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Med Surg > Critical Care - Shock > Flashcards

Critical Care - Shock Flashcards

1
Q

What is shock?

A

is a syndrome condition resulting from inadequate tissue perfusion and impaired cellular metabolism leading to cell dysfunction, cell death and organ failure. Cells experience hypoperfusion since the demand for oxygen and nutrients are deprived.

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2
Q

Decreased tissue perfusion can lead to:

A

hypoperfusion > impaired oxygen and glucose delivery > increasing cellular demand (oxygen and nutrients) and comsumption > impaired cellular metabolism

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3
Q

types of shock

A

hypovolemic
cardiogenic
obstructive
distributive

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4
Q

what is hypovolemic shock

A

caused by inadequate blood circulation volume or intravascular volume
oxygen delivery is impaired since RBC volume is decreased which carries oxygen

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5
Q

causes of hypovolaemic shock

A

non-haemorrhagic (not bleeding) - fluid shift (oedema) and severe dehydration (vomiting, diarrhoea and burns)

haemorrhagic (bleeding) - trauma, GI bleed, postpartum (after giving birth)

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6
Q

hypovolaemic shock transitions

A

decreased circulating volume > decreased venous return > decreased cardiac output > HYPOTENSION > decreased tissue perfusion > impaired cellular metabolism

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7
Q

S&S of hypovolaemic shock

A

HR - Tachy (compensates to increase blood flow)
Pulse - weak and thready
BP - hypotension
CO - decreased
CVP - decreased
SVR - increased due to vasoconstriction
O2 sat - low (decreased tissue perfusion)
Skin and Temp - cyanotic, cool and pale skin. cap refill is > 3 secs

oliguria
confused and agitated mental state (decreased blood circulation in the brain)

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8
Q

nursing treatments and intervention for hypovolaemic shock

A

Fluids and blood replacement
- crystalloids (normal saline) and colloids (albumin) if non-hemorrhagic
- RBCs or blood products for hemorrhagic

encourage fluids

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9
Q

what is cardiogenic shock?

A

-caused by inadequate cardiac pump function leading to low CO and SV or HR
-heart cannot pump enough blood to meet normal tissue perfusion
-caused by myocardial damage
-blood volume is adequate, however, the heart pump function is impaired causing fluid accumulation in the lungs (pulmonary oedema)

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10
Q

cardiogenic shock transitions

A
  1. decreased CO > compensatory RAAS (renin angiotensin aldosterone system) > increased blood volume > increased preload, SV and HR > systemic and pulmonary oedema > dyspnea
  2. decreased CO > compensatory catecholamine (neurohormone) > increased SVR, preload and HR > increased myocardial oxygen demand > decreased CO and EF (ejection fraction) > decreased tissue perfusion (ischaemia) > impaired cellular metabolism > myocardial dysfunction
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11
Q

S&S of cardiogenic shock

A

HR - Tachy (compensates to increase blood flow)
Pulse - weak peripheral pulses
BP - hypotension
CO - decreased
CVP - increased
SVR - increased due to vasoconstriction
O2 sat - low (decreased tissue perfusion)
Skin and Temp - cool and clammy skin. cap refill is > 3 secs

oliguria
confused and agitated mental state (decreased blood circulation in the brain) or sense of impending doom
jugular vein distention
chest pain
dyspnea (due to pulmonary oedema)

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12
Q

nursing intervention and treatment for cardiogenic shock

A

MI - agioplasty (procedure used to open blocked coronary artery)
thrombolytics (medication to dissolve blood clots)

Oxygen therapy

Vasopressors (adrenaline, dobutamine or dopamine) - increase vasoconstriction to increase blood circulation therefore increasing tissue perfusion

Diuretics - decrease heart workload and extra blood volume

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13
Q

pathologic conditions that cause cardiogenic shock

A

acute MI - cardiomyopathy, sepsis, myocarditis, pericarditis, aneurysm, dysrhythmias (impaired diastolic filling), contusion (blood capillary injury), metabolic abnormalities and papillary muscle rupture

cardiac obstructions due to pulmonary embolism, cardiac tamponade (pressure in the heart due to fluid accumulation between heart muscle spaces and pericardium), valvular disorders, tumours and arterial wall ruptures or defects

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14
Q

what is obstructive shock?

