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Shock Notes

covers shock stages, cardiogenic, hypovolemic, neurogenic, septic, ana...
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Nursing Care- Complex Health Problems II (11-63-375)

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SHOCK

A condition that results from decreased tissue perfusion ⇢ further resulting in CELL HYPOXIA ⇢ further resulting in Multi Organ Dysfunction Syndrome (MODS)

The CAUSE of SHOCK depends on the TYPE of SHOCK presenting!

Types of SHOCK

Septic shock: occurs due to a severe infection (gram +/- bacteria) Hypovolemic shock: occurs due to severe fluid volume loss Neurogenic shock: occurs due to severe damage to the neuro system e. Spinal Cord Injury Cardiogenic Shock: occurs due to a weak heart Anaphylactic shock: occurs due to an allergic reaction

Distributive Shock:

I. Anaphylactic shock II. Neurogenic shock III. Septic shock

Stages of Shock

1. Initial Stage
2. Compensatory Stage
3. Progressive Stage
4. Refractory Stage

INITIAL STAGE:

LOW CO = LOW amount of blood the Heart Pumps/min  cannot maintain tissue perfusion & O 2 demands of tissues/orrgans  The current tissue perfusion is inadequate & unable to support the tissues O 2 demands of the tissue/organ cells

BIG Takeaway: CELLS switch from AEROBIC METABOLISM  Anaerobic Metabolism

Anaerobic Metabolism produces waste products (LACTIC ACID) ⇢ Normally, the Liver is responsible in taking care of Lactic Acid.... ⇢ BUT, the Liver cells = poorly oxygenated

Lactic Acid accumulates in the blood  pH levels decrease  LACTIC ACIDOSIS

Normal Serum Lactate  <1 mmol/L Abnormal indicating Lactic Acidosis  >4 mmol/L

S&S are very subtle/minimal*

COMPENSATORY STAGE: still reversible  only if the cause
of shock is corrected!

Body’s attempt to fight against the results of Anaerobic Metabolism by:  Increasing CO & BP via  simulation of the SNS & Renin-Angiotensin System (RAS)

 Resulting in  INCREASED TISSUE PERFUSION (but with time limits)

How does the body try to compensate?
Body senses the DROP in BP & CO

Baroreceptors in the CAROTID SINUS & AORTIC ARCH  stimulate SNS SNS releases Catecholamines (e. Epinephrine & Norepinephrine)  VASOCONSTRICTION OCCURS  increases the BP & HR  increased tissue perfusion to VITAL ORGANS & Less tissue perfusion to non-vital organs!

Note:

Decreased BP & CO = Decreased CVP/RAP/Preload = Decreased Capillary Hydrostatic Pressure

This will signal the body to INCREASE VENOUS BLOOD RETURN by: SHIFTING FLUID from Interstitial Spaces  Intravascular Space (aka....... A natural fluid IV bolus)

Body is attempting to increase CO & BP = To increase in tissue perfusion!

d/t decreased tissue perfusion  impaired gas exchange  V/Q Mismatch  O 2 in blood is TOO LOW  Hyperventilation; Increased RR to raise O 2 levels

PROGRESSIVE STAGE of SHOCK

####### BIG TAKE AWAY:

Compensation failed = Drop in CO = Decreased tissue perfusion = Hypoxic Injury = Increased Capillary Permeability ⇢ flood gates are opened; ⇢ FLUID leaves Intravascular  Interstitial Space

Decreased CO:

Decreased Tissue Perfusion  Hypoxic Injury to Cells

 Cell begins to SWELL d/t INCREASED CAPILLARY PERMEABILITY  FLUID + PROTEIN SHIFT from INTRAVASCULAR  INTERSTITIAL SPACE RESULTING in MASSIVE EDEMA

Fluid Volume Depletion in the Intravascular Space = MASSIVE EDEMA throughout

Overall... there is Fluid Volume Depletion = Decreased CO & Decreased Tissue Perfusion!

