unprovoked seizure and a high probability of further seizures. Can be considered resolved if there is an age dependent diagnoses/component & they have passed that age OR they have remained seizure free for the past 10 years with no seizure medications for the last 5 years. Acute symptomatic seizure; - Seizure occurring at the time of, or in close temporal relationship with, a central nervous system or systemic insult. Also known as reactive or provoked seizure. Seizures are a symptom of another event. Aetiology: - Cerebrovascular, trauma, CNS infection, withdrawal, metabolic, toxic, other - In >65 YO, cerebrovascular disease, such as strokes cause ⅔ of seizures - Cerebrovascular disease: ischemia & hemorrhagic CVA/stroke, cerebral venous thrombosis, vascular malformation. - CNS infection: meningitis, encephalitis, cerebral malaria - Head injury: subdural haematoma, penetrating head injury, concussion, neurosurgery - Alcohol & medication withdrawal; suspected in pt with chronic abuse & occurs in 7-48 hours after last dose/drink - Metabolic: hypo/hyperglycaemia, hypo/hypernatremia, hypocalcaemia - Toxic: cocaine, antidepressants, antipsychotics, antihistamines, analgesics, alcohol intoxication (more common in overdose) - Other: eclampsia, febrile seizures, cerebral hypoxia Unprovoked seizure; - Occur in the absence of any precipitating factors or conditions. It is an inaccurate term as there are epileptic seizures that can be brought on by certain things such as light flashing lights or sleep deprivation, however it is not the sole precipitant. Epilepsy aetiology: - Genetic, structural, infectious, metabolic, immune, other - Genetic: a chromosomal or genetic abnormality (epilepsy from birth/young age) - Metabolic: genetic metabolic disorders eg. cerebral folate deficiency (epilepsy from birth/young age) - Immune; immune response causing central nervous system inflammation & is different from infectious, due to it antibody mediated. - Infectious: meningitis, encephalitis, cerebral malaria - Structural: CVA/stroke, TBI, tumours, vascular malformations, scarring from cerebral hypoxia Classification: - Created by the International League Against Epilepsy (ILAE) - Used to facilitate communication in clinical care, research & teaching Focal onset: unilateral, limited to one hemisphere at onset - Can be more discrete (more localised/unifocal) or more widely distributed & multifocal/hemispheric - Aware: the patient is fully aware of themselves & their environment throughout the entirety of the seizure - Impaired awareness: if awareness is impaired at ANY point throughout seizure - Motor: any ipsilateral tonus or clonus present (one side of the body) - Non motor:no motor activity, instead would present with sensory, cognitive, autonomic, emotional or behavioural arrest. - Interventions are required more heavily if the individual has impaired awareness at any point. - Jacksonian March: a focal motor seizure that has an orderly progression of seizure activity from the distal part of the limb toward the body, due to distribution of the anatomical areas in the primary motor cortex. Generalised onset: originating at one point then very rapidly progresses to bilateral involvement - Awareness is not used as classifies for generalised seizures as the vast majority have impaired awareness - Motor: For generalised motor seizures, motor activity will be bilateral from the onset - Specific descriptions of motor activity can described, but not required - Absent/non motor: present with sudden cessation of awareness and activity, tending to occur in younger patients & have a sudden start & stop. Usually display some automatic, non purposeful movements (lip smacking, hand movements) Focal to bilateral tonic clonic; - Starts unilaterally & then progresses to bilateral tonic-clonic movements Unknown onset: unknown if focal or generalised at onset - Onset of the seizure wasn't witnessed however further description explanation may be offered Unclassified: unwitnessed/all elements unknown - Nothing is known about the seizure, or it doesn't fit any of the other categories. Status epilepticus; Epidemiologically defined as: - A prolonged seizure >30 mins duration, OR - A series of seizures during which function is not regained between ictal events in a 30 minute period Clinically defined as: - >5 minutes of continuous seizure, OR - >2 discrete seizures between which there is incomplete recovery of