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M2 Cardiovascular > Shock - Kaiser > Flashcards

Shock - Kaiser Flashcards

1
Q

What defines shock?

A

1) Inadequate tissue perfusion, resulting in poor exchange of metabolic supplies and wastes.
2) A failure of oxidative metabolism involving either oxygen delivery, transport, or utilization.

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2
Q

How common is shock?

How dangerous is it?

A

Shock is the most frequent & substantial problem in critical care medicine.

Untreated, leads to multiorgan dysfunction & failure, and death.

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3
Q

What are the SIX types of shock, based on ETIOLOGY?

A

1) Septic (vasogenic)
2) Neurogenic
3) Obstructive
4) Traumatic
5) Cardiogenic
6) Hypovolemic
(“SNOTCH”)

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4
Q

What are the FOUR types of shock, based on HEMODYNAMIC findings?

A

1) Hypovolemic
2) Cardiogenic
3) Distributive
4) Obstructive

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5
Q

What are the two most lethal types of shock?

A

1) Cardiogenic (60%-90% mortality)

2) Septic (35%-40% mortality)

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6
Q

What are the four stages of shock?

A

1) Initial
2) Compensatory
3) Progressive
4) Refractory

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7
Q

What happens in the Initial stage of shock?

A

Hypoperfusion, tissue hypoxia, & lactic acidosis

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8
Q

What happens in the Compensatory stage of shock?

A

Cytokine release, hyperventilation, endogenous catecholamine release

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9
Q

What happens in the Progressive stage of shock?

A

Failing compensatory mechanisms. Worsening acidosis, capillary leakage, and organ dysfunction. Increased blood viscosity causing “sludging” of the microvasculature

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10
Q

What happens in the Refractory stage of shock?

A

IRREVERSIBLE organ damage, cell death, degradation of ATP to adenosine

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11
Q

What does the body do to increase blood flow to vital organs?

Why is peripheral pooling of blood sometimes seen with shock?

A

The body shunts blood away from the skin, acral regions, and the splanchnic system. CO/CI, RR, and tidal volume are increased. Urine production and gastrointestinal activity are reduced.

Eventually, metabolic (lactic) acidosis can lead to uncontrolled vasoconstriction and failure of precapillary sphincters. Blood ends up pooling in peripheral capillary beds and veins.

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12
Q

How does shock cause organ dysfunction in the:

1) Kidneys?
2) Liver?
3) GI tract?
4) Lungs?

A

1) Acute tubular necrosis leading to kidney failure
2) Liven congestion w/ increased enzymes & coagulopathy
3) GI ischemia & hemorrhage, peritonitis
4) ARDS (Acute Respiratory Distress Syndrome)

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13
Q

What defines Cardiogenic shock?

A

Protracted, severe malperfusion of tissues due to an ACUTE & critical reduction in heart pumping ability

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14
Q

How is Cardiogenic shock diagnosed?

A
  • By clinical & hemodynamic criteria

- Exclusion of other factors: Hypovolemia, Arterial hypoxia, Vasovagal reaction

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15
Q

In what context is Cardiogenic shock most often seen?

How lethal is it in this context?

A

In patients hospitalized with an acute MI, 5-10% develop Cardiogenic shock. (Only tiny % of pts w/ unstable angina w/o MI get Cardiogenic shock.)

Accounts for 50-90% of death in these pts.

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16
Q

What are the clinical signs of Cardiogenic shock?

A
  • In general: Signs of centralized circulation & organ dysfunction
  • Agitation
  • Pale, cool, clammy skin
  • Oliguria (reduced urine production: < 20ml/hr)
  • RV dysfunction (PE, RCA MI)
    • Elevated venous pressure, jugular distention
  • LV dysfunction (LAD/Cx MI, acute AI/MR)
    • Pulmonary edema
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17
Q

What hemodynamic parameters indicate Cardiogenic shock?

