20 cardiac failure & shock

8/13/2019 20 Cardiac Failure & Shock

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CHAPTER 20

HEART FAILURE AND

CIRCULATORY SHOCK

Essentials of Pathophysiology


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PRE LECTURE QUIZ

True/False Decreased cardiac output will lead to an increase inrenal blood flow and glomerular filtration rate.

The endothelins are potent vasodilators that arereleased from the endothelial cells throughout the

circulation. Myocardial hypertrophy is a long-term mechanism by

which the heart compensates for increased workload.

Afterload represents the force that the contractingheart must generate to eject blood from the filledheart.

Five major complications of severe shock are acuterespiratory distress syndrome, acute renal failure,gastrointestinal ulceration, disseminated intravascularcoagulation, and multiple organ dysfunctionsyndrome.

F

F

T

T

T


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PRE LECTURE QUIZ In __________ heart failure, blood backs up in

the systemic circulation, causing peripheraledema and congestion of the abdominalorgans.

The most common cause of ____________shock is myocardial infarction.

Examples of conditions that cause __________shock include loss of whole blood (e.g.,hemorrhage), plasma loss (e.g., severe burns),or extracellular fluid (e.g., gastrointestinal fluidslost in vomiting or diarrhea).

An increase in __________ rate is an early signof shock.

A life-threatening condition, acute __________edema is the most dramatic symptom of left heart

failure and is characterized by capillary fluidmoving into the alveoli.

cardiogenic

heart

hypovolemic

pulmonary

right


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STANDARD ECG WAVEFORM

Atrial Contraction

initiated

Ventricular

Contraction initiated VentricularRelaxation

Papillary Muscle

Relaxation

ST segment can indicate

ischemia or infarction


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ST SEGMENT ELEVATION

ST Depression

With a 12 lead ECG certain leads can be connected to each other

to reverse the R wave and accentuate the ST Elevation


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CORORNARY OCCLUSION

total occlusion of theproximal segment of left

anterior descending

artery, and

severe disease involvingthe proximal segment of

the obtuse marginal

branch

Angiogram
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TYPES OF HEART FAILURE

High-output versus low-output failure Is cardiac output high or low?

Systolic or diastolic failure

Is the heart failing to pump out enough blood,

or failing to accept enough blood from the

body and lungs?

Right-sided or left-sided failure Is the right or left side of the heart failing?


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MANIFESTATIONS OF HEART FAILURE

Effects of impaired pumping

Effects of decreased renal blood flow

RAA pathway

Effects of the sympathetic nervous

system

Angioplasty CABG
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MANIFESTATIONS OF HEART FAILURE

Orthopnea: StraightBreathing, ie. Must be

straight upright, or

difficult breathing occurs


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CONTROL OF HEART FUNCTION


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LEFT-SIDED HEART FAILURE

Systolic: LV doesnot pump enoughblood to body

Diastolic: LV doesnot accept enoughblood from lungs

Body lacks blood

Lungs fill with fluid

right

heart

lungs

left

heart

body

Blood Flow


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RIGHT-SIDED HEART FAILURE

Systolic: RV doesnot pump enoughblood to lungs

Diastolic: RV doesnot accept enoughblood from body

Body fills with blood

Lungs do not

oxygenate enough blood

right

heart

lungs

left

heart

body

Blood Flow


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QUESTION

Tell whether the following statement is true or

false:

The characteristic pink sputum produced is

pulmonary edema is tinged with blood.


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ANSWER

True

In pulmonary edema, the alveolar capillary

membrane is damaged, and blood from the

capillaries moves into the alveoli. The blood

from the capillaries causes the sputum

(produced from the lower respiratory tract) toappear pink or light red.


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TYPES OF SHOCK

Cardiogenic

Hypovolemi

c

Obstructive

Distributive

Septic


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BLOOD PRESSURE

BP = CO x PR

Which of the following affect CO, and which affect PR?Why?

