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Pathophysiology > Patho: Shock > Flashcards

Patho: Shock Flashcards

1
Q

What is shock?

A

Shock results from a decrease in circulating blood volume, leading to decreased tissue perfusion (Flow of blood to tissues) and general hypoxia.
In most cases, CO is low. (but not all)
Shock is most easily classified by the cause, which also indicates the basic patho and Tx.

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2
Q

Classifications of Shock

A

1) Hypovolemic: loss of circulating blood volume.
2)Cardiogenic: inability of the heart to pump the blood through the circulation.
A) Obstructive: interference w/ blood flow through the heart.
B)Distributive: Vessels aren’t working for delivery. Changes in peripheral Resistance leading to pooling of blood in ther periphery
- Neurogenic,
-Anaphylactic,
-Septic shocks.

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3
Q

How can blood pressure be affected by blood volume, cardiac contraction, and peripheral resistance?

A

BP is determined by blood volume, heart contraction, and peripheral resistance.-when one of these fails, BP drops.

1) When BP is low, it is difficult to maintain pressure within the distribution of the system.
2) If the force of the pump declines, blood flow slows, and venous return is reduced.
3) If peripheral resistance is altered by general vasodilation, which increased the capacity of the vascular system, it leads to a lower pressure within the system and sluggish flow.

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4
Q

Metabolic needs of cells

A
  • In people w/ shock, there is usually less CO and so blood flow through the microcirculation (blood flow through the capillaries) is decreased, leading to reduced oxygenation and nutrients for the cells; waste removal.
  • Less oxygen results in anaerobic metabolism and increased lactic acid production. Metabolic needs for the cells are not met.
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5
Q

Stages of Shock

A

1) Nonprogressive stage
2) Progressive stage
3) Irreversible Stage

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6
Q

Nonprogressive stage

A

A.k.a: Compensatory shock

  • Compensations are still working
  • Compensatory mechanisms prevent large changes in circulatory function.
  • Maintaining BP for pt.
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7
Q

Progressive stage

A

A.k.a Uncompensated Shock

  • Compensations are no longer working.
  • Shock becomes progressively worse.
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8
Q

Irreversible/decompensated Stage

A
  • No medical interventions are capable of allowing the pt to go back to normal.
  • Shock has progressed to an extent where all known forms of therapy are insufficient to provide life saving measures.
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9
Q

S/s of Nonprogressive/Compensatory stage shock.

A

-Anxiety and Restlessness:
from decreased O2 to the brain, meaning neurons are hypoxic. Decreased glucose and nutrients to the brain, meaining neurons don’t have a store of energy, no fats or glycogen to draw from.

-Thirst (CNS involement):
Compensation to increase blood volume b/c it’s low.-Tachycardia: body is trying to increase CO (CO= HRxSV). If BP is too low, and not enough blood is being delievered, the baroreceptors will notice and signal to compensate by pumping the heart faster.

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10
Q

S/s of Progressive Stage shock

A

-Lethargy/Weakness(CNS): decreased O2(hypoxic), decreased nutrients. The difference is that this is more long term.
Brain is tired, CNS isn’t firing and sending same signals, therefoe, the body is less awake and less alert. LOC will drop.
-Cool,moist, pale skin: Blood is shunting from the peripheral tissues. If not enough blood is circulatiing around the body, then the body will pull bood out of the integ system.
Cool feeling d/t no heart from blood.
Moist d/t being in fight or flight reponse; body expects you to be running around, so you get insensible perpiration
Ex: sweaty plams when shaking someones hand.-Low BP: compensation is failing, not enough to maintain BP. HR and thirst are not enough to compensate anymore.
-Tachycardia: Still trying to incr. CO to incr. BP.
-Weak pulse: BP is low and blood volume is down so pulse strength is no longer maintained.
-Tachypnea:
1)Body trying to reverse hypoxia and take in O2. 2)body is in metabolic acidosis d/t lack of O2 and blood flow (trying to compensate)
-Metabolic Acidosis: Lactic acid production from muscles d/t lack of O2.

