C/1) Rapid assessment of the critically ill

FIRST ASSESEMENT Alert, Responsive Responsive Unresponsive

no Secure Airway (Eschmark, Mayo-tube) no Ventilate ! (assisted, controlled)

AIRWAY - patent yes

BREATHING ? (breathing movement, sound) yes cyanosis ? O 2 -saturation

(+12 lead. ECG) no DISABILITY ? PAIN ? INJURY ? (assesement, management)

HYPOTENSION ? ARRHYTMIA (obtain blood pressure) (monitor ECG) no yes no SHOCK ALGORYTHM

A B C

give oxygen

CALL FOR HELP SEGTSG HVSA Cervical immobilization! Cerviklis immobilizci! Prior medical intervention? Orvosi beavatkozs (possible anaphylaxys?) (anaphylaxia lehetsge?) Intoxication? Decontaminate first! Intoxikci? Dekontaminci Emergency interventions: Srgs beavatkozs szks.sz.: surgical airway(conicotomia) sebszi lgt (conicotomy) PTX decompression PTX dekompresszi

CIRCULATION ? (pulse, capill.refill) no yes establish IV line

CPR
(BLS)

ARRHYTMIA ALGORYTHM

During the first assesement of a critically ill patient, the priority is the ABC vital signs. Always follow the rule: evaluate interveniate reasses. All parameters must be carefully monitored after reassesement, and the following parameter can be evaluated only after the prior ones are secured. Use algorythms (CPR, Shock, Arrhytmia) for stabilization. Call for help immediately. All trauma patient are supposed to have cervical injury untill the opposite is proved. If prior medication was used, anaphylaxis is also to be considered. Stop administering the drug immediately but LEAVE the needle in situ! If intoxication is suspected decontamination is to be done first. Watch out! Surgical airway is to be done on the scene if necessary by the first responder medical professional. Do not wait for surgeons or ICU staff.

BLS - Basic life support for everyone aim:

to maintain perfusion of vital organs until ALS can be started ALS Advanced life support for CPR teams aim: to get spontaneous circulation restarted PLS Prolonged life support in the ICU aim: to minimize neurological damage

Basic life support (BLS) algorithm:

Advanced life support (ALS) algorithm:

Drug dosages used during CPR:

DRUGS (all doses based on a 70 kg woman) Epinephrine 1:10,000 10 ml = 1 mg Atropine (0.6 mg/ml) Amiodarone (in 20 ml 5% dextrose) Bretylium tosylate 50 mg/ml Mexiletine 25 mg/ml Calcium gluconate 10% (0.225 mmol Ca/ml) Lidocaine 2% Adenosine Sodium bicarbonate 8.4%

IV-dose 0.1-1 mg

COMMENT and receptor stimulant Infusion 5 mg:500 ml saline (10 g/ml) Increases heart rate (blocks ACh receptors) Completely blocks the vagus nerve, used in asystole

1 mg 3 mg 300 mg second dose: 150 mg 500 mg 150 mg bolus 10 ml 100 mg 6 mg 50 ml 5 mg

Used in refractory fibrillation Membrane stabilisation, reduces tendency to tachyarrythmias Inotropic action Infusion 1.5 g:500 ml 3 mg/ml then 12 mg x 3 every 2 min Not as routine, only refractory cases, pH to be measured as soon as possible -blocker used for supraventricular arrythmias (SVT)

Metoprolol (1 mg/ml)

C/2) Circulatory shock states

Shock is a state with characteristic symptoms and signs where there is an imbalance between oxygen supply (oxygen delicery to tissues DO2) and demand which leads to tissue hypoxia. Definition: Progressive cardiovascular dysfunction independent from the etiology and resulting in a generalized inadequacy in tissue perfusion and oxygenation relative to metabolic requirements Shock is traditionally classified according to etiology: 1. 2. 3. 4. 5. Hypovolemic shock Cardiogenic shock Septic shock Anaphylactic shock less frequent (distributive shock) Neurogenic shock less frequent (distributive shock)

Symptoms of circulatory shock: The clinical picture observed with the different types of shock can be divided into 2 categories, depending on whether cardiac index is reduced (hypodynamic shock) or increased (hyperdynamic shock). Cardiac index (CI) is a vasodynamic parameter that relates the cardiac output (CO) to body surface area (BSA), thus relating heart performance to the size of the individual. The unit of measurement is litres per minute per square metre (l/min/m2). The index is usually calculated using the following formula:

CI=Cardiac Index, BSA=Body Surface Area, SV=Stroke Volume, HR=Heart Rate (The normal range of cardiac index is 2.6 - 4.2 L/min per square meter) a) Hypodynamic shock Hypovoemic and cardiogenic ashock are both usually associated with a low cardiac index. Blood pressure may be normal due to compensatory mechanisms. b) Hyperdynamic shock Septic shock is typically hyperdynamic,unless the patient is also hypovolemic Classic signs of shock:

Pallor the patient is pale Tachycardia HR is elevated as a compensation mechanism Tachypnea the patient is hyperventilating Poor tissue perfusion Oliguria is typical reduced urinary output Pulmonary edema may occur in cardiogenic shock (left ventricular failure) extreme dyspnea with inspiratory crepitations

In the clinical practice, these forms of shock may overlap. It is not uncommon for instance to find both hypovolemia and myocardial dysfunction in patients with septic shock Progression of circulatory shock (if left untreated): Cardiovascular dysfunction Tissue perfusion impairement Tissue hypoxia Progressive failure of cellular metabolism Organ dysfunction Multiple Organ Dysfunction Death Time dependency of shock: 1) Early phase: Compensated shock no organ disfunction is present (yet) reversible with treatment 2) Late phase: Decompensated shock hardly reversable organ dysfunction(s)

PATHOPHYSIOLOGY of shock
1. Cellular changes Tissue hypoxia ATP depletion Na-K pump failure Na / water influx cell swelling Progressively worsening lactic acidosis due to hypoxemia (metabolic acidosis) Intracellular Ca overload ( [Ca2+]i) mitochondrial damage (loss of calcium from mitochondria) leads to impaired oxidative phosphorylation, and may impair organ functions such as myocardial contracitility Mediator release / activation (vasodilating, cytotoxic) eicosanoids (AA) lipoxygenase leukotriens cyclooxygenase thromboxane, cytokines (TNF, IL-1, IL-6, etc) complement system (C3a, C5a), Nitric oxide (NO = EDRF) bradykinin, free oxygen radicals, neutrophil proteases 2. Changes in the microvasculature/capillary permeability

