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Medicine II: Emergency Medicine > Shock > Flashcards

Flashcards in Shock Deck (58):
1

Types of Shock

1. Pump failure = Cardiogenic shock
2. Release valve failure = Obstructive shock
3. Hose failure = Distributive shock
4. Water failure = Hypovolemic shock

2

What are the Causes of Hypovolemic Shock:

Low Volume due to Traumatic and Non-traumatic blood loss.

3

How do we treat Hypovolemic Shock?

An increase in maintenance fluid is inadequate to cause significant volume expansion during the resuscitative phase resuscitative phase Therefore Fluid must be given as a rapid BOLUS

4

What is a BOLUS?

Large volume administered over 15-20 minutes

5

What are the possible etiologies of Cardiogenic Shock (Pump Failure)?

• Acute M I
• CHF
• Bradyarrhythmias
• Tachyarrhythmias

6

What happens with Distributive Shock?

There is inappropriate vasodilation of peripheral blood vessels.

This can be caused by: Septic shock, Neurogenic shock, Anaphylaxis, pregnancy, etc.

7

Case Presentation: A 60 yo female with family, c/o SOB, fever. Family: pt confused. Her vitals are HR 130, T=39.8, RR 26, BP=80/30, MAP 55. On PE: No retractions are noted. Lungs have decreased BS, ABD: s/nt/nd, Ext: no edema and Neck: no JVD.

What is this patient experiencing?

Septic shock

8

What is SIRS?

Systemic inflammatory response syndrome

A clinical response arising from a nonspecific insult, including ≥2 of the following:
– Temperature ≥38oC or ≤36oC
– HR ≥90 beats/min
– Respirations ≥20/min
– WBC count ≥12,000/mm3 or
≤4,000/mm3 or >10% immature neutrophils

9

What is Sepsis?

SIRS with a presumed or confirmed infectious process

10

What is the association between Sepsis and Mortality?

Major cause of morbidity and mortality worldwide. Leading cause of death in noncoronary ICU (US)*

11

What are the Goals of therapy for sepsis?

Require consideration of both global and regional perfusion

Care received in the ED during the first 6 hours of presentation impacted mortality more than the rest of the hospital stay combined.

12

What was the outcome of Norepinephrine use in patients with sepsis?

Decreased mortality and was shown to be the sole factor associated with increased survival

13

What are other Vasopressors that could be used?

Phenylephrine, Vasopressin, Epinephrine

14

What are the effects of Phenylephrine?

Excellent vasoconstriction. No activation of beta receptors; no change in HR

15

What are the effects of Epinephrine?

Affects beta and alpha receptors

16

Case Presentation: A 65 yo male presents with 2 hours of crushing substernal CP radiating to the LUE with N/V, diaphoresis. His EKG is significant for 3mm ST elevation inf. leads.

What is this patient experiencing?

Cardiogenic Shock

17

Cardiogenic Shock

Pump failure is not reversed by body’s compensatory mechanisms.

Patient presents with SBP < 90mm Hg, or 25-30mm Hg below baseline and increased Heart Rate, SVR, PCWP

18

Shock: Risk Factors in AMI

Age > 65
Diabetes Mellitus
Multivessel CAD
Female Gender
Anterior Infarction
Previous angina, CAD, CHF

19

What is the association of Cardiogenic Shock with Mortality?

Leading cause of death for AMI who reach the hospital alive. Incidence remains constant over 20 years (Despite early PCI or CABG, shock mortality is 50%)

Half of deaths occur within the first 48 hours.

Clinical history (PMH) was inversely associated with short-term mortality. Shock was the most predictive of short-term mortality.

20

How do we treat Cardiogenic Shock?

Volume resuscitation (if pulmonary edema is absent) & Intubation to decreased the work of breathing

Get an angiography

21

Case Presentation: A 19 yo male was body surfing on Jersey Shore and hits his head. He can not move his extremities. His vitals are : BP 80/40, RR 18, HR:60 s/p 4 L IVNS.

What is this patient experiencing?

Neurogenic Shock

22

Case Presentation: 18 yo female stung by a bee. They are in Acute respiratory distress with BP 75/50, HR 130, RR 28. They present with Cold, clammy skin, perioral swelling.

What is this patient experiencing?

Anaphalactic Shock

23

What are the symptoms of Anaphylactic Shock?

Bronchospasm, Laryngeal edema, Cardiac dysrhythmia, Hypotension, Angioedma & Confusion

24

Why is Shock in Children Important to Consider? How do we treat them?

Because of their ability to compensate it can mask their shock. Failure may cause “sudden” cardiovascular collapse.

increased hypovolemia and hypothermia risks

Pallor, altered LOC, cool skin = shock UPO

Avoid massive fluid infusion, use 20 cc/kg boluses

25

Why is Shock in the Elderly Important to Consider?

