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NSCC 7320 > Hemodynamic instability > Flashcards

Hemodynamic instability Flashcards

1
Q

Abdominal aortic aneurysm

A

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

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2
Q

Capillary Fluid Dynamics

A

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)

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3
Q

Cardiogenic shock

A

arises from poor contractility

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4
Q

Colloid

A

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.

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5
Q

Crystalloid solutions

A

Crystalloid solutions contain small molecules (e.g. electrolytes) that pass freely through cell
membranes and vascular system walls.

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6
Q

Distributive shock

A

arises when vascular tone is disrupted (afterload) (e.g., in sepsis, severe anaphylaxis, or
from neurogenic causes)

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7
Q

Hypovolemic shock

A

arises from inadequate circulating volume and/or inadequate venous return to the heart.

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8
Q

Inotropic drugs

A 
alter contractility. Positive inotropes (e.g. dopamine, dobutamine) increase contractility & 
negative inotropes (e.g. beta blockers) decrease contractility.
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9
Q

Shock

A

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.

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10
Q

Vasoconstrictors

A

Vasoconstrictor drugs created vasoconstriction: arterial vasoconstriction results in
increased afterload; venoconstriction will contribute to increased preload (as it decreases
venous capacitance)

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11
Q

Vasodilators

A

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.

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12
Q

Chronotropes:

A

drugs that change the heart rate, some may also change heart rhythm

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13
Q

Inotropes:

A

Inotropes change the contractile force of the heart. Positive inotropes increase contractile force.
Negative inotropes decrease the contractile force

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14
Q

Beta 2 acts on

A

Beta2- lungs bronchiodilation

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15
Q

Beta 1 acts on

A

Beta 1 receptors- heart.

increases cardiac output and stroke volume by increasing heart rate, contractility.

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16
Q

Alpha 1 acts on

A

Activation of alpha 1 adrenergic receptors cause smooth muscle contraction which induces vasoconstriction.

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17
Q

Dobutamine

A

positive inotrope- increases contractility

Primary used for cardiogenic shock

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18
Q

Vasopressin

A

V 1- vasoconstriction

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19
Q

Epinephrine

A

works on alpha 1 and beta 1 and beta 2
Alpha 1- vasoconstriction
Beta 1 increases contractility
Beta 2- Bronchiodilation

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20
Q

Dopamine

A

Inotropic increases contractility and vassopressor

good for cardiogenic shock with hypotension

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21
Q

Collagen and elastin

A

responsible for giving the vessel strength and elasticity.

Finite life expectancy of collagen/elastin of 40 to 70 years

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22
Q

Abdominal aortic aneurysm definition

A

a permanent localized full thickness dilation of

the aorta that is 50% larger than the normal (2 cm)

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23
Q

Pathophysiology of AAA

A

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

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24
Q

AAA diagnostics

A

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

25
>5.5 cm AAA
consider surgery
26
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
27
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
28
Post-op issues of AAA repair GI issues
Colon ischemia/ ischemic colitis (usually involves the sigmoid colon) Paralytic ileus
29
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 ```
30
The first thing we address in hemodynamic instability?
preload
31
Shock definition
ACUTE, WIDESPREAD PROCESS OF IMPAIRED TISSUE PERFUSION THAT RESULTS IN CELLULAR, METABOLIC AND HEMODYNAMIC ALTERATIONS
32
Hypovolemic shock primary problem is
decreased preload
33
Cardiogenic shock the primary problem is
decreased contractility
34
Distributive shock the primary problem is
decreased afterload
35
Obstructive shock the primary problem is
increased afterload
36
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
37
Neural compensatory mechanisms
SNS-Baroreceptors
38
Hormonal compensatory mechanisms
RAAS, ACTH, ADH
39
Chemical compensatory mechanisms
Chemorecptors
40
Metabolic indicators of shock
SvO2, OER, lactate, pH & base deficit
41
‘balanced crystalloids
Plasmalyte/Normosol | RL
42
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
43
• Lactated ringers dangers
• Can make acidosis worse • Careful to give with underperfused liver (lactate≠ bicarbonate) • Careful with the K if decr UO
44
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
45
Give PRBC for Hgb under...
70 | Exception: w/ a documented history of ACS hgb <80 gm/L
46
Inotropes
(+) improve contractility sympathomimetic (beta 1 receptors) – dopamine, dobutamine, epinephrine inhibitor of phosphodiesterase breakdown leading to cAMP and calcium levels – milrinone
47
Milrinone:
phosphodiesterase inhibitor + inotrope with little chronotropic effect direct vasodilator
48
Dobutamine action
- predominantly Beta 1 effects - some Beta 2 – produces mild vasodilation - has chronotropic effects
49
Dobutamine is used to treat
HF– especially in hypotensive pts who can not tolerate vasodilator therapy
50
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 ```
51
vasopressors
improve afterload - by stimulating alpha receptorsnorepinephrine (levophed) & phenylephrine - by stimulating V1 receptors vasopressin
52
Levophed
strictly in clinical practice is alpha - onset 1-2 min - commonly ordered at 1 to 20 mcg/min
53
Levophed - side effects
* Hypertension * Angina or worse * Ischemia to limbs at high dosages
54
Phenylephrine
Alpha 1 agonist without beta agonist vasoconstriction
55
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
56
labetalol
alpha/beta adrenergic antagonist/blocker alpha prevents vasoconstriction beta prevents reflex tachycardia
57
hydralazine
a direct smooth muscle relaxant & a strong arterial vasodilator S.E. reflex tachycardia (avoid in ACS)
58
nitroprusside
>arterial than venous dilator faster action; S.E. cyanide toxicity
59
Nitroglycerin
>venous than arterial dilator

NSCC 7320 (9 decks)

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