Shock ppt (+obstructive)

Question 1

PAWP is high is Cardiogenic shock as the increased pressure in left ventricle due to backing up of blood.

Systemic Vascular Resitance is high in Cardiogenic Shock and Hypovolemic shock

Distributive = NAS (Neurogenic Shock, Anaphylactic, Septic Shock) = decreased systemic vascular resitance. Septic shock = normovolemic, sepsis, edema in tissue, vasodilation of the blood vessels - because of edema, oxygen is not reaching the tissue.

Answer 1

Obstructive shock = Pulmonary edema/ embolism/ tension penumothorax whic is putting pressure on the heart. So, there is no blood in the heart + its imability to contract => decrease in PAWP

Question 2

Shock Patho

Note*
Neurogenic = s/s Bradycardia, give Atropine
With other types : increased HR

Answer 2

*Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism

*Imbalance in supply/demand for O2 and nutrients

Question 3

Classification of shock
-Cardiogenic - heart
-Hypovolemic - systemic
-Distributive – neuro, anaphylactic, sepsis
-Obstructive – PE (Embolism)

Question 4

Low Blood FlowCardiogenic Shock

Answer 4

Definition
Systolic (pumping/ compress) or diastolic (pulmonary problem) dysfunction. E.g.: cardiomyopathy

Compromised cardiac output (CO)
↓ CO = not enough blood for circulation
(mortality rate = 60%)

Give fluids 1st before squeeze drugs – Digoxin, Dopamine (2.5 mg/kg)

Inotropic drugs like Digoxin to increase the contractility of the heart. IV fluids, Dopamine (inotropic drug)

Question 5

Low Blood FlowCardiogenic Shock

Answer 5

Precipitating causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems

Question 6

Cardiogenic shock

Early manifestations

Answer 6

Early manifestations
Tachycardia
Hypotension (BP ↓)
Narrowed pulse pressure -
Venous insufficiency – no perfusion to lower extremities.
↑ Myocardial O2 consumption

Question 7

Notes for cardiogenic shock

Answer 7

Physical assessment
Tachypnea, pulmonary congestion (right ventricle affected = filling insuffient, left side has more pressure – cor pulmonae)
*NCLEXPallor and cool, clammy skin #Exam#
Decreased capillary refill time (takes more than 3 – 5 secs to perfuse)
Anxiety, confusion (no prefusion with brain), agitation , restless
↑ Pulmonary artery wedge pressure = heart problem
Decreased renal perfusion and urinary output

Nursing Care# for cardiogenic shock???

Question 8

2. Hypovolemic Shock

Question 9

Hypovolemic Patho

Answer 9

Absolute hypovolemia: loss of intravascular fluid volume
Hemorrhage
GI loss (e.g., vomiting, diarrhea)
Fistula drainage
Diabetes insipidus
BURN
Hyperglycemia – 3 Ps (Polydipsia, Polyphagia, Polyuria)
Diuresis

Example no oxygen transportation to brain, and vital organs as no circulatory blood.

Question 10

Interventions hypovolemia

Answer 10

Relative hypovolemia
Results when fluid volume moves out of the vascular space into extravascular space (e.g., intracavitary space)
Termed third spacing

Nursing Interventions: - Lower HOB for perfusion

Question 11

Hypovolemic shock
Clinical Manifestations:

Answer 11

Clinical manifestations
Anxiety
Tachypnea
Tachycardia (HR ↑)
Hyperventilating
Increase in CO, heart rate
Decrease in stroke volume, PAWP, urinary output
If loss is >30%, ### blood volume should be replaced
##1 to know## 0.9% NS bolus
# Exam# Qn. How to do you know pt. is getting is better?
↑ u/o hourly = more fluid to be given as required
CBC to check for anemia H&H, lactic acid, ABG to check CO2 WNL

Question 12

3.Distributive ShockNeurogenic Shock| Septic| Anaphylactic

Question 13

Neurogenic Shock

Answer 13

Hemodynamic phenomenon
Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above
Can last up to 6 weeks
Heart Rate is low PNS !=SNS

Why Bradycardia with Neuro shock??
#Exam# Dominant is PNS with neurogenic => leads to Bradycardia

Question 14

Neurogenic shock patho

Answer 14

Can occur in response to spinal cord injury or spinal anesthesia
Results in massive vasodilation, leading to pooling of blood in vessels, tissue hypoperfusion, ultimately impaired cellular metabolism

Question 15

Neurogenic shock clinical manifestations

Answer 15

Clinical manifestations
Hypotension and bradycardia
Dry skin
Poikilothermia- taking on temperature of environment - Inability to regulate body temperature (resulting in heat loss) # Venous pooling. Blood not going back to heart

HALLMARK = Poikilothermia.
Give 0.9% NS to expand – able to distribute to body.