NEURO: Cells of the brain are not being perfused MAP < 60 mmHg; poor perfusion Decreased CPP ; poor perfusion to Cerebral Cells marks the changes in Mental Status slow speech, restless, anxious, agitated & may not respond to stimuli

####### LUNGS:

ARDS will develop d/t increased capillary permeability in the ALVEOLI SACS = collapse d/t fluid surrounding them Lungs loose elasticity Fluid in lungs (e. Crackles, Tachypnea, Low O 2 & Res Failure Intubation & Mechanical Ventilation may be required

####### CARDIO:

Decreased O 2 to Myocardial Cells = Muscle begins to die = Pump Failure Cardiac Dysrhythmias occur AMI/HF

KIDNEYS: Nephrons stop working  ACUTE TUBULAR NECROSIS (ATN)  RENAL FAILURE Renal failure Decreased UOP Increased BUN Increased Creatinine Metabolic Acidosis GI: Decreased O 2 to Mucosal cells that protect the lining of the stomach from acid  increases in acid  loses protective chemicals ⇢ ULCERS, Hemorrhage .. bad because clotting ability is compromised too because of Liver cell death

LIVER: Decreased O 2 to Liver Cells  Waste and Drug filtering is impaired! = BUILD UP of TOXIC WASTE (e. bilirubin, ammonia)

 Disseminated Intravascular Coagulation (DIC): Small clots will form in the vessels  further compromising blood flow to Organs)  Depletes the body’s platelets & clotting stores LEADS TO  Massive, Uncontrollable Bleeding

REFRACTORY STAGE : unmanageable & irreversible

All organs begin to fail and shut down permanently, everything that happened in previous stage is getting WORSE!

⇢ Decreased CPP ⇢ Increased WASTE ⇢ Decreased RR ⇢ Decreased Renal Function ⇢ DIC ⇢ Decreased CO

Pathophysiology of Hypovolemic Shock
What is happening in Hypovolemic Shock?

Major Depletion of Volume in the Intravascular System

⇢ relative or absolute cause

 this DECREASES the Amount of Venous Return to the heart

⇢ this is the amount of blood draining back to the heart

 this DECREASES Preload

⇢ the amount the ventricles stretch once their filled with blood).. won’t be stretching very much because there isn’t much fluid to fill them

 this DECREASES Stroke Volume

⇢ the amount of blood pumped by the left ventricle with each beat

 this DECREASES CARDIAC OUTPUT

⇢ this is the amount of blood the heart pumps per minute ⇢ 4 - 8 Liters/Minute.. = HR x SV) ⇢ If CO falls too low, the amount of blood that should be going to the organs/tissues cells per minute will drastically fall.

Remember the numbers: 15, 15-30, 30-40, 40%

What is happening to the blood pressure, heart rate, urinary output, mental status, and the skin?

STAGES of FLUID LOSS

Class I :
<15% of volume loss... to 750 mL in an adult

body can maintain STILL MAINTAIN the CO with this volume loss.

mainly Asymptomatic with this class.

⇢ HR normal ⇢ BP normal

⇢ RR normal ⇢ Skin pink, warm

⇢ Capillary refill normal (<2 seconds) ⇢ U/O/P normal (greater than 30 mL/hr)

Mental status: normal.. be a little anxious

Class II:

15-30% of volume loss...-1500 mL in an adult

CO  starting to FALL d/t volume loss

COMPENSATION via the SNS, Renin-Angiotensin System, and the Shunting of blood to vital organs & away from non-vital organs

⇢ HR will increase... (greater than 100 bpm)... to the effects of the SNS ⇢ BP Decreases but within normal limits (for now d/t vasoconstriction) ⇢ RR mildly increases (d/t low oxygen level in the body)

Class IV:

>40% of volume loss..... than 2,000 mL in an adult

Death is very near... very dynamic treatment!

The body is shutting down = fluid loss is SEVERE!

 Significant tachycardia (>140 bpm),

 increase respiratory (respiratory failure)  severe hypotension*

 anuria (no urine production)

Mental status: lifeless, coma

Signs and Symptoms of Hypovolemic Shock

Remember it depends on the % of volume loss, but in a nutshell:

Tachycardia Hypotension Cool/clammy skin Weak peripheral pulses Anxiety Decreased urinary output CVP: low PAWP/PCWP: low

Nursing Interventions for Hypovolemic Shock

Treatment goals:

 fluid resuscitation  correct underlying cause that is leading to the fluid loss e. Hemorrhaging  get the patient ready for surgery

Nursing Interventions  Monitor oxygenation & perfusion status of patient:  place on O 2

 may need intubation and mechanical ventilation,

Hemodynamic Status

 BP  HR  Rhythm

Tissue Perfusion to organs:

 Mental status  Urinary output ⇢ will need Catheter insertion monitor urinary output closely... ⇢ UOP needs to be greater than 30 mL/hr

If bleeding, hold firm, direct pressure.

