Shock Flashcards
what is shock
condition of inadequate perfusion to sustain normal organ function
what are the 5 main types of shock
hypovolaemic cardiogenic obstructive distributive cytotoxic
what is cytotoxic shock
uncoupling of tissue oxygen delivery and mitochondrial uptake
what can cause cytotoxic shock
CO poisoning CN poisoning (cyanide)
what is hypovolaemic shock
insufficient circulating volume to fill the circuit
what can cause hypvolaemic shock
blood loss
interstitial fluid
pure water deficit (severe dehydration -rare)
third space losses (interstitial/ extravascular/ extracellular)
what are the clinical features of hypovolaemic shock
depends on degree of hypovolaemia
- tachycardia
- hypotension
- tachypnoeic
- reduced urine output
- anxious -> confused and lethargic
who is most at risk in hypovolaemic shock
young people- as compensate very well and then crash
what are the compensatory mechanisms for hypovolaemic shock
baroreceptor reflexes
sympathetic mediated neurohormonal response
capillary absorption of interstitial fluid
hypothalamo-pituitary response
explain the baroreceptor compensatory mechanism for hypovolaemic shock
stretch sensitive receptors in the carotid sinus (CNIX) and aortic arch (CNX) sense decrease stretch
=decreased afferent input to medullary CV centres
=inhibition of parasympathetic (CNX) and enhanced sympathetic output
=increase HR and inotropy
explain the sympathetic mediated neurohormonal response compensatory mechanism for hypovolaemic shock
sympathetic chronotropy and inotropy from baroreceptor reflex
=release of circulating vasoconstrictors (adrenaline, angiotensin, norad, vasopressin)
=redirects fluid from peripheral and secondary organs
=lactic acidosis
=drives chemoreceptors to enhance response
in decompensatory stage circulating vasodilators also increased
explain capillary absorption as a compensatory mechanism for hypovolaemic shock
reduced capillary hydrostatic pressure causes inward net filtration of interstitial fluid
explain the hypothalamo-pituitary-adrenal response as a compensatory mechanism for hypovolaemic shock
internal baroreceptors mediate renin release from juxtaglomerular apparatus
resulting Ang II enhances vasoconstriction and ADH secretion
=enhances renal reabsorption of sodium and water
what is a increase in inotropy
increase in heart contractility
how does the heart increase its cardiac output
increase rate (nerves, hormones)
increase stroke volume (blood volume, vascular resistance)
or increase both
how does inotropy affect the frank starling curve
shifts it upwards- increases contractility
what happens to the frank starling curve in heart failure
failing heart has decreased contractility - curves shifts down
EDV increases to maintain SV but this results in pulmonary congestion
what does it mean when a patient is sensitive to fluids
given fluid when someone is hypovolaemic will have a much bigger effect - a small change in preload will result in a significant increase in contraction
this response lessens as the patient becomes more hypervolaemic
what do you need to consider before giving fluids
know what they are and the dose needed
consider constitution of patient
consider fluid and electrolyte balance
consider difference in fluid for resus and maintenance
what is cardiogenic shock
inability of the heart to pump to meet circulatory demands
myocardial dysfunction causing reduction in systolic function and cardiac output
what can cause cardiogenic shock
mostly complication of MIs acute valve lesion e.g acute mitral prolapse, MI affecting papillary muscle- valve prolapse myocarditis cardiomyopathy myocardial contusion (trauma)
what are the clinical signs of cardiogenic shock
(caused by poor forward flow): hypotension/ shock, fatigue, syncope
(backpressure): pulmonary oedema, elevated JVP, hepatic congestion
what is positive inotropy
increase in force of cardiac contraction regardless of preload
what increases inotropy physiologically
sympathetic nervous stimulation
what drugs increase inotropy
beta and dopaminergic agents
beta- dobutamine, adrenaline
dopamine- dopamine, dopexamine
others- milrinone/ levosimendan
when might you give inotropic drugs
when someone has cardiogenic shock after MI but also have pulmonary oedema due to heart failure
