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IPT: CC > Block 2 > Flashcards

Block 2 Flashcards

1
Q

BP = what two parameters?

A

CO x SVR

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2
Q

SVR is determined by what?

A

Radius of resistance vessels

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3
Q

Cardiac = what two parameters?

A

SV x HR

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4
Q

CO
SVR
SV
HR

Which one is directly influenced by preload, contractility, and afterload?

A

SV

SVR is proportional to Afterload

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5
Q

Increase of (preload/contractility/afterload) increases SV

A

All except afterload

Increased afterload decreases SV

Increased afterload will INCREASE SVR though

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6
Q

Cardiac output adjusted for body weight is known as..?

A

Cardiac Index

= CO/BSA

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7
Q

What is preload? Afterload?

A

Preload = pressure/volume in ventricles as they fill up

Afterload = the pressure the left ventricles have to overcome for blood to flow, resistance to blood flow

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8
Q

How do fluids and vasopressors affect preload/afterload?

A

Fluids will increase preload (diuretics will decrease it)

Anything that causes vasoconstriction (like vasopressors) will increase afterload (so vasodilation will decrease it)

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9
Q

Increased preload = Increased end diastolic volume = Increased contractility except in what patients?

A

Heart Failure, stroke volume hardly changes

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10
Q

What are the 4 types of shock?

A

Hypovolemic
Cardiogenic
Obstructive
Distributive

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11
Q

Distributive
Hypovolemic
Cardiogenic
Obstructive

Which one has vasodilation?

A

Distributive

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12
Q

Distributive
Hypovolemic
Cardiogenic
Obstructive

Which one has vasoconstriction?

A

Hypovolemic (arterial side usually)

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13
Q

Distributive
Hypovolemic
Cardiogenic
Obstructive

Which one has a formation of a pericardial tamponade?

A

Obstruction

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14
Q

Distributive
Hypovolemic
Cardiogenic
Obstructive

Which one is seen in patients with possible edema?

A

Cardiogenic

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15
Q

Distributive
Hypovolemic
Cardiogenic
Obstructive

Which one is caused by ventricular failure?

A

Cardiogenic

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16
Q

CVP
PCWP
CO
SVR

How does hypovolemic shock affect these values?

A

Low fluid, therefore CVP and PCWP decreased

CO is down as a result, but SVR will compensate (vasoconstriction) and increase

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17
Q

CVP
PCWP
CO
SVR

How does cardiogenic shock affect these values?

A

Fluid status is usually increased, so CVP and PCWP are increased.

CO is still down as a result and SVR will compensate by increasing

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18
Q

CVP
PCWP
CO
SVR

How does obstructive (pericardium tamponade) shock affect these values?

A

Same as cardiogenic but different from PE obstructive shock

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19
Q

CVP
PCWP
CO
SVR

How does obstructive (systolic contraction/PE) shock affect these values?

A

Pretty much the same as obstructive and cardiogenic, but PCWP may decrease or be normal

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20
Q

CVP
PCWP
CO
SVR

How does distributive shock affect these values?

A

No treatment = everything decreased

With treatment = everything increased except SVR

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21
Q

Immediate goals of:

MAP
CI

A

MAP > 65

CI >2.2

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22
Q

Immediate goals of:

Hgb
O2 sat
Lactate

A

Hgb > 7

O2 sat >92%

Lactate < 2

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23
Q

Osmolarity equation?

A

2xNa + (BUN/2.8) + (Glucose/18)

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24
Q

Compared to NS, what does LR have?

A

Less sodium

Potassium
Calcium

Less chloride

Lactate

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25
Q

Compared to NS, what does plasmalyte-A or Normosol-R have?

A

Less sodium (but more than LR)

Potassium (higher than LR)

Less chloride (even less than LR)

Magnesium
Acetate
Gluconate

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26
Q

How does administering albumin help with fluids?

A

Draws fluids from extravascular/intracellular space to intravascular space

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27
Q

What did the SAFE trial say?