consciousness Status epilepticus is a life threatening emergency requiring immediate intervention with a mortality rate up to 20%. - Excitotoxicity & hypoxia are thought to the two main elements behind its fatality - Excitotoxicity: excessive exposure to the neurotransmitter glutamate ot overstimulation of its membrane receptors, leading to neuronal injury or death - Increased duration of status epilepticus worsens the prognosis, with neuronal injury becoming irreversible after around 30 mins - Refractory status epilepticus: when the seizure continues post benzodiazepine administration Assessment: Questions for the witness: - Description of the event & onset? - How long did their seizure last? - For generalised or focal impaired awareness seizures, the patient wont remember the details & will initially be confused in their post-ictal state. Questions for patient; - Any symptoms leading up to the seizure? Any prodromal symptoms, causes, triggers? - Was there an aura? Funny sensation prior? - Personal or family history of seizures? - Compliance with anti-seizure medication? - Triggers? Exhaustion, overstimulation, concomitant illness? - History of multiple seizures? Physical examination - Head trauma - Oral trauma eg. tongue biting - Incontinence - Fever/stiff neck (meningism) - Focal neurological deficits eg. altered sensation or motor weaknesses & what came first - Injuries / broken bones from contractions Differential diagnoses: - Syncope: cardiac, vasovagal, orthostatic - Psychological: dissociative states, psychogenic non-epileptic seizures, panic attacks - Migraines: visual auras, hemiplegia, vertigo - Paroxysmal movement disorders: tics, tourettes - Sleep disorders: narcolepsy - Metabolic conditions: hypo/hyperglycaemic, hyponatremia, hypocalcaemia, hypomagnesemia, hyperthyroidism - Vascular conditions - Gastrointestinal conditions: esophageal reflux in neonates & infants - Traumatic: subdural hematoma, subarachnoid haemorrhage, TBI, brain abscess, meningitis, encephalitis Treatment: - First aid: recovery/side position, loosen clothing, avoid oral, - Protect the body during ictus - Airway patency: consider trismus, suction, NPA, oxygen - Benzodiazepines as required (midazolam IM 10mg, repeat once @5/60 if required) - The ILAE recommends pharmacological interventions should begin at the 5 minute mark - IV access if possible - MICA (IV midazolam, ETT) Treat & refer: If this is a typical, self limiting seizure and the patient has returned to normal baseline level of awareness, consider treat & refer if they are able to be monitored by a responsible adult. Do not proceed if: - Patient requires further in-hospital assessment/treatment (incomplete recovery, non epileptic cause, no diagnosis/first presentation, concurrent illness, midazolam administration, different to usual presentation) - Seizure was unwitnessed - Risk of recurrent seizure (history of multiple seizures, feeling of impending seizure, unable to be monitored by adult) - Pregnancy - Patient requests transport Strokes: Includes a group of disorders involving a sudden, focal interruption of cerebral blood flow that causes neurologic deficit. This interruption can be caused by a blockage (ischemic) or from a bleed (haemorrhagic). Neurological deficits can vary depending on which cerebral artery is affected and the area of the brain that artery supplies. Risk factors: - Age: ⅔ of strokes occur in >65 group & is 3x higher again in >85 - 1.4 times higher in males - Higher rates in the indigenous population - Tobacco smoking - Hypertension - Dyslipidemia - Previous transient ischemic attack - Atrial fibrillation - Diabetes Anatomy review: The blood vessels supplying the brain are two internal carotid arteries & two vertebral arteries - The carotid arteries contribute 80% of total cerebral blood flow Anterior circulation: - Anterior cerebral artery, middle cerebral artery & internal carotid arteries - Anterior cerebral artery: controls motor & sensory of trunk, hips, legs & genitals. - Middle cerebral artery: motor & sensory of hands, shoulders, arms, eyes, face, tongue as well as speech areas; Broca’s (expressive speech/output of speech = aphasia/dysphasia) & Wernicke’s (receptive speech/understanding = comprehension of own & others speech) Posterior circulation: - Posterior cerebral artery & basilar artery (fed by vertebral arteries) - Posterior cerebral artery: visual cortex - Basilar artery: feeds