Shock - Emergency Approach- Part II

Cardiogenic shock - etiology Contractility: AMI Aneurysm LV Cardiomiopathy Myocardium contusion Acute myocarditis LV dysfunction (toxics, drugs) Arrhythmia/ AVB

Cardiogenic shock - etiology Mechanic problems: Post partum Acute mitral regurgitation capillary muscles break/dysfunction ASo HCM Aorta dissection Ventricular septum break Pre partum Mitral stenosis Atria mixom Massive pulmonary embolism Heart break with tamponade Aorta dissection with pericardia tamponade Pericardia tomponade

Pathophysiology- Shock in AMI

Physiopathology AMI classes- Forrester: I- CO normal + preload normal ( reperfusion treatment)- mortality 3 % - II- CO normal + pulmonary edema (vasodilatations, diuretic)- mortality 9 % III- low CO, normal preload (volume, inotrop positive)- mortality 23 % IV- low CO, preload high ( inotrop positive, vasodilatation) - mortality > 50 %

Clinic framework Cardiac disease signs: angina pain, dispnea, asthenia Shock signs Signs of acute left ventricular insufficiency and right acute ventricular insufficiency

Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia. Hypotension due to decrease in cardiac output. A rapid, weak, thready pulse due to decreased circulation combined with tachycardia. Cool, clammy, and mottled skin (cutis marmorata), due to vasoconstriction and subsequent hypoperfusion of the skin. Distended jugular veins due to increased jugular venous pressure. Oliguria (low urine output) due to insufficient renal perfusion if condition persists. Rapid and deep respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis. Fatigue due to hyperventilation and hypoxia. Pulmonary edema, involving fluid back-up in the lungs due to insufficient pumping of the heart.

Diagnosis Physical exam Ecg 12 leads Thoracic radiography – pulmonary overloading, ICT Arterial gases Myocardium enzymes Transthoracic and trans esophageal echocardiography Hemodynamic invasive monitoring

Treatament Cardiac diseases: trombolysis, PTCA, cardiovascular surgery APE: mechanic ventilation, vasodilatators, diuretic Positive inotropic support: dopamine, dobutamine, aortic contra pulsation balloon Emergency surgeries

Neurogenic shock - definition Hypotension and bradycardia appeared after acute lesion of the spine with sympathic influx interruption Spinal shock – temporary loss of medullar reflex activity appeared after a total spine lesion Epidemiology – close traumas (car, motobike accidents), open traumas (white weapons, fire weapons)

Physiopathology Traumatic event: spine compression, dilaceration Medullar secondary lesions (days, weeks)-ischemia, local arterial lesions, intra-arterial thromboses Sympathic tonus loss with emphasis on the parasympathic one Hypotension, bradycardia

Clinic framework Traumatic context (close or open) Hypotension with warm and dry teguments, possibly hypothermia Bradycardia Lesion upper than T1- blocking of whole SNVS Lesion T1-L3 – partial interruption of SNVS Different framework in penetrative trauma (hemorrhagic component)

Treatament A- with cervical spine protection B- ventilation, oxygenation C- fluids resuscitation: crystalline solutions D- neurological evaluation E- secondary evaluation of a patient with trauma Corticotherapy metilprednisolon 30 mg/kg during the first hour then 5,4 mg/ kg/h ,23h Vasopressor support - dopamine, dobutamine

Obstructive shock Cardiac tamponade Tension pneumotorax Massive Pulmonary Embolism How to recognize? How to treat?

Tromboliza sau embolectomie high risc PE (shock or hypotension) CT available immediate * no yes Echocardiography R V distension CT available no yes CT CT no availble* alte teste sau pacient instabil pozitiv negativ Cercetarea altor cauze Tromboliza/ embolectomia nejustificate Tratamentul specific al EP este justificat Tromboliza sau embolectomie Cercetarea altor cauze Tromboliza/ embolectomia nejustificate