1) indicationofintubation

A. Airway patency B. Requirement for positive pressure ventilation due to pulmonary disease (ie, hypoxia or hypercarbia) C. Significant cardiovascular compromise, shock D. Neurologic-seizures, weakness, head injury
2) Hyperk+treatment Mild/modarate forms: limitation /stop K intake resins (ion chelation) diuretics Severe forms: emergency treatment antagonization of membrane effects and decreased plasma level by redistribution calcium gluconate / chloride Na bicarbonate glucose + insulin K removal resins diuretics hemodialysis stop K intake

3) Parametersofhypovolimecshock Heartrate=increased ArterialBloddPressure=decreased CardiacOutput=decreased CentralVenousPressure=decreased PulmonaryArteryocclusionpressure=decreased Systemicvascularresistance=increased OxygenArterialVenousdifference=increased MixedVenousBloodOxygensaturation=decreased 2)Ecgsignsofhypok+ Flat T wave U wave wide QRS complex ST depression Atrial and ventricular rhythm disturbances 3)causesofhypovolemia Dehydratrion,Bleeding,Vomiting,severeBurnsandDrugssuchasDiuretics,Vasodilators

1)classificationofshock

Hypovolemic shock

shock

reduction of effective circulating blood volume (hypovolemia) Cardiogenic shock reduction of cardiac output induced by primary cardiac causes Extracardiac obstructive shock reduction of cardiac output induced by extracardiac primary Causes Distributive shock maldistribution of blood flow caused by vasodilation

2)signsofrespiratoryfailure respiratory signs: hyperventilation with tachypnea hyperventilation may lead to hypocapnia cardio-circulatory signs: adrenergic response: cardiac output + tachycardia cold extremities + profuse diaphoresis the arterial pressure increases (initially) cyanosis cardio-circulatory deterioration: bradycardia , decreased cardiac output, decreased arterial pressure and cardiac arrest. central nervous system signs: fatigue and decreased mental capacity impressive restlessness, then stupor and coma

2)parametersofcardiogenicshock Heartrate=increased ArterialBloddPressure=decreased CardiacOutput=decreased CentralVenousPressure=increased PulmonaryArteryocclusionpressure=increased Systemicvascularresistance=increased OxygenArterialVenousdifference=increased MixedVenousBloodOxygensaturation=decreased 3)treatmentofacuterenalfailure Treatment of the causative disease Circulanting blood volume restoration Volemic solutions (see hypovolemic shock) Correction of cardiac output and renal perfusion inotropic drugs (dobutamine, dopamine) Removal of the nephrotoxic drugs Fluid-electrolyte and nutritional support Infection prophylaxis Dialysis (when necessary) Obstacle removal (when necessary)

1)respiratoryalkalosis Respiratory alkalosis the primary (non compensatory) decrease of PaCO2 CAUSES Hypoxemia Pulmonary diseases: ARDS, pneumonia, pulmonary edema, pulmonary embolism, pulmonary fibrosis_ FiO2 high altitude, closed spaces Congenital cardiac diseases Anemia, blood hypotension Stimulation of respiratory center psychogenic hyperventilation (fear, effort) CNS diseases: trauma, tumors, ICHT, brain stem diseases Pulmonary deseases: pneumonia, asthma, pulmonary embolism Other causes salicilate intoxication SIRS, sepsis liver failure pregnancy Hyperventilation during mechanical ventilation

2)causesofacuterespiratoryfailure upper airway obstruction (nasopharinx, larynx, trachea) airway obstruction by the tongue coma, anaesthesia, head trauma, etc. foreign bodies, fluids blood, aspirated gastric content, drowning neck and facial trauma laryngeal or tracheal tumors infections laryngitis, epiglotytis obstruction of bronchi aspiration of gastric content, drowning

1)respiratoryfailuretypes - hypoxemic RF PaO2 < 60mmHg PaCO2 </= 40mmHg Synonyms: Type I RF Partial RF Nonventilatory RF - hypoxemic-hypercapnic RF PaO2 < 60mmHg PaCO2 > 45 mmHg Synonyms: Type II RF Global RF Ventilatory failure

2)epinephrineaction Stimulatesalpha,beta1andbeta2adrenergicreceptorsresultinginrelaxationofsmoothmuscleof thebronchialtree,cariacstimulationanddilationofskeletalmusclevasculature.

