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Flashcards in Surgery 2.1 (3-6) - Sheet1 Deck (111):
1

What are the different forms of shock?

Hypovolemic Shock (Hemorrhagic)

Cardiogenic Shock

Vasodilatory Shock (Septic)

Neurogenic Shock

2

When does Hypovolemic/Hemorrhagic Shock occur?

It is present when marked reduction in oxygen delivery results from diminished cardiac output secondary to inadequate to vascular volume.

3

Hypovolemic/Hemorrhagic Shock is the most common cause of...

Shock in the surgical or trauma patient.

4

Which type of shock is most common in regards to external loses?

Hemorrhagic is the most common (external loses)

5

Why is there a marked reduction in oxygen delivery?

This results from diminished cardiac output secondary to inadequate vascular volume.

6

What can cause a decrease in effective circulating volume?

Internal redistribution of extracellular fluid from intravascular to extravascular space (3rd space)

7

Is shock still considered to be a medical diagnosis?

Shock remains a clinical diagnosis despite technological advances.

8

What are some clinical signs of Hypovolemic/Hemorrhagic Shock?

Some signs are an agitated patient pallor, cold clammy extremities, tachycardia, weak or absent peripheral pulse and hypotension.

9

How much blood loss is associated with Hypovolemic/Hemorrhagic Shock?

Clinical sign are apparent at least 25-30% blood loss.

10

What is considered to not be accurate in regards to measuring one's index of shock?

BP is not an accurate index of shock

11

What are some signs of Hypovolemic/Hemorrhagic Shock?

Initially, the patient is anxious, appears tired and depending on the degree of shock, can be extremely restless or frankly comatose.

12

How much blood loss is needed to produce little in regards to obvious symptoms?

15% blood loss (700-750mL for 70kg pt) may produce little in terms of obvious symptoms.

13

How much blood loss would be required for mild tachycardia, tachypnea and anxiety?

30% blood loss (1.5L)

14

How much blood loss results in hypotension, marked tachycardia, confusion?

>30% blood loss

15

How much blood loss is needed for it to be considered life threatening and generally requires operative control of bleeding?

40% blood loss

16

What is ABG?

Metabolic acidosis (lactic academia)

17

How are the serum electrolytes?

Nearly always normal

18

Why is serum creatinine important?

useful for evaluation of renal function

19

When is hematocrit most likely to occur?

Normal within few hours of trauma

20

How could one check for Hypovolemic/Hemorrhagic Shock?

Ultrasound or diagnostic peritoneal lavage.

Thoracentesis or abdominal tip.

21

What are the appropriate priorities in regards to dealing with Hypovolemic/Hemorrhagic Shock?

Secure the airway

Control the source of bleeding

Intravenous volume resuscitation

22

What are other forms of treatment?

Identify the body cavity harboring active hemorrhage.

Blood transfusion, O2 inhalation

Early intra operative intervention to correct intraabdominal or intrathoracic blood loss.

23

What is cardiogenic shock?

Cardiogenic shock is circulatory pump failure.

24

What can cardiogenic shock lead to?

It can lead to diminished forward flow and subsequent tissue hypoxia.

25

What is the name of the criteria for "cardiogenic shock"?

It is called "Hemodynamics criteria".

26

List the three components of hemodynamics criteria.

1.) Sustained hypotension (i.e. SBP <90mmHg for at least 30 mins).

2.) Reduced cardiac index, (,2.2 L/min per square meter).

3.) Elevated pulmonary artery wedge pressure (>15mmHg).

27

What happens to the Myocardial diastolic function when cardiogenic shock occurs?

The Myocardial diastolic function becomes impaired.

28

What is the mortality rate of cardiogenic shock?

50% - 80%

29

What is the most common cause of cardiogenic shock?

Acute, extensive MI is the most common cause of cardiogenic shock.

30

When cardiogenic shock occurs, it causes significant damage to which part of the heart?

It causes damage to the Left ventricle in 40% of cases.

31

In what percentage of cases is damage found to the Left ventricle when a patient dies from cardiogenic shock?

In 40% of cases, patients dying from cardiogenic shock has found damage to the Left ventricle.

32

Cardiogenic shock complicates what percentage of acute MI's?

It complicated 5-10; most common cause of death in patient hospitalized with acute MI).

33

What is mandatory to minimize mortality?

Acute MI, expeditious restoration of cardiac output.

34

What happens with increased time to restoration of coronary blood flow?

