Hemodynamic Instability Flashcards
1
Q
hemodynamic instability
A
- created by influences on preload (inadequate blood flow), contractility (poor), and afterload (changes in vascular tone)
- can be short or long lasting or progress to shock
2
Q
is preload decreased or increased with low/high CVP?
A
low CVP = decreased preload
high CVP = increased preload
3
Q
if you can see JVD and hear S3 heart sounds, what does that mean in terms of preload?
A
increased
4
Q
primary indicators of preload
A
CVP, JVD, S3, POCUS, crackles
5
Q
secondary indicators of preload
A
skin turgor, mucous membranes, I&O, daily weights
6
Q
afterload indicators
A
pulse pressure, dBP, cap refill, colour/temp of limbs, pulses
7
Q
pulse pressure and relation to afterload?
A
narrow = increased afterload
wide = decreased afterload
8
Q
contractility assessment indicators
A
EF >60%, medical history, lytes, starling’s law
9
Q
aortic aneurysm
A
a permanent localized dilation of the aorta that is 50% larger than normal
10
Q
classifications of AA
A
ascending, descending, abdominal
11
Q
abdominal aortic aneurysm
A
- occurs below diaphragm
- categorized in relation to renal arteries: infra and suprarenal
12
Q
what are the arteries of the aorta?
A
superior mesenteric, renal artery, inferior mesenteric
13
Q
what does the superior mesenteric artery perfuse?
A
small bowel and large bowel (except colon)
14
Q
what does the renal artery perfuse?
A
both kidneys
15
Q
what does the inferior mesenteric artery perfuse?
A
colon/rectum
16
Q
most common sites of aortic aneurysms
A
- below renal arteries
- above renal arteries
- involving both aorta and iliac crest
- abdominal-thoracic
17
Q
how does AAA form?
A
degenerative process of elastin and collagen
fibers and smooth muscle fibers resulting in:
- thinning of the medial layer of the aorta
- loss of strength/ elasticity/structural integrity
- eventual dilation or aortic wall
18
Q
predisposing factors for AAA
A
- more common in males
- familial link evident
- increased age >50
- smoking
- CAD
- HTN
- COPD
19
Q
how to recognize AAA
A
- routine physical
- one time screening for males who smoked
- vague abdo/back pain
- symptoms from AAA pressing on organs
20
Q
common symptoms reported
A
- vague abdo pain
- low back pain
- n/v
- ischemia from embolization of distal
circulation - abdo pain + hypoTN = pulsatile mass = rupture
21
Q
rupture mortality rate and triad of symptoms
A
- 50-90%
- Some chance of surviving if leak is slow or bleed occurs in retroperitoneal cavity
- triad = abdo pain, hypoTN, pulsatile mass
22
Q
AAA relative risk
A
Relative risk of size (diameter) vs rupture in year. when greater than 5.5cm then surgery is indicated
23
Q
factors that best predict rupture possibility
A
size of aneurysm, including diameter and length
24
Q
diagnostic tests for AAA
A
U/S, CT scan, angiography
25
what is the goal of surgical repair for AAA?
Repair and restore aortic lumen integrity and prevent fatal blood loss and ischemia to vital organs due to rupture
26
what are 2 surgical options for AAA?
- OPEN surgical repair
- Endovascular aneurysm repair (EVAR)
27
nursing priorities post-op
Dysrhythmias:
- cardiac monitoring, ECG changes (rhythm, rate, ST/ QT Analysis
- electrolyte optimization
- maintain MAP and SBP goals
Fluid Imbalances
- optimize pre-load
- What TYPE of Fluid do you need?