Question 16

3.2 Anaphylactic shock

Answer 16

Acute, life-threatening hypersensitivity (allergic) reaction to drug, chemicals, food, bee sting, snake venom.
*Massive vasodilation
*BP ↓ Circulatory failure from massive dilation.

Release of vasoactive mediators
↑ Capillary permeability
*Laryngeal spasm, Bronchospasm with release of cytokines
*#1st med: Epinephrine <inject at 90 degree and stay for 10 secs injected.
*Repeat epipen repeat every 15 mins until your pt. becomes better.
*Injected on outer later aspect of thigh.
*After epi give corticosteroids.

Question 17

Anaphylactic shock - clinical manifestations

Answer 17

Clinical manifestations
Anxiety, confusion, dizziness
Sense of impending doom
Chest pain
Incontinence

Question 18

Anaphylactic shock clinical mani

Answer 18

Clinical manifestations
Swelling of lips and tongue, angioedema
Wheezing, stridor due to laryngeal edema
Flushing, pruritus, urticaria
**Respiratory distress (#1: ABG) and circulatory failure

Question 19

3.3 Sepsis
SIRS #1 cause of shock*

s/s: ↑ HR, ↓BP, ↑RR, #1.Still give fluids then give #2.NorEpi (Levophed) === increase in fluid, the BP does not go up. High metabolic acidosis, we have to keep giving fluids. Fight the metabolic acidosis, give G tube or NG tube feeding.

Answer 19

Sepsis: systemic inflammatory response to documented or suspected infection
Severe sepsis: sepsis complicated by organ dysfunction
MOD diseases
RF: Aspiration Pneumonia, gum infection, UTI, Burns
Cytokines + Vasodilation with increased permeability => leak infectious matter from capillaries.

Question 20

Septic shock

Answer 20

Septic shock
Presence of sepsis with hypotension despite fluid resuscitation
Presence of inadequate tissue perfusion resulting in hypoxia

Question 21

Septic Shock clinical manifestations

Answer 21

Clinical manifestations
↑ Coagulation and inflammation
↓ Fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Hyperdynamic state: increased CO and decreased SVR

Question 22

Septic shock notes

How do you know shock is resolved?
Answer: ↑BP, u/o > 30 mL/hr, Capillary refill < 3 secs

Clinical manifestations
Tachypnea/hyperventilation
Results in respiratory alkalosis
Respiratory failure develops in 85% of patients
↓ Urine output
Altered neurologic status
GI dysfunction, GI bleeding, paralytic ileus

Answer 22

Three major pathophysiologic effects
Vasodilation massive => cold clammy skin
Maldistribution of blood flow
Myocardial dysfunction
Decreased ejection fraction
Ventricular dilation

Tissue Hypoperfusion and GI affected, so give PPI (protonix)
As a nurse you should > Assess the abdomen, eye, brain, urinary

Question 23

4. Distributive Shock

PE (Embolism), Abd. Compartment Syndrome*

Answer 23

Develops when physical obstruction to blood flow occurs with decreased CO
Caused by restricted diastolic filling of right ventricle from compression
Abdominal compartment syndrome- abdominal pressure compresses inferior vena cava

Question 24

Obstructive Shock - s/s

Answer 24

Patient will experience:

Decreased CO
Increased afterload
Variable left ventricular filling pressure
**Pulses Paradoxes
**JVD distention
Rapid assessment and immediate treatment are important

Question 25

Stages of Shock in short

Question 26

Diagnostics of shock

Answer 26

Thorough history and physical examination
No single study to determine shock (~swimming~)
Blood studies
Elevation of lactate
Base deficit
12-lead ECG, continuous ECG monitoring
Chest x-ray (cardiomyopathy)
Hemodynamic monitoring (H&H ↓)

Question 27

Successful management

Interventions to control or eliminate cause of decreased perfusion
Protection of target and distal organs from dysfunction
Provision of multisystem supportive care

Answer 27

Address the cause, Fluids, Norepi (Levophed), Oxygen, Mechanical Ventilation (ET), Patent airway (especially)with analyphylatic shock with laryngeal edema,
Identification of patients at risk for developing shock
Integration of patient’s history, physical examination, and clinical findings to establish a diagnosis