A
  • Systolic BP < 90mmHg, or a BP drop of > 30mmHg for > 30min
  • Increased LVEPD (PAWP > 15mmHg)
  • Reduced cardiac index (< 2.2 L/min/m2)
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18
Q

What is LVEPD? What cardiovascular parameter does it share a direct relationship with?

A

Left Ventricular End-Diastolic Pressure.

Related directly to PRELOAD.

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19
Q

What is PAWP / PCWP / PWP / PAOP?

A 
Pulmonary Artery Wedge Pressure
aka
Pulmonary Capillary Wedge Pressure
aka
Pulmonary Wedge Pressure
aka
Pulmonary Artery Occlusion Pressure
(Yup. They are ALL THE GODDAMNED SAME)
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20
Q

What is the PAWP closely related to?

A

(From Wiki) Due to the high compliance of the pulmonary circulation, under normal conditions the PAWP can be taken as an indirect measurement of Left atrial pressure and thus the LVEDP.

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21
Q

Name some myocardial etiologies of Cardiogenic shock.

A

1) Acute MI
2) Myocarditis
3) DCM
4) RV pump failure
5) Myocardial depression after cardiac arrest / bypass
6) Myocardial depression in septic shock

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22
Q

Name some mechanical etiologies of Cardiogenic shock.

A

1) Acute mitral insufficiency
2) Acute aortic insufficiency
3) Ventricular septum rupture
4) Ventricular free wall rupture
5) Ventricular aneurysm
5) Obstruction of LV outflow tract (aortic stenosis)
6) Obstruction of LV inflow tract (mitral stenosis)
7) Obstruction of RV outflow tract (PE)

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23
Q

Describe the cycle of progressive pathology in ischemic Cardiogenic shock

A

1) Decreased perfusion leads to
2) Cardiac injury, causing
3) Decreased stroke volume, leading to
4) Increased catecholamine release, which causes
5) Increased heart rate, which adds to the
1) Decreased perfusion
etc.

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24
Q

What happens to the duration of diastole during Cardiogenic shock?

A

Decreases due to compensatory tachycardia.

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25
Q

What causes the excessive myocardial oxygen consumption in Cardiogenic shock?

A

(Compensatory) tachycardia and increased myocardial wall tension.

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26
Q

What activates the sympathetic nervous system to compensate during Cardiogenic shock?
What specific effects does this activation produce?

A

Activation trigger: critical decrease in STROKE VOLUME

Effects:

1) Increased HR
2) Increased RR
3) Activation of RAAS
4) Baroreceptor-mediated ADH-release

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27
Q

What is the END RESULT of compensatory activation of the sympathetic nervous system during Cardiogenic shock?

Is this good or bad?

A

Increased pre- and afterload

Initially good (it's compensatory!), but in protracted shock, ALL primary useful compensatory mechanisms lead to FURTHER increase in myocardial oxygen use and shock progression. 
Leads to fluid retention, pulmonary edema, hypoxemia, worsening myocardial function.
28
Q

What TESTS are useful in the diagnosis of Cardiogenic shock?

A

1) 12-channel EKG
2) Echocardiography
3) Chest X-ray
4) Arterial blood gas (& Venous)
5) Basic chem, CBC, & cardiac enzyme panels
6) Serial lactate levels (indicates perfusion)

29
Q

Which can be detected in the serum longer following a STEMI: cardiac troponin or CK-MB? How long can each be detected?

A

Troponin can be detected up to 7-8 days after.

CK-MB can only be detected up to about 2 days after.

30
Q

An echocardiogram is fast, easy, and can be routinely used at the bedside. What diagnoses can it help make?

A

Aside from shock, useful for several severe conditions:

  • Papillary muscle rupture
  • Ventricular rupture
  • Pericardial tamponade
  • Pulmonary embolism
31
Q

What’s the general flow of cardiogenic shock management?