Emboli/Thrombus
- CWMS lower limbs
Endo Leak/bleeding
- MAP/ Hgb/surgical site ax
Hypoperfusion/Ischemia
- monitor EOP
28
common post op complications from AAA
- dysrhythmias
- embolization
- fluid imbalances
- longer cross clamp
- bowel ischemia, kidney hypoperfusion
29
shock definition
occurs when widespread inadequate end-organ perfusion persists to the point that it results in disruption of cellular function
30
continuum of shock
- changes in determinants of CO
- hemodynamic instability
- shock
31
SNS comp mechanism
- stimulates adrenal glands to release CATECHOLAMINES
(e.g. Norepinephrine and epinephrine)
- alpha, beta 1 and beta 2 receptors are stimulated
32
alpha 1 receptors will ____ preload and ____ afterload
increase for both
33
beta 1 receptors will ____ HR and _____ contractility
increase for both
34
beta 2 receptors will ___ airway resistance, ___ ventilation; ___ preload and afterload
decrease, improve, decrease
35
types of shock
hypovolemic, cardiogenic, distributive, obstructive
36
hypovolemic shock
decreased preload
37
cardiogenic shock
decreased contractility
38
distributive shock
decreased afterload
39
what is the end result of ALL shocks?
inadequate tissue perfusion
40
how common is obstructive shock?
not common; rare type making up 1-2% of cases. caused by blood clot, fluid around heart, high pressures in chest from lung injury (ie, tension pneumothorax)
41
hypovolemic shock causes
- bleeding
- vomiting
- diarrhea
- decreased PO intake
- diabetes insipidus
42
hypovolemic shock hemodynamics (change in, cause/consequence/compensation)
preload: decreased, cause
afterload: increased, compensation
contractility: decreased, consequence
HR: increased, compensation
CO: decreased, consequence
43
how to fix hypovolemic shock?
fluids, blood products, crystalloids
44
cardiogenic shock causes
- ACS/MI
- dysrhythmia
- CHF
- myocarditis
- myocardial contusion
- diseased valves
45
cardiogenic shock hemodynamics
preload: inc, conseq
afterload: inc, comp
contractility: dec, cause
HR: inc, comp
CO: dec, consequence
46
how to fix cardiogenic shock?
is there too much fluid? = diuretics
too much afterload? = vasodilators
weak heart? = inotropes/betablockers
really weak heart? = IABP, VAD, ECMO
47
distributive shock types
anaphlyaxis, neurogenic, sepsis (most common)
48
distributive shock hemodynamics
preload: dec, conseq
afterload: dec, cause
contractility: dec, conseq
HR: inc, compensation
CO: inc or dec, conseq
49
how do we fix distributive shock?
leaky vessels = fluids
low vascular tone = vasopressors
loss of autonomic tone = compression stockings/abdo binder
sepsis = abx/steroids
50
why is effective assessment important?
essential to early detection of hemodynamic changes, O2 supply and demand, and
inadequate tissue perfusion and critical to preventing and supporting early intervention
51
assessment of shock includes....
ECG (HR), arterial pressure, CVP, MAP/pulse pressure
52
MAP
- gold standard for treatment goals
- important to look at whole picture, not just number
53
metabolic indicators
lactate, pH, ScVO2
54
lactate
marker of tissue hypoxia – byproduct of anaerobic metabolism. levels take 12-24 hours to clear and may have an upswing once good tissue perfusion
occurs
55
pH
in conjunction with metabolic acidosis
56
assessment of shock important points
when looking at MAP always look at pulse pressure. HR is highly nonspecific. EOP take hx into account. trend lab values
57
manipulating cardiac output
1. what caused decrease in CO
2. appropriate tx
3. re-evalute tx.
4. re-assess pt
58
do you always give fluid first in shock?
yes unless they're in HF
59
management of hypovolemic shock
restore circulating volume. obtain and maintain IV access (central line). admin fluids as fast as possible. frequent charting of VS, labs, interventions
60
fluid therapy is guided by the following desired outcomes:
- Replacement of current ongoing fluid losses
- Restoration of previous fluid losses
- Maintenance of normal fluid requirements
- Prevention of anticipated procedure-related hypotension
61
type of fluid therapy chosen is influenced by ?