The extent of myocardial salvage possibly decreases exponentially.

35

What happens to the degree of coronary flow after percutaneous transluminal coronary angioplasty?

It correlates within hospital mortality.

36

What are some examples of the degree of coronary flow after percutaneous transluminal coronary angioplasty correlating within hospital mortality?

33% mortality with complete reperfusion; 50% mortality with incomplete reperfusion; and 85% mortality with absent reperfusion.

37

What is cardiogenic shock caused by?

Myocardial ischemia that causes myocardial dysfunction.

38

What causes the stroke volume to decrease?

When sufficient mass of the left ventricular wall is necrotic or ischemic and fails to pump.

39

What happens when sufficient mass of the left ventricular wall is necrotic or ischemic and fails to pump?

It causes the stroke volume to decrease.

40

What disease do most cardiogenic shock patients have?

A majority have multivessel disease with limited vasodilator reserve and pressure dependent coronary flow in multiple areas of heart.

41

During cardiogenic shock, what happens to myocardial diastolic function?

Myocardial diastolic function is impaired.

42

What is one result from myocardial ischemia?

Decreased compliance results form myocardial ischemia.

43

What are the causes of cardiogenic shock?

1.) Acute MI - Pump Failure, Mechanical Complications (acute mitral regurgitation, acute ventricular septal defect [VSD], free wall rupture, pericardial tamponade).

2.) Arrhythmia, End-stage cardiomyopathy, Myocarditis, Severe myocardial contusion.

3.) Left ventricular outflow obstruction - Mitral stenosis, Left atrial myxoma.

4.) Acute mitral regurgitation, Acute aortic insufficiency, Metabolic causes, Drug reactions

44

Why is it important to have rapid identification of the Px with pump failure and an institution of corrective action?

They are both essential, including history and PE (for the Px with pump failure) in preventing the ongoing spiral of decreased cardiac output from injury causing increased myocardial O2 needs that cannot be met.

45

What happens when increased myocardial O2 needs cannot be met?

It leads to progressive and unremitting cardiac dysfunction.

46

What causes of hypotension must be excluded?

Hemorrhage, Sepsis, Pulmonary embolism, Aortic dissection.

47

What are some signs of circulatory shock?

Hypertension, cool and mottled skin, depressed mental status, tachycardia, and diminished pulse.

48

What does a cardiac exam test for?

Dysrhythmia, precordial heave, or distal heart tones.

49

What are two examples of cardiac exams?

Electrocardiogram and urgent Echocardiography

50

What are some other useful diagnostic tests?

Chest radiographs, Arterial blood gas (ABG), electrolytes, CBC, and cardiac enzymes.

51

When would a doctor consider more invasive cardiac monitoring?

Although it's generally not necessary, it is done to exclude right ventricular infarction, hypovolemia, and possible mechanical complications.

52

What is the purpose of cardiac exams?

To identify cardiac dysfunction or acute heart failure in a susceptible patient.

53

What happens when there is a blunt traumatic injury?

Hemorrhagic shock from intra-abdominal bleeding; intra-thoracic bleeding from fracture (both must be be excluded before implicating cardiogenic shock from blunt cardiac injury).

54

Do many or few patients with cardiac injury develop cardiac pump dysfunction?

Few patients with blunt cardiac injury will develop cardiac pump dysfunction.

55

What is the status of diagnosing blunt cardiac injury?

Establishing the diagnosis of blunt cardiac injury is secondary to excluding other etiologies for shock and establishing that cardiac dysfunction is present.

56

What can help uncover evidence of diminished cardiac output and elevated pulmonary artery pressure?

Invasive hemodynamic monitoring with pulmonary artery catheter.

57

What are the steps to need to treat cardiogenic shock?

1.) Adequate airway is present and ventilation is sufficient.

2.) Support of the circulation (intubation, mechanical ventilation - are often required [if only to decrease work of breathing and facilitating sedation of the patient])

3.) Maintenance of adequate oxygenation.

4.) Electrolyte Equilibrium

5.) IV pain medication intravenously

6.) Antiarrhythmic drugs, pacing or cardioversion

7.) Early consultation with cardiology.

8.) Inotropic support

9.) Dobutamine

10.) Dopamine

11.) Epinephrine

12.) Phosphodiesterase inhibitors Amrinone and Milrinone

13.) Intra-aortic Balloon Pump

14.) Anticoagulation and aspirin given for acute MI

15.) Beta blockers

16.) Nitrates

17.) ACE mediated vasoconstrictive effects

18.) Stent

19.) Bypass Grafting

58

What are two IV pain medications that are given intravenously?