Blood volume Heart rate

Vasoconstriction

Angiotensin II

Aldosterone

Epinephrine

Histamine


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SCENARIO:

Mr. M was injured in a motorcycle accident. On his arrival at the hospital he presented

with bleeding from the right leg,restlessness, pallor, sweating, elevated heartrate, weak pulse, rapid breathing, and lack ofbowel sounds; his blood pressure wasslightly elevated

Question:

What has happened to this patients:

Stroke volumeCardiac output

Sympathetic nervous system


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SCENARIO (CONT.)

Although he was given 6 units of blood,Mr. M got worse

He became lethargic and his bloodpressure began to fall; he still had no

bowel sounds or urine productionQuestion:

The intern ordered epinephrine, and Mr.Ms blood pressure increased. Why?

Later, you overhear the resident tellingthe intern that was not the besttreatment. Why not, if it raised Mr. Msblood pressure?


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SCENARIO (CONT.)

Mr. Ms blood pressure went up a bit

He has been moved out of the ICU

Question:

His chart says you should do a 24-hour

urine collection. Why?


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SCENARIO (CONT.)

Mr. M appears to be improving

He sleeps quite a lot, but his blood pressure hasremained stable; he had a little urine production; and hedid not eat his supper

Checking on him in the evening, you notice that he isslightly flushed, his respiration rate is a little high, andhis temperature is elevated

Question:

What is happening to his peripheral resistance?

What do you expect his heart rateto be like? Why?


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DISTRIBUTIVE OR VASODILATORY SHOCK

Blood vessels dilate

There is not enough blood to fill the circulatory

system

Blood flow decreases

Less blood is returned to the heart

Less blood is circulated to the body


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QUESTION

Which type of shock is caused by low bloodvolume?

a. Cardiogenic

b. Hypovolemic

c. Distributive

d. Septic


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ANSWER

b. Hypovolemic

Hypo(low) volemia(blood volume) occurs

when a patient has lost blood due to trauma,surgery, or third space fluid loss.


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CAUSES OF DISTRIBUTIVE SHOCK

Decreased sympathetic activity: neurogenicBrain or spine injury; anesthetics; insulin

shock; emotion

Vasodilator substances in blood

Type I hypersensitivity (anaphylactic shock)

Inflammatory response to infection (sepsis)

Vessel damage from severe hypovolemia


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MECHANISM OF

TYPE I

HYPERSENSITIVITY

Mast cell

Mast cell

degranulates

IgE attachesto mast cell

Allergen

attaches

to IgE

Allergen

Granules released:Histamine,

acetylcholine, kinins,

leukotrienes, and

prostaglandins allcause vasodilation


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ANAPHYLAXIS

Systemic response to the inflammatorymediators released in type I

hypersensitivity

Histamine, acetylcholine, kinins, leukotrienes,

and prostaglandins all cause vasodilation

What will happen when arterioles vasodilate

throughout the body?

Acetylcholine, kinins, leukotrienes, and

prostaglandins all can cause

bronchoconstriction

SEPSIS OR SYSTEMIC INFLAMMATORY


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RESPONSE SYNDROME (SIRS)

Inflammatory mediators released into thecirculation

Tumor necrosis factor

InterleukinsProstaglandins

Cause systemic signs of inflammation

Fever and increased respiration, respiratoryalkalosis, vasodilation, warm flushed skin

Activate inflammatory pathways

Coagulation, complement



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RESPONSE SYNDROME (SIRS) (CONT.)

Discussion:

Why is septic shock called distributive?

In the later phases of septic shock, bloodvolume decreases. What part of the

inflammatory process explains this?