3)septicshocksignsandsymptoms Clinical signs : Hyperthermia or hypothermia Tachycardia Tachypnea Altered mental status (septic encephalopathy ) Arterial hypotension Warm extremities Large pulse wave Good colour return to the nail bed Full peripheral veins Oliguria

Symptoms
Septic shock can affect any part of the body, including the heart, brain, kidneys, liver, and intestines. Symptoms may include:

Cool, pale extremities High or very low temperature, chills Lightheadedness Low blood pressure, especially when standing Low urine output Palpitations Rapid heart rate Restlessness, agitation, lethargy, or confusion Shortness of breath

2)acuteprerenalFailuretreatment - early and agressive treatment of the causative disorder for normalisation of renal perfusion before occurance of ischemic damage Hemodynamic optimization: normalisation of intravascular volume, cardiac output and systemic vascular resistance - by volemic repletion, inotropic and vasoactive drugs Promotion of urinary output with diuretics (manitol, furosemid)

3)traumapatientairwaymanagement When to suspect cervical spine injury? Know the mechanism of injury Strangulation Fall Deceleration or acceleration s.o. Traumatic signs At the cephalic extremity In the cervical region In the region of thorax (the superior 1/3) Above the nipple line Maintain the head in neutral position 3)cpralgorithm

 1)airwaymanagement Should be applied in case of any unconscious victim; Should precede assessment of spontaneous breathing; Should be maintained during assessment of spontaneous breathing; Should precede artificial ventilation; Should be maintained during artificial ventilation; DURING BASIC LIFE SUPPORT: Safety position Head tilt Chin lift Head tilt and chin lift Jaw thrust Jaw thrust and mouth opening Head extension, mouth opening, chin lift (Safar maneuver / triple airway maneuver); Finger sweep maneuver to remove foreign solid/liquid material in the airway DURING ADVANCED LIFE SUPPORT: Airway devices Endotracheal tube placement 1)renalfailureclassification Prerenal acute renal failure Reduction of renal blood flow Intrinsic acute renal failure Agression of renal parenchyma (toxic, ischemic, imunological, etc) Postrenal acute renal failure Urinary tract obstruction

2)respiratoryacidosis Respiratory acidosis the primary (noncompensatory) elevation of PaCO2 The primary disturbance: PaCO2 > 45mmHg (hypercapnia) Compensatory disturbance change: HCO3 > 27mmol CAUSES : all conditions resulting in type II respiratory failure RESPIRATORY ACIDOSIS Mechanisms: alveolar hypoventilation severe ventilation/perfusion mismatch

3)causesofprerenalfailure Reduction of effective circulant blood volume Hypovolemia caused by hemorrhage Hipovolemia caused by non-hemorrhagic losses Low cardiac output Cardiogenic shock or extracardiac obstructive shock Chronic heart failure Ischemic, toxic, dilated cardiomyopathy Cardiac disrhytmias, etc. Blood flow maldistribution Excessive vasodilatation ( septic shock, excess of antihypertensive drugs) Cirrhosis 1)defibrillationtechnique Patient positioning Rescuer positioning Electrode position Clear order Energy Checking for efficiency

2)parametersofsepticshock Heartrate=increased ArterialBloddPressure=decreased CardiacOutput=increased CentralVenousPressure=decreasednormal PulmonaryArteryocclusionpressure=normal Systemicvascularresistance=decreased OxygenArterialVenousdifference=decreased MixedVenousBloodOxygensaturation=increased 3)ph,hco3,co2metabolicacidosis = increased H+ concentration due to acids acumulation or alkali loss (base deficit BE > -2mEq/l) Primary disturbance: HCO3 < 24mmol/l Compensatory change: PaCO2< 35mmHg