NURS 400 Exam 2: Shock/Sepsis/Mods (A Crisis in
Tissue Perfusion/Oxygenation) – Questions &
Solutions
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Terms in this set (89)
Case Study: Mrs. Leaf Mrs. Leaf is a 56 year old women admitted to the ED
with a diagnosis of UGI bleed after being found in a
pool of blood, unconscious, and hypotensive. She is
intubated and placed on a ventilator, an arterial line
and CVC are inserted and fluid is administered. She
is transferred to the ICU with these VS and lab: BP
106/88, HR 115, RR 18, Temp 97, CVP 2, SVR 1478, Hgb
8.4
Shock - A Syndrome A physiologic state of inadequate cellular
oxygenation (O2 demand exceeds O2 supply).
1.) Resulting from ineffective tissue perfusion.
2.) Resulting in widespread cellular dysfunction and
death.
Shock is a SYNDROME as there is not a single
clinical test that can tell us one has this disease. This
is a cellular phenomenon that occurs when we have
higher oxygen demand than we have oxygen
supply.
,Shock - A Syndrome (continued) What exactly is "ineffective tissue perfusion?"
1.) The purpose of tissue perfusion is to supply
(deliver) oxygen (O2) to the cells → Oxygen Delivery
(DO2).
2.) So that the cells can "use" the O2 to create energy
(aerobic metabolism) → Oxygen consumption (VO2).
Cellular O2 Supply
Shock Syndrome: Etiology 1.) Inadequate volume: Hypovolemic ("Cold
[ineffective tissue perfusion] & Dry [dry in
intravascular space]").
2.) Inadequate pump: Cardiogenic ("Cold [ineffective
tissue perfusion] & Wet [intravascular hypervolemia]".
3.) Maldistribution of Volume: Distributive ("Warm")
→ We have adequate volume inside the body but it is
in the wrong place. It is out in the third space or
interstitium instead of the vascular space.
→ Caused primarily by vasodilation so they are
actually warm!
Notice that both hypovolemic and cardiogenic are
"cold" while distributive is warm - a very
distinctively different type of shock.
,Focus on Hypovolemic & Cardiogenic Shock Syndrome: Initial threat to perfusion
Shock (decreased CO; in hypovolemic decreased preload
and cardiogenic inadequate SV) → Compensation
(ANS, hormonal & chemical stimulation).
1.) Despite the what is causing the threat, the body is
going to respond to try and stay alive.
→ In hypovolemic shock our preload is too low,
causing a stroke volume that is too low.
→ In cardiogenic shock we have an inadequate
stroke volume resulting in an inadequate CO which is
accompanied by a high preload because of the
neurohormonal activation which will contribute to a
drop in SV.
, Compensation 1.) ANS Stimulation: Activation of the alpha and beta
receptors.
→ Increased sympathetic tone leads to increased
HR/contractility.
→ This is why you see the symptoms of tachycardia,
increased DBP, cool & clammy, mottling, and
decreased capillary refill.
2.) Hormonal Stimulation:
→ Epi and norepi leads to and augments the ANS
response.
→ ACTH leads to glucocorticoids leads to increased
glucose.
→ Renin-angiotensin-aldosterone leads to ??
→ This leads to all the same symptoms that you have
above plus fluid retention, decreased urine output,
and decreased K+.
3.) Chemical Stimulation:
→ Hyperventilation leads to respiratory alkalosis.
→ This is to try and increase the oxygen level in the
blood.
Notice: Many of the early "S&S" of shock are
actually signs of attempted compensation. They do
not tell you what the problem is, they tell you that
your patient is in trouble.
Compensated Shock Compensatory mechanisms may produce normal
hemodynamic values even when tissue perfusion is
compromised! Hypotension is a late sign!
Tissue Perfusion/Oxygenation) – Questions &
Solutions
Save
Terms in this set (89)
Case Study: Mrs. Leaf Mrs. Leaf is a 56 year old women admitted to the ED
with a diagnosis of UGI bleed after being found in a
pool of blood, unconscious, and hypotensive. She is
intubated and placed on a ventilator, an arterial line
and CVC are inserted and fluid is administered. She
is transferred to the ICU with these VS and lab: BP
106/88, HR 115, RR 18, Temp 97, CVP 2, SVR 1478, Hgb
8.4
Shock - A Syndrome A physiologic state of inadequate cellular
oxygenation (O2 demand exceeds O2 supply).
1.) Resulting from ineffective tissue perfusion.
2.) Resulting in widespread cellular dysfunction and
death.
Shock is a SYNDROME as there is not a single
clinical test that can tell us one has this disease. This
is a cellular phenomenon that occurs when we have
higher oxygen demand than we have oxygen
supply.
,Shock - A Syndrome (continued) What exactly is "ineffective tissue perfusion?"
1.) The purpose of tissue perfusion is to supply
(deliver) oxygen (O2) to the cells → Oxygen Delivery
(DO2).
2.) So that the cells can "use" the O2 to create energy
(aerobic metabolism) → Oxygen consumption (VO2).
Cellular O2 Supply
Shock Syndrome: Etiology 1.) Inadequate volume: Hypovolemic ("Cold
[ineffective tissue perfusion] & Dry [dry in
intravascular space]").
2.) Inadequate pump: Cardiogenic ("Cold [ineffective
tissue perfusion] & Wet [intravascular hypervolemia]".
3.) Maldistribution of Volume: Distributive ("Warm")
→ We have adequate volume inside the body but it is
in the wrong place. It is out in the third space or
interstitium instead of the vascular space.
→ Caused primarily by vasodilation so they are
actually warm!
Notice that both hypovolemic and cardiogenic are
"cold" while distributive is warm - a very
distinctively different type of shock.
,Focus on Hypovolemic & Cardiogenic Shock Syndrome: Initial threat to perfusion
Shock (decreased CO; in hypovolemic decreased preload
and cardiogenic inadequate SV) → Compensation
(ANS, hormonal & chemical stimulation).
1.) Despite the what is causing the threat, the body is
going to respond to try and stay alive.
→ In hypovolemic shock our preload is too low,
causing a stroke volume that is too low.
→ In cardiogenic shock we have an inadequate
stroke volume resulting in an inadequate CO which is
accompanied by a high preload because of the
neurohormonal activation which will contribute to a
drop in SV.
, Compensation 1.) ANS Stimulation: Activation of the alpha and beta
receptors.
→ Increased sympathetic tone leads to increased
HR/contractility.
→ This is why you see the symptoms of tachycardia,
increased DBP, cool & clammy, mottling, and
decreased capillary refill.
2.) Hormonal Stimulation:
→ Epi and norepi leads to and augments the ANS
response.
→ ACTH leads to glucocorticoids leads to increased
glucose.
→ Renin-angiotensin-aldosterone leads to ??
→ This leads to all the same symptoms that you have
above plus fluid retention, decreased urine output,
and decreased K+.
3.) Chemical Stimulation:
→ Hyperventilation leads to respiratory alkalosis.
→ This is to try and increase the oxygen level in the
blood.
Notice: Many of the early "S&S" of shock are
actually signs of attempted compensation. They do
not tell you what the problem is, they tell you that
your patient is in trouble.
Compensated Shock Compensatory mechanisms may produce normal
hemodynamic values even when tissue perfusion is
compromised! Hypotension is a late sign!