Question 28

Interprof. Care - Oxygenation

Answer 28

Oxygen and ventilation
Increase supply
Optimize CO with fluid replacement or drugs
Increase hemoglobin by transfusion
Increase arterial oxygen with supplemental oxygen and mechanical ventilation
Abx, Dopamine, Digoxin
#Exam# Bradycardia give atropine

Question 29

Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = volume expansion

Answer 29

Exam### Two large-bore IV catheters , intraosseous access device, or central venous catheter

Isotonic crystalloids (e.g., normal saline, lactated Ringers can increase Lactic acid) and colloids (e.g., albumin)

Infiltrated = Cold skin, Pale as well.
Stop IV, and new IV site.

Question 30

Volume expansion - shown by

Answer 30

Fluid responsiveness is determined by clinical assessment
Vital signs = BP high. MAP > 65 mmHg
Cerebral and abdominal pressures
Capillary refill < 3 secs
Skin temperature
Urine output > = 30 mL/hr

NCLEX NG : What are the abnormal VS you should follow-up????

Question 31

Complications of large volume infusion

Answer 31

Two major complications of large volumes
Hypothermia
Coagulopathy - too much volume (fluids) , warm up the patients
Persistent hypotension after adequate fluids
Fluids first, Vasopressor may be added

Question 32

Fluid resuscitation

Answer 32

Warm crystalloid and colloid solutions
Replace clotting factors

Question 33

Drug therapy

Primary goal of drug therapy = correction of decreased tissue perfusion
Vasodilator therapy (e.g., For MI = chest pain = cardiogenic shock = vasodilate your blood vessel which are blocked = nitroglycerin, nitroprusside)
Decrease afterload
Achieve/maintain MAP >65 mm Hg

Answer 33

Primary goal of drug therapy = correction of decreased tissue perfusion
Vasopressor drugs (e.g., norepinephrine)
Achieve/maintain MAP >60 to 65 mm Hg
Reserved for patients unresponsive to fluid resuscitation
Continuously monitor end-organ perfusion

Question 34

GI function

Nutrition is vital to decreasing morbidity from shock
Start enteral nutrition within first 24 hours
Parenteral nutrition used only if enteral feedings contraindicated

Start trophic feeding- slow drip of small amounts of enteral nutrition
Weigh patient daily
Monitor serum protein, total albumin, prealbumin, BUN, glucose, electrolytes

Answer 34

Give Food immediately, tackled metabolic acidosis, functioning of GI – stimulate motility of stomach.

Enteral nutrition preferred than TPN due to infection, and making GI function.

Question 35

II. Interprofessional CareCardiogenic Shock

Hemodynamic monitoring
Drug therapy
Nitrates to dilate coronary arteries
Diuretics to reduce preload)
Vasodilators to reduce afterload
β-adrenergic blockers to reduce HR
Circulatory assist devices
Circulatory assist devices
Decrease SVR and left ventricular workload
Intraaortic balloon pump
Ventricular assist device (VAD)
Heart transplantation

Answer 35

Overall goal: restore blood flow to myocardium by restoring balance between O2 supply and demand
Cardiac Cath = Angioplasty with stenting
Until the cath is performed…..monitor CO = SV * HR
Emergency revascularization
Valve replacement

Question 36

III. Interprofessional CareHypovolemic Shock

Answer 36

Management focuses on stopping loss of fluid and restoring the circulating volume
Fluid resuscitation is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss)

Question 37

IV. Interprofessional CareSeptic Shock Management =

Antibiotics should be started within first hour
After cultures are obtained (e.g., blood, wound exudate, urine, stool, sputum)
Broad-spectrum antibiotics are given first
More specific antibiotics may be ordered once the organism identified

Answer 37

Septic Shock Management:

Fluid replacement to restore perfusion
Hemodynamic monitoring
Vasopressor drug therapy
Exogenous vasopressin for patients refractory to vasopressor therapy

#1. Fluids, Vasopressor
# Culture and ABX within 1 hour of septic shock
Corticosteroids - antiinflammatory
Kidney Function monitor: make sure Cr not high, check u/o

Question 38

Septic Shock - Drugs

**Insulin rejection from body
Gluconeogensis, give insulin subq =

**Malox - mild
H2 Receptor blockers
Aggressive PPIs (Protonix)
***DVT Prophylaxis, SCD, Heparin

Answer 38

Glucose levels <180 mg/dL
Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole [Protonix])
Deep vein thrombosis prophylaxis (e.g., heparin, enoxaparin [Lovenox])

Question 39

IV. Interprofessional CareNeurogenic Shock

In spinal cord injury: spinal stability
Treatment of hypotension and bradycardia with vasopressors and atropine
Fluids infused cautiously as hypotension generally is not related to fluid loss
Monitor for hypothermia

Answer 39

Chest pain with Vasopressor
Make sure you are not killing the pt.
#So call HCP, and titrate vasopressor to low.

