Hypovolaemic shock/ fluid loss

• Explain the Renin-Angiotensin Mechanism? Step 1-3, stimulus, receptor, control center

  1)Stimulus- Low blood pressure, sympathetic division stimulation

  2)Receptor- The juxtaglomerular (JG) apparatus responds to stimuli

  3)Control center- The JG apparatus releases renin enzyme into the blood 4)Renin activates angiotensin to angiotensin I, and angiotensin converting enzyme(ACE) converts angiotensin I to angiotensin II
• Renin-Angiotensin mechanism steps 5-6, effectors(4 of them) and net effect?

  5) Angiotensin II cause: Systemic blood vessels to vasoconstrict which increases peripheral resistance & increased BP, kidneys-decreases glomerular filtration rate (GFR) & decreases urine output to maintain blood volume & BP, Hypothalamus activates thirst center to increase fluid intake =increases blood volume and bp, it also releases ADH =maintains blood volume & decreases urine output, Adrenal cortex releases aldosterone = maintains blood volume & decreases urine output

  6) Net effect- Increased Bp
• Explain the actions of Aldosterone?step 1-3,stimulus, receptor and control center?

  1)Stimulus:Angiotensin II, decreased Na+ blood plasma levels and increased K+ blood plasma levels

  2)Receptor: The adrenal cortex responds to stimuli

  3)Control center: The adrenal cortex releases aldosterone into the blood
• Explain aldosterone step 4-5, effectors and net effect?

  4)Effectors, Aldosterone binds to effectors to cause: In the kidneys there is an increase in K+ secretion into tubular fluid(H+ can be substituted for K+ in conditions of low pH), increases Na+/H20 reabsorption into blood, decreases Na+/H20 and increases K+ lost in urine

  5)Net effect: Blood plasma Na+ maintained; blood plasma K+ decreases. Blood volume and BP are maintained by decreasing urine output
• What is hypovolaemic shock? why does it occur? what does it manifest as?

  “occurs when there is inadequate intravascular fluid volume which leads to inadequate tissue perfusion”

  Manifestations:

  • Decreased Blood Pressure

  • Increased heart rate, respiratory rate • Pallor, cool and clammy skin

  • Decreased urine output

  • Anxiety, Confusion, Agitation
• explain the chart of what acute bleeding causes?

  Hypovolemic shock

  
• Explain the four classes of hemorrhagic shock classification?

  Class I, Class II, Class III, Class IV

  
• Explain the pathophysiological rationale for shock through vital signs?

  Increased heart rate: SNS increases heart rate to maintain cardiac output despite despite decrease in SV (stroke volume)to support perfusion of O2 to major organs and tissues

  Decreased BP:

  Increased respiratory rate: To compensate for decreased available O2 to tissues and increase acid production from anerobic respiration and decreased urinary output results in increased H+ ions – trying to reduce CO2

  Skin is pale, cool and clammy: caused by vasoconstriction caused by RAAS occurring to vasoconstrict and increase BP
• Treatments for shock?

  IV Fluids:

  • Crystalloids

  • Contain substances in solution that can pass through the

  intravascular/interstitial membrane

  • Usually used for replacement or maintenance fluids: Plasma-lyte, Normal Saline, D5W

  ,Lactated Ringers

  -Plasma expanders: Albumin, Gelfusine=act to keep fluid in vessels for longer
• How does hypovolaemic shock occur? How can fluid be lost?

  Due to a haemorrhage is the most common cause but can also occur through fluid loss including blood loss, plasma loss and or loss of interstitial fluid. Blood is lost from bleeding organs or wounds however the circulating volume can be reudced by plasma loss e.g. burns, damaged tissue, fluid loss from renal impairment or inadequate fluid intake.
• what does the loss of fluid in hypovolaemic shock do to the body?

  firstly loss of fluid leads to a reduction in circulatory fluid in the blood vessels=insufficent amount of blood returning to the heart. This poor venous return causes a decrease in cardiac output thus leads to a decrease in blood pressure= decrease in tissue perfusion and thus impairs cellular metabolism and causes shock

  
• Explain the pathophysiology of shock?

  Shock is a severe syndrome that can cause death and is characterized by inadequate tissue perfusion=impaired cellular metabolism. Shock manifests in many diseases and traumatic injuries and is a state of insufficient oxygenation and perfusion to vital organs and tissues throughout the body. Causes of shock vary but the end results are the same=cellular hypoxia/damage is the same for all
• Explain the 1st stage of shock?

  stage 1 aka compensatory/non progressive stage of shock:

  -sufficent BP is needed to adequately perfuse cells with O2 and nutrients, shock starts when BP is unable to do this and thus the body begins a series of compensatory mechanism.

  -during this stage the patient is not at imminent risk of death and shock can be reversed with proper interventions

  -Compensatory mechanisms:neural, hormonal and chemical are initiated to restore homeostasis and maintain blood flow to vital organs like heart, brain and kidneys.
• What is the clinical presentation of hypovolaemic shock?vital signs, urine output, skin, mental status

  heart rate= Tachycardia

  RR=Tachypnoea

  Blood pressure= Hypotension

  Urine output=decreased

  Temperature= normal

  Skin= Cool and pake

  Mental status= restless and anxious
• explain the neural compensatory mechanism from stage 1 of shock?SNS what does it do?

  the sympathetic nervous system(SNS) regulates blood flow and pressure by its ability to increase heart rate and total peripheral resistance. During shock the baroreceptors and chemoreceptors located in the carotid sinus and aortic arch detect the reduction in BP and impulses are relayed to the vasomotor center in the medulla oblongata
• Explain the hormonal compensatory mechanism from stage 1 shock? SNS and adrenal medulla?