If showing Signs and Symptoms of Hypovolemic
Shock

place in Modified Trendelenburg position  HOB flat & feet elevated @ 45’ increases venous return to heart and CO

Obtain IV access

 at least 2 IV sites that are large bore  needed for rapid fluid delivery and other medications....  many patients with Severe Hypovolemic Shock (especially ones who are not responding to fluid treatment) will have a central line and hemodynamic monitoring to monitor CO and fluid replacement

Collect labs:  hgb, hct (blood level),  lactate level (status of cell’s metabolism),  blood gases (acidosis?),  electrolytes,  bun, and creatinine

Severe Hypovolemic Shock Lab Values:

 Central Venous Pressure (low)  PAWP/PCWP (low)

⇢ risk of Anaphylactic RXN ⇢ monitor for fluid overload

***If giving large amount of fluids, need to WARM them.

WHY? If not warmed, it can lead to Hypothermia, and this will alter clotting enzymes. Keep the patient warm, but not to the point of sweating.

Blood and Blood Products:
Packed Red Blood Cells (PRBC)
Platelets or Fresh Frozen Plasma (FFP):
PRBCS: helps replace fluid and provides the patient with hemoglobin,

which will carry oxygen to deprived cells

(Crystalloids and Colloids can’t do this)....

May be used when the patient is:

⇢ not responding to Crystalloid Fluid Challenge ⇢ experiencing Severe Bleeding/Severe Hypovolemic shock

Platelets: for uncontrolled bleeding to help with Thrombocytopenia
Fresh Frozen Plasma: for when the patient needs clotting factors

monitor for transfusion reaction with these products

Cardiogenic Shock

What is Cardiogenic Shock? the heart CANNOT pump enough blood to meet the perfusion needs of the body.

Therefore, the heart does not pump enough blood throughout the body, which will: ⇢ Decrease CO and this leads  Decrease in tissue perfusion and oxygen supply to the organs/tissue’s cells.

NOTE: this is NOT an issue with a loss of blood volume like in some of the other types of shock.

Blood volume is Normal! However, because the heart has experienced a decrease in its ability to function properly, that blood volume starts to back up and leads to congestion in the LUNGS & Right side of the body (keep this in mind for when we review the signs and symptoms).

Signs and Symptoms of Cardiogenic Shock

by body systems:

Heart:

⇢ Is weak + not pumping blood forward or filling efficiently.... LEADS to:

Back flow of blood from the left side of heart  lungs  Pulmonary Congestion

⇢ Crackles ⇢ Dyspnea ⇢ Increased RR ⇢ Low Oxygen ⇢ Increased HR

....... it progresses, blood will back flow from the lungs  Right side of the heart

⇢ Neck Veins Distention d/t an increase in Venous Pressure ⇢ High CVP ⇢ Chest Pain  ⇢ Decrease perfusion to heart muscle via the Coronary arteries ⇢ Hypotension: Systolic blood pressure less than 90 mmHg or 40 mmHg from baseline for at least 30 minutes ⇢ Weak Peripheral Pulses

If on hemodynamic monitoring may have:

o Decreased C I < 2 L/min/m o Increased (PCWP) > 18 mmHg

o Increased CVP

 most meds are titrated and the patient is on hemodynamic monitoring to assess certain pressures in the heart)

⇢ decrease fluid overload

 via diuretics

⇢ maintain oxygen status d/t pulmonary edema

 will need mechanical ventilation

Nurse’s Role:

⇢ Hemodynamic monitoring ⇢ Maintain mechanical ventilation (will need to help with respiratory failure) ⇢ Central line placement for medication ⇢ Monitoring, assessing for signs of adequate tissue perfusion:  mental status, blood pressure, heart rate, rhythm, urine output, skin color and capillary refill, lung sounds etc.

⇢ Monitoring of labs:

⇢ high cardiac markers  ex: elevated troponin (this substance is released if there is injury to heart cells), ⇢ increased BNP  this substance is released by the cells that make up the ventricles when they stretch due to high blood volume) ⇢ Pulmonary Edema on CXR (white blobs) ⇢ Echocardiogram  Will show a low ejection fraction ⇢ Lactate > 4 mmol/L o cells will switch from aerobic to anaerobic metabolism which will produce lactic acid o Metabolic acidosis ⇢ drop in blood ph < 7.