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11
Q

S/s of Irreversible/decompensated stage shock

A
  • Stupor/confusion/coma: Sever lack of O2, neurons shut down and are completely unable to metabolize.
  • Arrythmias: lack of O2 and glucose leds to myocardial cell death. Metabolic acidosis is happenings, so kidneys will try to get rid of H+ to rbing pH back up. H+ shifts out of cells, and to maintain electrical neutrality, K+ gets shifted into cells and pt ends up hyperkalemic.
  • Bradycardia: Blood volume is low, heart is dying. No longer tachycardia, heart is in state of dysrhythmia/arrhythmia.
  • Metabolic acidosis: has progressed and is unfixed by renal mechanism. b/c body can’t breathe and release CO2
  • Acute respiratory distress syndrome: Muscles for breathing need glucose and can’t work anaerobically for very long so mucles go into state of paralysis.
  • Multiple thrombi: clot formation in bloodstream from clotting cascade in this phase. d/t Disseminated intravascular coagulation
  • Acute renal/liver failure: both organs fail d/t complete lack of ATP
  • Paralytic ileus: GI tract stops moving d/t absence of smooth muscle contractions and neuronal function. Halts nutritional intake.
  • GI hemorrhage: as Gi tract stops moving, edema occurs which leads to rupture and hemorrhage.
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12
Q

Compensated Shock Compensation

A

Compensation starts as soon as BP drops.
1)SNS and Adrenal Medulla are stimulated to increase the HR, force of contractions, and systemic vasoconstriction. Causes bronchodilation, leads to incr. peripheral vascular resistance, and decr. in capillary flow in some capillary beds like the GI tract.
2)Renin is secreted to activate angiotensin (vasocontrictor), and aldosterone (from adrenal gland) to incr. blood volume.
3)Increased secretion of ADH (to hold onto water) also promotes reabsorption of water from the kidneys to increase blood volume and acts as a vasoconstrictor.
4)Glucocorticoids are secreted that help stabilize the vascular system.
5)A decrease in perfusion and incr. in acidosis leads to a chemoreceptor response, this response increases the rate and depth of ventilation.
Acidosis stimulates resps, incr. O2, and decr. CO2 lvl.Pt may have decr. cap refill and cool skin b/c the blood is shunted from the skin to the vital organs.

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13
Q

Uncompensated Shock Compensation

A

Compensation occurs when the body is no longer able to maintain systemic BP as the compensatory mechanisms fail, systolic and dystolic pressures drop and cerebral flow decreases.

  • systolic drops before distolic b/c systolic usually depends more on blood volume.
  • the decrease in systolic compared to dystolic can lead to a narrow pulse pressure to the point where it may not longer be detectable.
  • PCO2 may drop; however PCO2 usually stays normal.
  • Effects of the cardiovascular system include a decreased preload and an increased rate of contraction cause by catcholamine stimulation.
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14
Q

In uncompensated shock, why might the myocardial strength be decreased?

A

1) Ischemia: from a reduction of circulating RBC’s, a lower oxygen saturation pressure (PO2) and decreased coronary perfusion b/c of hypotension (especially diastolic hypotension)
2) Cardiodepressant substances can depress heart function in late shock.
3) Necrosis of myocardium can result from ischemia.
4) Decr. preload can lead to decr. contractility (decr. venous return)
5) Acidosis can lead to decreased contractility
6) Cardiac rhythm disturbances can result from hypoxia.

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15
Q

Irreversible/decompensated Shock Compensation.

A

The progression of cellular ischemia and necrosis and organ death (even with oxygenation and perfusion restored) indicate irreversible shock which is fatal.
-Thrombi form in the microcirculation further reducing venous return and CO
-Fluid shifts to ISF as more cytokines are released from damaged cells. (edema)
-Cells and vitals organs begin to die d/t lack of energy
-Membrane pumps fail (Na/K pump) ***
-Organelles in cells breakdow, necrosis is unavoidable. (losing the mitochondria= no ATP)-Eventually everything dies.
Decompensation may occur suddenly or is delayed from 1day-3wks after onset of shock.

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16
Q

What are the Irreversible Shock Complications?

A

1)Acute renal failure
2)Adult Respiratory Distress Syndrome (ARDS): d/t pooling of blood and alveolar damage.3)Hepatic failure d/t cell necrosis.
4)Parlytic ileus and stress or hemorrhagic ulcers.
5)Disseminated intravascular coagulation (DIC)(over active proteins that controls blood clotting) as the clotting process is initiated.
6)Depression of cardiac function by the oxygen deficit, acidosis and hyperkalemia, and myocardial depressant facor released from ischemic pancreas.
Eventually cardiac arrhythmias and ischemia develop, perhaps resulting in cardiac arrest.B/c of multi organ failure, shock becomes irreversible and death occurs.

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17
Q

General Treatment of Shock

A

The primary problem, whatever it is, must be tx’d quickly to prevent decompensation.
-The oxygen supply should be maximized.
-Use of vasoconstrictors and vasodilators depends on situation.
Ex: -Epinephrine reinforces the heart and contricts blood vessels.
-Dopamine and dobutamine increae heart function and, in low doses, dilate renal blood vessels, which may prevent acute renal failure.