Morphine sulfate or fentanyl

59

When would one be prescribed antiarrhythmic drugs, pacing or cardioversion be given?

For dysrhythmia and heart block.

60

When would one consider early consultation with cardiology?

It would be essential in current management of cardiogenic shock, particularly in the setting of acute MI.

61

When would one use inotropic support?

May be indicated to improve cardiac contractility and cardiac output if profound cardiac dysfunction exists.

62

What is Dobutamine and what is its purpose?

Primarily stimulates cardiac beta 1 receptors to increase cardiac output.

But may also vasodilation peripheral vascular beds; thus lowering peripheral resistance and lower systemic BP through effects on beta 2 receptors.

Ensuring adequate preload and intravascular volume is essential prior to instituting therapy with dobutamine.

63

What is Dopamine and what is its purpose?

Stimulates alpha 1 receptor = vasoconstriction

May be preferable to dobutamine in treatment of cardiac dysfunction in hypotensive patients

Tachycardia and increased peripheral resistance from dopamine infusion may worsen myocardial ischemia (titration of both dopamine and dobutamine infusion may be required in some patients)

64

What is Epinephrine and what is its purpose?

Stimulates alpha and beta receptors and may increase cardiac contractility and heart rate.

May have intense peripheral vasoconstrictor effects that impair further cardiac performance.

65

What are phosphodiesterase inhibitors Amrinone and Milrinone and what are their purposes?

May be required on occasion in patients with resistant cardiogenic shock.

66

What is an Intra-aortic Balloon Pump and what is its purpose.

For mechanical circulatory support.

67

What are the purpose of beta blockers?

To control heart rate and myocardial O2 consumption.

68

What is the purpose of nitrates?

To promote coronary blood flow through vasodilation

69

What are the effects of ACE mediated vasoconstriction?

Increases the myocardial workload and myocardial O2 consumption.

70

What is a stent?

A small mesh tube inserted in narrow/weak arteries.

71

What is bypass grafting?

It is known as CABG/Coronary artery bypass grafting; It is a surgical intervention that improves blood flow due to plaque buildup in CHD.

72

What is Septic/Vasodilatory Shock?

It is the failure of vascular smooth muscle to constrict appropriately.

73

What is the most commonly encountered form?

Septic shock is the most commonly encountered form.

74

What are some characteristics of Septic/Vasodilatory shock?

Peripheral vasodilation and resistance to treatment with vasopressors.

75

What does it mean (or represent)?

It can represent the final common pathway for profound and prolonged shock of any etiology.

76

What is septic shock?

By-product of the body's response to invasive or severe localized infection.

77

What is the mortality rate of septic shock?

30-50% mortality rate.

78

What is a general causes of septic shock?

Typically from bacterial or fungal pathogens.

79

What is the vasodilatory effect?

Due in part to the upregulation of the inducible form of nitric oxide synthase in the vessel wall.

80

What are the causes of Vasodilatory Shock?

Systemic response to infection.

Non Infectious systemic inflammation (pancreatitis, burns)

Anaphylaxis

Acute adrenal insufficiency

Prolonged, severe hypotension (hemorrhagic shock, cardiogenic shock, cardiopulmonary bypass)

Metabolic (Hypoxic lactic acidosis, carbon monoxide poisoning)

81

What were some attempts to eradicate the pathogens?

Immune and other cell types elaborate soluble mediators that: enhance macrophage and PMN killing effector mechanisms, increase procoagulant activity, increase fibroblast activity to localize invaders, and increase microvascular blood flow to enhance delivery of killing forces.

82

How is the progression of the disease described?

It is described as complex.

83

How does the disease progress?

A severe infection moves from a systemic inflammatory response syndrome (SIRS) to sepsis and severe sepsis to septic shock.

84

What happens if septic shock is left untreated?

It can lead to lead, with or without multiple organ dysfunction syndrome (MODS).

85

When is it best to treat septic shock?

It is important to recognize the problem as early as possible and treat it accordingly.

86

What is the mortality rate for sepsis?

16-20% mortality rate.

87

What is the mortality of septic shock?

20-50%; varies based on the type of infectious organism, underlying illness or complication, timing and the kind of antimicrobial therapy and degree of system failure present.