Edema diffusion distance

cellular hypoxia flow Edema

Sludging of blood flow microvascular thrombosis ( consumption!) Precapillary sphincter constriction Postcapillary shincter constriction filtration pressure Precapillary sphincter dilates (!) filtration Cellular hypoxia AV shunt

3. Organ dysfunctions

Heart / circulation BP , HR coronary perfusion

myocardial ischemia

Contractility , CI circulatory failure

Brain confusion, apathy, coma

altered sensory function

GI tract GI mucosal ischaemia barrier function impaired Bacterial and toxin translocation (to bloodstream) septic complications

Stress ulcer

Lungs Hyperventilation (due to acidosis) Oxidative burst leukocyte migration pulmonary Epithel dysfunction alveolar protein excretion ARDS (shock lung) PVR R-L shunt hypoxaemia

Kidneys GFR oliguria Acute tubular necrosis ARF (shock-kidney)

Mortality from circulatory shock: Depends largely on the etiology Hypovolemic shock has a considerably lower mortality compared to both cardiogenic and septic shock. Mortality from septic shock, even with adequate therapy, is approx. 40-60%, while mortality from cardiogenic shock may be even higher than this (50-80 %)

MOST IMPORTANT COMPENSATORY MECHANISMS

Sympathetic activation Vasoconstriction Redistribution of blood flow toward the vital organs Tachycardia Respiratory compensation of metabolic acidosis Hyperventilation

CLINICAL PRESENTATION (independent from etiology)

Manifestation of tissue hypoxia - early sign!

metabolic acidosis, lactate level cyanosis (peripherial !) mottled skin (cutis marmorata) prolonged capillary refill time (exc. hyperdinam septic s.)

Manifestation of compensatory mechanisms

depends on etiology sympathico-adrenerg stimulation pallor, sweating, cold extremities (cold knees: temp. difference between the thigh and the knee) narrowed pulse pressure hypervantilation

Manifestation of organ dysfunctions

Circulatory: hypotension, tachycardia Renal: oliguria, anuria Brain: altered sensorium, confusion, coma

DO NOT FORGET about the other organ dysfunctions!

Liver (altered metabolism, lactate-metabolism, etc!) GI tract (impaired absorption, stress ulcer, translocation !) The clinical presentation of circulatory shock is slighlty different according to the different etiologies.

MANAGEMENT of circulatory shock Finding the cause of circulatory shock may be done by a few simple blood tests such as CBC, clotting parameters, electrolytes, urea, creatinine, arterial blood gases, lactate, troponin and blood cultures, in addition to an ECG and a chest film Treat the cause Stabilize vital parameters and peripherial circulation urgent and well organized management is required frequent (or even continous) reasessment needs therapeutic and diagnostic processes MUST proceed in parallell 1) VENTILATION and OXYGENATION airway, breathing high flow O2 by face-mask to improve arterial oxygen saturation and tissue oxygenation intubate and ventilate immediately if SaO2 < 90 % or GCS < 9 Exclude PTX ! (trauma cases!) 2) VOLUME RESUSCITATION optimizing cardiac preload and restoring circulating volume large bore peripherial IV cannulae -several litres may be needed in hypovolemic and septic shock external haemorrhage to be controlled by pressure or surgically urgent thoracotomy aortic cross-clamping if needed Volume resuscitation in hypovolaemic shock: GENERAL RULE: The fluid to be administered should most closely match the fluid lost Cristalloid vs colloid debated some claim that colloids increase mortality with 3- 4 % not the type of fluid but the volume and time is important Small volume resuscitation (SVR) - hyperosmolar fluid (100 ml of 7.4% NaCl + HAES) saline7,5% /dextran 70 recommended - rapid administration if possible - 10 X volume expansion effect subsequent cristalloid administration is mandatory - on field trauma victims survival improved Blood transfusion Invasive monitoring: A pulmonary artery catheter (PAC) may be very useful in the differentiation between the different types of shock: (Early intubation also allows for insertion of invasive hemodynamic monitoring devices such as PAC)
Septic shock Cardiac index (CI) Pulmonary artery occlusion pressure (PAoP) Central venous pressure (CVP) Systemic vascular resistance (SVR) Oxygen delivery to tissues (DO2) Normal or Normal or Cardiogenic shock Normal or Hypovloemic shock

C/3) Hypovolemic shock

Is commonly the result of hemorrhage, but may also be due to excessive fluid loss from GI-tract and urinary tract and may alkso be caused by massive burns.

Relative or absolute reduced circulating volume (by 25 30 %) - 10,5-12,6 L (!) Hemorrhage (loss of blood) investigations should include peritoneal lavage, abdominal ultrasound, spiral CT and invasive monitoring of CVP should be replaced by transfusions Electrolyte disturbances can be severe Severe burn (loss of plasma) Dehydration: vomiting, ileus, diabetic coma, etc. (loss of water) Oxygen delivery to tissues (DO2) is reduced due to reduced cardiac output, anemia and hypovolemia Diminished cardiac output is due to reduced cardiac preload In the early phases of hypovolemic shock, tissues are able to extract more oxygen from the blood due to the reserve capacity (see topic B/5) When this reserve capacity is exhausted; oxygen debt develops, and its severeity is determined by the level of blood lactate which develops as a consequence Fluid resuscitation is usually the primary aim in the management of hypovolemic shock, but sometimes, as in the case of trauma and hemorrhage, surgical interventions to stop bleeding and further blood loss precedes this

C/4) Sepsis, septic shock

Progressive mismatch between tissue oxygen demand and supply secondary to systemic immune response (SIRS) In septic shock, microbial components are recognized by soluble cell-bound receptors such as CD14 and toll-like receptors, which stimulates the release of pro-inflammatory cytokines such as TNF-, IL-1 and IL-6, in addition to anti-inflammatory cytokines such as IL-10, IL1ra and TNF-receptors, generation of complement, activation of coagulation cascade and platelet aggregation. There is also increased generation of arachidonic acid metabolites, reactive oxygen species and nitric oxide (NO) The combined effect of all these changes is vasodilation, increased cardiac output despite reduced contractility and a reduced effective intravascular volume secondary to increased capillary permeability. However, oxygen delivery to tissues (DO2) is actually supranormal in septic shock, mainly as a result of increased cardiac output Distributional circulatory insufficiency Relative hypovolaemia Secondary myocardial dysfunction Hyperdynamic, hypodynamic pattern Treatment involves