A

1) Optimize Milieu (I assume this means electrolyte and metabolite balances, etc?)
2) Control heart rate & rhythm
3) Optimize preload
4) Enhance contractility
5) Normalize systemic vascular resistance (SVR) (can be increased or decreased!)

32
Q

Name five treatments or drugs that are useful for improving coronary perfusion in Cardiogenic shock.

A

1) Vasopressors (NE, phenylepinephrine)
2) Inotropics (dobutamine, epinephrine, milrinone)
3) IABP (Intra-Aortic Balloon Pump)
4) LV or RV assist device (LVAD, RVAD)
5) When acute MI is cause: immediate angiography and revascularization.

33
Q

Name 3 inoconstrictor drugs (inotrope + vasoconstriction).

A

1) Norepinephrine
2) Epinephrine
3) Dopamine

34
Q

Name 3 inodilator drugs (inotrope + vasodilation).

A

1) Dobutamine
2) Milrinone
3) Isoproterenol

35
Q

Sepsis arises from a combination of what two major factors?

A

1) Infection
and
2) Systemic Inflammatory Response Syndrome (SIRS)

36
Q

Which is worse: severe Sepsis or Septic shock?

A

Septic Shock is worse; it follows severe sepsis in terms of progression.

37
Q

What four criteria are typically used to diagnose Systemic Inflammatory Response Syndrome (SIRS)?

A
  • Tachypnea
  • WBC either 12,000
  • HR > 90bpm
  • Fever > 38C (100.4F) or Hypothermia < 36C (96.8F)
38
Q

Name four possible manifestation of inadequate organ function/perfusion seen in Sepsis.

A

1) Mental state alteration
2) Hypoxemia (PaO2 < 72mmHg)
3) Elevated plasma lactate level
4) Oliguria ( < 30ml/hr for at least 1hr)

39
Q

What differentiates severe sepsis from regular sepsis?

A

Severe = sepsis with tissue hypoperfusion or organ dysfunction. Aside from various lab and test benchmarks, a common finding is sepsis-induced HYPOTENSION.

40
Q

What differentiates septic shock from severe sepsis? What does this differentiating factor present in spite of?

A

Septic shock = severe sepsis with persistent arterial hypotension (Systolic BP < 90mmHg or > 40mmHg below baseline DESPITE ADEQUATE FLUID RESUSCITATION!

41
Q

Is bacteremia always seen in septic shock?

A

No! Only 30-50% of cases.

42
Q

What is the differences between primary MODS (Multi-Organ Dysfunction Syndrome) and secondary MODS?

A

Primary MODS: Direct result of the insult

Secondary MODS: Consequence of the host response

43
Q

Both septic and vasodiliatory shock feature severe hypotension. What are some things that cause them?

A

1) SIRS
2) Pancreatitis
3) Burns
4) Anaphylaxis
5) Acute adrenal insufficiency
6) Cardiopulmonary bypass
7) CO poisoning

Others…

44
Q

What are septic shock campaign bundles?

A

Groups of tests and treatments to be completed within 3 hours and 6 hours of presentation.

45
Q

In sepsis, what tests and treatments are to be completed within 3 hours?

A

1) Measure lactate level
2) Obtain blood cultures prior to antibiotics
3) Give broad spectrum antibiotics
4) Give crystalloid for hypotension or elevated lactate

46
Q

In sepsis, what additional tests and treatments are to be completed within 6 hours, after all 3 hour criteria are met?

A

5) Apply vasopressors to maintain MAP > 65mmHg if fluids are not enough
6) Measure venous pressure CVP and venous oxygen saturation (ScVO2)
7) Remeasure lactate if initial lactate was elevated

47
Q

What are the targets for resuscitation in sepsis?

A

1) CVP >8mmHg
2) ScVO2 (venous oxygen saturation) > 70%
3) normalize lactate levels

48
Q

Behind antibiotics, what is the most important, first-line treatment for severe sepsis and septic shock?