88

What initiates the syndrome?

It is initiated by the host's innate immune system.

89

What is the difference between sepsis and septic shock?

An infection that is widespread throughout the bloodstream is called sepsis (or septicemia) and can lead to severe symptoms and life threatening conditions called septic shock.

90

When does sepsis occur?

Sepsis occurs when pathogenic microorganisms cross host barriers and overwhelm defenses.

91

What are the key pathogens in sepsis?

Gram negative bacteria, such as: E. Coli, K. Pneumonia, P. Aeruginosa, and N. meningitides.

92

What are some of the causative agents of sepsis?

Gram positive organisms, such as: S. aeurus, coagulas-negative staphylococcus, S. Pneumonia, Strept. Pyogenes, and Enterococcus Rickettsia, viruses, fungi, and polymicrobial sepsis.

93

In neonates, what is sepsis most likely caused by?

It is most likely caused by group B strept., E. coli bearing a pathogenic K1 capsule, Klebsiella sp. And Enterobactes sp.

94

What happens to the patient as the disease progresses?

The patient generally experiences both earlier symptoms along with organ dysfunction, hypoperfusion or hypotension.

95

Are there any other observed perfusion abnormalities?

Confusion or altered mental status, elevated plasma lactate levels and oliguria (decreased urine output <30cc).

96

What is sepsis?

systemic inflammatory response to infection.

97

What is severe sepsis?

sepsis with one or more dysfunctional organ systems.

98

What is Systemic Inflammatory response syndrome (SIRS)?

syndrome in which inflammatory mediators released, particularly cytokines such as TNF, secondary to an infectious and/or traumatic insult cause the patient to present with at least 2 of the ff. conditions.

99

What are the ff. conditions?

Body temperature can increase above 38 degrees Celsius; Tachycardia (>90bpm); Tachypnea (>20 breaths/min); WBC > 12k < 4k

100

What is Compensatory anti-inflammatory response syndrome (CARS)?

syndrome in which anti-inflammatory mediators release overcompensates for the systemic inflammatory response to an infection and/or traumatic insult leading to a state of immunosuppression.

101

What are the indicators of moderate sepsis?

Body temperature > 38 degrees Celsius or < 36 degrees Celsius

HR > 90
RR > 20 or PCO2 , 32
WBC . 12k
Urine output: 1cc/1kg/hr

102

What is severe sepsis?

sepsis-associated with lactic acidosis, oliguria, acute alteration of mental status.

103

What is septic shock?

Sepsis-induced hypotension despite adequate fluid resuscitation with multiple organ dysfunction (MODS). Hypotension and hyperperfusion secondary to pathophysiological alteration.

104

What are some signs that indicate Vasodilatory Shock?

Evidence of infection and systemic signs of inflammation (sepsis)

Hypoperfusion with signs of organ dysfunction (severe sepsis)

Significant evidence of hypoperfusion and systemic hypotension (septic shock)

105

What should one do if they suspect Vasodilatory Shock?

Aggressively search for infection

Inspect all wounds

Evaluate all intravascular catheter or other foreign body

Obtain an appropriate culture

106

What else should be done to evaluate Vasodilatory Shock?

Adjunctive imaging studies.

107

What forms of diagnostic assessment should be done?

CBC and differential

Coagulation status (PT or a PTT, fibrinogen, FDP, d-dimer

Serum electrolyte level renal and hepatic function

ABG Analysis

Elevated serum lactate level

urinalysis and culturing

Gram staining

Blood Culture

108

How does Vasodilatory Shock manifest?

Enhanced cardiac output

Peripheral vasodilation
Fever
Leukocytosis
Hyperglycemia
Tachycardia
Confusion, malaise, oliguria, or hypotension

109

What are some forms of treatment for Vasodilatory Shock?

Fluid resuscitation and restoration of circulatory blood volume with balanced salt solutions.

Empiric antibiotics
Surgical drainage
Vasopressors (catecholamines, arginine, vasopressin).

110

What are some expensive forms of treatment?

Immune Modulation

111

What are some forms of Immune Modulation? (expensive)

Anti-endotoxin antibodies

Anti-cytokine antibodies

Cytokine receptor antagonist

Immune enhancers

Non-isoform specific nitric oxide synthase inhibitor

Oxygen radical scavenger

Activated protein C - promotes fibrinolysis and inhibits thrombosis and inflammation

Corticosteroids - still controversial