Patho: Shock Flashcards
What is shock?
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.
Classifications of Shock
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.
How can blood pressure be affected by blood volume, cardiac contraction, and peripheral resistance?
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.
Metabolic needs of cells
- 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.
Stages of Shock
1) Nonprogressive stage
2) Progressive stage
3) Irreversible Stage
Nonprogressive stage
A.k.a: Compensatory shock
- Compensations are still working
- Compensatory mechanisms prevent large changes in circulatory function.
- Maintaining BP for pt.
Progressive stage
A.k.a Uncompensated Shock
- Compensations are no longer working.
- Shock becomes progressively worse.
Irreversible/decompensated Stage
- 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.
S/s of Nonprogressive/Compensatory stage shock.
-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.
S/s of Progressive Stage shock
-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.
S/s of Irreversible/decompensated stage shock
- 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.
Compensated Shock Compensation
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.
Uncompensated Shock Compensation
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.
In uncompensated shock, why might the myocardial strength be decreased?
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.
Irreversible/decompensated Shock Compensation.
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.
What are the Irreversible Shock Complications?
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.
General Treatment of Shock
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.
What is Hypovolemic Shock?
Results from fluid loss of about 15-20% (1L)
Diminshed blood loss does not allow for aqeuate filling of the vascular compartment.
Etiology of Hypovolemic Shock
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)
Hypovolemic Shock compensatory mechanisms
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.
S/s of Hypovolemic shock
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.
Tx of Hypovolemic Shock
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)
What is Cardiogenic Shock?
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.
Etiology of Cardiogenic Shock
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.