Fluid resiscitation Surgical drainage of infected fluid collections Systemic antibiotics (Cefuroxime 1,5g/8h if no clue to possible source, or Gentamicin + antipseudomonal penicillin, e.g. Timentin) Large dose steroids (e.g. 30-120 mg/kg methylprednisolone) given within 24 h of onset improved hemodynamics, but not the survival rate L-NMMA (N-methyl-L-arginine) is a non-selective NO-synthase inhibitor which is very promising in the treatment of septic shock (since NO contributes to vasodilation). Italso reduces the need for Noradrenaline needed. Increased mortality has been seen in phase III trials however (due to increased systemic and pulmonary vascular resistance), and a selective NO-synthase inhibitor may be a better alternative in the future Vasopressin can be used in case of refractory hypotension (despite high doses of catecholamines) not routinely used Activated protein C (APC) promotes fibrinolysis and inhibits thrombosis and inflammation. In patients with sever sepsis, infusion of APC reduces mortality by 6 % Hemofiltration used frequently to manage severe metabolic acidosis, and it probably removes inflammatory and vasoactive cytokines as well

C/5) Anaphylaxia, anaphylactic shock

Anaphylactic shock (and neurogenic shock) is also referred to as distributive shock There is a mismatch between circulating blood volume and vascular bed capacity resulting in a relative hypovolemia secondary to generalized vasoparalysis of anaphylactic origin

Anaphylactic shock Neurogenic shock (spinal lesion) Toxic shock syndrome (TSS)

C/6) Cardiogenic shock

Reduced cardiac output (CO) secondary to reduced contractility myocardial infarction 40 % loss of myocardial functional mass irregular or critically altered ventricular contractions arrhytmias VT, SVT, AF, bradyarrhytmias... severe valvular dysfunction, haemodynamic disturbance papillary muscle rupture, septal wall rupture Oxygen delivery to tissues (DO2) is reduced due to reduced cardiac output, anemia and hypovolemia Diminished cardiac output is due to reduced cardiac contractility In the early phases of cardiogenic shock, tissues are able to extract more oxygen from the blood due to the reserve capacity (see topic B/5) When this reserve capacity is exhausted; oxygen debt develops, and its severeity is determined by the level of blood lactate which develops as a consequence ECG is invaluable sinceit may reveal te nature of the shock e.g. a large MI Treatment includes Fluid resuscitation Vasoactive drugs - an inodilator, such as Dobutamine or Milrinone can be used An inoconstrictor such as Adrenaline or Dopamine is generally preferred in case of severe hypotension Thrombolysis, Angioplasty, PTCA or CABG are treatments of coronary disease IABP an intraaortic balloon pump provides a useful bridge to surgery (buys time) in cardiogenic shock caused by papillary muscle rupture and ischemic ventricular septal defects

Obstructive shock may occur due to

cardiac tamponade constrictive pericarditis pulmonary embolism (PE) pneumothorax (PTX)

C/7) Volume replacement therapy

When replacing fluids in case of volume resuscitation, the choice stands between colloids, crystalloids or blood products (artificial or human) The fluids added will end up in a given body fluid compartement based on its osmolarity. A high osmolarity fluid will remain in the bloodstream (expanding effective circulating volume), while an isotonic or hypotonic solution will be distributed also to the ECF more or less. The osmotic pressure generated by a solute is proportional to the number of solute molecules (or ions) and is independent of the size of the molecules/ions. Colloid osmotic pressure (COP) is the osmotic pressure exerted by macromolecules of colloid solutions. a) Colloids Colloids are plasma expanders used to expand the blood volume. When added, they expand only the intravascular volume (plasma with blood cells) with the volume infused. There are two types of colloids; plasma derivatives and synthetics

Human albumin solution (plasma derivative)

Contains > 95 % human albumin. It is considered as the ideal colloid since albumin is the naturally occuring substance responsible for plasma oncotic pressure physiologically. It is very expensive and has a short shelf-life (about 1 year). In addition, concerns have been raised about risk of rare infections (e.g. Creutzfeld Jacobs) and increased mortality (6 %) when used in volume resuscitation

Gelatins (synthetic) made from bovine collagen

They are relatively inexpensive and have long shelflives. However, their plasma-expanding effects last for only 90-120 minutes. Anaphylactic reactions may occur with gelatins

Dextrans (synthetic) polysaccharides made from sucrose

Made as Dextran 40 (Mw: 40 kDa) and Dextran 70 (Mw: 70 kDa). They are stable and have long shelf-lives. Dextran 70 is used as a plasma substitute in hypovolemia and its plasma expanding effects last for at least 6 h. Dextran 40 is used in some types of surgery, such as vascular, neuro and plastic surgery since it has an anti-sludging effect. It canalso be used in hypovolemia, but has the risk of causing renal failure since it may become lodged inside renal tubules. Dextrans aso have side effects on hemostasis which include dilution of clotting factors, reduced clot strength, increased fibrinolysis, increased plasminogen activation and impairment of platelet function anticoagulant side-effects

Hydroxyethyl starches (synthetic) produced from D-glucose polymers

HES solutions are made in different molecular weights. They may cause anaphylactoid reactions and coagulopathies.

Hypertonic solutions (600 1800 mOsm) both as colloids and crystalloids

These solutions are now used in a variety of clinical situations. They are used in small volume resuscitation, using small volumes of hypertonic solutions which cause a considerable amount of fluid to be relocated to the intravascular compartment. They also minimize tissue edema, and may reduce cerebral edema. They are usually given as single doses

b) Crystalloids Crystalloids are much cheaper than colloids and they are therefore extensively used. They are simple solutions which will expand not only the plasma/blood (intravascular) compartment, but will also increase the interstitial volume compartment (of ECF) to some extent since they are not restricted to the blood vessels. Glucose (when added) will be distributed to all body fluid compartments. Crystalloids will expand the intravascular compartment, but 3 times as much volume (generally) is needed compared to colloids to replace lost fluid. Hypertonic solutions are recommended for fluid resuscitation (e.g. glucose 25/50 %) Hypotonic solutions are useful in hypertonic dehydration states, but they may worson cerebral edema. Solution Glucose 5% Glucose 25% Glucose 50% Saline 0,9% Glucose-saline Ringer solution Plasmalyte B Osmolarity (mOsm) pH 252 (hypotonic) 1260 (hypertonic) 2520 (hypertonic) 300 (isotonic) 282 (isotonic) 309 (isotonic) 298,5 (isotonic) 3,5-6,5 3,5-6,5 3,5-6,5 5,0 3,5-6,5 5,0-7,5 5,5 Na+ (mM) K+ (mM) Cl- (mM) glucose 154 30 147 140 4 5 154 30 156 98 50 mg/l 250 mg/l 500 mg/l 40 mg/l -

c) Blood products (plasma derivatives)