Hemodynamic Monitoring:
Pulmonary Artery Wedge Pressure/Pulmonary Capillary
Wedge Pressure (PAWP/PCWP)

⇢ INCREASED in Cardiogenic Shock ⇢ >18 mmHg  blood is backing up in the heart and lungs; hence not being pumped out and creating a high pressure in the L

a pulmonary artery catheter (Swan-Ganz catheter) is inserted through the right side of the heart via a vessel and the catheter is wedged in the Pulmonary Arterial Branch and a balloon is temporarily inflated to

measure Left Atrial Filling Pressure.
Central Venous Pressure (CVP): used to measure the pressure in

the R. Atrium and Superior Vena Cava via Catheter

⇢ INCREASED in Cardiogenic Shock ⇢ Normal CVP is 2 - 6 mmHg or 8 -12 mmHg depending on source

WHY? The back flow of blood to the right side of the heart (right atrium into venous circulation) leads to Venous Congestion, which increases the CVP

Medications: a combination of medications can be given and

medications vary depending on the cause of the Cardiogenic Shock and the patient’s response.

Diuretics: Cardiogenic shock is one of the 2 types of shock that DOES

NOT have a decrease in Blood Volume (the other is NEUROGENIC SHOCK

 Patients with Cardiogenic Shock = a backup of fluid in the lungs from an injured heart that is failing to pump blood forward.

Diuretics will help remove extra fluid volume via the kidneys decrease the PRELOAD (amount ventricles stretch at the end of diastole) = DECREASE in WORK of CONTRACTION

⇢ watch the fluid status of the patient, ⇢ renal function ⇢ worsening hypotension

e. with Furosemide... K level “hypokalemia“....

⇢ increases Stroke Volume because it decreases the Afterload, so it’s easier for the heart to pump blood forward so CO increases!

by dilating the coronary arteries = cardiac workload
decreases

⇢ CAUSES HYPOTENSION and may not be used if the patient is Severely Hypotensive (monitor blood pressure very closely).

E. Nitroglycerin or Sodium Nitroprusside

IV Fluids:

Normal Saline (if even used) is used with extreme caution due to Pulmonary Edema that may be present.

A fluid challenge is majorly used for the other types of shock when blood volume is the issue.. in Cardiogenic Shock blood volume is not the issue.

Intra-Aortic Balloon Pump

⇢ device placed to help improve coronary artery blood flow and increase cardiac output.

How?

A catheter is inserted through a vessel (ex: femoral artery) up through a section of the aorta.

A balloon attached to the catheter will inflate and deflate during systole (contraction) and diastole (relaxation).

When the balloon deflates during systole. it creates a suction-like pressure that will draw blood out of the weak heart and into the coronary arteries and systemic circulation (hence increasing cardiac output and blood supply to the heart muscle).

When the balloon inflates during diastole. it will create pressure that will push blood into the coronary arteries (hence further increasing blood supply to the heart muscle).

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Shock Notes

Course: Nursing Care- Complex Health Problems II (11-63-375)

23 Documents
Students shared 23 documents in this course

University: University of Windsor

Was this document helpful?
SHOCK
A condition that results from decreased tissue perfusion
⇢ further resulting in CELL HYPOXIA
⇢ further resulting in Multi Organ Dysfunction Syndrome (MODS)
The CAUSE of SHOCK depends on the TYPE of SHOCK presenting!
Types of SHOCK
Septic shock: occurs due to a severe infection (gram +/- bacteria)
Hypovolemic shock: occurs due to severe fluid volume loss
Neurogenic shock: occurs due to severe damage to the neuro system
e.g. Spinal Cord Injury
Cardiogenic Shock: occurs due to a weak heart
Anaphylactic shock: occurs due to an allergic reaction
Distributive Shock:
I. Anaphylactic shock
II. Neurogenic shock
III. Septic shock
Stages of Shock
1. Initial Stage
2. Compensatory Stage
3. Progressive Stage
4. Refractory Stage
INITIAL STAGE:
LOW CO = LOW amount of blood the Heart Pumps/min
cannot maintain tissue perfusion & O2 demands of tissues/orrgans
The current tissue perfusion is inadequate & unable to support the
tissues O2 demands of the tissue/organ cells
BIG Takeaway: CELLS switch from AEROBIC METABOLISM
Anaerobic Metabolism
Anaerobic Metabolism produces waste products (LACTIC ACID)
⇢ Normally, the Liver is responsible in taking care of Lactic Acid….
⇢ BUT, the Liver cells = poorly oxygenated
Lactic Acid accumulates in the blood pH levels decrease LACTIC
ACIDOSIS

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