cerebellum, controlling balance, and brain stem, controlling crucial functions - Vertebral arteries; feeds both posterior & basilar regions Ischemic strokes: An episode of neurological dysfunction caused by a focal CNS infarction - 87% of all strokes - Penumbra: the infarcted portion is known as the core or umbra. The surrounding area that is hypo-perfused and ischemic is known as the penumbra (the salvageable portion). Approximately 1.9 million neurons die per minute in hypo-perfused ischemic penumbra. Small vessel occlusion: Occlusion of the small cerebral arteries that supply the deeper structures of the brain (¼ ischemic strokes) - Predominantly caused by vascular pathologies: - Thickening of the artery walls & hypertrophy of the smooth muscle, narrowing the vessel - Atheroma & stenosis - Can technically be caused by an emboli, but is uncommon - Smaller vessels mean smaller infarcted core, however can still be fatal - S&S; - Hemiparesis: one sided weakness - Dysarthria: difficulty speaking with motor function - Altered sensation - Ataxia: discoordinated movements & trouble walking - Combination of sensory & motor Can be treated with thrombolysis, but efficacy depends on mechanisms behind the stroke Large vessel occlusion: (LVO) Occlusion of any of the large cerebral arteries/intracranial vessels, including the basilar artery (BA), the internal carotid artery (ICA) and the middle cerebral artery (MCA). Approximately 50% of ischemic strokes - Some definitions included posterior cerebral artery (PCA), anterior cerebral artery (ACA), and vertebral artery (VA). - Around 80% of LVOs affect anterior circulation - Causes include: - Primary atherosclerosis - Extracranial artery atherosclerotic embolism: atherosclerosis that shoots off an embolism, primarily in the lower arteries - Cardioembolic events (atrial fibrillation): valvular disease, embolism from aorta - Cryptogenic (unknown) - Disproportionate contributor to mortality & morbidity. LVOs are responsible for 60% of post ischemic stroke dependence & death & 90% of post ischemic stroke mortality Can be treated with thrombolysis or endovascular clot retrieval (ECR) Anterior circulation strokes Posterior circulation strokes 75-80% of strokes 20-25% of strokes 91% FAST positive 60% FAST positive (more challenging to diagnose & more often missed) Common symptoms: Common symptoms: - Hemiparesis/hemiplegia (one side) - Vertigo - Altered conscious state - Headache - Ipsilateral sensory deficit (same side) - Ataxia - Facial palsy - Hemiparesis - Dysarthria - Blurred vision - Dysarthria Sensitive symptoms: specific to anterior Sensitive symptoms: specific to posterior - Aphasia (associated with eyes) - Gaze palsy - Nystagmus - Hemi-environmental neglect (usually - Oculomotor palsy left) - Horner's syndrome: drooping eyelid, miosis, facial anhidrosis - Diplopia - Quadrantanopia: quarter field vision loss Transient Ischemic attacks (TIAs): Transient episode of neurological dysfunction caused by a focal brain, spinal cord or retinal ischemia, without acute infarction - Stroke symptoms - Sudden onset - Typically only lasts minutes, but can last hours - Post TIA, the risk of stroke within 3 months has been reported to be around 20%, with 50% of those within 2 days All potential TIA patients must be transported to hospital. TIAs can't be diagnoses prehospitally, imaging is still required, and early intervention reduces the risk of stroke by 80% Haemorrhagic stroke: An episode of focal neurological dysfunction caused by a focal collection of blood in the CNS that is not caused by trauma - 13% of all strokes - Poor morbidity & mortality (30 day mortality rate = 35-52%) Intracerebral haemorrhage: A focal collection of blood within the brain parenchyma or ventricular system - A bleed that it is the cerebrum area - ⅔ of hemorrhagic strokes - Substantial displacement of the brain parenchyma may cause elevation of ICP and potentially fatal herniation syndromes. The buildup of blood can push the brain across. - 50% will have an altered GCS, with overt GCS = worse outcome predictor - 50-70% wil have a headache & 6-7% will have seizures - Causes can include: - Chronic hypertension: puts pressure on vascular system & causes aneurysms which can burst - Cerebral amyloid angiopathy: condition where amyloid (protein) builds up on the walls of the arteries in the brain, which weakens the walls & makes them more susceptible to breaking - Anticoagulation