Hemodynamic instability Flashcards
Abdominal aortic aneurysm
A localized dilatation of the abdominal aorta exceeding the normal diameter by more than 50 percent. If occurs above the kidneys it is referred to as ‘suprarenal’, while those occurring below the kidneys are referred to as ‘infrarenal
Capillary Fluid Dynamics
Normally, capillary walls are permeable to water and solutes, but not to larger molecules like proteins. The movement of water through the capillary walls is controlled by two pressures: hydrostatic pressure and colloid osmotic pressure (also referred to as oncotic
pressure)
Cardiogenic shock
arises from poor contractility
Colloid
A colloid solution has a high molecular weight (generated by large molecules in the solution)
: in the presence of normal capillary walls, a colloid solution tends to remain in the
intravascular compartment, thereby generating an oncotic (or colloid osmotic) pressure.
Crystalloid solutions
Crystalloid solutions contain small molecules (e.g. electrolytes) that pass freely through cell
membranes and vascular system walls.
Distributive shock
arises when vascular tone is disrupted (afterload) (e.g., in sepsis, severe anaphylaxis, or
from neurogenic causes)
Hypovolemic shock
arises from inadequate circulating volume and/or inadequate venous return to the heart.
Inotropic drugs
alter contractility. Positive inotropes (e.g. dopamine, dobutamine) increase contractility & negative inotropes (e.g. beta blockers) decrease contractility.
Shock
acute, widespread process of impaired tissue perfusion that results in cellular, metabolic
and hemodynamic alterations.” Urden et al., 2022. Shock can arise from disruption of any
of the three primary determinants of cardiac output (preload, afterload and contractility).
Types of shock include hypovolemic (preload) , cardiogenic (contractility) and distributive
(afterload). The common denominator of all types of shock is inadequate tissue perfusion
that occurs when an imbalance develops between cellular oxygen demand and cellular
oxygen supply.
Vasoconstrictors
Vasoconstrictor drugs created vasoconstriction: arterial vasoconstriction results in
increased afterload; venoconstriction will contribute to increased preload (as it decreases
venous capacitance)
Vasodilators
Vasodilator drugs exert vasodilating effects on either arterial or venous vasculature (or
both). Venodilation will reduce preload (d/t increased venous capacitance); arterial
vasodilation will decreased afterload.
Chronotropes:
drugs that change the heart rate, some may also change heart rhythm
Inotropes:
Inotropes change the contractile force of the heart. Positive inotropes increase contractile force.
Negative inotropes decrease the contractile force
Beta 2 acts on
Beta2- lungs bronchiodilation
Beta 1 acts on
Beta 1 receptors- heart.
increases cardiac output and stroke volume by increasing heart rate, contractility.
Alpha 1 acts on
Activation of alpha 1 adrenergic receptors cause smooth muscle contraction which induces vasoconstriction.
Dobutamine
positive inotrope- increases contractility
Primary used for cardiogenic shock
Vasopressin
V 1- vasoconstriction
Epinephrine
works on alpha 1 and beta 1 and beta 2
Alpha 1- vasoconstriction
Beta 1 increases contractility
Beta 2- Bronchiodilation
Dopamine
Inotropic increases contractility and vassopressor
good for cardiogenic shock with hypotension
Collagen and elastin
responsible for giving the vessel strength and elasticity.
Finite life expectancy of collagen/elastin of 40 to 70 years
Abdominal aortic aneurysm definition
a permanent localized full thickness dilation of
the aorta that is 50% larger than the normal (2 cm)
Pathophysiology of AAA
degeneration of elastin and collagen fibers, loss of smooth muscle fibers causes
thinning of the medial layer &
loss of structural integrity pressure dilation of affected area
INCREASED VOLUME AND PRESSURE
AAA diagnostics
Ultrasound - diagnose and track progression
CT scan - detail of AAA relative to surrounding structures
Angiography
• CT is better
• If aneurysm has thrombosis no dye will enter so will
not know size
• Good at determining if surrounding vascular
anatomy is affected
• Dye risk > AKI
> 5.5 cm AAA
consider surgery
Open repair of AAA facts
• Pt is heparinized
• Distal cross clamp first to prevent plaque traveling to feet
• Clot is removed along with any plaque or debris
• If iliac arteries are involved a “Y” graft is used if not just a
regular tube graft
Post-op issues of AAA repair Hemodynamics
• CAD, dysrhythmias, CHF
• Watch for rhythm changes & ischemic changes on monitor
(ST monitoring)
• Assess cardiac function & systemic perfusion (preload)
• Minimize workload of the heart (pain control & mobility)
• S & S of ACS and MI
Fluid overload:
• Excessive weight gain > increase in myocardial oxygen demand
• 3rd spacing of fluid (lungs too)
• Increased preload
Fluid overload in combination with CAD can lead to MI, angina, heart
failure, pneumonia, respiratory failure
• Fluid loss: excess bleeding, reperfusion injury, or 3rd space fluid shifts
Post-op issues of AAA repair GI issues
Colon ischemia/ ischemic colitis (usually involves the sigmoid colon)
Paralytic ileus
Post OP AAA nursing responsibilities
Find out: intra-op events, EBL, I & O intra-op, clamping
time, sedation
Telemetry monitor (ECG, ST, QT analysis) Arterial line (SBP, DBP, MAP) CVC with CVP transduced IV access Assess lower leg pulses (TP, DP) by Doppler, skin color Assess surgical dresssing Urine output CBC, BUN, Crea, electrolytes
The first thing we address in hemodynamic instability?