Fresh frozen plasma (FFP) Contains normal plasma levels of clotting factors, albumin and immunoglobulins. A unit is typically 200-250 ml. 4 packs are sufficient for a 70 kg individual. It is kept at temps. Of 50 C to preserve its coagulant levels. FFP is used for the replacement of multiple coagulation factor deficiencies such as liver failure, anticoagulant overdosing and coagulopathies associated with massive blood transfusions. Cryoprecipitate Prepared from FFP from a pool of 6 or so donors in every pack. It contains about 50 % of the FFP's coagulant activity. It is given in case of massive hemorrhages and DIC to correct coagulation deficiencies. Factor VIII Used to treat Hemophilia A and von Willebrands disease Factor IX prothrombin concentrate Contains factors II, VII, IX and X, prepared from plasma. Used to treat hemophilia B (factor IX deficiency) and to correct bleeding disorders caused by anticoagulant overdoses. Other plasma concentrates Immunoglobulins Whole human blood used for replacement of blood loss

Volume resuscitation of circulatory shock states For relative hypovolaemia: - treat the cause antihistamin for anaphylaxis antibiotics, plasma exchange, HD for septic shock - vasoconstrictors adrenalin (epinephrine) for anaphylaxis noradrenalin (norepinephrine) for septic shock - give IV fluid immediately cristalloid for anaphylaxis (1000 2000 ml) less cristalloid for sepsis (capillary leakage!, ARDS!) Cardiogenic shock - fluid challenge 300 ml cristalloid / 10 min CVP ?

C/8) Diagnosis and management of acute MI

Coronary artery disease (CAD) is the background of all types of angina and of myocardial infarctions (both STEMI and NSTEMI). It is polygenic and multifactorial in origin.

Etiology of Coronary artery disease (and of STEMI):

a) Non-modifiable risk factors: 1. Increasing age degenerative changes cause increased risk with increasing age 2. Male gender female sex-hormones postpone the development of CAD 3. Family history significant when CAD is present in a male first degree relative < 55 years 4. Ethnic origin e.g. South Asians have a higher prevalence of CAD than Europeans b) Modifiable risk factors: 1. Smoking increases risk of CAD by 50% (and mortality from IHD by 60%) 2. Hypertension - hard to define precisely (complex relationship) 3. Dyslipidemia low HDL and high triglycerides with average cholesterol levels 4. Diabetes Mellitus vascular damage in long run + often presents w/ metabolic syndrome 5. Metabolic syndrome Obesity, insulin resistance, moderate hypertension, dyslipidemia, 6. Physical inactivity, high calorie diet, psychological stress

Clinical symptoms:

Chest pain usually similar to angina, but of greater severity, longer duration and the pain is not relieved by administration of nitrates Atypical pain may be present; e.g. epigastric, or radiating to the back (indicates aneurysm) Silent infarcts - may occur in elderly, diabetics, hypertensives and females Presents with dyspnea (acute pulmonary edema), syncope or coma from arrhythmias, acute confusion states (mania/psychosis), diabetic hyperglycemia, cardiogenic shock or CNS manifestations similar to stroke

Diagnosis:

History (anamnesis) assess risk factors, family predisposition, life style etc. Biochemical markers elevated Troponin-T+I, CK-MB, LDH and ASAT (see topic9) ECG-signs:

1. ST-segment elevation occurs within minutes and may persist for upt to 2 weeks (persisting ST-elevation after 1 month indicates formation of a LV aneurysm) 2. Pathological Q-waves indicate significant abnormal electrical conduction, but is not synonymous with irreversible myocardial damage. It may take hours or days to develop and it usually persists throughout life (and is thus an ECG-sign of old MI) 3. ST-segment depression in other leads than the ones showing ST-elevation; indicates ischemia in territories other than the infarcted area. It implies an overall poorer prognosis. 4. PR-segment depression/elevation indicate atrial infarction; most patients will experience abnormal atrial rhythms such as atrial fibrillation/flutter, wandering atrial pacemaker and AV-nodal rhythms 5. T-wave inversion immediate or delayed; presists after the ST-elevation has resolved 6. Non-diagnostic changes include new LBBB or RBBB, tachyarrhythmias, transient tall peaked T-waves or T-wave inversion, axis shift (extreme righ/left) or AV-block

MANAGEMENT of uncomplicated STEMI 1. Immediate stabilizing measures and assessment: (as for NSTEMI and unstable angina)

Continuous ECG monitoring (single rhythm-strip on monitor) with easily available defibrillator and medications Aspirin give 200 mg orally (not IM since it causes a rise in CK-MB and risk of bleeding) Rapid examination to exclude hypertension, note presence of murmurs and exclude pulmonary edema (or treat it if present) 12-lead ECG should be obtained and reported within 10 min (see diagnosis of MI) Administer: a) Oxygen - 2-5 L/min for at least 2-3 hours. Hypoxemia is frequently seen post-MI due to ventilation-perfusion abnormalities secondary to left ventricular failure (remember to reduce oxygen tension if presence of COPD) b) Diamorphine 2,5-10 mg IV for pain relief (and improves respiration due to lack of pain) c) Metoclopramide 10mg IV for nausea (caused by Diamorphone) d) Nitrates spray unless hypotensive may relieve chest pain. However; use with caution in inferior MI's (esp. With right ventricular infarction) as venodilation may impair right ventricular filling and precipitate hypotension. Nitrate therapy is purely symptomatic and has no effect on mortality rates

Correction of electrolyte disturbances: Both low potassium and low magnesium may be arrhythmogenic and must be supplemented

2. Strategies to limit infarct size:

a) -blockade early administration of -blockers will decrease infarct size, reduce mortality and risk of early malignant arrhythmias. All patients (including PCI and thrombolysis patients) should receive -blockers early. Those patients will benefit most from this that have an elevated BP, sinus tachycardia, tachyarrhythmias (e.g. AF) or have ongoing or recurrent pain/ reinfarction. Use short-acting agent (e.g. metoprolol 1-2g IV, every 1-2 min) or use esmolol ultrashort acting if intolerance to -blockade is suspected) b) ACE inhibition should be given within the first 24 h of presenting symptoms. Patients with large infarcts (high risk, esp. anterior infarcts), previous MI, heart failure and elderly patients wil benefit most from this. c) Reperfusion

REPERFUSION STRATEGIES of STEMI Rapid reperfusion is the cornerstone of current management of STEMI. It is marked by normalization of ST-segments on ECG. Primary PCI (percutaneous coronary intervention) and Thrombolysis are the main reperfusion strategies.

