Wk 7: Shock Flashcards
Define shock
= inadequate tissue perfusion (=hypoperfusion), resulting in impaired cellular respiration, metabolism and function.
(Pefusion= volume/time over amount of tissue e.g. 20ml/min/100g tissue)
This occurs due to an imbalance between supply and demand of oxygen and nutrients.
O2 delivered < O2 required
**life-threatening
Explain cellular respiration
When tissue has adequate perfusion-> O2 is used to convert glucose to ATP/energy to fuel cellular function (aerobic metabolism)
C6H12O6 + 6O2 –> 6CO2 + 6H2O + ATP (36 molecules)
Glucose + Oxygen –> Carbon Dioxide + Water + Energy
Explain anaerobic metabolism
= where the cells are deprived of oxygen-> produce only 2 ATP molecules instead of 36 and additionally produce lactic acid-> contributed to cell damage
Explain how impaired oxygen leads to organ failure/shock
-> impaired O2 delivery to cells (hypoperfusion)
-> anaerobic metabolism commences (+lactic acid)
-> ↓ production of ATP (Energy)
->loss if cell membrane permeability
-> Na+/K+ pump lost
-> fluid shifts
->lysosomal enzymes released
-> Cellular death and organ failure
Explain how impaired delivery and use of glucose leads to shock
-> impaired delivery and use of glucose by the cell
-> another source of energy is accessed
-> increasing acidosis (?due to lactic acid)
-> protein depletion
-> impaired cellular metabolism
What are reasons hypoperfusion can occur?
- decreased circulating volume of blood thus not able to get O2 to the cells (Hypovolemic)
- poor heart contractility (cardiogenic)
- obstruction in CVD (obstructive)
- fluid obstructs perfusion between blood and cells (distributive)
What are the three pathophysiological stages of shock?
- compensatory
- Progressive
- irreversible/refractory
Explain what occurs in the compensatory stage of shock
- Neural, hormonal and biochemical compensatory mechanisms are activated to overcome the consequences of anaerobic metabolism and maintain homeostasis/ tissue perfusion.
- decreased CO (presenting as decreased BP) stimulates baroreceptors and chemoreceptors which active the SNS= vasoconstriction + release of nor-adrenaline and adrenaline= increased myocardial contractility and thus oxygen consumption= coronary arteries dilate.
- Blood flow to most essential organs (heart and brain) is maintained
- decreased blood flow to the non-vital organs, such as kidneys, GI tract, skin and lungs as is diverted or shunted.
- Renin-angiotensin-aldosterone system activated due to decreased renal blood flow. Angiotension 2= atrial and venous vasoconstriction= increased vennous return to heart (+ increases BP)
- Antidiuretic hormone (ADH) released by stimulation of adrenal cortex when increased Na+ and water reabsorption + K+ excretion by kidneys= increased serum osmolarity-> release of AHD from posterior pit gland to increase water reabsorption by the kidneys, thus further increasing blood volume= increase in Co and thus BP
- shunting blood away from the lungs results in psychological dead space where air can not participate in gaseous exchange= Arterial oxygen decrease= compensatory increase of rate and depth of respirations
- decreased blood flow to GI= impaired mobility + slowing perilstalsis= increased risk of paalytic ileus.
- decreased flow to skin= cool and clammy (**in early septic shock they feel hot due to fighting infection)
-
At what stage of shock can a to recover from shock?
- Compensatory
Explain the pathophysiology of the Progressive stage of shock
-> Compensatory mechanisms fail
-> decreased ATP production
-> Hypoxia of vital organs as CO + BP begins to fall
-> Decreased cellular perfusion and tissue ischemia
-> Failure of Na+-K+ pump
-> altered cell membrane permeability= leakage of
fluid and protein out of the vascular space into the surrounding
interstitial space= increase is systemic interstitial oedema
-> metabolic acidosis
-> Decreased cardiac output and thus myocardial perfusion
-> arrhythmias, myocardial ischemia and possible MI
-> pulmonary ateriorlies contrict= increased PA pressure= worsening decreased ventilation and PQ mis match-> fluid moves form pulmonary space to interstitial space= oedema, bronchoconstriction and a decrease in functional residual capacity + decrease compliance.