  stimulation of the sympathetic nervous system causes the adrenal medulla to release the catecholamines (epinephrine and norepinephrin), which increase heart rate and force contractions to improve cardiac output. The coronary arteries vasodilate to increase blood flow to the heart and meet its increasing demands for O2. the rate and depth of respirations will also increase to try and increase gaseous exchange and O2 levels in the blood.
• what occurs during the hormonal compensatory mechanism of stage 1 shock? hint RAAS angiotensin


  A decrease in cardiac output will also impact the renal system which will detect a decrease in blood flow and pressure to the kidneys. Causing the kidneys to release renin which will convert angiotensinogen into angiotensin I which is metabolized onto angiotensin II, a powerful vasoconstrictor= its presence will cause the release of the hormone aldosterone from the adrenal gland causing the reabsorption of sodium from the renal tubule= retention of water to help increase the falling blood volume.
• what is another hormonal compensatory mechanism for stage 1 shock? posterior pituitary

  Stimulation of the posterior pituitary gland causes the release of anti diuretic hormone(ADH) aka the vasopressin hormone which increases the amount of water reabsorbed by the kidney tumbles thus the patient may produce small volumes of urine or in more severe cases may not produce any at all(Anuria).
• In simple terms explain the renin angiotensin mechanism?

  Hypovolaemic shock

  
• describe the chemical compensatory mechanism for stage 1 shock? hint:CO, blood flow and chemoreceptors

  a reduction in cardiac output= decrease in blood flow to the lungs, which is detected by the chemoreceptors in the aorta and carotid arteries= causing an increase in rate and depth of respirations, however this hyperventilation causes a reduction in CO2 which impacts blood flow and O2 levels to the brain=causing confusion and restlessness. The 2nd stage of shock will begin if the compensatory mechanisms haven’t overcome the shock and will begin to fail
• Explain stage 2 shock? How does it occur an describe the beginning?

  Stage 2 shock aka Progressive/decompensated shock

  -occurs when the the body’s initial compensatory responses fail to restore an adequate BP and tissue perfusion.

  -During the beginning of of progressive shock the patients life can be saved if treatment is timely and appropriate, only if the cause of the shock has been corrected e.g. a haemorrhage, the body’s compensatory mechanisms wont’ cope with the continuing decrease in cardiac output and BP= thus vital organs will not be perfused & tissue damage can occur.
• describe what the systemic circulation does during stage 2 shock?

  The systemic circulation will continue to vasoconstrict aiming to shunt blood to vital organs, this is at the expense of micro circulation= causing ischaemia of the extremities.
• explain cellular metabolism during stage 2 shock?

  -impaired cellular metabolism occurs due to lack of O2 and nutrients this causes the cells to switch from aerobic to anaerobic metabolism=produces lactic acid= metabolic acidosis.

  -prolonged anaerobic metabolism=reduction in production of adenosine triphosphate(ATP)=failure of the sodium-potassium pump=sodium ions accumulate in the cell=swelling and deterioration in cells function
• what happens with histamine and bradykinin during stage 2 shock?hint: not good, hypoxia

  As shock progresses, histamine and bradykinin both have vasodilation properties are released= decreasing the peripheral vascular resistance=continued reduction in blood returning to the heart= causing further decrease in cardiac output and BP=cellular hypoxia.

  -Hypoxia causes depression of the vasomotor center in the medulla and the sympathetic nervous system=decrease in consciousnes, patient become restless and confused, abdominal dissension and paralytic ileus and pancreas becoming ichaemic
• What is stage 3 shock?

  aka irreversib;e/refractory stage of shock

  -during this stage the continued decrease in BP and heart rate= inadequate tissue perfusion= failure of body to respond to therapy=organ failure=death in a matter of hours
• Explain briefly the physiological changes and clinical presentation of stage 1 shock?

  Compensatory

  
• explain briefly the physiological changes and clinical presentation of stage 2 shock?

  Progressive

  
• explain briefly the physiological changes and clinical presentation of stage 3 shock?

  Irreversible

  
• Lo5: explain why patients skin may be cool and clammy after fluid loss?

  Write after lecture
• Lo5: why does pulse increase during hypovolaemic shock?

  Anwser
• Lo5:why does bp decrease during hypovolaemic shock?

  Anwser
• Lo5: what are the signs and symptoms of hypovolaemic shock?

  Anwser
• Lo5: explain the three stages of hypovolaemic shock?

  Anwser
• Lo5: how does perfusion link to hypovolaemic shock?

  Answer
• Lo5: what is the renin angiotensin aldosterone cycle, what causes this to kick into action and why?

  Anwser
• Explain the flow chart of RAAS compensatory mechanism?

  Stage 1 shock or fluid loss in general

  low BP stimulates SNS(sympathetic nervous system) specifically the juxtaglomular apparatus which secretes renin the first stage in RAAS, which promotes secretion of angiotensin that then prompts secretion of angiotensin 1 where ACE converts to angiotensin II, nothing before this step of forming angiotensin II will be active in terms of maintain body fluid

  
• hypovoloaemic explanation from lecture?

  the overall effect of hypovolaemia which can lead to hypovolaemic shock, is that you aren’t getting enough oxygen perfusion to your organs and tissue cells, the body can’t function properly if the fluid loss isn’t fixed so give patient fluids, if this doesn’t work metabolic acidosis will occur as their cells aren’t getting enough oxygen so they revert to anaerobic respiration causing a build up in lactic acid causing acidosis