Thrombolysis: is the breakdown (lysis) by pharmacological means, of blood clots

The principle is to stimulate fibrinolysis by plasmin through infusion of analogs of tissue plasminogen activator (tPa), the protein that normally activates plasmin. Reperfusion occurs in 50-70% of patients who receive thrombolysis within 4 hours of onset of pain, resulting in reduced mortality, LV dysfunction, heart failure, cardiogenic shock and arrhythmias. However, a drawback of thrombolysis is that the coronary anatomy needs to be established before treatment begins (this is done simultaneously with PCI procedures). The time-aspect is essential and thrombolysis should be performed within 4 hours of onset of pain. Indications for thrombolysis: Typical history of cardiac pain within 12 h and ST-elevation in 2 contiguous leads. Choice of thrombolytic agent: Different strategies exist, use the local one. 1. Streptokinase (SK) no need for routine heparinization since it comes with an increased risk of bleeding. Allergic reactions and hypotension may occur with streptokinase 2. Recombinant tissue type plasminogen activator (rtPa) administered with routine heparine. It has a greater reperfusion capacity and a marginally higher 30-day survival rate than Streptokinase. However, it comes with an increased risk of hemorrhage. 3. Other agents available: Reteplase, Tenectaplase, APSAC (anistreplase) Complications of thrombolysis: Bleeding (in 10%), Hypotension (common with SK), Allergic reactions (also common with SK: rashes, low-grade fever, nausea, headaches, flushing), Intracranial hemorrhage (0.3% w/SK, 0.6% w/rtPa), Rerfusion arrhythmias (usually short, self-limiting), Systemic embolization (may be the result in cases of a thrombus in the left atrium, left ventricle or within an aortic aneurysm)

Primary PCI:

the current gold standard of reperfusion in STEMI

Results in reduced mortality, LV dysfunction, heart failure, cardiogenic shock and arrhythmias, same as with thrombolysis. However, primary PCI produces superior long term results. Another advantage is the above-mentioned that PCI simultaneously assesses coronary anatomy by angiography at the same time as the clot is removed. Elderly patients (>65 yrs) are best managed by PCI since thrombolysis is associated with increased risk of cardiac rupture.
Indications for primary PCI: All patients with chest pain and ST-elevation ao with new LBBB, or when thrombolysis is contraindicated Complications: Bleeding from arterial puncture site, stroke, recurrent infarction, need for emergency coronary artery bypass graft (CABG very rare)
Procedure: Vascular access is gained via the femoral or radial artery and a catheter is inserted here. Upon reaching the coronary arteries, a contrast material is injected and the anatomy of the coronaries is revealed by fluoroscopic Xray technique. A ballon is located on the catheter tip which is surrounded by a graft consisting of a metal mesh. The balloon is inflated, stretching the graft which is left in place opening the coronary and thus restoring local blood flow (referred to as PTCA percutaneous transluminal coronary angioplasty see topic 15)

C/9) Complications of acute MI, diagnosis and management

Complications include:

Continuing chest pain is not necessarily angina. A bruised sensation and

muskuloskeletal pains are common in the first 24-48 hours. Esp. in patients who have received chest compressions or repeated defibrillatory shocks. Other causes of continued pain include:

1. Recurrent infarction - includes bort extension of zone of infarct and a new infarct at a separate location. Usually associated with a recurrent ST-elevation. Cardiac enzymes may be over twice that of the values of the first infarction 2. Post-infarction angina angina that develops within 10 days of MI. Treated as ordinary angina, but if still hospitalized, perform new catheterization and revascularization 3. Pericarditis presents as sharp, pleuritic, positional chest pains, usually 1-3 days post- MI. A pericardial friction-rub may be audible. ECG-changes are rarely seen. Treat with aspirin. 4. Pericardial effusion most common with anterior MI's, esp. if complicated by heart failure. Tamponade is rare and is the result of cardiac rupture and/or hemorrhagic effusions. Treatment includes aspiration of the fluid with a large gauge needle.

Fever is commonly seen and peaks 3-4 days post-MI. Associated with increased
leukocyte-count and CRP. Other causes of fever should be considered (infection, thrombophlebitis, venous thrombosis, drug reactions, pericarditis) and treated by cause.

New systolic murmur:

1. Ventricular septal defect (VSD) classically seen 24 hours post-MI (highest risk) or within first 10 days (affects 2-4% of patients) Clinical features a rapid deterioration with a harsh pansystolic murmur (maximal at lower sternal edge), poor perfusion and pulmonary edema. Echocardiography is used to diagnose (2-D or Color Doppler). Treatment is stabilization (continuous monitoring, vasodilators, inotropes if severely hypotensive (dobutamine or adrenaline), possibly intra-aortic balloon for counter pulsation) before finally surgical closure of the septal defect. 2. Acute Mitral valve regurgitation (MR) is caused by ischemia of papillary muscles conneted to the mitral valve. Dysfunction or partial rupture is seen 2-10 days post-MI. Complete rupture is usually fatal. Most commonly associated with inferior MI's. Diagnosis is made by echo, and treatment is with vasodilators (e.g. nitroprusside) before surgical or replacement of the mitral valve. 3. Pseudoaneurysm and free wall rupture demonstrated in 3-6% of STEMI patients. Leads to sudden death in 67% of cases. Some patients present subacutely with cardiogenic shock allowing time for intervention. Pericardial effusion and tamponade are other features that may be discovered, e.g. by echo. Patients who have previously undergone thrombolysis have a decrease risk. Needs urgent discussion by surgeons to find surgical treatment.

Arrhythmias - include tachyarrhythmias (ventricular tachycardia, accelerated

idioventricular rhythm, ventricular premature beats, ventricular fibrillation and Torsades de Pointes), AV-block ectopics and bradycardia treat with proper antiarrhythmic drugs.

