NRSG 327 Week 4

What is shock

A syndrome characterized by decreased tissue perfusion and impaired cellular metabolism

Results in an imbalance between supply and demand of oxygen and nutrients for the cells

Syndrome

Cluster of different symptoms

A group of symptoms that occur together

Patients at risk to develop shock

Trauma patients

Immunocompromised patients

Children

Elderly

Patients with lots of comorbidities

CO = ?

HR x SV

Stroke volume

Amount of blood ejected from heart with each beat

3 components of stroke volume

Preload, afterload and contractility

Normal CO

5000 mL/min (avg)

Preload

Volume of blood in the ventricles by the end of diastole

Ability of ventricles to stretch, relax and fill

Determined by venous return

Diseases that affect preload

Cardiac inflammation (peri, myo or endo- carditis), hypovolemia, anemia

Contractility

Ability of heart myofibrils to change their strength of contraction

What is contractility determined by?

Preload (starling's law)

Stimulatory affect of SNS

External factors that impact amount of Ca in myocardial cell

Starling's law

The force or tension in a myofibril (contractility) depends on how much that myofibril is stretched (preload)

As you increase the volume infused into a heart, the CO increases. It reaches a point where further volume decreases CO.

What diseases affect contractility

MI, HF, atherosclerosis, electrolyte imbalances, cardiomyopathy

Afterload

Force or strength/resistance against which the ventricles have to pump to eject the blood

3 Vs of afterload

Vessel tone, valves, viscosity

What diseases affect afterload

Sepsis, anaphylaxis, neurogenic trauma

MAP = ?

(SBP + 2(DBP))/3

Classifications of shock

Hypovolemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic)

Hypovolemic shock

Loss of volume from intravascular fluid as well as blood loss

Cardiogenic and obstructive shock

Shocks due to the pump

Due to ineffective pumping of the heart and insufficient perfusion and deliver of oxygen to cells

Distributive shock

Shocks due to the pipes

Due to ineffective distribution of blood volume in the vessels

cause by vessel dilation and inadequate delivery of oxygen

Stages of shock

Initial, compensatory, progressive, refractory

Initial stage of shock

Little to no s/s

Lactic acid build-up due to switching of metabolism from aerobic to anaerobic

Compensatory stage of shock

Body starts to try to compensate and is successful for a little while

Hypotension is a classic late sign

Nursing interventions usually start here

Progressive stage of shock

AKA uncompensated

Signs and symptoms become obvious, heading towards MODS

We must act right. away

Refractory stage of shock

AKA irreversible

Patient will experience MODS and die

3 main compensatory stage mechanisms

Neural, bio-chemical and hormonal

Neural mechanism

SNS activation

Increase HR, BP and RR

Flushing, sweating, muscle tightening/tense up, pupil dilation

Bio-chemical mechanism

Activated by H+, O2 and CO2 concentrations

Work to balance CO2 and H+ out

Hormonal mechanism

RAAS activation

ADH is producted

Decreased UOP

What happens in the neural response

Body senses that there is decreased pressure through baroreceptors

Releases epinephrine and norepinephrine to cause vasodilation

What happens in the biochemical response

Chemoreceptors sense that there is a drop in pH and O2 and an increase in CO2

Increase hydrogen and oxygen and decrease CO2

RAAS system

Activated by decreased kidney perfusion

Renin -> angiotensinogen -> angiotensin 1 -> angiotensin 2

Stimulates ADH and aldosterone

Early signs of compensated shock

Pale, cool skin

Increase RR with normal WOB and SpO2

Thirst

Slight restlessness, mild confusion, decreased concentration, increased glucose

Mild tachycardia, weak peripheral pulses, normal to slightly low BP

Decreased UOP

Labs to take during progressive shock

Lytes, ABG, lactate, liver enzymes, renal panel, cardiac panel, coags

MODS Neuro symptoms

Decreased LOC, confusion, hallucinations, "off" behaviour, word salad, fluctuating between tiredness and coming-to

MODS resp symptoms

Irregular RR, decreased RR, varying paces of breathing (rapid/shalow), O2 sats dropping, decreased air entry to bases, crackles

MODS cardiac symptoms

Pale, delayed cap refill, HR may still be high but can begin to see it drop, dysrhythmias, BP drops, cool, clammy, grey/ashen look

MODS GI symptoms

Hypoactive, can see ileus

MODS Liver symptoms

Increased enzymes

MODS GU symptoms

UO decreased and is much more concentrated

A client who was in an automobile collision is now in hypovolemic shock. Why is it important for the nurse to take the client's vital signs frequently during the compensatory stage of shock?

Arteriolar constriction occurs

Hypovolemia is a preload problem, so the body will try to constrict everything

During the progressive stage of shock, anaerobic metabolism occurs. The nurse expects that initially anaerobic metabolism causes?

Metabolic acidosis

Due to increased lactic acid from anaerobic metabolism

Difference between cardiogenic and obstructive shock

Cardiogenic = systolic dysfunction, inability to pump blood forwards

Obstructive = diastolic dysfunction, affects ability of LV or RV to relax and fill

Risk factors for cardiogenic shock due to an MI

Age, hypertension, DM, multivessel coronary artery disease, prior MI or angina, prior dx of HF, left bundle-brach block

What drug class should be avoided in cardiogenic shock?

Vasopressors

Why are inotropes good in cardiac shock + examples of drugs

Target myocardium more than other drugs do

Dobutamine, milrinone, levophed

DX for

pH = 7.47

PaCO2 = 30

HCO3 = 22

pH = basic

PaCO2 = basic

HCO3 = normal

Respiratory alkalosis, uncompensated

DX for

pH = 7.25

PaCO2 = 30

HCO3 = 17

pH = acidic

PaCO2 = basic

HCO3 = acidic

Metabolic acidosis, partially compensated

DX for

pH = 7.05

PaCO2 = 56

HCO3 = 14

pH = acidic

PaCO2 = acidic

HCO3 = acidic

Mixed acidosis

Principles of treating shock

Treat underlying cause

Increase supply (O2, CO and Hgb)

Decrease demand (normothermia, activity, sedation/analgesia)

CVS Symptoms of cardiogenic shock

Decreased cap refill, ?chest pain, increased MVO2, increased cardiac markers, hypoperfusion, palpitations, syncope, hypotension, tachycardia, raised JVP, peripheral edema, quiet or adventitious heart sounds

GI symptoms of cardiogenic shock

Decreased bowel sounds, NV, increased BG

Neuro symptoms of cardiogenic shock

Decreased CVP, anxiety, confusion, agitation, disorientation

Pulmonary symptoms of cardiogenic shock

Crackles, cyanosis, tachypnea, wheezes, dyspnea

Renal system symptoms of cardiogenic shock

Increased sodium and water retention, decreased renal blood flow and UOP, increased BUN

Skin symptoms of cardiogenic shock

Cool, clammy, pallor