Critical care lecture 2 (shock, SIRS, MODS) Flashcards
1
Q
What is shock
A
physiologic state characterized by significant reduction of systemic tissue perfusion from decreased tissue oxygen delivery
2
Q
if prolonged oxygen deprivation continues without compensation, what could the complications be
A
cellular hypoxia and derangement of critical biochemical processes that could turn into systemic consequences
3
Q
what are the determinants of systemic tissue perfusion
A
cardiac output and systemic vascular resistance
4
Q
blood pressure
A
pressure against the wall of a blood vessel exerted by circulating blood and is a major factor in tissue oxygenation and perfusion
5
Q
vasoplegic
A
patient who is extremely vasodilated
6
Q
mean arterial pressure
A
average pressure seen in the systemic circulation (or organs)
7
Q
what is the normal range of MAP
A
70-100mmhg
8
Q
what are the determinants of cardiac output (amount of blood pumped by the left ventricle each minute)
A
- heart rate
- stroke volume
9
Q
what are the detrminants of stroke volume
A
- pre-load
- after-load
- contractility
10
Q
what is the normal cardiac output
A
4-8L/min
11
Q
what is cardiac index
A
cardiac output but takes into account body surface
12
Q
pre-load
A
- amount of stretch exerted on the myocardial fibers at the end of distaole which represents the volume of blood in the ventricle
- uses pressure to estimate volume
13
Q
afterload
A
- ventricular wall tension or stress during systolic ejection or as the resistance against which the ventricle pump blood
14
Q
what is the difference between Blood pressure and afterload
A
Blood pressure is the force against artery and afterload is the reistance the blood encounters to pump
15
Q
A
16
Q
what happens if there is no resistance
A
no flow of blood
17
Q
contractility or inotropy
A
ability of the myocardium to contract that is independent of afterload and preload
18
Q
what can affect contractility
A
- electrolytes
- level of fitness
- damage to myocardium
- obstruction
19
Q
what is the broad-spectrum of what a shock state looks like
A
- unmet metabolic demands
- tissue hypoxia that leads to cells death
- anaerobic metabolism with high levels of lactate
- organ dysfunction
- supply and demand for oxygen is imbalanced
20
Q
inital stage of shock
A
- a trigger events causes cardiac output to decrease and tissue perfusion decreases
21
Q
compensatory stage of shock
A
- helps increase cardiac output and oxygen dilvery
- increase HR and contractility, vasoconstricton, abdnormal redirection of blood (shunting) to vital organs
- hormonal compensation (vasoconstrictionand fluid retention)
- adrenal medulla stimulated to release epinephrine and norepinephrine
22
Q
progressive stage of shock
A
- compensatory mechanisms inadequate
- major dysfunction of organs
- low blood flow, poor tissue perfusion, metabolic waste build up
23
Q
refractory stage of shcok
A
- shock stage is so deep that death is inevitable
- intractable circulatory failure and death
24
Q
early stages of shock
A
- fever and chills
- skin warm and flushes
- tachycardia and tachypnea
- known as warm shock
25
late stages of shock
- vasoconstriction
- decrease urine output
- decrease CO
- hypotension
- known as cold shock
26
how do patients with DIC present
- fluid overloaded
- purpura and petechiae
- limbs can become necrotic
27
cardiogenic shock
inability of the heart to pump because of contractility issue
28
Hypovolemic shock
loss of circulating or intravascular volume (no RBC to transport oxygen)
29
obstructive shock
mechanical barrier to blood flow blocking oxygen delivery (PE or cardiac tamponade)
30
distributive shock
maldistribution of circulating blood volume
31
what are traditional clinical manifestations of shock
- hypotension
- oliguria from shunting of renal blood flow to other organs
- cool and clammy skin from vasoconstriction
- abnormal mental status
32
absolute hypotension
SBP less than 90mmhg
33
relative hypotension
drop in SBP by 40mmhg
34
what are the global indicators of shock from blood sample
- arterial Ph showing metabolic acidosis
- serum lactate above 5mmol and combines with acidodis
- base excess and base deficit greater or less than 3mmol/l
- venous oxygen saturation of 60% or less
