11 17 2014 Shock Flashcards

1
Q

What is Shock?

A

A physiological state characterized by a significant systemic reduction in tissue perfusion leading to cellular hypoxia

* Cellular Energy Deficit!! ** Decrease in ATP

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2
Q

4 causes of systemic Hypotension and their pathology

A
  1. Myocardial Pump Failure —–> Decrease in CO
    - due to MI, Ventricular Arrhythmia, compression (cardiac tamponade), Pulmonary Embolism
  2. Trauma —– > Decrease in CO
    - hemorrhage, fluid loss form burns
  3. Vascular injury —> 3rd spacing : edema/ ascities –> decrease effective circulating volume
    - Due to anesthesia or secondary to spinal cord injury
    - also seen in HTN/ Heart failure, pancreatitis
  4. Atrial vasodilation and venous blood pooling due to systemic immune response – Anaphylactic Shock
    - decrease in vascular tone = endothelial cell activation = Hypercoagulative state –> Intravascular coagulation
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3
Q

What are the two important compensatory mechanisms to Hypoperfusion? What is their overall outcome?

A
  1. Baroreceptor Response
  2. Renin-Angiotensin system

= Increase SNS, release catecholamines, increase ADH, and increase RAAS

  • retain water and increase contractility of heart to increase CO
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4
Q

Baroreceptor Response role in increasing perfusion:

A

Decreased arterial pressure is sensed in carotid sinuses and aortic arch (baroreceptors).

These usually sense high blood pressure and stimulate Vagal nerve to try to depress CO.

When pressure is low, these structure’s funciton are inhibited

=disinhibition of SNS

  • increase in vascular constriction and increase in heart rate and contractility
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5
Q

Renin- Angiotensin Aldosterone System role in increasing perfusion:

A
  1. low blood pressure is sensed in Juxtaglomerular cells – secrete Renin in response
  2. Renin catalyzes Angiotenisinogen – AI ( ACE –>) –> AII
  3. AII binds to AT1 ( Angiotensin II Type 1 Receptor) = Systemic vasoconstriction;

Also binds in Posterior Pituitary = release of Vasopressin ( activates aquaporins to increase reuptake of fluids)

Also binds to AT1 in Medulla of Adrenal Gland = Release of Aldosterone = increase in Na+ uptake and K+ excretion. Also aids in the reuptake of fluid

= Net water resorption

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6
Q

What is the benefit of the compensatory response?

A

Metabolic rates of heart and brain are high!

  • critically dependent on blood flow for oxygen delivery

Fall in CO results in diversion of blood from nonessential vascular beds ( skin, muscle, GI) to heart and brain.

* peripheral constriction

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7
Q

Common clinical findings with tissue hypo perfusion?

A
  • Cool, clammy skin, pale or grey color

( periopheral vasoconstriction)

  • Metnal status changes : agitation/ anxiety; sense of impending doom, confusion, and obtundation ( loss of conciousness)
  • Metabolic Acidosis
  • due to hypoperfusion —> causes tachypnea ( hyperventilation) to try to compensate for decrease in pH — compensation is to increse release of CO2
  • liver will have a hard time clearing lactate
  • anerobic metabolism rapidly worsenes acidemia
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8
Q

What are the classifications of shock?

A
  1. Low Cardiac Output
    - Cardiogenic
    - Hypovolemic
    - Obstructive
    - Pericardial Tamponade
    - Tension Pneumothorax
  2. Norma/ high cardiac output
    - Septic shock
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9
Q

What are the causes for cardiogenic shock and pathophysiology?

A

Primary pump failure

  • MI

Cardiomyopathy

  • Arrhythmia (ventricular)
  • Valvular Heart Disease
  • Pulmonary Embolism

Pathophysiology

All which lead toreduce cardiac output and low blood pressure AND:

  • Increase in LVEDV
  • Increased LA pressure
  • Increase pulmonary capillary pressure
  • Increase pulmonary Edema
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10
Q

Cardiogenic Shock

For the following define CV findings and Physical findings

  1. Filling pressure
  2. Peripheral vascular resistance
  3. Cardiac output
  4. Contractility
A
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11
Q

What are the causes of Hypovolemic Shock?

A

Intravasuclar volume depletion

  • loss of blood cell mass (trauma)

**- Loss of plasma volume, 3rd spacing **

  • burn injury

Essential derangement = decreased preload

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12
Q

Hypovolemic Shock

For the following define CV findings and Physical findings

  1. Filling pressure
  2. Peripheral vascular resistance
  3. Cardiac output
  4. Contractility
A
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13
Q

Causes of Obstructive Shock?

A

Impaired venous return

  • Pericardial Tamponade
  • Tension pneumothorax

Essential derangement = decreased preload

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14
Q

Beck’s Triad and what does it signify?

A
  1. Hypotension
  2. Muffled Heart Sound
  3. Jugular Venous Distension

* Clinical features of pericardial tamponade

  • also include: Tachycardia and pulsus paradoxus
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15
Q

What is Pulsus paradoxus?

A

Abnormally large declinde ( > 10mmHg) in systemic arterial pressure that occurs with inspiration

Inspiration you decrease thoracic pressure– normal heart you would increase venous return.

With accute pericadial tampanode, there is higher pressure on the heart so when right ventricle fills, the septum buldges into LV

= decrease in Stroke volume due to a decrease in LV volume

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16
Q

Obstructive Shock– Pericardial Tamponade

For the following define CV findings and Physical findings

  1. Filling pressure
  2. Peripheral vascular resistance
  3. Cardiac output
  4. Contractility
A
17
Q

Clinical features of Tension pneumothorax?

A
  • absent breath sounds
  • Jugular venous distension
  • tracheal ( and mediastinum) deviation
    - shift of heart to one side = pressure on veins adn they can’t fill = increase in backflow
18
Q

Septic Shock

For the following define CV findings and Physical findings

  1. Filling pressure
  2. Peripheral vascular resistance
  3. Cardiac output
  4. Contractility
A
19
Q

What is septic shock characteristic – terms of why it happens? What is the clinical presentation?

What initiates sepsis?

A

Decrease in peripheral vascular resistance despite increased vasopressors ( vasoconstriction)

Clinical picture:

  • CO is increased; peripheral blood flow in increased, impaired peripheral oxygen utilization; deminished response to catecholamines
  • Fever, tachycardia, GI dysfunction, Disorientation, confusion, elevated blood lactate or glucse

Initated by “danger singlans”

  • Pathogen associated molecular patterns ( PAMPs) – LPS, Flagellin, Fimbria, DNA
  • toll receptor family; Nod receptor family
20
Q

Differentiate between Cardiogenic shock, Hypovolemic Shock, Obstructive Shock, and Septic Shock based on:

  1. BP
  2. HR
  3. SKIN
  4. LUNGS
  5. Heart
  6. JVD
A