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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
Q

> 5.5 cm AAA

A

consider surgery

26
Q

Open repair of AAA facts

A

• 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
Q

Post-op issues of AAA repair Hemodynamics

A

• 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
Q

Post-op issues of AAA repair GI issues

A

Colon ischemia/ ischemic colitis (usually involves the sigmoid colon)
Paralytic ileus

29
Q

Post OP AAA nursing responsibilities

A

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
Q

The first thing we address in hemodynamic instability?

A

preload

31
Q

Shock definition

A

ACUTE, WIDESPREAD PROCESS OF IMPAIRED TISSUE PERFUSION
THAT RESULTS IN CELLULAR, METABOLIC AND HEMODYNAMIC
ALTERATIONS

32
Q

Hypovolemic shock primary problem is

A

decreased preload

33
Q

Cardiogenic shock the primary problem is

A

decreased contractility

34
Q

Distributive shock the primary problem is

A

decreased afterload

35
Q

Obstructive shock the primary problem is

A

increased afterload

36
Q

Initially, compensatory mechanisms are ______ and then in hemodynamic instability they start to ____

A

Initially, compensatory mechanisms are EFFECTIVE and then in hemodynamic instability they start to PERPETUATE DYSFUNCTION

37
Q

Neural compensatory mechanisms

A

SNS-Baroreceptors

38
Q

Hormonal compensatory mechanisms

A

RAAS, ACTH, ADH

39
Q

Chemical compensatory mechanisms

A

Chemorecptors

40
Q

Metabolic indicators of shock

A

SvO2, OER, lactate, pH & base deficit

41
Q

‘balanced crystalloids

A

Plasmalyte/Normosol

RL

42
Q

Normal saline

A

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
Q

• Lactated ringers dangers

A

• Can make acidosis worse
• Careful to give with underperfused liver
(lactate≠ bicarbonate)
• Careful with the K if decr UO

44
Q

D5W

A
  • 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
Q

Give PRBC for Hgb under…

A

70

Exception: w/ a documented history of ACS hgb <80 gm/L

46
Q

Inotropes

A

(+) improve contractility

sympathomimetic (beta 1 receptors) – dopamine,
dobutamine, epinephrine

inhibitor of phosphodiesterase breakdown leading to
cAMP and calcium levels – milrinone

47
Q

Milrinone:

A

phosphodiesterase inhibitor
+ inotrope with little chronotropic effect
direct vasodilator

48
Q

Dobutamine action

A
  • predominantly Beta 1 effects
  • some Beta 2 – produces mild vasodilation
  • has chronotropic effects
49
Q

Dobutamine is used to treat

A

HF– especially in hypotensive pts who can not tolerate vasodilator therapy

50
Q

Dopamine

A
  • 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
Q

vasopressors

A

improve afterload

  • by stimulating alpha receptorsnorepinephrine (levophed) & phenylephrine
  • by stimulating V1 receptors
    vasopressin
52
Q

Levophed

A

strictly in clinical practice is alpha

  • onset 1-2 min
  • commonly ordered at 1 to 20 mcg/min
53
Q

Levophed - side effects

A
  • Hypertension
  • Angina or worse
  • Ischemia to limbs at high dosages
54
Q

Phenylephrine

A

Alpha 1 agonist without beta agonist

vasoconstriction

55
Q

Vasopressin

A

• 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
Q

labetalol

A

alpha/beta adrenergic antagonist/blocker

alpha prevents vasoconstriction
beta prevents reflex tachycardia

57
Q

hydralazine

A

a direct smooth muscle relaxant & a strong arterial vasodilator
S.E. reflex tachycardia (avoid in ACS)

58
Q

nitroprusside

A

> arterial than venous dilator
faster action;

S.E. cyanide toxicity

59
Q

Nitroglycerin

A

> venous than arterial dilator

NSCC 7320 (9 decks)

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