Pump failure Hypotension, Cardiac failure or Cardiogenic shock

No pharmacological treatment is necessary if the patient is well perfused peripherally. Try to correct any arrhythmia, hypoxia or acidosis. Arrange an echo to rule out mechanical reasons for hypotension (e.g. MR, VSD or ventricular anurysm)

C/10) Cardiac arrhythmias and management

Atrial fibrillation (AT)
This is the most common sustained cardiac arrhythmia with a prevalence of 0,5 1,0% of the general population. 5-10% of people over 65 years suffer from atrial fibrillation. Te consequence of this arrhythmia is that electrical activity in the atria is chaotic so that coordinated contraction of the atria is impaired, and the atria dilate. No P-waves are seen on the ECG, ventricular rate is highly irregular (irregularly irregular pulse) and the baseline has an irregular zig-zag-pattern

Etiology:
Atrial fibrillation is a common end-point for many forms of cardiac disease. 1. 2. 3. 4. 5. 1. 2. 3. 4. 5. 6. 7. Common causes: Hypertension long term consequence Left ventricular failure of any cause Coronary artery disease (CAD) Mitral or tricuspid disease Hypertrophic cardiomyopathy Potentially reversible causes: Alcohol binge excessive alcohol consumption over a short period of time Hyperthyroidism Acute MI acute pericarditis myocarditis Exacerbation of pulmonary disease, pulmonary embolism Cardiac surgery

Symptoms and signs: Palpitations dyspnea fatigue presyncope/syncope chest pains irregularly irregular pulse

Management of atrial fibrillation:

a) Rate control - first line drugs include -blockers and non-DHP calcium channel blockers such as Diltiazem or Verapamil. A pacemaker may also be implanted. b) Rhythm control - maintenance of sinus rhythm should be attempted with drugs such as Sotalol, Quinidine and Flecainide. Amiodarone is the most effective at this, but is not tolerated by 25% of patients. A pacemaker may also be implanted. c) Anticoagulation due to the constantly fibrillating, non-contracting atria, thrombi may form inside them. These thrombi may embolize and cause MI's and cerebral infarction. Anticoagulation therapy includes Aspirin and Warfarin. INR shuld be kept at 2.0-3.5.

Ventricular tachycardia (VT): Classification:

The most important distinction is the presence or absense of structural heart disease. Impaired LV function is the strongest predictor of a poor prognosis. a) Normal heart VT (benign VT) 1. Right ventricular outflow tract (RVOT) tachycardia This is due to automatic firing of the firing cells of the RVOT. ECG shows a pattern of LBBB with strongly inferior axis. Palpitation sare related to exercise. Treatment - -blockers or Verapamil 2. Fascicular tachycardia its mechanism is uncertain, but it arises from the left posterior fascicle of the conducting fibers of the heart. b) VT with impaired LV function: Any cause of impaired LV function can cause a VT. Common causes are CAD, dilated cardiomyopathy, and hypertrophic cardiomyopathy. These VT's are caused by re-entry phenomena around fibrous scars and/or diseases myocardium. VT may rapidly deteriorate into ventricular fibrillation, and these patients may die suddenly!

Clinical features:
Symptoms: Palpitations Chest pain Presyncope/syncope Dyspnea Pulmonary edema Sudden death

Management:

Long term antiarrhythmic treatment: -blockers reduce arrhythmias and prevent sudden cardiac death Amiodarone and Mexilitine have no effect on prognosis, but may reduce nr. of VT's Lidocaine for prevention and termination of VT Procainamide - for prevention and termination of VT Magnesium - for prevention and termination of VT Defibrillator (DC shock) -for prevention and termination of VT Radiofrequency ablation (electrophysiological procedure) only possible when VT is slow and hemodynamically well tolerated Implantable cardiac defibrillators have dramaticaly improved survival for these patients

1. 2. 3. 4. 5. 6.

C/11) Pulmonary embolism

Pulmonary embolism (PE) is an extremely common and highly lethal condition that is a leading cause of death in all age groups. A good clinician actively seeks the diagnosis as soon as any suspicion of PE whatsoever is warranted, because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of the disease. Unfortunately, the diagnosis is missed more often than it is made, because PE often causes only vague and nonspecific symptoms. Deep vein thrombosis (DVT) and PE are much more common than usually realized. Most patients with DVT develop PE and the majority of cases are unrecognized clinically. Untreated, approximately 1/3 of patients who survive an initial PE die of a future embolic episode. This is true whether the initial embolism is small or large. Most cases of PE are diagnosed at autopsy, and most who die of PE have not had any diagnostic workup or treatment of the disease. In most cases, the diagnosis has not even been considered, even when classic signs and symptoms are documented in the medical chart. Sadly, appropriate diagnostic and therapeutic management often is withheld even when the potential diagnosis of PE has been considered explicitly and documented in the chart. Pulmonary thromboembolism is not a disease in and of itself. Rather, it is an often fatal complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. Under pathological conditions, microthrombi may escape the normal fibrinolytic system to grow and propagate. PE occurs when these propagating clots break loose and embolize to block pulmonary blood vessels. Thrombosis in the veins is triggered by venostasis, hypercoagulability, and vessel wall inflammation. These 3 underlying causes are known as the Virchow triad. All known clinical risk factors for DVT and PE have their basis in one or more elements of the triad. Risk factors for pulmonary embolism: a) Primary hypercoagulable states

Antithrombin III deficiency Protein C and/or S deficiency Resistance to activated protein C (inherited factor V Leiden mutation)

Hyperhomocysteinemia Lupus anticoagulant (antiphospholipid antibody)

b) Secondary hypercoagulable states

Immobility Smoking Surgery Oral contraceptives Trauma Burns Malignancy Patients with limb paralysis Pregnancy Heart failure Obesity Indwelling catheters in great veins and the right heart

Patients who have undergone gynecologic surgery, those with major trauma, and those with indwelling venous catheters may have DVTs that start at any location. For other patients, venous thrombosis most often involves the lower extremities and nearly always starts in the calf veins, which are involved in virtually 100% of all cases of symptomatic spontaneous lower extremity DVT. Although DVT starts in the calf veins, it already has propagated above the knee in 87% of symptomatic patients before the diagnosis is made.