They have Poor cardiovascular condition and Rapid decompensation making Sepsis more likely

Hypoperfusion can cause: CVA, AMI, Seizures, Bowel Infarctions, or Renal failure

Difficult to diagnose because: They present with Weak pulses, Altered sensorium, Hypertension masking hypoperfusion, Beta-blockers masking hypoperfusion

Fluid infusion may produce volume overload/CHF

26

Why is Shock in OB Patients Important to Consider? How do we treat them?

• Pulse increases 10 to 15 bpm
• BP lower than in non-pregnant patient
• Blood volume increased by 45% (Slower onset of shock signs/ symptoms)
• Fluid resuscitation requires greater volume
• Oxygen requirement increased 10 to 20%
• Pregnant uterus may compress vena cava, decreasing venous return to heart. (Place women in late-term pregnancy on left-side)
• Fetus can be in trouble even though mother looks well-perfused
• Parodoxical bradycardia 

27

What is Anaphylactic Shock?

One of the most frightening causes of shock is the patient in anaphylaxis where the airway is obstructing, ventilation is compromised with bronchospasm, and the blood pressure is low.

28

Complications of Anaphylactic Shock:

Treatment should be aggressive and proactive. The airway is at risk in anaphylaxis due to angioedema, tongue or laryngeal edema. Patients with anaphylaxis are likely to be among the most challenging with regard to airway management. These patients can rapidly deteriorate and become "can't intubate, can't ventilate" airway disasters.

29

What is Septic Shock?

Septic shock is a clinical syndrome complicating infections caused by an exaggerated release of inflammatory mediators causing widespread organ dysfunction. The hallmark is the systemic inflammatory response syndrome (SIRS) (two or more of (1) temperature >38° C or 90 bpm, (3) respiratory rate > 20 breaths per minute, or PaCO2 < 32 (4) WBC > 12,000 cell/mm3 or < 4000 cell/mm3 or > 10% bands).

30

What is Neurogenic Shock?

a distributive shock in which there is a loss of vascular tone due to paralysis from a cervical cord spinal lesion can cause hypotension, shock & bradycardia.

peripheral vasodialtion

31

Define shock:

State of severe reduction in tissue perfusion characterized by decreased cellular oxygen delivery and utilization as well as decreased removal of metabolic waste products

Shock State exists whenever VO2 is inadequate for tissue needs or when dependent on DO2→ DO2 =oxygen delivery

**REMEMBER: Presence of normal vital signs DOES NOT exclude shock

32

What are the possible Etiologies of Shock?

Hypovolemic, obstructive, cardiogenic, distributive

33

What are clinical clues to shock?

unsuspected trauma, unsuspected or known pregnancy, new meds, allergies, overdose, or depression, drug interactions, travel history, tampon use

34

Determine if there is a reversible condition present:

Is there traumatic blood loss?
Is there nontraumatic blood loss?
Is there a dysrhythmia?
Is there a tension pneumothorax?
Is there cardiac tamponade?
Is there evidence of massive pulmonary embolism?
Is there overt anaphylaxis?
Is the spinal cord injured?
Is the problem with SVR?

35

Is there traumatic blood loss?

Stop visible hemorrhage, look for cavitary bleeding in the chest (CXR, ultrasound (U/S)), abdomen (FAST exam), or pelvis from pelvic fracture or disruption or long-bone fracture. If pelvic or long-bone fractures are present, immobilize these injuries and consider pneumatic antishock trousers (PAST) for additional stabilization.

36

Is there nontraumatic blood loss?

Check for a pulsatile abdominal mass (abdominal aortic aneurysm, AAA) or perform bedside U/S of the abdomen; check for GI bleed (hematemesis or melena).

37

What is the management for Shock?

a. Aggressive approach→ resuscitation with oxygen delivery ASAP.

Signs of a successful resuscitation include improvement in BP, improved mentation, decreasing lactate, resolving metabolic acidosis, urine output > 1 cc/kg/h, and improved skin perfusion

VOLUME resuscitation with crystalloid to 40 mL/kg; Dobutamine to get cardiac output to goal

38

Preshock symptoms can be subtle (may be compensating early so don’t have hypotension):

1. Pale, cool moist skin (in hypovolemic and cardiogenic shock).
2. Pulse pressure narrows
3. Blood is shunted to the heart and brain
4. Tachycardia and urine volume decrease, agitation (20-30% volume loss)
5. Pulmonary edema in L-sided heart failure and peripheral edema and JVD in R-sided heart failure (cardiogenic)
6. In full-blown shock, patients become agitated and finally decrease their mental status. Hypotension occurs and may be profound. The patient has tachypnea until respiratory failure occurs and has a metabolic acidosis due to elevated lactic acid from anaerobic metabolism. At the cellular level, tissue oxygen extraction is maximal and is reflected in decreased mixed venous O2 saturation. Multiple organ failure follows. Irreversible shock follows if treatment is not aggressive.