what is an intra-aortic balloon pump
given to people in cardiogenic shock to due heart failure after an MI
- inflates during ventricular diastole to increase diastolic pressure and increase coronary artery perfusion
- deflates during systole to decrease systolic pressure (reduces the pressure the heart has to beat against lowering myocardial wall stress and O2 demands)
what is obstructive shock
involves a physical obstruction to either the heart of great vessels = reduced preload and cardiac output
mainly affects cardiac filling rather than ejection
what is the treatment for obstructive shock
depends on cause:
PE- anticoagulation +/- thrombosis
cardiac tamponade- pericardial drainage
tension pneumothorax- decompression and chest drainage
what are the causes of obstructive shock
PE- stops blood getting back from lungs
tamponade and tension pneumothorax- heart compressed and unable to fill
what does a PE look like on echo
dilated, hypokinetic RV (right side not contracting well due to high pressure)
bowing of interventricular septum to the left (less pressure on left side)
hyperkinetic RV apec (McConnels sign)
what does a pericardial effusion/ tamponade look like on echo
fluid accumulation in pericardial sac
compresses each of the chamber
impairs cardiac filling and contraction in all four chambers
why does a tension pneumothorax cause obstructive shock
air trapped in pleural cavity increases intrathoracic pressure- if this higher than venous pressure wont get cardiac filling
also displacement of mediastinal structures by air impairs cardiac filling and function
what is disruptive shock
Significant reduction in SVR beyond the compensatory limits of increased cardiac output
(circuits too big)
aka vasodilatory/ warm shock
generally high cardiac output but insufficient to maintain forward perfusion
what are the subtypes of distributive shock
septic- bacterial endotoxin mediated capillary dysfunction
anaphylactic- mast cell release of histaminergic vasodilators
neurogenic- loss of thoracic sympathetic outflow follow spinal injury
what is the role of sympathetics in blood vessels
tonically constricts them
how can you detect hypoperfusion in septic shock before hypotension occurs
shown in rising lactate levels
what is the management for septic shock
sepsis 6 + vasopressors after usually 2 bags of fluid with no response
what is anaphylactic shock
uncontrolled activation and degranulation of mast cells
=release of histamine
=uncontrolled widespread vasodilation
=distributive shock
how does adrenaline help in anaphylatic shock
acts as a vasoconstrictor and a mast cell stabiliser
what test confirms analphylaxis
serum mast cell tryptase levels
what is neurogenic shock
form of distributive shock
commonly follows spinal cord/ central trauma
=loss of sympathetic tone
=hypotension
also = unopposed vagal tone= inappropriate bradycardia
(this can be exacerbated by suction, PR exams as these stimulate the vagal nerve)
what is the treatment for neurogenic shock
dopamine + vasopressors
what is spinal shock
NOT SAME AS NEUROGENIC SHOCK
loss of spinal reflexes following a cord transection (can be temporary)
cord transection above what level causes you to loose sympathetic function
T1/2
why does the vagus nerve still work in a cord transection
as is a cranial nerve
what are the reversible causes of cardiac arrest
4H’s
- hypovolaemia
- hypoxia
- hypokalaemia/ hyperkalaemia
- hypothermia
4T’s
- tamponade
- tension pneumothorax
- thrombosis
- toxins
why are recoils important in CPR
release of intrathoracic pressure allows blood to be sucked into the chest before it is pushed out again
what are the four rhythms you can get in cardiac arrest
shockable: VF (will not have a pulse), pulseless VT
non shockable: pulseless electrical activity (could be normal rhythm but no pulse), asystole
what usually causes pulseless electrical activity
hypovolaemia- will have sinus tachycardia on ECG but no pulse
what usually causes asystole
(bad)
severe hypoxia
usually an end stage for other forms of arrest
associated with significant brain damage if do resuscitate
what usually causes the shockable rhythms of arrest
acute MI
toxins
electrolyte abnormalities