Studies suggest that nearly every patient with thrombus in the upper leg or thigh will have a PE if a sensitive enough test is done to look for it. Current techniques allow us to demonstrate PE in 6080% of these patients, even though about half have no clinical symptoms to suggest PE. Thrombus in the popliteal segment of the femoral vein (the segment behind the knee) is the cause of PE in more than 60% of cases. PE can arise from DVT anywhere in the body. Fatal PE often results from thrombus that originates in the axillary or subclavian veins (deep veins of the arm or shoulder) or in veins of the pelvis. Thrombus that forms around indwelling central venous catheters is a common cause of fatal PE. The belief that calf vein DVT is only a minor threat is outdated and inaccurate. DVT of the calf is a significant source of PE and often causes serious morbidity or death. In fact, one third of the cases of massive PE have their only identified source in the veins of the calf PE is the third most common cause of death in the US, with at least 650,000 cases occurring annually. It is the first or second most common cause of unexpected death in most age groups. The highest incidence of recognized PE occurs in hospitalized patients. Autopsy results show that as many as 60% of patients dying in the hospital have had a PE, but the diagnosis has been missed in about 70% of the cases. Surgical patients have long been recognized to be at special risk for DVT and PE, but the problem is not confined to surgical patients. Prospective studies show that in the absence of prophylaxis acute DVT may be demonstrated in any of the following:

General medical patients placed at bed rest for a week (10-13%) Patients in medical intensive care units (29-33%) Patients with pulmonary disease kept in bed for 3 or more days (20-26%) Patients admitted to a coronary care unit after myocardial infarction (27-33%) Patients who are asymptomatic after coronary artery bypass graft (48%)

Mortality: Massive PE is one of the most common causes of unexpected death, being second only to coronary artery disease as a cause of sudden unexpected natural death at any age. Approximately 10% of patients in whom acute PE is diagnosed die within the first 60 minutes. Of the remainder, the condition eventually is diagnosed and treated in one third and remains undiagnosed in two thirds. Patients who survive an acute PE are at high risk for recurrent PE and for the development of pulmonary hypertension and chronic cor pulmonale, which occurs in up to 70% of patients and carries its own attendant mortality and morbidity. Symptoms of PE: Symptoms that should provoke a suspicion of PE must include

Chest pain Chest wall tenderness Back pain Shoulder pain Upper abdominal pain Syncope, hemoptysis Shortness of breath (dyspnea) and tachypnea (96%) Painful respiration New onset of wheezing Any new cardiac arrhythmia Any other unexplained symptom referable to the thorax

The classic triad of signs and symptoms of PE (hemoptysis, dyspnea, chest pain) are neither sensitive nor specific. They occur in fewer than 20% of patients in whom the diagnosis of PE is made, and most patients with those symptoms are found to have some etiology other than PE to account for them. Of patients who go on to die from massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have hemoptysis. Nonetheless, the presence of any of these classic signs and symptoms is an indication for a complete diagnostic evaluation. Many patients with PE are initially completely asymptomatic, and most of those who do have symptoms have an atypical presentation. Patients with PE often present with primary or isolated complaints of seizure, syncope, abdominal pain, high fever, productive cough, new onset of reactive airway disease ("adult-onset asthma"), or hiccups. They may present with new-onset atrial fibrillation, disseminated intravascular coagulation (DIC), or any of a host of other signs and symptoms. Pleuritic or respirophasic chest pain is a particularly worrisome symptom. PE has been diagnosed in 21% of young, active patients who come to the ED complaining only of pleuritic chest pain. These patients usually lack any other classical signs, symptoms, or known risk factors for pulmonary thromboembolism. Such patients often are dismissed inappropriately with an inadequate workup and a nonspecific diagnosis, such as musculoskeletal chest pain or pleurisy. Signs of PE: Massive PE causes hypotension due to acute cor pulmonale, but the physical examination findings early in submassive PE may be completely normal. Initially, abnormal physical findings are absent in most patients with PE. After 24-72 hours, loss of pulmonary surfactant often causes atelectasis and alveolar infiltrates that are indistinguishable from pneumonia on clinical examination and by x-ray. New wheezing may be appreciated. If pleural lung surfaces are affected, a pulmonary rub may be heard. The spontaneous onset of chest wall tenderness without a good history of trauma is always worrisome, because patients with PE may have chest wall tenderness as the only physical finding.

Investigations of suspected PE:

D-dimer a normal D-dimer excludes a PE, however an delevated D-dimer is not specific for PE. It is also elevated in case of trauma, post-surgery, DIC, malignancies, acute MI's, pneumonia and in heart failure (non-specific) Arterial blood gases a normal blood gas profile does not exclude PE, but hypoxemia and hypercapnia may indicate a PE (non-specific). Metabolic acidosis is found in case of shock ECG classical signs of PE: (found in 2/3) tachycardia, a pathological Q-wave + inverted T-wave in lead 3, deep S-wave in lead 1 and sometimes a P-pulmonale is present (S1Q3T3 is classical but uncommonly found) Chest film often normal or only slightly abnormal classically demonstrates an enlarged right side of heart + Hampton's hump and Westermark sign Ventilation/perfusion (V/Q) scanning an important method in PE diagnosis It determines whether there are areas within the lung which are mismatched with respect to perfusion vs ventilation Results are given as a normal, high-, moderate- or low-risk of a PE A normal lung scan effectively excludes a PE no treatment needed

Spiral CT rapid scan using contrast may reveal a proximal PE with high accuracy. It is also possible to scan peripheral veins of limbs in search of a thrombus. In addition, with CT-scans, alternative diagnoses such as pneumonia, emphysema, pulmonary masses, pleural effusion and mediastinal adenopathy can be made Echocardiography right ventricular hypokinesia with apical sparing is pathognomonic for a PE. Ventricular function and flow velocity can also be examined this way MRI promising method, but of limited use Pulmonary angiography the only test which can exclude a PE with relative certainty. It is safe to perform, even in high-risk patients. However, it is unavailable in many hospitals. Also, there is now a trend-shift towards less invasive methods such as spiral CT Search for DVT with Doppler US

Management of pulmonary embolism

a) Massive PE (hemodynamically unstable)

Mortality of patients with both a PE and hypotension is 30 % despite treatment Attempts should be made to remove the embolus urgently with surgical/endoscopical embolectomy or medical thrombolysis

b) Moderate PE (hemodynamically stable, but with evidence of RV dysfunction)

Patients have a higher mortality when RV dysfunction is present Thrombolysis is usually performed, although somewhat controversial Further embolization should be removed with anticoagulation (Heparin; LMWH)

c) Mild PE (hemodynamically stable, with no evidence of RV dysfunction)

These patients have normal blood pressure and normal RV function Prevention of further embolizations is the primary goal Methods to remove embolus is unliely to have any benefit

Recommended doses for thrombolytic agents used to treat PE: These agents all activate plasminogen to form plasmin, which dissolves blood clots These agents provide about the same results and are about equally good

rtPA (TPA) 10 mg bolus followed by 90 mg over 2 h Urokinase 4400 U/kg bolus (10 mmin) followed by 4400 U/kg pr h for 12h Streptokinase 250 000 U to 500 000 U (15 min) followed by 100 000 U/h for 24 h Reteplase 10 U boluses 30 min apart

Additional therapy:

Oxygen therapy oxygen saturation must be maintaned at an appropriate level Analgesics such as morphine are given for pain also improves respiratory efforts IV fluids may be given, but not excessively may worsen RV function ICU monitoring with ECG, BP measurements, pulse oxymeter, CVP measurements etc.