CI = Venous pooling = PNS =Bradycardia = Pt. Hyperthermia= Put pulse ox forehead and ears.

Question 40

III. Interprofessional CareAnaphylactic Shock Mgmt

Minimum intervention:
Stabilize Neck, ensure patent airway w/o intervention like ET

Aggressive fluid replacement
Usually crystalloids
IV corticosteroids if significant hypotension persists after 1–2 hours of aggressive therapy
**Hypotension = fluid leak to intervascular space = vasodilation
**BS monitor:
With corticosteroid administration , check for BS (blood sugar)

Answer 40

Epinephrine, diphenhydramine, ranitidine (Zantac)
**Give epi every 15 mins till the shock resolves or BP comes up.

Maintain a patent airway
Nebulized bronchodilators
Aerosolized epinephrine
Endotracheal intubation or cricothyroidotomy may be necessary

Question 41

IV. Interprofessional CareObstructive Shock

ABCs
Airway
Breathing
Circulation

Focused assessment of tissue perfusion
Vital signs
Peripheral pulses
Level of consciousness
Capillary refill
Skin (e.g., temperature, color, moisture)
Urine output

Brief history
Events leading to shock
Onset and duration of symptoms
Health history
Medications
Allergies
Vaccinations, recent travel

Answer 41

Primary strategy is early recognition and treatment to relieve obstruction
Mechanical decompression to release compartment syndrome
Thrombolytic therapy, know where clot is?
Thrombolytic therapy
Radiation, debulking to remove tumor, or removal of mass
Decompressive laparotomy – passively

Question 42

Nursing Management

Question 43

Nursing Dx

Goals
Evidence of adequate tissue perfusion
Restoration of normal or baseline BP
Recovery of organ function
Avoidance of complications from prolonged states of hypoperfusion

Answer 43

Ineffective peripheral tissue perfusion and risk for decreased cardiac tissue perfusion, ineffective cerebral tissue perfusion, ineffective renal perfusion, impaired liver function, and ineffective GI perfusion
Anxiety

Question 44

When assessing a patient in shock, the nurse recognizes that the hemodynamics of shock include
a.normal cardiac output in cardiogenic shock.
b.increase in central venous pressure in hypovolemic shock.
c.increase in systemic vascular resistance in all types of shock.
d.variations in cardiac output and decreased systemic vascular resistance in septic shock.

Answer 44

Answer: D
Rationale: Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. Patients may be normovolemic, but because of acute vasodilation, relative hypovolemia and hypotension may occur. The ejection fraction is decreased for the first few days after the initial insult. Because of a decreased ejection fraction, the ventricles will dilate to maintain stroke volume. The ejection fraction typically improves and ventricular dilation resolves over 7 to 10 days. Persistence of a high CO and a low SVR beyond 24 hours is an ominous finding and is often associated with increased development of hypotension and MODS. Systemic vascular resistance (SVR) increases in cardiogenic and hypovolemic shock; SVR decreases in neurogenic, anaphylactic, and septic shock. Cardiac output decreases in cardiogenic shock. Central venous pressure decreases in hypovolemic shock.

Question 45

The nurse is caring for a critically ill patient. The nurse suspects that the patient has progressed beyond the compensatory stage of shock if what occurs?
a.Increased blood glucose levels
b.Increased serum sodium levels
c.Increased serum calcium levels
d.Increased serum potassium levels

Answer 45

Answer: D
Rationale: Hyperkalemia occurs in the progressive phase of shock when cellular death liberates intracellular potassium. Hyperkalemia will also occur in acute kidney injury and in the presence of acidosis.

Question 46

The nurse is caring for a patient in septic shock. Which hemodynamic change would the nurse expect?
a.Increased ejection fraction.
b.Increased mean arterial pressure.
c.Decreased central venous pressure.
d.Decreased systemic vascular resistance.

Answer 46

Answer: D
Rationale: Patients in septic shock will have a decreased systemic vascular resistance, decreased ejection fraction, and decreased mean arterial pressure. Decreased central venous pressure (preload) is expected in hypovolemic or obstructive shock.