Lecture

• general things that cause shock are inadequate Cardiac output and blockage to flow
• Cardiac tamponade causes fluid filling around the pericardium of the heart. This can cause diastolic heart failure as the space the heart has to fill and contract is reduced..
• A tension pneumothorax consists of massive atelectasis and is a one valve in which air can get in and can't get out. It can lead to diastolic heart failure as air compresses on the hard and makes it difficult to pump
• No perfusion to the cells(shock) means decreased flow/pressure, decreased O2, decreased glucose/nutrients and decreased CO2 removal
• Decreased CO2 removal in shock causes: acidosis which causes vasodilation(worsening shock symptoms).It also alters H+ levels which affects K+, causing transient hyperkalemia
• In shock, Na/K pump fails due to hypoxemia so Na+ pools inside the cell which causes hydrotropic swelling. As this progresses, the cell bursts and mitochondria gets broken down; this releases cytochrome c to activate apoptosis
• In shock, there's an increase in anaerobic metabolism which causes: a decrease in pH decreasing cardiac contractility, decrease in vascular responsiveness and an increase in NO(potent vasodilator)
• Failure of autoregulation in shock causes malperfusion within the vascular system, meaning that blood will not be going towards where its needed most.
• Shock causes an increased immune response which causes increased capillary permeability(histamines). This causes fluids to go into interstitial spaces and it decreases vascular volume
• The 3 stages of shock are: compensatory, progressive and refractory
• Compensatory shock is the earliest stage of shock and its not easy to identify.
• Within compensatory shock: HR is within 60-100, BP might be decreased but its within normal parameters and pulse pressure should be normal/narrow.
• Within compensatory shock, decreased perfusion causes increased osmolarity, baroreceptor stimulation to signal the SNS, chemoreceptors increase the resp rate/volume and ADH increases responsiveness to catecholamines
• Clinical manifestations of compensatory shock are: narrowed pulse pressure, tachycardia, tachypnea, oliguria(decreased urine output due to sns stimulation), altered mentation and mydriasis
• Progressive/decompensating stage of shock occurs when compensatory mechanisms are ineffective. This when vital signs are falling outside of normal range.
• In the progressive stage of shock, the myocardial depressant factor gets released by the pancreas. It also gets released in pancreatitis.
• In the progressive stage of shock, metabolic acidosis occurs which worsens oxygenation. Respiratory acidosis also occurs but metabolic is greater
• In progressive shock, the increased SNS stimulation increases preload but also MVO2 which is bad looks frfr
• S/S of progressive shock : tachycardia/dysrhythmias, hypotension, LOA/LOC changes, thrombi and oliguria
• Refractory shock is when tx doesn't work and is irreversible.
• Refractory shock has a widened pulse pressure(at the very end the systolic catches up to the bottomed out diastolic). It's seizure/coma/death type shit
• In refractory shock, there's: cell anoxia/death, loss of vasomotor tone, continued released of myocardial depressant factor, bradypnea/apnea, and organ failure
• S/S of refractory shock: bradycardia to asystole, respiratory arrest, ashen colour, dependent lividity and pupils are fixed and dilated
• Complications of shock are: acute renal failure(ARF), Multiple organ dysfunction syndrome(MODS), acute respiratory distress syndrome(ARDS) and disseminated intravascular coagulation(DIC)
• In ARF, there's decreased renal perfusion leading to decrease GHP(renal BP) and GFR which leads to acute tubular necrosis(ATN). This causes urine output to diminish which allows toxins to build up. Is potentially reversible if treatment is given early enough
• MODS occurs when there's dysfunction in 2 or more systems. Its associated with systemic inflammatory response system(SIRS).The key to this is the mitochondria organelle. Primarily due to trauma but can occur secondarily due to sepsis
• ARDS occurs often due to inflammation and sepsis. It manifests in non-cardiogenic pulmonary edema, decreased compliance and refractory hypoxemia
• DIC is common with sepsis and obstetrical problems. It refers to abnormal clot formation which uses up clotting factors, making patients prone to bleeding
• S/S of DIC depend on location and severity. Can result in intracranial hemorrhage, vascular obstruction and organ/system obstruction. It causes oozing hemorrhages like: IV sites, hemoptysis, hematuria and wounds
• Cardiogenic shock is decreased contractility and pump failure. Most commonly is an MI but could be these other things that cause decreased CO: arrhythmia's, valve disease and ventricular rupture
• Obstructive shock refers to when the heart is prevented from pumping by a mechanical obstruction. Examples are pulmonary embolisms, cardiac tamponade and tension pneumothoraxes. This type of shock can sometimes overlap with cardiogenic shock
• Beck's triad for cardiac tamponade: JVD, hypotension and muffled heart sounds
• Hypovolemic shock is inadequate blood volume for tissue perfusion. It's divided into either hemorrhagic or non-hemorrhagic
• Non-hemorrhagic hypovolemic shock occurs due to dehydration, loss of plasma proteins and overuse of diuretics
• Stage 1 hemorrhagic shock: only skin signs and tachycardia
• Stage 2 hemorrhagic shock: responsive to fluid treatment
• Stage 3 hemorrhagic shock: hypotensive shock with less signs of responsiveness to treatment
• Stage 4 hemorrhagic shock: shock with signs of ischemia to the brain/heart or total blood loss volume >40%
• Stage 5 hemorrhagic shock: cardiac arrest due to exsanguination
• Distributive shock is caused by anaphylaxis, neurotrauma and sepsis