35
what are general interventions to optimize oxygen delivery
- treating the underlying cause
- oxygen therapy to increase pulmonary gas exchange
- fluid administration
- blood transfusin depending on hgb levels
- vasopressors, inotropes and vasodilators
36
what are general interventions to decrease oxygen consumption
- decreasing total body work - neuromuscular blocking agents and sedation
- reducing pain and anxiety
- maintain normothermia
- maintaining normal serum glucose level
37
what happens to cardiac variable in hypovolemic shock
- increase systemic vascular resistace
- decrease cardiac output
- decrease stroke volume
- decrease pre-load
38
what is absolute hypovolemia and examples of causes
- no fluid in the body at all
- ex - blunt trauama, upper or lower GI bleed, rupture hematoma etc
39
relative hypovolemia
blood remains the body but it is in the wrong place
ex: vasodilation with sepsis and third spacing
40
what does the general head to toe assessment look like with a aptient who has hypovolemix shock
- anxiety, agitation and confusion
- tachypnea, delayed cap refill and flat neck veins
- decreased or absent bowel soudns with increased abdo. girth
- decreased urine output
- pallor, cool, clammy skin with dry mucous memebranes
- changes in HCT, HGB, specific gravity and lactate
41
how does hypovolemic shock affect hemodynamic parameters
- increase heart rate
- decrease pulse pressure
- decrease blood pressur
- increase systemetic vacualr resistance
- decrease cardiac output
- decrease in oxygen sats
42
how should tissue perfusion be restored in hypovolemic shock
- large gauge PIVs need to be inserted
- fluid and blood repletion
- hemodynamic support and monitoring
43
what needs to be kept in mind when fluid resuscitating patients in hypovolemic shock
- fludis should be warmed during infusion to prevent hypothermia
- RL and NS are used as first-line therapy
44
what are complications when it comes to fluid resuscitation with crystalloid and colloids
- dilutional coagulopathy (replacement with not enough clotting factor)
- thrombocytopenia
- hypothermia
- increased hemorrhae
- decrease blood viscocity
- pulmonary edema
- Intracranial hypertension
45
what are complications with fluid resuscitation with PRBCs
- acidosis
- left shift on the oxyhemoglobin curve which causes oxygen to be more affinitive for hgb
- hyperkalemia
- immunologic and infectious complications
46
what is the general collaborative management for hypovolemis shock
- indetify and stop the source of fluid loss
- administer fluid or blood replacement
- assess the response to therapy
- prevent and watch for complication while giving support
47
what are the various causes of cardiogenic shock
1. decreased contractility
2. impaired filling - diastolic dysfunctioning
3. impaired emptying - systolic dysfunction
48
what will you find on lung examination for cardiogenic shock
- diffuse crackles
- pulmonary congestion
- edema on CXR
49
what would you find on a cardiac examination for cardiogenic shock
- new murmur or soft heart sounds
- recent or current ischemia on ECG
- chest pain or palpitations
- thready, rapid pulse, narrow pulse pressure
50
what are the assessment findings from diagnositc studies for cardiogenic shock
- systolic blood pressure less than 90mmhg
- MAP less than 70mmhg
- cardiac index less than 2.2L/min
- pulmonary arteries occlusion pressure greater than 15 mmhg
- decreased in an outs
- decreased arterisl oxygen saturation
- respiratory alkalosis
- elevated creatinine kinase, cardiac troponin and BNP
- enlarged heart and pulmonary congestion on XR
51
what affects does cardiogenic shock have on hemodynamic paramters
- increased HR
- pulse pressur edecrease
- BP decrease
- SVR increase
- pre-load equal or increase
- CO decrease
- ozygen decrease
52
how would you manage the different variable of cardiogenic shock
- if pre-load is too low, fluids mays be used
- if pre-load is too high - diuresis maybe necessary
- positive inotropes and vasopressors can help with contractibility
- arrhtyhmia control
- potassium, calcium and magnesium replacement to help w damaged myocardial muscle
53
how would you manage decrease left ventricular workload for cardiogenic shock
