Shock Flashcards
how is shock a syndrome and not a disease?
a syndrome is a group of symptoms which CONSISTENTLY OCCUR TOGETHER, or a condition characterized by a set of associated symptoms. A syndrome only becomes a disease when paired with a definitive cause.
because shock alone is not a causative agent, rather it is caused by an agent, it is therefore a syndrome and not a disease.
define the four types of shock: cardiogenic, obstructive, hypovolemic, distributive.
cardiogenic: Cardiogenic shock is a clinical condition of inadequate tissue (end-organ) perfusion due to the inability of the heart to pump an adequate amount of blood.
obstructive: Obstructive shock is caused by physical obstruction of circulation either into or out of the heart.
hypovolemic shock: characterized by diminished blood volume such that there is inadequate filling of the vascular compartments.
distributive shock: characterized by a loss of blood vessel tone, enlargement of the vascular compartment, and displacement of the vascular volume away from the heart and central circulation.
discuss the outcomes of impaired tissue oxygenation at the cellular level
cells will surely lose function if there is low oxygenation, and can even die if the oxygenation is inadequate for long periods of time.
explain why kidney function would be compromised in most forms of shock
shock often lasts longer than 15-20 minutes, and the kidneys can only take severe ischemia (non-perfusion of the kidneys) for 15-20 minutes.
furthermore, the renal tubes are particularly vulnerable to ischemia.
clinical signs of hypovolemic shock
ways to restore blood volume
thirst, increased HR, cool and clammy skin, decreased arterial bp, decreased urine output, change in pigmentation.
Tx directed to correcting or controlling the underlying cause.
give o2, IV medications, and IV infusions of blood.
discuss the outcomes of impaired tissue oxygenation at the cellular level
the cells and tissues die after a considerable amount of time
explain anaphylactic shock: causes and outcomes
causes: medication reactions (penicillin), foods (nuts and shellfish), insect venoms.
outcomes: can die without treatment (epi pen or removal of the inciting agent or etc.), so getting treatment quickly is a priority because the airways are closing and you don’t have time to sit around.
clinical manifestations and treatment measures for septic shock
CM: hypotension, warm/flushed skin, decrease in SVR, hypovolemia d/t arterial and venous dilation and leakage of plasma within the interstitial spaces and fever.
Tx: control of the causitve agent and support circulation.
antibiotic therapy
airway management–mechanical ventilation if needed
central venous access to give medicines
CBCs and other tests to indicate severity
blood cultures from two different sites to give best antibiotic.
describe clinical signs of obstructive shock and pulmonary embolism.
obstructive shock: elevated right heart pressure, elevation of CVP (central venous pressure), jugular venous distension.
pulmonary embolism: dyspnea, tachypnea (RR >20) , tachycardia (BPM >100), pleuritic chest pain, anxiety/apprehension, cough, haemoptysis (coughing up blood), leg pain, clinically evident DVT (10% of patients)
describe clinical signs of cardiaC tamponade and tension pneumothorax.
cardiac tamponade:
BECK’S triad:
1. low Blood pressure in the arteries
2. mufflEd heart sounds
3. swollen or bulging neCK veins (neck veins distended)
also low bp, chest pain, dyspnea, tachypnea, discomfort that’s relieved by sitting or leaning forward.
tension pneumothorax: chest pain, shortness of breath, rapid breathing, and a racing heart, followed by shock
doctors can usually diagnose based on person’s hx, symptoms, and exam results. Emergency treatment is needed.
regarding hypovolemic/hemorrhagic shock, list the compensatory mechanisms to maintain circulatory function and blood volume
sympathetic-mediated responses: tachycardia, vasoconstriction (to increase blood return to the heart).
to restore blood volume: absorption of fluid from the interstitial spaces, conservation of sodium and water by the kidneys and thirst (ADH stimulates this).
decrease in renal blood flow and glomerular filtration rate to activate RAAS, which results in an increase of sodium reabsorption by the kidneys.
septic shock: explain the pathogenic mechanisms. start with infection.
suspected or proven infection: this is when a pathogenic microorganism enters the body and starts an infection process. then the systemic inflammatory response happens.
(diffuse endothelium dysfunction and impaired microvascular function)
systemic inflammatory response: this is the immune system in overdrive because there is an invader and the invader must be killed.
severe sepsis with organ dysfunction: when the imflammatory response goes on for too long, the body gets tired because it has been on such high alert for so long of a time. This leads to organs (probably the kidneys and such) FAILING because they are quite tired and don’t have enough “energy” to carry out their normal processes d/t being on high alert and conserving energy.
INFECTION–>SYSTEMIC INFLAMMATORY RESPONSE—>ORGAN FAILURE
link endothelial cell dysfunction to some major consequences in septic shock: capillary leak, peripheral vasodilation, and impaired tissue perfusion
capillary leak: if the endothelial cells are dysfunctional, then the capillaries would leak because the endothelial cells wouldn’t be there to regulate what can go in or come out.
peripheral vasodilation: if dysfunction, the periphery of the body would vasodilate because there is nothing to regulate them.
impaired tissue perfusion: tissues would not be perfused because the cell is broken and cannot help perfuse the tissues.
discuss clinical signs of improvement for patients with septic shock
signs for improvement would be a reversal of symptoms–no hypotension, skin a normal temperature and not flushed, SVR back to normal, no hypovolemia, no fever, WBC count down.