C/12) Acute heart failure; diagnosis and treatment

C/13) Emergency pacemaker therapy

C/14) Cardioversion and defibrillation

Electrical cardioversion:
Electrical cardioversion is a procedure in which an electric current is used to reset the heart's rhythm back to its regular pattern (normal sinus rhythm). The low-voltage electric current enters the body through metal paddles or patches applied to the chest wall. Cardioversion is used in case of:

Atrial fibrillation and/or flutter that has not stopped on its own or after a trial of antiarrhythmic medications has failed. Ventricular tachycardia or fibrillation - as an emergency procedure to correct a fast heart rhythm that is causing low blood pressure, chest pain, or heart failure. Other Supraventricular Tachycardias (SVT's)

A DC cardioverter is used (defibrillator). The procedure requires sedation (if patient is not already unconcious due to cardiovascular collapse) and pain killers are also given. Suggested initial energies used for cardioversion:

Atrial fibrillation: Atrial flutter and other SVT's: Sustained VT: Ventricular fibrillation:

50-100 J 50 J 200 J 200 J (up to 360 J)

Implantable cardioverter defibrillation (ICD) therapy

The first devices were designed in the 1980's. Nowadays, they are implanted by transvenous insertion and are placed in the pectoral region. These devices use complex sensing algorithms for detection of lectrical signals (such normal sinus thythm and abnormal rhythm patterns) and consist of a pulse generator , a lithium silver vanadium oxide battery, a sensing circuit, an electrical filter and a shocking coil. They are designed to minimize myocardial injury and to prevent sudden cardiac death. The electrodes of the device are designed to both detect rhythms/arrhythmias and to administer shocks when apropriate. A possible problem arises when atrial fibrillation is present or occurs. AF causes the device to become confused by the chaotic electrical activity of the atria, even though it is designed to filter out electrical noise such as the electrical activity of skeletal muscles. AF must therefore be treated medically in such patients to support the function of the ICDdevice. To decrease the likelihood of inapropriate shocks, modern devices are equipped with detection enhancement programs. These include: Rate stability - evaluates R-R intervals to recognize AF Electrogram morphology to distinguish normal QRS from abnormal one Sudden onset criteria gradual onset of sinus tachycardia according to autonomic nerve signals. The patient teherefore will enjoy a practicaly normal physiological heart beat: bradycardia when resting and faster rhythms and tachycardia with exercise Sustained rate duration will prevent a tachycardia to persist for a longer period, preventing VT's (a problem occurs when distinguishing sinus tachycardia from ventricular tachycardia) ICD therapy includes two types of activity: a) Antitachycardia pacing (ATP) b) Defibrillation They thus act as both pacemakers and defibrillators

C/15) Diagnosis of cardiac and respiratory arrest and management

C/16) Drugs of CPR

DRUGS (all doses based on a 70 kg woman) Epinephrine 1:10,000 10 ml = 1 mg Atropine (0.6 mg/ml) Amiodarone (in 20 ml 5% dextrose) Bretylium tosylate 50 mg/ml Mexiletine 25 mg/ml Calcium gluconate 10% (0.225 mmol Ca/ml) Lidocaine 2% Adenosine Sodium bicarbonate 8.4%

IV-dose 0.1-1 mg

COMMENT and receptor stimulant Infusion 5 mg:500 ml saline (10 g/ml) Increases heart rate (blocks ACh receptors) Completely blocks the vagus nerve, used in asystole

1 mg 3 mg 300 mg second dose: 150 mg 500 mg 150 mg bolus 10 ml 100 mg 6 mg 50 ml 5 mg

Used in refractory fibrillation Membrane stabilisation, reduces tendency to tachyarrythmias Inotropic action Infusion 1.5 g:500 ml 3 mg/ml then 12 mg x 3 every 2 min Not as routine, only refractory cases, pH to be measured as soon as possible -blocker used for supraventricular arrythmias (SVT)

Metoprolol (1 mg/ml)

INOTROPIC SUPPORT Inotropic support is rarely needed in hypovolemic shock since fluid replacement alone is usually sufficient to restore cardiac output and blood pressure. Vasoactive drugs may be very important however in both septic and cardiogenic shock to improve tissue perfusion and oxygenation and to reverse tissue hypoxia. An inodilator, such as Dobutamine or Milrinone can be used in these cases. An inoconstrictor such as Adrenaline or Dopamine is generally preferred in case of severe hypotension. However, adrenaline causes hyperglycemia, hypokalemia and hyperlactatemia. Therefore, when measuring blood lactate levels, the previous use of adrenaline should be taken into account. When cardiac preload is optimized, the use of a vasopressor inotrope such as Noradrenaline is recommended. DIURETICS Furosemide may be used (in a bolus 10-80 mg, or continuous infusion of 3 10 mg/h) to induce natriuresis as a renal protective measure to reduce the incidence of renal failure after a period of circulatory shock. This can only be done when the patient is adequately volume replaced to prevent hypovolemia.

C/17) Cerebral resuscitation

C18) Electrotherapy during CPR

Defibrillation:
The termination of VT/VF within 5 seconds after delivering an electric shock

Involves depolarization of critical myocardial mass The aim is to achieve restoration of physiological pacemaking In-hospital defibrillation should be started within 3 min Efficacy of defibrillation decreases by 7-10 % / minute of delay!

Procedure: 1 shock in every cycle Monophasic device (was used until 1980's) : 360 J pr shock Biphasic device (newer model) : 150 360 J pr shock Immediately resume CPR after the shock for 2 minutes Correct reversible causes during this period (see algorithm) Brief rhythm assessment follows, with or without addition of medications The 1st shock is > 90 % successful If it is unsuccessful, check the equipment and electrodes + give antiarrhythmic agents

3-phase model of CPR:

1) Electric phase 5 minutes With defibrillation; survival is > 65 % 2) Circulatory phase 5-10 minutes BLS should be performed first (90 seconds), then defibrillation again; survival is 15-55 % 3) Metabolic phase Suspended animation survival is 0-25 % AED: An Automated External Defibrillator or AED is a portable electronic device that automatically diagnoses the potentially life threatening cardiac arrhythmias of ventricular fibrillation and ventricular tachycardia in a patient, and is able to treat them through defibrillation, the application of electrical therapy which stops the arrhythmia, allowing the heart to re-establish an effective rhythm. AEDs are designed to be simple to use for the layman, and the use of AEDs is taught in many first aid, first responder and basic life support (BLS) level CPR classes.