preload
Shock definition
ACUTE, WIDESPREAD PROCESS OF IMPAIRED TISSUE PERFUSION
THAT RESULTS IN CELLULAR, METABOLIC AND HEMODYNAMIC
ALTERATIONS
Hypovolemic shock primary problem is
decreased preload
Cardiogenic shock the primary problem is
decreased contractility
Distributive shock the primary problem is
decreased afterload
Obstructive shock the primary problem is
increased afterload
Initially, compensatory mechanisms are ______ and then in hemodynamic instability they start to ____
Initially, compensatory mechanisms are EFFECTIVE and then in hemodynamic instability they start to PERPETUATE DYSFUNCTION
Neural compensatory mechanisms
SNS-Baroreceptors
Hormonal compensatory mechanisms
RAAS, ACTH, ADH
Chemical compensatory mechanisms
Chemorecptors
Metabolic indicators of shock
SvO2, OER, lactate, pH & base deficit
‘balanced crystalloids
Plasmalyte/Normosol
RL
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 pre-load and cardiac output
• Lactated ringers dangers
• Can make acidosis worse
• Careful to give with underperfused liver
(lactate≠ bicarbonate)
• Careful with the K if decr UO
D5W
- Hypotonic as body consumes dextrose making the sol’n hypotonic
- Used mainly in CC for mixing
- Not for fluid replacement
- Can be used when there is water deficit
Give PRBC for Hgb under…
70
Exception: w/ a documented history of ACS hgb <80 gm/L
Inotropes
(+) improve contractility
sympathomimetic (beta 1 receptors) – dopamine,
dobutamine, epinephrine
inhibitor of phosphodiesterase breakdown leading to
cAMP and calcium levels – milrinone
Milrinone:
phosphodiesterase inhibitor
+ inotrope with little chronotropic effect
direct vasodilator
Dobutamine action
- predominantly Beta 1 effects
- some Beta 2 – produces mild vasodilation
- has chronotropic effects
Dobutamine is used to treat
HF– especially in hypotensive pts who can not tolerate vasodilator therapy
Dopamine
- higher doses have alpha effects; non- specific beta effects
- usual range is 1-20 mcg/kg/min
beta or moderate 4-10 mcg/kg/min (increases cardiac output) alpha >10 mcg/kg/min - side effects: • Hypertension • Tachycardia > can happen at any dose
vasopressors
improve afterload
- by stimulating alpha receptorsnorepinephrine (levophed) & phenylephrine
- by stimulating V1 receptors
vasopressin
Levophed
strictly in clinical practice is alpha
- onset 1-2 min
- commonly ordered at 1 to 20 mcg/min
Levophed - side effects
- Hypertension
- Angina or worse
- Ischemia to limbs at high dosages
Phenylephrine
Alpha 1 agonist without beta agonist
vasoconstriction
Vasopressin
• Acts on V1 receptors – located on blood vessels vasoconstriction
• Acts on V2 receptors – located on the collecting tubules in the kidney
ADH effect
• In shock : 20 units in 100 ml at 0.04 units/min IV infusion
• Do not titrate, run at fixed dose
labetalol
alpha/beta adrenergic antagonist/blocker
alpha prevents vasoconstriction
beta prevents reflex tachycardia
hydralazine
a direct smooth muscle relaxant & a strong arterial vasodilator
S.E. reflex tachycardia (avoid in ACS)
nitroprusside
> arterial than venous dilator
faster action;
S.E. cyanide toxicity
Nitroglycerin
> venous than arterial dilator