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TYPES OF SHOCK


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GUT BARRIER FAILUREdecreased

perfusion

of the gut

bacteria and

toxins escape

inflammatoryresponse

bacterial

endotoxins

in blood

and lymph

inflammatory

mediators in blood

and lymph

vasodilation


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SEPTIC SHOCK

vasodilation

decreased

peripheralresistance

decreased

blood pressure

SEPTIC SHOCK40% mortality


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SEPTIC SHOCK

Also called systemic

inflammatory response

syndrome(SIRS)

Inflammatory mediators also

increase the metabolic rate

of tissues, so they needmore oxygen

The role of the endothelium insevere sepsis and multiple organ

dysfunction syndrome


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(Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organdysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from

http://www.blood journal.org/cgi/content/full/101/10/3765.0)

inflammatorymediators

vascular endothelial cells

respond and:

promoteclot

formation

createadhesivemolecules

more WBCs move out into

the tissues and release moreinflammatory mediators

produce more

vasodilation

substances (NO)

more

vasodilation

The role of the endothelium in severe sepsis andmultiple organ dysfunction syndrome


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SEPTIC SHOCK (CONT.)

Despitethe prompt implementation of

appropriate antibiotic therapy, sepsis

mortality remains high, in the range of

28% to 50%.

(Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organdysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, fromhttp://www.blood journal.org/cgi/content/full/101/10/3765.0)

Second, patients with culture-positive and

culture-negative sepsis or septic shock have

comparable mortality rates.


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SEPTIC SHOCK (CONT.)

Third, administrationof anti-endotoxin

antibodies in large, clinical trials did not

improve survival.

(Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organdysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, fromhttp://www.blood journal.org/cgi/content/full/101/10/3765.0)


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QUESTION

Which type of shock is the result of a severeallergic reaction?

a. Cardiogenic

b. Obstructive

c. Anaphylactic

d. Septic


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ANSWER

c. Anaphylactic

Anaphylactic shock is caused when

inflammatory mediators are released (type Ihypersensitivity reaction). The mediators

include histamine, acetylcholine, kinins,

leukotrienes, and prostaglandins, all of which

cause vasodilation.

The main function of protein C is its


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ACTIVATED PROTEIN C

Drotrecogin alpha - a recombinant form of humanactivated protein C that has anti-thrombotic, anti-inflammatory, and profibrinolytic properties - a

treatment for severe sepsis

Blocks clotting

Blocks inflammation

Increases survival of the most seriously ill

sepsis patients

May cause bleeding!

The main function of protein C is its

anticoagulant property as an inhibitor

of coagulation factors V and VIII


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COMPLICATIONS OF SHOCK

Scenario:A doctor has been called in to treat Mr. M and

has started him on fluid and antibiotics

You are warned to watch him carefully for any

signs of respiratory distress

Question:

Why would blood pressure imbalances

cause respiratory distress?


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COMPLICATIONS OF SHOCK (CONT.)

Acute respiratory distress syndrome

Acute renal failure

Gastrointestinal complications

Disseminated intravascular

coagulation

Multiple organ dysfunction syndrome


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ACUTE RESPIRATORY DISTRESS SYNDROME

(ARDS)

Exudate enters alveoliBlocks gas exchange

Makes inhaling more difficult

Neutrophils enter alveoliRelease inflammatory mediators

Release proteolytic enzymes


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ACUTE RENAL FAILURE (ARF)

Renal vasoconstriction cuts off urineproduction

Acute renal failure

Continued vasoconstriction cuts off renal

oxygen supply

Renal tubular cells die

Acute tubular necrosis


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DISSEMINATED INTRAVASCULAR COAGULATION

(DIC)

coagulationpathways

activated

clots inmany

small

blood

vessels

microinfarcts,

ischemia

plateletsand

clotting

proteins

used up

bleeding

problems

MULTIPLE ORGAN DYSFUNCTION SYNDROME


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MULTIPLE ORGAN DYSFUNCTION SYNDROME

(MODS)

The most frequent cause of death in thenoncoronary intensive care unit

Mortality rates vary from 30% to 100%

Mechanism not known


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QUESTION

Tell whether the following statement is true orfalse:

Treatment for ARDS often includes breathing

assistance using mechanical ventilation.


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ANSWER

TrueBecause alveoli are filled with exudate and

blood that has leaked from the capillary, the

surface area available for gas exchange isgreatly reduced. Most patients will require

ventilatory support until the process

reverses. ARDS has a high mortality rate

because it is difficult to ventilate these

patients.

20 cardiac failure & shock

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