- vasodilators to reduce SVR and LEVDP
- narcotic analgesics and sedatives to decrease myocardial oxygen deman
- intra-aortic balloon pump
- mechanical ventilation to increase oxygen saturation and improve oxygen delivery tot he tissue
- schedule physical care to ensure period of rest to minimize myocardial energy
| hemodynamic monitoring
54
what are the multiple causes of obstructive shock
- massive PE
- tension pneumothorax
- severe constrictive pericarditis
- pericardial tamponade
- severe pulmonary hypertension
55
what is the clinical presentation of a patient with obstructive shock
- hypotension
- distended neck veins
- no signs of fluid overload or reduced pre-load
56
what does a tone problem include
- cardiac output is normal or high
- theri is a problem with systemic vascualr resistance where the vessels are so dilated that there is no blood flow
57
what happens to cardiac variable with distributive shock states
- ALOT of decrease in SVR
- increase cardiac output
- increase contractility
- increase heart rate
58
anaphylactic shock and septic shock
vasodilation results from the presence of vasodilating substances in the blood
59
neurogenic shock
vasodilation results from a loss of sympathetic innervation to the blood vessels
60
sepsis
micro-organism entering the body
61
septic shock
systemic inflammatory response due to microorganisms enteing body
62
SIRS
clinical syndrome of dysregulated inflammation and activation of thrombotic cascade
63
what is the criteria for a patient to be diagnosed with SIRS
2 or more of the following:
- temp above 38 or below 36
- respiratory rate over 20/min or partial carbon below 32
- heart rate above 90
- white blood cells above 12,000 or below 4000
64
septic shock
- sepsis associated with hypotension despitae adequate fluid resus along with the presence of perfusion abnormalities that include lactic acidosis, oliguria and an acute alteration in mental status
65
pathophysiology of sepsis
- microorganism enters body and stimulates inflammatory/immune system
- containment failure by the body
- endothelial damage and coagulation dysfunction
- systemic/metabolic alterations
- apoptosis due to hypoxemia
66
what are the two most common organs to be affected by Sepsis
cardiovascular system and lungs
67
clinical manifestatios with sepsis and septic shock
- increase inflammation and coagulation
- increase cardia output and decrease SVR
- tachypnea, hyperventilation, alkalosis then acidosis later state
- temperature dysregulation
- decrease urine output
- altered neurological status
- GI dysfunction
68
what are the components apart of NEWS
- respiration rate
- spo2
- air or oxygen
- systolic blood pressure
- pulse
- conciousness
- temperature
69
what effect does septic shock have on hemodynamic parameters
- increase HR
- decrease pulse pressure
- decrease blood pressure
- decrease SVR
- decrease pre-load
- increase, same or decrease cardiac output
70
what is the hour one bundle for sepsis and septic shock
- measure lactate level - (remeasure of lactate level is greater than 2mmol/L)
- obtain blood cultures before adminstering antibiotics
- administer broad spectrum antibiotics
- begin rapid administration of crystalloid for hypotension or lactate
- apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP greater than 65mmhg
71
if sepsis is present how long should antibiotics be adminstered at
within 1 hour of recognition
72
when should antibiotics be given when sepsis is possibly but shock is absent
withing 3 hours if there is a concern for infection
73
what should be used as a first-line vasopressor
norepinephrine
74
what are the hemodynamic goals of septic shock patients
- target MAP of 65mmhg
- invasive monitoring using arterial blood pressure
- if there is no central acess copnsider initatiing vasopressor PIV
75
if MAP is inadequate despit low-moderate with norepinephrine what should be done
adding vasopressin
76
what is the collaborative management of septic shock
- fluid resuscitation (RL or NS)
- vasopressors and inotropes
- supplemental oxygen
- anticoagulants
- IV corticosteroids
- antibiotics after cultures are obtained
- promote nutrition
- hemodynamic monitong (cardiac variable, temp, blood glucose and lactate)
77
what is anaphylactic shock