A

Crystalloids for fluid resuscitation!

49
Q

What vasopressors are used in septic shock?

A

1) NE 1st choice

2) Epinephrine when additional vasoconstriction needed

50
Q

What is recommended in case of myocardial dysfunction during septic shock?

A

Inotropic support - most often DOBUTAMINE

51
Q

What are three causes of hypovolemic shock?

A

1) Traumatic / hemorrhagic shock
2) Burns
3) Dehydration

52
Q

What are DAMPs?

A

Damage Associated Molecular Patterns

Similar to PAMPS, released in response to tissue damage. Recognized by many of the same receptors (PRRs) and activate similar signaling pathways (pro-inflammatory)

53
Q

What are the four classes of hemorrhage? How much blood is lost in each?

A

Class I: 750ml (2000ml (>40%)

54
Q

Is a decrease in systolic blood pressure always noted with hemorrhagic shock?

A

SBP is typically decreased only in Classes III and IV

55
Q

What are some other findings in hemorrhagic shock?

A

1) Increased RR (compensate for lactic acidosis and low oxygen content)
2) Decreased urine production (oligouria)
3) Pale and/or cool extremeties
4) Altered mental state

56
Q

What mental state is a hemorrhagic shock patient likely to be in depending on the Class?

A

Class I: Agitated +
Class II: Agitated ++
Class III: Disoriented / Confused
Class IV: Obtunded / Lethargic

57
Q

What is most important therapy in hemorrhagic shock? What are two examples of this therapy?

A

Volume therapy!

1) Crystalloid solutions
2) Colloid Solutions (Hydroxyethyl starch / HAES)

58
Q

What is a serious potential side effect of hydroxyethyl starches (HAES)?

A

Renal failure

59
Q

What is pathological supply dependence on oxygen delivery?

A

Tissues normally have a reserve of oxygen to draw off of. Below a critical level of oxygen delivery (DO2), such as in hemorrhagic shock, reserves become depleted and anaerobic metabolism occurs. Below this critical point, oxygen consumption (VO2) is said to be dependent upon delivery (DO2).

60
Q

What is obstructive shock? What are two common causes?

A

Subtype of Cardiogenic shock, results from mechanical impediment to circulation.
Causes:
1) PE
2) Tension pneumothorax

61
Q

What is neurogenic shock? What typically causes it?

A

Profound vasodilation of arterial and venous blood vessels. Causes massive BP drop w/ reflex tachycardia.

Caused by injury of brain, brain stem, or spinal cord

62
Q

What is anaphylactic shock? What causes it?

A

A type of distributive shock with vasodilation and relative hypovolemia - in short, the tissues that need more blood flow don’t get it due to a pathological redistribution of blood volume.
Causes: IgE-dependent, IgE-independent (physical, chemical, or osmotic induced)

63
Q

Describe the five classes of anaphylactic shock

A

Class 0: Local, limited, cutaneous rxn.
Class I: Disseminated cutaneous & mucosal rxn with systemic sxs (agitation, headache)
Class II: Hemodynamic dysregulation, dyspnea, vomiting, defecation
Class III: Shock, severe dyspnea w/ bronchospasm, obtundation, vomiting, defecation
Class IV: Respiratory & circulatory arrest (vital orgam failure)

64
Q

What therapies are used for anaphylactic shock?

A

1) For volume: crystalloid/colloid solutions

2) For vasoconstriction: EPINEPHRINE, norepi, vasopressin

65
Q

How does epinephrine treat anaphylactic shock?

A

1) beta agonist: bronchodilation
2) positive inotrope / chronotrope
3) anti-inflammatory
4) alpha mimetic at high doses: vasoconstriction

66
Q

In what two types of shock does the Cardiac Index increase? In what two types does it decrease?

A 
Increase:
1) Neurogenic
2) Septic
Decrease:
1) Cardiogenic
2) Hypovolemic

M2 Cardiovascular (40 decks)

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