Hemodynamic Instability Flashcards
hemodynamic instability
- 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
is preload decreased or increased with low/high CVP?
low CVP = decreased preload
high CVP = increased preload
if you can see JVD and hear S3 heart sounds, what does that mean in terms of preload?
increased
primary indicators of preload
CVP, JVD, S3, POCUS, crackles
secondary indicators of preload
skin turgor, mucous membranes, I&O, daily weights
afterload indicators
pulse pressure, dBP, cap refill, colour/temp of limbs, pulses
pulse pressure and relation to afterload?
narrow = increased afterload
wide = decreased afterload
contractility assessment indicators
EF >60%, medical history, lytes, starling’s law
aortic aneurysm
a permanent localized dilation of the aorta that is 50% larger than normal
classifications of AA
ascending, descending, abdominal
abdominal aortic aneurysm
- occurs below diaphragm
- categorized in relation to renal arteries: infra and suprarenal
what are the arteries of the aorta?
superior mesenteric, renal artery, inferior mesenteric
what does the superior mesenteric artery perfuse?
small bowel and large bowel (except colon)
what does the renal artery perfuse?
both kidneys
what does the inferior mesenteric artery perfuse?
colon/rectum
most common sites of aortic aneurysms
- below renal arteries
- above renal arteries
- involving both aorta and iliac crest
- abdominal-thoracic
how does AAA form?
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
predisposing factors for AAA
- more common in males
- familial link evident
- increased age >50
- smoking
- CAD
- HTN
- COPD
how to recognize AAA
- routine physical
- one time screening for males who smoked
- vague abdo/back pain
- symptoms from AAA pressing on organs
common symptoms reported
- vague abdo pain
- low back pain
- n/v
- ischemia from embolization of distal
circulation - abdo pain + hypoTN = pulsatile mass = rupture
rupture mortality rate and triad of symptoms
- 50-90%
- Some chance of surviving if leak is slow or bleed occurs in retroperitoneal cavity
- triad = abdo pain, hypoTN, pulsatile mass
AAA relative risk
Relative risk of size (diameter) vs rupture in year. when greater than 5.5cm then surgery is indicated
factors that best predict rupture possibility
size of aneurysm, including diameter and length
diagnostic tests for AAA
U/S, CT scan, angiography
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
what are 2 surgical options for AAA?
- OPEN surgical repair
- Endovascular aneurysm repair (EVAR)
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
common post op complications from AAA
- dysrhythmias
- embolization
- fluid imbalances
- longer cross clamp
- bowel ischemia, kidney hypoperfusion
shock definition
occurs when widespread inadequate end-organ perfusion persists to the point that it results in disruption of cellular function
continuum of shock
- changes in determinants of CO
- hemodynamic instability
- shock
SNS comp mechanism
- stimulates adrenal glands to release CATECHOLAMINES
(e.g. Norepinephrine and epinephrine) - alpha, beta 1 and beta 2 receptors are stimulated
alpha 1 receptors will ____ preload and ____ afterload
increase for both
beta 1 receptors will ____ HR and _____ contractility
increase for both
beta 2 receptors will ___ airway resistance, ___ ventilation; ___ preload and afterload
decrease, improve, decrease
types of shock
hypovolemic, cardiogenic, distributive, obstructive
hypovolemic shock
decreased preload
cardiogenic shock
decreased contractility
distributive shock
decreased afterload
what is the end result of ALL shocks?
inadequate tissue perfusion
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)
hypovolemic shock causes
- bleeding
- vomiting
- diarrhea
- decreased PO intake
- diabetes insipidus
hypovolemic shock hemodynamics (change in, cause/consequence/compensation)
preload: decreased, cause
afterload: increased, compensation
contractility: decreased, consequence
HR: increased, compensation
CO: decreased, consequence
how to fix hypovolemic shock?
fluids, blood products, crystalloids
cardiogenic shock causes
- ACS/MI
- dysrhythmia
- CHF
- myocarditis
- myocardial contusion
- diseased valves
cardiogenic shock hemodynamics
preload: inc, conseq
afterload: inc, comp
contractility: dec, cause
HR: inc, comp
CO: dec, consequence
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
distributive shock types
anaphlyaxis, neurogenic, sepsis (most common)
distributive shock hemodynamics
preload: dec, conseq
afterload: dec, cause
contractility: dec, conseq
HR: inc, compensation
CO: inc or dec, conseq
how do we fix distributive shock?
leaky vessels = fluids
low vascular tone = vasopressors
loss of autonomic tone = compression stockings/abdo binder
sepsis = abx/steroids
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
assessment of shock includes….
ECG (HR), arterial pressure, CVP, MAP/pulse pressure
MAP
- gold standard for treatment goals
- important to look at whole picture, not just number
metabolic indicators
lactate, pH, ScVO2
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
pH
in conjunction with metabolic acidosis
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
manipulating cardiac output
- what caused decrease in CO
- appropriate tx
- re-evalute tx.
- re-assess pt
do you always give fluid first in shock?
yes unless they’re in HF
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
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
type of fluid therapy chosen is influenced by ?
origin of volume of loss, BW, pt condition, physician preference
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)
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
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
D5W
- hypotonic, body consumes dextrose
- used mainly for mixing
- not for fluid replacement
- can be used when there is water deficit
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)
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
other fluids used
- 0.45NS used when Na is too high for .9NS
- 2/3 1/3 not used
when do you transfuse?
less than 70 Hgb
if ACS is present then less than 80 Hgb
what will you generally see with hemodynamics when giving fluids?
increased preload, CO and decreased HR
vasoactive drugs
- inotropes = alter contractility
- vasodilators = either arterial or venous
- vasoconstrictors = increased afterload
what drugs are inotropes?
dopamine, dobutamine, epi, milrinone
what drugs are vasoconstrictors?
norepi/phenylephrine
what drugs are vasodilators?
nitro, hydralazine, sodium nitroprusside
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
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
milrinone
- positive inotrope
- increases contractility
- causes vasodilation and decreases afterload
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
levophed
- vasoconstrictor
- alpha receptors
- common dose = 1-20mcg/min
- must use central line
- side effects: HTN, angina, ischemic limbs
- titrated to MAP goal
phenylephrine
- vasoconstrictor
- Potent, synthetic direct-acting sympathomemetic with strong alpha and weak beta
- elevates BP
- infusion or small bolus doses
- short acting
vasopressin
- ADH hormone
- works on vasopressin receptors V1 and V2
- V1 causes vasoconstriction
- V2 causes increase preload
nitro
- vasodilator
- more venous dilating
- reduces preload, CO, dilates coronary arteries
- IV infusion
- mild arterial dilation but only at high doses
sodium nitroprusside and hydralazine
vasodilator, more arterial, reduce afterload, relax smooth muscle
how do you titrate IV drugs?
increase infusion in small dosages to achieve affect evaluating outcome with each increment increase
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
HTN common parameters
keep sBP < 160 or MAP <110
common drugs for HTN
labetalol or hydralazine
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
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
what is the goal of treating HI and shock?
to improve EOP
what AKI are you at risk for in hypovolemic shock?
prerenal