medications - Vascular malformations - Secondary to ischemic strokes - Can be a gradual or sudden onset, depending on specific mechanisms/cause - S&S: depend on location of the bleed - Headache, nausea, vomiting, altered conscious levels, weakness or numbness, vision loss, seizures Subarachnoid haemorrhage: Bleeding into the subarachnoid space (the area between the arachnoid membrane and the pia mater of the brain or spinal cord) - ⅓ of haemorrhagic strokes - Patient typically presents with thunderclap headache, usually the worst headache of their lives & is often associated with photophobia & nuchal rigidity (blood surrounds brain & spinal cord, mimicking meningitis) - Almost 50% present with profound loss of conscious - Focal neurological deficits often present either at the same time as the headache or soon after - Causes include: - 85% due to aneurysm rupture (berry aneurysms) - 15% varied causes: include vascular malformations Treatment can include conservative treatment including BP & ICP control or neurosurgical decompression **ischemic strokes block a specific & localised portion of the brain, whereas a haemorrhagic stroke presents more with global symptoms due to the pressure build up of the blood on the brain (global symptoms & altered conscious / < GCS 8) Assessments: Stroke screening tools: - Face arm speech time/test (FAST) (public predictor for ischemic strokes) - National institutes of health stroke scale 8 (NIHSS-8) - Melbourne/metropolitan ambulance stroke screen (MASS) - HUNTER 8 - Field assessment stroke triage for emergency destination (FAST-ED) - Recognition of stroke in the emergency room (ROSIER) FAST: - Face: ask the person to smile & does one side of the face droop? - Arms: is one arm weak or numb? Raise both arms, does one drift downward? - Speech: is speech slurred? Is a simple sentence repeated correctly? - Time: Time of onset? Identified 70-90% of strokes, however missed up to 40% of posterior circulation More complex stroke assessments: - More details FAST (level of facial palsy, hemiparesis, dysarthria) - Level of consciousness - Eye assessment - Visual/sensory neglect or extinction - Modified Rankin scale: assesses the patient's premorbid function, if a high score, pt is unlikely to receive interventions Good measure of stroke severity, predict LVOs & lesion size Facial motor assessment: - Top half (above eyes) = bilateral innervation - Forehead wrinkling, brow movement, eye squeeze - Bottom half (below eyes) = unilateral innervation - Smile, nasolabial fold, tongue protrusion Facial palsy: - Partial palsy: unilateral lower face motor deficit - Complete palsy: unilateral upper & lower face motor deficit (likely to be a lower motor neuron affected = brain stem = posterior stroke OR stroke mimic such as bell’s palsy) Motor associated further assessments - Limb hemiplegia: can't move their limbs against gravity (can't lift limb up) - Limb hemiparesis: can't sustain limb against gravity (up to 10 seconds) - Dysarthria: difficulty speaking (due to loss of motor control) - Dysphagia: difficulty swallowing (due to loss of motor control) - Gaze abnormality: restricted ocular motion past midpoint (H test) (one eye can't track past midpoint) Sensory associated further assessments - Dysphasia/aphasia: language difficulties (expressive or receptive) - Visual or sensory neglect: unilateral lack of response to stimuli (cant feel or see on certain side) (if you do it on one side, they cant feel/see that side & have complete neglect of that hemisphere) - Visual or sensory extinction: unilateral lack of response to stimuli only when both sides are stimulated simultaneously (can only feel/see one side when tested = extinction of one side when tested simultaneously Missed signs: - Vertigo - Diplopia: double vision - Ataxia: difficulty coordinating movements Lateralisation of the brain functions: Certain functions are only in one hemisphere - Language centres are more often in majority of patients in the left hemisphere (not all the time, but majority) - If you have right side motor deficit (hemiplegia) that is controlled by the left hemisphere, you might also see difficulties with language - If you have right hemisphere infarction, there will be left motor deficit, with right sided neglect Blood pressure: - 80% of stroke patients will present with hypertension, which can be due to dysregulation from injury, or compensation due to increased ICP - Any changes to systemic pressure can change the impact of expansion of the ischemic core (penumbra - core). If pressure is too low, the core might get greater, or if the pressure is too high, the haemorrhage might grow. If ICP pressure is increasing, in order to maintain CPP, systemic BP must increase, however if systemic BP is too high it can be contributed to poorer outcomes. - It also might change which intervention is available for the patient, so note changes to BP & handover this information. Cerebral perfusion pressure (CCP) = mean arterial pressure (MAP) - intracranial pressure (ICP) - CPP: pressure required to maintain cerebral perfusion - MAP: diastolic BP + ⅓ of systolic-diastolic - ICP: pressure inside your skull due to the rigid capsule preventing expansion. This increases with any oedema or intracranial bleeding. Stroke mimics: 1. Post ictal / seizures - Todd’s paresis, gaze deviation, decrease levels of awareness - To rule out stroke: history of seizures, or seizure witnessed prior to stroke symptoms (whichever one came first) 2. Migraine: - Up to 25% of migraine sufferers will have focal neurological symptoms, & hemiplegic migraines exist. Most migraines are self resolving but some can suffer permanent neurological changes: - To rule out stroke: history of migraines & presents exactly like current presentation 3. Metabolic: - Dysglycaemia can cause hemiparesis. More common in HHS due to encephalopathy. Hypernatremia, hyponatremia, hepatic encephalopathy & thyroid storm may also cause focal neurological deficits. - To rule out stroke: BSL. Most stroke guidelines require normal BSL (if BSL is fixed & stroke symptoms remain = can rule in stroke) 4. Bell’s Palsy: - Temporary, unilateral paralysis of the face usually due to trauma or infection to the facial nerve (CN7) - To rule out stroke: good history taking, no other stroke symptoms, 5. Functional neurological disorder: - Presents with limb weakness, numbness, or speech disturbances - To rule out stroke: Clinical signs demonstrate inconsistency and reversibility (often through distraction) 6. Brain tumours; - Gliomas, meningiomas, adenomas 7. Cerebral infections: - Meningitis, encephalitis ** Err on the side of caution. If you cannot entirely rule a mimic in, a stroke must be considered. Treatment: 1. Early identification 2. Timely transport to appropriate hospital with notification (stroke unit & reperfusion therapies) - Monitor BP (too hypertensive might not be eligible for thrombolysis) - Consider: - Large bore IV cannula (imaging & medications in-hospital) - MICA for intubation of the unconscious patient (try not to delay transport) - Antiemetics to minimise gagging & vomiting (prophylaxis for ICP) - Treat seizures with benzodiazepines/midazolam - Oxygen in the hypoxic patient (high flow can be associated with worse outcomes of not required) Definitive assessment: Brain imaging: - Shows ischemic VS hemorrhagic - Aids decision of treatment pathway & timeline - Non contrast CT: shows haemorrhage & some mimics such as tumours (favoured & available, but not good at identifying posterior circulation strokes) - CT angiogram: contrast dye shows image of cerebral vessels, showing which artery is occluded during an ischemic stroke. - CT perfusion: measured cerebral blood flow & cerebral blood volume within cerebral tissues. Shows the penumbra & core of the stroke using dye. Definitive treatment Ischemic stroke: - Thrombolysis - Tenecteplase or alteplase are most commonly used. - Used in all ischemic stroke patients within 4.5 hours of symptoms onset. If CT perfusion imaging shows salvageable penumbra, thrombolysis can be administered up to 9 hours post symptom onset. - Less successful in LVOs, however, should be given in conjunction with ECR. - 6% of thrombolysis pts were at risk of ongoing haemorrhage which can form into haemorrhagic stroke = risky procedure but risk VS benefits. Why BP should be lower than 185. - Endovascular clot retrieval: - Technique where they enter the groin & femoral artery with a catheter & under x-ray they find the site of the clot, cross through the clot & capture it with a mesh cage, using vacuum suction to pull out & remove the clot. - Only able to treat LVOs & will be considered up to 24 hours post symptom onset. - Improved 90 day functional independent rates from 13-50%. - Only available at specific hospitals. Haemorrhagic stroke: - Conservative treatment: - Maintain balance