hypersensitivity reaction that occurs due to inflammatory pathways
78
IgE antibody mediated systemic anaphylaxis
- food
- medicines
- venoms
- blood products
79
80
nonimmunologic anaphylactoid
- not IgE mediated but indistinguishable clinically but seen in opiods, NSAID and contrast
81
82
what are early clinical manifestation of anaphylactic shock
- generalized erythema
- uticaria (hives)
- pruritis
- anxiety and restlessness
- dyspnea
- wheezing
- chest tightness
- feeling or warthm
- nausea and vomiting
- angioedema
- abdominal pain
83
what are later clinical manifestations of anaphylactic shock
- stridor
- laryngeal edema
- severe bronchoconstriction
- hypotension leading to ciruclatory collapse
- deterioration of level of conciousness
- unresponsiveness
- hemodynamic parameter changes
84
what are the effects that anaphylactic shock has on hemodynamic parameters
- increase heart rate
- decrease pulse pressure
- decrease blood pressure
- decrease svr
- decrease pre-load
- decrease cardio output
- decrease oxygen
85
what is the management of mild anaphylactic management
- oxygen
- S/C or IV administration of anti-histamin
- possibly IM epinephrine injection to reverse the vasodilation and bronchoconstriction
86
what is the management of severe anaphylactic reactions
- administration of epinephrine, corticosteroids, bronchodilators
- potentially intubation and mechanical ventilation (intubate before it gets worse)
- vasoconstrictors and positive inotropic agents for patients who are experiencing circulatory collapse
87
what is the dosage for adults in epinephrine if iV acess is not available
- 0.01mg/kg Im into anterolateral thigh and proceed to obtain IV acess
88
what the dosage of epinephrine if IV acess **IS** available
- administer epinephrine 0.1mg IV infusion pump over 5 minutes
- inititate the infusion at 1-4mcg/min (max rate 10mcg/min) for the lowest effective concentration
- stop the infusion 30 minutes after signs and symptoms have resolved
89
neurogenic shock and most common causes
- loss of suppression of sympathetic tone
- disruption of the sympathetic nervous system usually due to severe cervical or upper thoracic spinal cord injury
90
what is the clinical presentation of neurogenic shock
- hypotension
- bradycardia
- warm and dry skin
- altered mental state
- oliguria
91
what effec does **neurogenic shock** have on **hemodynamic parameters**
- low CVP and pre-load
- low systemic vascualr resistance
- low stroke volume or cardiac output
- normal cardiac chamber
- temperature dysregulation
- respiratory dysfunction
92
what is observed with perfusionw hen there is a spinal cord injury
- normal perfusion or vasoconstriction above the level of the injury
- vasodilation with warm and dry extremities are present below the injury
93
what effects does neurogenic shock have on hemodynamic parameters
- everything decreases
94
what is the collaborative management of **neurogenic** shock
- spine stabilization
- atropine for bradycardia
- careful fluid resuscitation and use of vasopressors
- maintain airway patency
- maintain normothermia
95
what should be monitored when there is an ICP monitor present
- use CPP as a target instead of only MAP
- CPP should be above 70mmhg
96
if there is no ICP management what should be done
- taregt MAP 85-90 for 5-7 days
97
what is the assessment of the respiratory system with MODS
- alveolar edema
- decrease in surfactant
- increase in shunt
- V/Q mismatch
- end result is ARDS
98
what is the assessment of cardio in MODS
- myocardial depression and massive vasodilation
99
what is the assessment of acute renal failure in MODS
- hypoperfusion
- activation of renin-angiostension-aldosterone system
100
what is the assessment of the GI system in MODS
- decreased motility
- abdo distention
- decrease perfusion and risk for ulceration
- potential for bacterial translocation
101
hypermetbaolic state
- hypo or hyper glycemia
- catabolic state
- liver dysfunction
- lactic acidosis
102
what is the collaborative management of MODS
- maximize oxygen delivery above 95%
- maximize cardiac output
- decrease oxygen deman and minimize oxygen consumption of tissues
- nutritional and metabolic support
- support any failings organs