origin of volume of loss, BW, pt condition, physician preference
62
options for fluid therapy
- Blood or blood products (packed cells, fresh frozen plasma,
albumin)
- Artificial colloid solutions (voluven, pentaspan) (not as
common anymore)
- Crystalloid solutions (NS, D5W, LR, plasmalyte)
63
albumin
- most abundant protein in the blood- maintains oncotic
pressure
- produced in the liver
- can be transfused (5%-25%)
- used in volume resuscitation along with other factors
64
normal saline
- isotonic
- used for fluid replacement and resuscitation
- most effective when given rapidly
- if given too slow will re-distribute in tissues
and not increase preload and CO
65
D5W
- hypotonic, body consumes dextrose
- used mainly for mixing
- not for fluid replacement
- can be used when there is water deficit
66
plasmalyte
- mimics human plasma in its content of electrolytes, osmolality, and pH
- shares the same problems as most other crystalloid fluids
(fluid overload, edema with weight gain, lung edema, and worsening of the intracranial pressure)
67
lactated ringers
- Used mainly in OR when there is a loss of whole blood as LR
has electrolytes in it
- Not used very much in CC as contains lactate and can make
acidosis worse shifting Oxy-HGB curve
68
other fluids used
- 0.45NS used when Na is too high for .9NS
* 2/3 1/3 not used
69
when do you transfuse?
less than 70 Hgb
if ACS is present then less than 80 Hgb
70
what will you generally see with hemodynamics when giving fluids?
increased preload, CO and decreased HR
71
vasoactive drugs
- inotropes = alter contractility
- vasodilators = either arterial or venous
- vasoconstrictors = increased afterload
72
what drugs are inotropes?
dopamine, dobutamine, epi, milrinone
73
what drugs are vasoconstrictors?
norepi/phenylephrine
74
what drugs are vasodilators?
nitro, hydralazine, sodium nitroprusside
75
dopamine
- inotrope
- nonspecific beta effects; higher doses have alpha effects
- inc contractility, CO, SV
- side effects: HRN, tachycardia
- not used as often
- 1-20mcg/kg/min
76
dobutamine
- inotrope
- predominantly beta 1 and slight beta 2
- little effect on HR
- usually doesn't cause tachycardia
- dose range 2.5-5mcg/kg/min
- doctors set dose, not adjusted
- monitor results via BW
77
milrinone
- positive inotrope
- increases contractility
- causes vasodilation and decreases afterload
78
epinephrine
- inotrope
- Produced by the adrenal gland as part of the body’s response
to stress
- stimulate both alpha and beta receptors depending on dose
- 1-2 mcg/min will bind with beta which will increase HR and
contractility = increased CO
- dose increased = inc afterload d/t alpha receptor stimulation
79
levophed
- vasoconstrictor
- alpha receptors
- common dose = 1-20mcg/min
- must use central line
- side effects: HTN, angina, ischemic limbs
- titrated to MAP goal
80
phenylephrine
- vasoconstrictor
- Potent, synthetic direct-acting sympathomemetic with strong alpha and weak beta
- elevates BP
- infusion or small bolus doses
- short acting
81
vasopressin
- ADH hormone
- works on vasopressin receptors V1 and V2
- V1 causes vasoconstriction
- V2 causes increase preload
82
nitro
- vasodilator
- more venous dilating
- reduces preload, CO, dilates coronary arteries
- IV infusion
- mild arterial dilation but only at high doses
83
sodium nitroprusside and hydralazine
vasodilator, more arterial, reduce afterload, relax smooth muscle
84
how do you titrate IV drugs?
increase infusion in small dosages to achieve affect evaluating outcome with each increment increase
85
things to remember for inotropes
- MUST HAVE enough fluid on board (if low CVP, and attempt
inotrope you will simply ask heart to contract harder without giving it preload, increasing myocardial demand and O2 needs)
- use lowest dose
- don't respond to every change in pressure when titrating
- watch for side effects
86
HTN common parameters
keep sBP < 160 or MAP <110
87
common drugs for HTN
labetalol or hydralazine
88
labetalol
- Blocks alpha receptors
- Blocks beta receptors to prevent reflex tachycardia (that might increase BP again)
- In post op AAA repair, want to control BP to prevent risk of
surgical bleeding
- Relaxes smooth muscles in arterial walls
- Typical dose 5mg iv
89
sodium nitroprusside
- Vasodilator relaxes arterial and venous smooth muscle to
decrease afterload and preload; afterload reduction arterial
effect > venous
- Infusions: 0.5-8 mcg/kg/min
90
what is the goal of treating HI and shock?
to improve EOP
91
what AKI are you at risk for in hypovolemic shock?
prerenal