of BP - Osmotherapy & hyperventilation can be trialled in those with oedema or increased ICP - BGLs kept in normal range (40 years) - Other associated conditions or features (head trauma, illicit drug use, toxic exposure, headache on awakening, precipitated by cough/exertion/sexual activity) - Previous headache history with progression or change in frequency, severity or clinical features Life threatening causes of secondary headaches: - Trauma to the head or neck - CVA or cerebral vasculitis - Tumours & increased ICP - Seizures - Medications or positions (Nitrates = vasodilation, carbon monoxide) - Infections (meningitis, encephalitis) - Hypertension, dehydration, renal or thyroid problems Treatment: - Gentle handling, reduce stimulus (lights, noise, sirens) - Non-narcotic analgesia (paracetamol) - Antiemetics (prochlorperazine) - Raise the head of the stretcher 30 degrees to help decrease ICP - Transport to a neuro centre if the patient has any red flags Neurogenic shock: Shock occurring in the setting of normal blood volume (normovolemic hypotension) - Refers to the haemodynamic instability that occurs in the setting of a spinal cord injury at the level of T6 & above, and is related to the loss of sympathetic tone to the peripheral vasculature & heart - Significant loss of sympathetic division past T6, but large preservation of parasympathetic, leaving the spinal column much higher than the level of injury. The result being that the loss of sympathetic tone prevents the usual ability to control the peripheral vascular and increase the firing rate & contraction of the heart. - Involves the loss of innervation to the Celiac ganglion, which results in an inability to stimulate the adrenal glands to release catecholamines (adrenaline & noradrenaline) with resulting loss of vascular tone and decreased inotropy (contractility) & chronotropy (heart rate). Signs & symptoms: - Hypotension - Bradycardia (inability to mount a tachycardic response) - A possible sweat line (pale & sweaty above injury line and dry & flushed below injury line) - Hypothermia **not to be confused with spinal shock which is associated with lower body paralysis & anaesthesia & an absence of pain & the presence of unexpected calmness - (spinal shock) Dysfunction of the spinal with the loss of reflexes and sensory & motor function below the level of injury VS (neurogenic shock) the distributive shock & haemodynamic changes that are apparent in the spinal cord patients Treatment: - BLS & spinal immobilisation - Conservative fluid challenge to help support perfusion - Vasopressors (adrenaline, noradrenaline or dopamine infusion) (MICA) Autonomic dysreflexia: Uninhibited or exaggerated sympathetic response to noxious stimuli below the level of injury, leading to diffuse vasoconstriction & hypertension & severe headache - Usually occurs in patients with spinal cord injuries above T6 - Typical stimuli include bladder distension, bowel impaction, pressure sores, bone fracture, occult visceral disturbances or sexual activity - The parasympathetic activity that occurs when the rise in BP is detected by the baroreceptors in our carotid bodies & aortic arch results in a compensatory bradycardia & vasodilation above the injury, but is not usually unable to control hypertension that continues to escalate Signs & symptoms: - Normal SBP for an individual with a spinal cord injury above T6 is 90-110mmHg. An increase of 20-40mmHg above this can suggest the diagnosis, and it is not uncommon to see profound hypertension (>200) in AD. - Bradycardia is common, as well as pounding headaches, nausea, anxiety, blurred vision & nasal obstruction - Profuse sweating and flushing abode the lesion (often face/neck/shoulders), with goosebumps below the injury - The severity of attacks ranges from asymptomatic hypertension to hypertensive crisis continuing by profound bradycardia, cardiac arrhythmias or arrest, intracranial haemorrhage & seizures Treatment: - Monitoring of blood pressure - Positioning of patient upright to orthostatically lower blood pressure - Removal of tight fitting garments - Searching for & correcting noxious inciting stimuli - Bladder distension, pressure areas, wounds, ingrown toenails, fractures - Nitrates (GTN 300-600 mcg, repeat @ 10/60 intervals) Malignant hyperthermia: Though rare, it is a severe, life threatening, hyperthermic response to medications, usually triggers by the combination of an