-> fluid moves intracappillary= decreased functional residual space + decreased surfactant production= tachypnoea, crackles + increased WOB
-> decreased GI perfusion = decreased ability to absorb nutrients+ ischemia of musosal barrier-> increased risk of gastric ulcers and gastric bleeding
-> increased risk of migration of bacteria from GI to blood
-> increased risk of developing disseminated intravascular coagulation (DIC)
-> Acute renal failure due to renal tubular ischemia secondary to prolonged hypoerfusion (**can be worsened by certain medxs e.g. certain antibiotics, anaesthetics and diuretics) = decreased urine output, increased blood urea nitrogen and serum ceratine= metabolic acidosis occurs from kidneys inability to excrete acids (especially lactic acid) and reabsorb bicarbonate
-> liver loses functional ability so jaundice can insure + increased waste in blood + loss of immune abilities so bacteria builds up
-> Disseminated intravascular coagulation= fribronltics consume clotting factors and platetes= bleeding form many orrifaces
-> Aggressive management required to prevent multip organ dysfunction syndrome (MODS)
**pts are admitted to ICU
** Mental state changes!
Explain the pathophysiology of the refectory stage of shock
- Compensatory mechanisms are overwhelmed
- Severe tissue hypoxia with ischemia, necrosis and death of the cell occurs
- Build up of toxins
- including lactic acid from decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism contributes to increased cap permeability and dilation
-> fluid moves to IS space
-> loss of IV volume= worsening hypotension + tachycardia + decreased coronary blood flow
-> myocardial depression= declining CO= cerebral BF connot be maintained= cerebral ischemia - Multi-organ failure
-> The failure of the liver, lungs
and kidneys results in an accumulation of waste products, such lactate, urea, ammonia and carbon dioxide.
->The failure of one organ system affects several other organ systems. - Recovery unlikely
What are the four types of shock, their general cause and comment on their dynamic nature?
- Hypovolaemic shock (loss of intravascular volume)
- Cardiogenic shock (pump failure)
- Distributive shock (systemic vasodilation)
- Obstructive shock (physical obstruction of blood circulation)
- may be in isolation or in combination with multifactorial shock
**note that shock may be due to an issue with the pump (cardiogenic), the tank (hypovolemic) or the pipes (obstructive or distributive)
What are some causes of hypovolemic shock?
= anything that causes a loss of fluid and low volume in IV space.
- occurs with 15% of IV volume lost. Compensated bu the average adult until this point (average adult= ~750ml)
- Absolute fluid loss= fluid lost from the body e.g vomiting, haemorrhage, diruesis
- Relative fluid loss= fluid lost from Iv space e.g third spacing
Different causes;
External
- trauma
- haemorrhage (whole blood)
- vomiting/diaphoresis (interstitial fluid)
- diabetes insipidus
- diuresis
Internal
- burns (plasma)
- dehydration
- ascites (third spacing in abdomen)
-peritonitis
- third spacing of fluid (ascites - often from liver failure where albumin is not being produced and this cant maintain IV BV cause fluid can escape vessels)
What what point do the levels of hypovolemia shock develop?
When total circulating volume is decreased by aprox 15%
At 15-20% total fluid loss SNS is activated= increased CO, HR, RR
> 30% lost- compensatory mechanisms fail
> 40%= irreversible tissue damage
What are the clinical manifestations of hypovolemic shock? and why might each of these be occurring?
- Restless, anxious, confused, agitated (cerebral hypoperfusion)
- Tachypnoea (decreased pulmonary functional capacity/VQ mismatch)
- Hypotension (patients may initially be hypertensive when compensation occurs) (decreased IV volume)
- Tachycardia (compensatory mechanisms SNS stimulation to overcome dressed BV and ensure perfusion)
- Weak thready or absent peripheral pulses (BF shunting to vital organs)
- Poor skin turgor (poor perfusion/dehydration)
- Cool, clammy, moist skin (blood diverted to vital organs)
- pale (due to blood loss) * particularly under eye lids
- Decreased UO (RAAS initiation + K+ sparing)
- Marked thirst (RAAS)
- Acidosis (beginning of anaerobic metabolism)
Explain the pathophysiology of hypovolemia shock
- low fluid volume in IV space= low pre-load/pre-load/LVEDV (heart filling)
- preload- afterload= SV and when PL is decreased= decreased SV= decreased CO
- SNS responses to baroreceptors recognising decreased BP= vasoconstriction occurs to compensate for decreased CO by attempting to increase preload
How is hypovolemic assessed/diagnosed?
Assessment of bloods
- lactates (indicating cell oxygenation status/? in anerobic)
- ABG (arterial blood gases to assess O2 of blood)
- complete blood count (? low haemoglobin or low heamotricrit)
What is the treatment of hypovolemic shock?
Goals: Maintain BP, blood volume, blood contents and treat cause
- IV fluids (to maintain BP)
- pressors (to vasoconstrict for BP)
- give blood transfusion, platelets, coag factors with FFP, albumin (blood contents)
- treat major problem (surgery)
What are the causes of cardiogenic shock?
= anything causing inadequate cardiac output.
**occurs in the presence of adequate IV volume (unlike hypovolemic shock does)
- issues in either diastolic or systolic action
- mortality rate is very high, up to 60%
- reduced contractility/muscular dysfunction (wall stiffness)
*MIs are the most common cause of cardiogenic shock - inadequate filling
- arrhythmias e.g. AF= ineffective contraction of the stria
- structural/failure of forward flow (valvular issues)
What are some clinical manifestations of cardiogenic shock?