A
  • CO is decreased as circulation is blocked into the heart and its vessels
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15
Q

cause of obstructive shock

A

-pulmonary embolism (blocked pulmonary artery)
-tension pneumothorax (accumulation of air in the pleural cavity causing pressure in the lungs)
-pericardial tamponade (accumulation of fluid around the sac of the heart)
-abdominal compartment syndrome (increased pressure in the abdomen that restricts blood flow)

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16
Q

nursing intervention and treatment to obstructive shock

A

-treating the cause of obstruction (surgical procedure)
-oxygen therapy and fluid resuscitation
-cardiac medications

17
Q

what is distributive shock? and its transitions

A

-caused by leaky and widespread vasodilation of the blood vessels leading to decreased peripheral vascular resistance or SVR and blood pressure, therefore leading to decreased tissue perfusion and relative hypovolemia.

septic (bacterial toxins) anaphylactic (antigen) neurogenic (decreased vascular tone) > release of chemical mediators > (myocardial dysfunction) (bronchoconstriction and vasodilation or vascular leakage) > excessive vasodilation > decreased peripheral vascular resistance > decreased CO > hypotension > decreased tissue perfusion > impaired cellular metabolism

18
Q

types of distributive shock

A

septic shock (severe infection)
anaphylactic shock (allergic reaction)
neurogenic shock (damage to nervous system)

19
Q

what is septic shock

A

-occurs when severe infection triggers the body a cascade of systemic inflammatory response (fever)
-oxygen demand and consumption of the cells are high impairing cellular metabolism
-glucose metabolism and consumption of cells will also increase

20
Q

causes of sepsis

A

pneumonia
urosepsis (untreated UTI)
bacteria
intra-abdominal infections (pancreatitis)
wound infection
invasive procedures
indwelling medical devices (catheters)

21
Q

pathophysiology of sepsis

A
22
Q

S&S of sepsis

A

HR - tachy
pulse - bounding
CO - increased (vasodilation)
BP - hypotension
CVP - low
SVR - low (vasodilation)
O2 sat- high, however can cause hypoxia due to deprived tissue perfusion
Skin and Temp- initially warm and flushed, however when BP drops skin becomes cool, pale and mottled
RR - high due to hypoxia

23
Q

nursing treatment and intervention for sepsis

A

-early detection and treatment of sepsis can prevent deterioration and death
-broad spectrum abx
-fluid resuscitation
-vasopressors (adrenaline)
-neuromascular blockade agents and sedation (decrease metabolic demands and provide comfort)
-stress ulcers medications (PPIs)

24
Q

what is anaphylactic shock?

A

occurs from severe allergic reaction where blood vessels leak and excessive vasodilation causes intravascular volume pooling in the peripheral blood vessels. As blood vessels accumulate in the peripherals, tissue perfusion to vital organs is reduced.

25
Q

causes of anaphylactic shocks

A

allergic reactions to:
food (peanuts)
medications
insects (bee stings)
latex
exercise-induced anaphylactic

26
Q

anaphylactic shock transitions

A

foreign substance (antigen) > systemic antigen-antibody reaction (IgE) > mast cells release potent vasoactive substance (histamine/bradykinin) > activates inflammatory cytokines > causing Vasodilation and capillary permeability.

27
Q

S&S of anaphylactic shock

A

HR- tachy
pulse- rapid but weak pulse
CO- decreased due to capillary permeability where fluid is leaving the intravascular spaces
BP- hypotension
CVP- low
SVR- vasodilation
O2 sat- low
Skin and Temp- generalised flushing
RR- increased and laboured due to bronchoconstriction (narrowed airway) resulting in SOB, wheezing, coughing and inability to speak

cardiac dysrhythmias or arrest
N&V
itching, rashes, hives
feeling of impending doom

28
Q

Nursing treatment or intervention to anaphylactic shock

A

*remove the allergen
EPIPEN (adrenaline) - to cause vasoconstriction and bronchodilation
high flow oxygen
antihistamines
fluids
strict monitoring as anaphylaxis may recur after treatment