inhaled anaesthetic and a depolarising neuromuscular blocker Signs & symptoms: - Muscular rigidity, especially of the jaw (often first sign) - Tachycardia or other dysrhythmias - Tachypnoea - Acidosis - Shock - Hyperthermia, with temp usually >40, but can progress to extremes >43 - Hypercapnia, as detected by an increased EtCO2 - Urine may appear brown or bloody if rhabdomyolysis and myoglobinuria have occurred Treatment: - Stop causative drug - Aggressive cool the patient - Immediate transfer to hospital for dantrolene to stop the hyperthermia Extrapyramidal reactions: The pyramidal system: - At the back of our brain are two medullary pyramids. Some of our motor tracts go through the pyramids (pyramidal tracts) & some do not (extrapyramidal tracts) There are 2 pyramidal tracts which both have neurons that start in the upper part of the brain (cerebral cortex). Some go from the brain to the cranial nerves to modulate facial movement via the corticobulbar tract & some go from the brain to large voluntary muscles & control body movement via the corticospinal tract The extrapyramidal tracts have neurons that start in the lower part of the brain (brainstem). These tracts control involuntary motor reflexes, walking & complicated movements (especially of our hands) and control our posture. Extrapyramidal reactions: serious neurological symptoms that may occur after initiation of antipsychotic drugs. - Drug induced movement disorders that are seen in patients taking antipsychotics & dopamine receptor blocking agents - Acute dystonia: - Manifests as involuntary muscle contraction & abnormal muscle posturing, affecting muscles of the neck, jaw, eyes, face & tongue, making it difficult to breath, swallow & speak - Occurs within hours of taking the medication - Treated with anticholinergics - Akinesia: Parkinson like syndrome - Collection of symptoms describing things like tremor, muscle rigidity, slowing of movements, changes of gait etc. & generally appear within a few days of taking the medication - Treated with dopamine agonists - Akathisia: - Inability to sit still & motor restlessness, leading to repetitive movements, usually of lower limbs, with leg crossing, swinging or shifting - Tardive dyskinesia - Manifests as involuntary, repetitive movements of the face & tongue - Occurs within months of the medication - Often permanent, not painful, but can cause difficulties chewing & talking Acute dystonic reactions: - Involuntary, sustained muscle contractions causing abnormal posture and/or repetitive twisting motions - Common causes included drugs, genetics, or for reasons unknown - Laryngospasms & failure of respiratory muscles are the most concerning short term features Management: - Anticholinergics, antihistamines, benzodiazepines & beta blockers are all used in various ways to treat these EP reactions - Most reactions are not immediately life threatening, however, reactions with laryngospasm or respiratory failure will require MICA (intubation & pharmaceutical treatment) - Benztropine is a drug made up of atropine & diphenhydramine used to treat acute dystonic reactions & is carried by most ICPs Neuroleptic malignant syndrome: - Severe & life threatening adverse drug reactions occuring with neuroleptic/antipsychotic drugs - Can be triggered by haloperidol Signs & symptoms: - Motor abnormalities: - Patients may have generalised, severe muscle tremor or rigidity (& less often, dystonias or chorea). Reflex responses tend to be decreased - Altered mental status: - Usually one of the earliest manifestations is a change in mental status, often an agitated delirium, which may progress to lethargy or unresponsiveness - Hyperthermia: - Temperature is usually >38 & often >40 - Autonomic hyperactivity: - Autonomic activity is increased, tending to cause tachycardia, arrhythmias, tachypnea, diaphoresis, labile BP (suddenly changes from normal to high) or hypertension Treatment: - Aggressive cooling - In-hospital management will usually involve medically supervised cessation of the causative drug & administration of dantrolene to stop the hyperthermia Parkinson's disease: Neurodegenerative disorder - Brain produces an aberrant protein that forms into permanent fibres, called Lewy bodies, which interfere with many functions of the CNS, including with the dopamine producing parts of the motor centres, which can lead to Parkinsons

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