- Increased respiratory rate (pulmonary congestion, systemic + pulmonary oedema secondary to increased PL, SV + HR from RAAS increasing PV after being stimulated by low CO and the release of Catecholamines (NA + A))
- Increased work of breathing (WOB) (pulmonary congestion, systemic + pulmonary oedema secondary to increased PL, SV + HR from RAAS increasing PV after being stimulated by low CO and the release of Catecholamines (NA + A))
- Possible crackles or acute pulmonary oedema (APO) on chest auscultation (pulmonary odeema)
- Tachycardia ( due to RAAS lifting BV and catecholamine initation)
- Hypotension (increased myocardial requirements in the presence of hypoperfusion= ↓ CO= ↓ BP)
- Distended neck veins (raised JVP) (due to blood backing up into the the venous system)
- Cool, clammy, pale skin (as blood is diverted to important rogans)
- Prolonged capillary refill time
- Decreased urine output
- Confusion (cerebral hypoxia)
- Anxiety (?cerebral hypoxia + ?decreased flow in coronary arteries)
- angina (as heart is starved for O2)
How is cardiogenic shock diagnosed?
- PCWP= pulmonary capillary wedge pressure (used to assess left ventricular filling, represent left atrial pressure, and assess mitral valve function) (measured by catheter place in pulmonary arteries to assess back pressure from heart)
- CO/ cardiac index (CO/Body s:a) used to standardise a pats cardiac output
- serum lactate (failure of cells to use oxygen/anabolic)
- ABG (oxygenation)
- troponins
- CXR
- ECG (?MI, arrhythmias)
- Echo/heart u/s to assess contractility
Explain the treatment of cardiogenic support
- Administration of O2 (to support cellular oxygenation)
- CV system support
- increase systemic vascular resistance with vasopressors (norepinephrine, epinephrine to get vasoconstriction)
- increased heart contractility with meds - repair heart/problem (e.g. if they have occluded vessels in the heart, repair that or valves if they are the issue)
What are the three types of distributive shock?
- Septic shock
- Anaphylactic shock
- Neurogenic shock
What is the cause of distributive shock?
= excessive vasodilation and impaired distribution of blood flow.
Define septic shocks and what causes it?
= occurs when a pt develops sepsis (septic material in the blood) and the inflammatory mediators that are released cause widespread vasodilation, compromised vessel permeability, tachycardia, decreased myocardial contractility and decreased tissue perfusion.
(bacteria has entered the bloodstream which triggers an inflammatory response. This activates the release of inflammatory mediators)
What are the clinical manifestations of septic shock?
- Tachypnoea
- Hypoxia
- Hypotension (persistent despite fluid resus so often need vasopressors)
- Systemic oedema
- Tachycardia
- Increased temperature
- Decreased urine output
- Hot clammy skin
- Confusion
- Agitation
Explain the pathophysiology of cardiogenic shock
-> CO is reduced
1. stimulates the release of compensatory RAAS and antidiuretic hormone -> shifts to ensure adequate or increased BV
2. stimulated release of catecholamines (adrenaline and nr-adrenaline) compensatory release leading to
- increasing SVR leading to
-> and secretly resulting in
-> increased preload, SV and HR
-> increasing the effects of systemic and pulmonary oedema= dyspnoea
-> causing increased myocardial requirements= ↓ CO and ↓ ejection fraction
-> lowers BP
-> ↓ tissue perfusion
-> ends with impaired cellular metabolism
Another view;
Ineffective forward flow of blood
- decreased SV-> decreased CO-> decreased cellular O2 supply-> ineffective tissue perfusion-> impaired cellular metabolism
and
Inneffective ventricular emptying-> increased pulmonary pressures-> pulmonary oedema-> decreased oxygenation-> decreased cellular oxygen supply-> ineffective tissue perfusion-> impaired cellular metabolism.
Explain the pathophysiology of septic shock
- identified as Gram-negative organism= release of endotoxins
- identified as Gram-positive organism= release of exotoxins
-> act as triggering molecules activating- CNS and endocrine systems->hyper metabolic state= increased cellular demand-> decreased tissue perfusion= shock
- complement system
- coagulation cascade
- Kinin system
- neutrophil, endothelial and monocyte-macrophage cell activity
-> all contribute to the release of endogenous mediators
-> which are tumor necrosis factor-alpha; interleukins-1
-> resulting in the release of proinflammatory cytokines
-> causes endothelial cell damage leading to - hypotension due to peripheral vasodilation
- decreased systemic vascular resistance
- decreased myocardial function (myocardial depression)
- lactic acidosis
- leucopenia
- thrombocytopenia
- vascular leakage due to increased capillary permeability
- pulmonary congestion
- micro- emboli formation
- tissue necrosis
-> decreased cellular oxygen supply
-> Decreased tissue perfusion
-> eventually causing organ dysfunction