39

What happens with Anaphylactic Shock?

The airway is obstructing and ventilation is compromised due to bronchospasms. BP is low.

40

What is the treatment for Anaphylactic Shock?

If pt is advancing rapidly, early intubation is necessary

Epinephrine for bronchospasm or beta-agonist aerosol, H1 and H2 blockade, steroids

41

What is Septic Shock?

Exaggerated release of inflammatory mediators causing widespread organ dysfunction

42

What are the hallmarks of Septic Shock?

SIRS→ 2 or more of increased vital signs (pulse, temp, respiratory rate) or leukocytosis.

43

Treatment of Septic Shock:

Resuscitation, targeted Abx, abscess drainage, early endotrachial intubation. Central venous and arterial monitoring (CVP and MAP)

Immunocompromised pt: 3rd or 4th generation cephalosporin

44

When diagnosing Neurogenic Shock what do we have to keep in mind?

Hypotension should not be assigned as being due to neurogenic shock until other causes of traumatic shock (hemorrhage) has been ruled out!

45

Signs and Symptoms of Neurogenic Shock

Clinically, patients with neurogenic shock present with warm skin, hypotension (often marked if the patient is tilted in reverse Trendelenburg), and a variable tachycardia response (in a patient with a cervical spine level of injury).

46

Treatment of Neurogenic Shock

Fluid challenge, getting Mean Arterial Pressure to > 90 mmHg.

If fluid replacement is not working, then administer vasopressors (with alpha activity). (Dopamine & Phenylepherine)

47

What are the different causes of Obstructive Shock?

Tension pneumothorax, pericardial tamponade, and massive PE.

48

What are the signs and symptoms of Tension pneumo?

Tension pneumothorax is a clinical not radiographic diagnosis characterized by unilateral decreased breath sounds, unilateral chest hyperresonance, and tracheal deviation in the setting of respiratory distress and shock.

49

Treatment of Tension pneumo:

Treatment is immediate needle decompression followed by chest tube thoracostomy placement.

50

What is the etiology of Pericardial tamponade?

Uremia and cancer cause a gradual effusion usually

51

What are the signs and symptoms of Pericardial tamponade?

Symptoms include hypotension, elevated right side pressures (JVD) pulsus paradoxus (a fall in systolic blood pressure in inspiration), and Kussmaul's sign (increased jugular venous pressure on inspiration).

52

What is the treatment for Pericardial Tamponade?

Bedside U/S is extremely sensitive in detecting pericardial fluid and can be instrumental in guiding pericardiocentesis, although in the patient in extremis, blind pericardiocentesis might be lifesaving.

53

Signs and symptoms of a Pulmonary Embolism:

Massive pulmonary embolism presents as chest pain, syncope, tachypnea, and hypotension with signs of acute right ventricular overload with JVD and ECG changes.

54

Treatment of a PE:

Fluid administration might worsen right ventricular failure and should be given only cautiously. Blood pressure should be augmented with an appropriate vasopressor such as norepinephrine 0.5–1 g/min titrated to response. Immediate surgical embolectomy is sometimes effective but not usually feasible. Shock complicating pulmonary embolism is an indication for thrombolytics if no other contraindication exists.

55

Neurogenic Shock Per Mr. I

Injury to the spinal cord at the level of the cervical or thoracic vertebrae causes peripheral sympathetic denervation. The loss of sympathetic arterial tone results in decreased systemic vascular resistance and blood pressure. Loss of sympathetic innervation to the heart (T1 through T4 cord levels) leaves the parasympathetic cardiac innervation via the vagus nerve unopposed, resulting in bradycardia, or an absence of reflex tachycardia. In general, patients with neurogenic shock are warm, peripherally vasodilated, and hypotensive with a relative bradycardia. Patients tend to tolerate hypotension relatively well, as peripheral oxygen delivery is presumably normal. Bradycardia is characteristic but not universal. Loss of sympathetic tone and subsequent inability to redirect blood from the periphery to the core may cause excessive heat loss and hypothermia.

The diagnosis of neurogenic shock should be one of exclusion. Certain clues—such as bradycardia and warm, dry skin—may be evident, but hypotension in the trauma patient can never be presumed to be caused by neurogenic shock until other possible sources of hypotension have been excluded.

56

What is obstructive shock?

Problem with SV d/t mechanical obstruction to preload, causes are hypovolemic or cardiogenic shock

57

How do we treat obstructive shock?

needle decompression, chest tube, pericardiocentesis
- Fluids, pressors, inotropes

58

How do we treat distributive shock?`

vasoconstrict the patient