A

ICU patients, fluid resuscitation with albumin vs NS

No difference in 28-day mortality

Subgroup analysis with traumatic brain injury had a higher mortality with albumin (but wasn’t the focus of the trial)

Use crystalloids (NS) for initial resuscitation vs colloids)

Another study (CRISTAL) showed the same results except they did it with more crystalloids and colloids

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28
Q

What have studies shown about using more balanced crystalloids (LR, plasma-lyte) vs NS?

A

No mortality differences, but less AKI in LR, plasma-lyte groups

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29
Q

Activation of alpha 1 and 2 in the vascular smooth muscle/CNS cause vaso(constriction/dilation)

A

Alpha 1 = constriction

Alpha 2 = dilation in CNS, constriction in vascular space

30
Q

Activation of beta 1 and 2 in the vascular smooth muscle cause vaso(constriction/dilation)

A

Beta 1 = increased chronotropy (cardiac muscle)

Beta 2 = dilation

31
Q

Activation of dopamine and phosphodiesterase in the vascular smooth muscle cause vaso(constriction/dilation)

A

Dopamine = constriction

Phosphodiesterase = dilation

32
Q

Activation of vasopressin 1 and 2 in the vascular smooth muscle cause vaso(constriction/dilation)

A

1 = constriction

2 = increases blood volume (water retention in kidneys)

33
Q

Activation of alpha receptors have more of an affect on (CVP/SVR)

A

SVR; constriction of vascular smooth muscles typically occur on the arterial side

Venous side (CVP) doesnt change shape much

34
Q

Vasopressin

V1 vs V2 receptors

Which one increases SVR? What does the other one do?

A

V1

V2 - increased blood volume

Both ultimately increases arterial pressure

35
Q 
Norepi
Epi
Phenylephrine
Vasopressin
Dopamine
Dobutamine
Isoproterenol
Milrinone

Which drug can cause reflex bradycardia?

A

Phenylephrine

It targets only alpha and body will compensate by lowering HR

36
Q 
Norepi
Epi
Phenylephrine
Vasopressin
Dopamine
Dobutamine
Isoproterenol
Milrinone

Which drug has differing receptor effects depending on dose?

A

Dopamine

Low - Dopamine and small beta 1

Medium - Dopamine, Beta 1 and small beta 2

High - Dopamine, Beta 1,2, and alpha

37
Q

What receptors do norepi and epi target?

A

Norepi - alpha + beta 1

Epi - alpha, beta 1 + 2

38
Q 
Norepi
Epi
Phenylephrine
Vasopressin
Dopamine
Dobutamine
Isoproterenol
Milrinone

Which drug is a PDE3 inhibitor?

A

Milrinone

39
Q

What targets do dobutamine and isoproterenol target?

A

Both target beta 1 and 2

Dobutamine however targets alpha which can sort of prevent hypotension

40
Q 
Norepi
Epi
Phenylephrine
Vasopressin
Dopamine
Dobutamine
Isoproterenol
Milrinone

Which drugs could cause hypotension?

A

Dobutamine
Isoproterenol
Milrinone

41
Q

How is cardiogenic shock treated?

A

Treat the underlying cause

Small amounts (250-500ml) of crystalloids in absence of pulmonary edema

Diuretics (caution)

Norepi is first line

You may do norepi + another vasopressor + inotropes (watch for hypotension)

Mechanical devices if nothing else works

42
Q

Cardiogenic shock goal?

A

MAP >60-65mmHg

43
Q

What did the SOAP II trial show?

A

Higher mortality rate with dopamine use in cardiogenic shock. That’s why dopamine is not recommended in treatment

Also causes more arrhythmias

44
Q

How is distributive shock treated?

A

Crystalloids and then norepi as first line BUT you may add vasopressin or epi on top

Target MAP is at 65mmHg

Steroids can be used but is controversial

Antimicrobials within 1 hr for 7-10 days

45
Q

What condition is common in distributive shock?

A

Sepsis

46
Q

What is the SIRS criteria?

A

Must be ≥2 to be qualified for sepsis

Temp >38 or <36
HR>90
RR>20
WBC>12 or <4

47
Q

What does the SOFA score look into?

