Shock

-Stages of Hemorrhagic Shock

Initial stage
Nonprogressive stage
Progressive stage
Refractory stage
Lactic Acidosis: Lactate acid is produced due to anaerobic respiration
- Lactate accumulates faster than it is reduced
- This happens when the demand for O2 is higher than what is available

Compensatory stage
750 to 1500 ccs 15% to 30% total blood volume loss
Restless and anxious
MAP decreases by 10 to 15 mm Hg
Kidney and hormonal adaptive mechanisms are activated
- Increased in HR and BP
- Not enough to maintain adequate perfusion to the viral organs
Tissue hypoxia in nonvital organs
Acidosis

Sustained decrease in MAP of more than 20 mm Hg from baseline
1500 to 2000 ccs or 30% to 40% total blood volume loss
HR of at least 120
- The heart is not able to fill all the way → less blood present during contraction → less O2 and less perfusion to other tissues and organs
Tachypnea
- 30 to 40 breaths per minute
- Hyperventilating
Lower pulse pressure → decreased perfusion
Vital organs develop hypoxia
- Kindyes
  - RAAS activation
- Brain
  - Agitated, confused
Life-threatening emergency
Immediate interventions are needed
Conditions causing shock need to be corrected within 1 hour of the onset of the progressive stage

More than 2 L of blood or greater than 40% of total blood
Severe hypotension
Severe tachycardia
- Over 140
Severe tachypnea
Prolonged Cap refill
Lethargy that can lead to unconsciousness
Skin is cool to touch
Too much cell death and tissue damage result from too little oxygen reaching the tissues
- Irreversible
The body can no longer respond effectively to interventions, and shock continues
There is irreversible cell and tissue death

Metabolites are released from dead cells
Microthrombi form in various locations throughout the body, depending on the specific circumstances of the infection and the individual's health status
MODS occurs first in the liver, heart, brain, and kidney

Caused by a decrease in Intravascular Volume
Decreased MAP stimulates baroreceptors
Stimulation of SNS → tachycardia, increased contractility
- Sympathetic Nervous System
Increased cardiac output temporarily
Coronary arteries dilate → lower BP
Decreased tissue perfusion

Control the source of the blood loss
Replace the volume loss
Colloids: Increase serum osmotic pressure and pull fluid from the interstitial space back into the vascular system
- Ex: Albumin, Dextran, Hetastarch
Crystalloids: Isotonic solutions that increase BP
- Ex: Normal Saline, Lactated Ringers
Blood Products: Replace the blood loss
- Never mix with glucose or hypotonic solutions bc→ clots
- Ex: Packed RBCs, Whole Blood

Beta-adrenergic agonists (positive Inotropic)
- A. Norepinephrine
  - Stimulates SNS
- B. Dobutamine
  - Stimulates beta 1 receptors
  - Also increases cardiac output
- C. Dopamine
  - Different effects depending on dosage
    - 2 mcg/kg/min (Low dosages)- dilates real and mesenteric arteries and ↑ renal perfusion
      - Also increases urinary output
    - 5mcg/kg/min (Moderate dosages)- ↑ HR, contractility and cardiac output
    - 10mcg/kg/min (High dosages)- ↑ vasoconstriction
Vasodilators- Decreases the workload of the heart, ↓ preload, and ↓ afterload
- Afterload: Force the heart has to pump against to eject blood = SVR (systemic vascular resistance)
- Preload: The amount of blood in the heart's ventricles before contraction. Preload is also known as the end-diastolic volume (EDV)
- A. Nitroprusside
- B. Nitroglycerin

The Intra-aortic balloon pump (IABP)
- Increases blood flow to the heart
- Decreases O2 requirements of the heart
- Increases afterload
- Increases cardiac output
Mobility restricted
Pedal pulses
- May not be able to palpate, but can auscultate with a Doppler
- Pulse MUST be present
  - If not it means IABP has migrated

Caused by problems that impair the ability of the normal heart muscle to pump effectively
- Heart muscle is healthy but there is a mechanical obstruction
- Mimic S/Sx of Cardiogenic Shock
Causes
- a. Pulmonary embolism
- b. Cardiac tamponade: Accumulation of fluid of pericardium
  - BP and cardiac output drop
  - Normal pressure on the L side of the heart: 6-12
  - Normal pressure on R of the heart: 2-5
    - Both will be high and the same with cardiac tamponade
      - Ex: 20
  - Can occlude pulmonary arteries and cause sudden death

Pulmonary Embolism
- Heparin
Fibrinolytic Therapy
- Streptokinase
- Alteplase
- tPA
Cardiac Tamponade
- Pericardiocentesis
- Pericardial window
  - Diverts fluid into another compartment of the body like the abd
- Drain

Abnormally expanded vascular space
- Blood volume has not been lost. It has been distributed to interstitial spaces
- Fluid leaks out of compartments
Septic, anaphylactic, and neurogenic shock are examples of distributive shock
- All 3 = vasodialation

Relative hypovolemia: Increased volume in the compartments. Volume has not changed but the vascular compartment expanded and needs more volume to be filled

Capillary leaking → increased cardiac output
Little to no cyanosis, warm extremities
All tissues have some degree of hypoxia
Microthrombi formation is extensive
Amplified systemic inflammatory response
- Neutrophils are the first cells that arrive at the site of infection
Anaerobic metabolism continues
WBC drops to 3000
- Normal is 5-10 K
- Indication of being in normal sepsis for too long
- Bone marrow cannot produce more WBCs