29
Q

stages of shock

A
  1. Compensatory- mechanism that initiates restoring homeostasis and blood flow to vital organs
    *neural - baroreceptors and chemoreceptors in the carotid sinus and aortic arch detects decreased BP and signals vasomotor in the medulla oblongata to increase HR and SVR
    *hormonal- SNS increases the release of catecholamines (adrenaline) to increase HR and CO. The coronary arteries will dilate to increase blood flow to the heart. RR will also rise to increase gas exchange and O2 levels in the blood. RAAS is also activated as BP decreases.
    *chemical - hyperventilation occurs since blood flow to the lungs is decreased (detected by chemoreceptors in aorta and carotids) causing a decreased in CO2 levels affecting blood circulation (O2) in the brain therefore causing confusion and restlessness.
  2. Progressive- compensatory responses fail to restore adequate BP and tissue perfusion.
    *cells switch from aerobic to anaerobic metabolism due to absence of O2 leading to build up of lactic acid progressing to metabolic acidosis
  3. Irreversible - progressive inadequate tissue perfusion and low BP and HR can lead to multiple organ failure since the body can no longer respond to any form of treatment. Death arise within hours.
30
Q

What is neurogenic shock?

A

caused by dysfunction or imbalance between sympathetic (causes constriction of the smooth muscles) and parasympathetic stimulation.

This kind of shock mainly experiences parasympathetic overstimulation causing excessive vasodilation for extended period.

31
Q

Causes of neurogenic shock

A

spinal cord injury (above T6, cervical)
TBI
anaesthesia complications (spinal anaesthesia)
opioids and sedative overdose
autonomic nervous system disorder
insulin reaction

32
Q

S&S of neurogenic shock

A

HR- brady (since SNS is impaired to compensate in increasing HR)
BP- hypotension (due to vasodilation)
CO- low
CVP- low
SVR- low (vasodilation)
O2 Sat- low
Skin and Temp- dry and warm extremities (venous blood pooling) and hypothermia warm extremities but cold body

33
Q

nursing intervention and treatment for neurogenic shock

A

*depending the cause of the shock
spinal cord injury - protect the spine with cervical collar, backboards and log-rolling
intubation and mechanical ventilation
head elevation
IV fluids

*watch for clotting risks - administer compression devises and antithrombic agents
vasopressors (adrenaline)

34
Q

S&S of poor tissue perfusion

A

restlessness or confusion
hypotension
weak peripheral pulses
tachycardia
rapid, shallow respirations
oliguria (<20 ml/h)
systemic venous and pulmonary oedema
narrowing pulse pressure (difference of SBP and DBP)
dysrhythmia
cyanosis and mottling (red-purplish marbling of the skin)
S3 and S4 heart sounds
hyperglycaemia

35
Q

shock in children is similar to adults and contributing factors are mostly caused by

A

severe dehydration
haemorrhage
progressive heart failure
sepsis

36
Q

in pedia, shock is present when there are sings of poor tissue perfusion regardless of

A

blood pressure (shock may be present whether bp is high, normal or low)

37
Q

causes of shock in pedia

A

hypovolaemic - GI losses, renal losses, haemorrhage, third spacing (accumulation of fluid in the interstitial spaces)
distributive shock - septic or anaphylactic shock, neurogenic or spinal shock
cardiogenic shock - CHD (congenital heart defects), arrhythmia, valvular disease, cardiomyopathy, myocarditis
obstructive shock - cardiac tamponade, pulmonary embolus, tension pneumothorax, obstructive congenital heart lesions (aortic stenosis)

38
Q

common S&S of shock in pedia and infants

A

initial irritability followed by lethargy
tachypnoea (fast RR), hyperpnoea (increased respiratory effort such as gruntling and retractions)
mottled and pallor skin
tachycardia
cool skin and prolonged capillary refill
weak peripheral pulses
metabolic acidosis
decreased central venous O2 sat

39
Q

general nursing management of patient in shock

A

assess V/S using EWS and ABCDE
immediate haemodynamic support (to manage poor tissue perfusion) - O2 therapy, ABGs (due to metabolic acidosis), fluid resuscitation (blood if hemorrhagic), aseptic insertion of IDC (to monitor response to therapy)
medications to improve cardiac function, CO and restore normal organ perfusion (vasopressors, antiarrhythmics)

12 lead ECG
blood tests

Med Surg (7 decks)

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