Prognosis: Good in early stages.Mortaility rates incr. when they reach decompensatd shock.

18
Q

What is Hypovolemic Shock?

A

Results from fluid loss of about 15-20% (1L)

Diminshed blood loss does not allow for aqeuate filling of the vascular compartment.

19
Q

Etiology of Hypovolemic Shock

A

May be from blood loss, plasma loss, or ECF loss.

Ex:vomiting, diarrhea.Can also result from:

  • Inernal hemorrhage-Burns: Fluid shift into ISF creating edema in the area of the burns and lose the water that goes there b/c you can’t maintain it.
  • Peritonitis: Third space accumulation (Ex: Ascites)
20
Q

Hypovolemic Shock compensatory mechanisms

A

SNS mediates responses to maintain CO and BP:

  • Tachycardia, incr. cardiac contractility, vasocontriction
  • Venous return to the heart is increased to incr. Blood volume
  • Fluid is absorbed from interstitial spaces
  • water and salt are conserved by the kidney d/t activation of the renin-angiotensin-aldoterone system-the feeling of thirst is induced.
  • ADH secretion can be induced by a 10-15% drop in blood volume.
  • Intracellular volume decreases as water is drawn out of the tissues into the capillaries.
  • Vasoconstriction of blood vessels to nonessential organs increases
  • if prolonged, this can cause tissue damage and cellular death.
21
Q

S/s of Hypovolemic shock

A

Thirst incr.
HR cool and clammy skin
decr. in arterial BPdecr. in U/O to keep fluid in to incr. BP

(Note: Decr BP, is usually a late sign as the body attemps to preserve blood pressure for as long as it can. )

Collapse of blood vessels can occur with severe dehydration.
Hematocrit blood tests to se severity of dehydration.
Lactate lvls and arterial pH determine extent of acidosis
Urine output decreases as blood is shunted away from the kidneys and towards the heart and brain.

22
Q

Tx of Hypovolemic Shock

A

Focused on correcting/controlling the underlying cause while improving tissue perfusion.
Cerebral flow MUST be maintained at all costs.
-O2 can be administered to lessen hypoxemia.
-Replace fluid loss w/ IV administration of fluid or blood.
-whole blood, plasma, and electrolyes is required (but check values of RBC’s and electrolytes first)

23
Q

What is Cardiogenic Shock?

A

Failure of the heart to pump blood adequately.
Critical decrease in tissue perfusion caused by the loss or redistribution of intravascular fluid.
It results from when blood vessels fail to provide the peripheral tissue+organs with enough blood.

24
Q

Etiology of Cardiogenic Shock

A

Patients have lost 40% of the cardiac muscle mass of the left ventricle needed for effective contraction.

  • Acute attack from damage to heart tissue d/t an MI.
  • ineffective pumping d/t cardiac arrhthmias
  • Mechanical defects after an MI like: ventricular septal defects, ventricular aneurysms, acute disruption of valvular function or problems with open heart Sx.
  • Ischemic tissues (pancreas) may produce substances that impair cardiac function, such as MI depressant factor.
25
Q

Patho of Cardiogenic Shock

A
  • Failure to eject blood from the heart, hypotension and inadequate CO.
  • there is usualy increased systemic vascular resistance which contributes to the condition.
  • Preload is increased, leading to an increase in end-systolic volume (Blood remaining after systole –> ventricle contradictive)
26
Q

S/s of Cardiogenic Shock

A
  • Often show heart failure**
  • Includes Cyanosis of the lips, nails, and skin.
  • Systemic and pulmonary capillary pressures increases as a result of volume overload and blood pooling.
27
Q

Tx of Cardiogenic Shock

A

1) Need to Improve CO2)Need to reduce heart workload and O2 demands of the myocardium and preserve oxygen perfusion.
3) Need to properly regulate fluid balance to maintain blood volume and filling rate on the heart without causing pulmonary congestion –> resp problems.

4) Pharmalogical Tx:-Vasodilators decr. venous return to the heart, and reduce vascular resistance against which the left ventricle must pump (making workload easier for the heart)
- At high doses: Nitroglycerin will also dilate the arterial beds, further lowering systemic resistance.
- Cathecholamines will do 2 things:
1) Increase contractility of the heart
2) Act as vasodilators, therefore must be used with caution. And dose properly w/ vasodilators.

(Note: Cathecholamines are hormones released from the adrenal glands)

28
Q

What is Obstructive Shock?

A 
A subclass of Cardiogenic Shock.
-Occurs with mechanical obstruction of blood through the central circulation of closed veins, the heart or lungs.
29
Q

Etioloy of Obstructive Shock

A

-Pulmonary embolism, aortic aneurysms,cardiac tamponade, pneumothorax, atrial myxoma or evisceration of the thoracic cavity d/t a ruptured diaphragm.
Anything that will block flow.