A

Organ failure assessment (used in the newest sepsis scoring assessment)

48
Q

Whats in the qSOFA scoring?

A

RR≤22bpm

Altered mentation

SBP≤100mmHg

≥2 suggest poor outcome

49
Q

How much crystalloid should you give in distributive shock and for what reason?

A

30ml/kg

For hypotension or lactate ≥4

50
Q

What is the ACTH stimulation test?

A

Uses cosyntropin to stress adrenal glands to measure increased cortisol levels

≤9 is insufficient

51
Q

What did the CORTICUS study show?

A

When given 50mg q6hrs x 5 days it reversed shock quicker but also increased hyperglycemia

52
Q

What did the HYPRESS trial show?

A

Corticosteroids for refractory shock only

53
Q

If patient needs steroids, what is the dose?

A

50mg q6 hrs

or

100mg q8 hrs

54
Q

Pros and cons of angiotensin 2 drugs?

A

Improve MAP within 3 hours but tapers off

AE of thrombotic and peripheral ischemia

55
Q

Obstructive shock treatment?

A

Modest fluids (diuresis for pulmonary HTN, fluids for PE)

Vasopressors (NE)

Thrombolytics for MASSIVE PE; Alteplase 100mg (90 for stoke) over 2 hrs

56
Q

Hypovolemic shock treatment?

A

<1.5 L of isotonic crystalloids

Adjunct vasopressors if life-threatening hypotension

Hemostatic resuscitation eat at least 2 erythrocyte like 1 plasma:1 PLT

57
Q

Distributive
Hypovolemic
Cardiogenic
Obstructive

Which one contains sepsis, neurogenic, and immune mediated shock?

A

Distributive

58
Q

What are the indications for mechanical ventilation?

A

Hypoxia

Hypoventilation

Respiratory fatigue (anxiety, dyspnea, status asthmaticus)

Seizures
GCS<8

59
Q

What is FiO2?

A

Fraction of inspired oxygen

Ranges from 21% (environmental air) to 100%

60
Q

What does the TLC ventilator mean?

A

Trigger - when breath starts

Limit - how fast breath enters

Cycle - when breath changes from inhalation to exhalation

61
Q

What does the continuous mandatory ventilation do?

A

Ventilator does all the work

Patient cannot trigger own breath

62
Q

Which ventilator option is mode of choice for ARDS?

A

Assist-control ventilation

63
Q

What does a assist-control ventilation do?

A

Assist pt to a full breath. Triggers when pt tries to inhale, if there is no breath, then it’ll act as a continuous mandatory ventilator

Causes hyperventilation and respiratory alkalosis

64
Q

What is a synchronized intermittent mandatory ventilator?

A

No assistance when patient triggered breath occurs

Allows them to contribute to their own respiratory effort

65
Q

What is a pressure support ventilator?

A

Full spontaneous respiratory effort by patient

66
Q

What is continuous positive airway pressure?

A

No inspiratory assistance

Can be given to intubated or non-intubated pt via mask

67
Q

What are the noninvasive ventilators?

A

BiPAP (usually for acute care)

CPAP

68
Q

ARDS is caused by a triad of symptoms which are:

A

Dyspnea

Tachypnea

Hypoxemia

69
Q

What is the Berlin Definition of ARDS?

A

Within 1 week

BILATERAL opacities

Not explained by HF or fluid overload

PaO2:FiO2 <300

Mild 201-300

Severe ≤100

Moderate inbetween

70
Q

Risk Factors of ARDS?

A
  1. Pneumonia
  2. Sepsis
  3. Trauma
71
Q

Mechanical ventilation and ARDS?

TV
PaCO2
PEEP

A

Tidal volume = 4-6ml/kg IBW

Permissive hypercapnia using A/C mode (PaCO2 50-55mmHg

PEEP of 5cm H20

72
Q

What are the pharmacological treatments used in ARDS?

A

Nimbex

EARLY use of low/moderate dose of methylprednisolone or decadron

IPT: CC (7 decks)

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