30
Q

S/s of Obstructive Shock

A
  • Elevated right BP
  • Impaired venous return to the heart.
  • increased venous pressre
  • Jugular vein distension.
31
Q

Tx of Obstructive Shock

A

Focused on correcting the cause of the disorder, usually with Sx.
-Thrombolytic drugs may also be used to remove a pulmonary embolus.

32
Q

What is Distributive Shock?

A

A.k.a Normovolemic Shock.
-Caused by a loss of blood vessel tone, enlargement of the vascular compartment and displacement of the vascular volume away from the central circulation.
-Capacity of the vascular system expands so much that the normal blood volume is not enough to fill the vessel system.
Loss of vessel tone has two major causes:
1)Sympathetic control of vasomotor tone is lost.
2)Presence of vasodilator substances in the blood.

33
Q

What is Neurogenic Shock?

A

Caused by decreased sympathetic control of blood vessel tone d/t a defect in the vasomotor center in the brainstem, or sympathetic outflow to the blood vessels. Ex: brain injury

-Nervous system output can be interrupted by brain injury, depressant action of meds, general anesthesia, hypoxia b/c of lack of O2 going to the neurons, decreased glucose uptake, pain or fear.

-Spinal shock (compression of the nerves of the spine when there is an injury to the spine) is a form of neurogenic shock that present in ppl w/ a spinal cord injury.
Can cause paralysis of the legs.HR is slower b/c the heart cannot make it beat fast d/t the defect of the vasomotor center.Is rare and transitory.

34
Q

What is Anaphylactic Shock?

A

Presents during severe systemic allergic reactions.

  • occurs when vasodilators, Ex: Histamine, are released into the circulation. Results in drop in BP.
  • Arterioles and venules dilate and capillaries have increased permeability.
  • Accompanied by laryngeal edema and bronchospasm, circulatory collapse, hives, contraction of GI and uterine smooth muscle.
35
Q

Causes of Anaphylactic Shock

A

Reactions to allergens: meds, foods, insect venom.

  • The onset depends on the person, the rate and quantity of antigen exposure.
  • Blood pools in periphery (B/c of vasodilation) and BP drops and pulse is weak.
  • Airway obstruction can occur b/c of laryngeal edema or bronchial spasm.
36
Q

S/s of Anapylactic shock, or “warning signs”

A 
Dyspnea
swelling
hives
apprehensive/restless
itching
coughing
choking
abdominal
 discomfort
37
Q

Tx of Anaphylactic Shock

A
  • Immediate removal of allergen or attempts to decrease its absorption.
  • Monitoring and maintenance of cardiovascular and respiratory function

Pharmacological Tx:
-Epinephrine: First med administered in an allergic reaction.
Functions to contrict blood vessels, relax smooth muscle of the bronchioles, and help the heart beat faster.

Antihistamines and corticosteroids:
To maintain CO.
Prevention is preferable to Tx.
Wear medic alert braceletes to inform medical peprsonnel of their sensitivites.

38
Q

What is Sepsis/Septic Shock?

A

Systemic infection.

  • Associated with severe infection and release of inflammatory mediators (Gram - bacteria and others)
  • Commonly associated with pathological complications including pulmonary insufficiency, disseminated intravascular coagulation (DIC)(overclotting) and multiple organ system dysfunction.
39
Q

S/s of Sepsis/Septic Shock

A

First signs:
-mild hyperventilation
-respiratory alkalosis
-changs in personality and behaviour d/t reduced blood flow to the brain.-fever-Vasodilation
-warm flushed skin
-tachycardia
Often present with hypovolemia, and decreased BP b/c of arterial venous dilation and leakage of plasma into the interstitial spaces.

40
Q

Tx of Sepsis/Septic Shock

A

Focus on the causative agent and support of circulation.
-Specific antibiotic must be administered to deal with the inavading pathogen.

  • Cardiovascular function must be maintained through:
    1) fluid administration and
    2) Tx with vasopressor agents.
  • Insulin can be used to Tx hyperglycemia, but the mechanism of insulin action is unknown.
  • Antimicrobials and glucocorticoids are necessary with septic shock (antibitocs)(So, Give antibiotics, and maintain cadrio function)
41
Q

Epidemiology of Sepsis

A

Occur freqeuently in very sick pts.
incidence has increased d/t increased awareness and correct Dx.
much more immunocompromised pts

advanced tx have not really helped fatality rate.

Pathophysiology (7 decks)

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