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Shelley Hart Alverno College- MSN 621 [email protected]

Shelley Hart Alverno College- MSN 621 [email protected]

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Shelley HartAlverno College- MSN 621

[email protected]

Click on any underlined words for an in depth explanation Use the arrows at the bottom of the page to move around

the tutorial Use this arrow to move forward:

Use this arrow to move backward:

Use this button to return to the beginning of the show:

Understand the pathophysiology of cardiogenic shock

Explain the compensatory mechanism for low oxygenation to the tissues

Identify the what you see as signs and symptoms of cardiogenic shock

Identify the nursing interventions for the assessment and management of cardiogenic shock

Would you like to learn more about the physiology of the heart?

Click here for a heart link :

Usually there is a myocardial injury and a loss of contractility of the heart

Then the heart is unable to provide enough oxygen to the body resulting in poor tissue perfusion to the major organs

http://www.getbodysmart.com/ap/circulatorysystem/heart/menu/menu.html

Sheffield, 2008

Why?◦ Impaired blood flow to the coronary arteries

How does this look?◦ Blood flow is blocked either by a clot or plaque in

various degrees, so part of the artery is blocked or most of it is blocked

◦ ECG will show changes T wave inversion, ST segment elevation or abnormal Q wave

When can you diagnose this problem ?◦ Timing of serum cardiac marker elevation

Porth,2005,p.539

ST wave elevation-First changes seen-Abrupt onset and chest pain-Signal that heart muscle is damaged

Abnormal Q wave-No depolarizing-necrotic /damaged heart tissue-change in conduction

ST

Normal ECG waveform

Q wave

1 mm

T wave

T –wave inversion-disruption in repolarization-may be earliest sign of Myocardial injury

Adapted from: ER Club of NYU School of Medicine,2007.

Enzymes within the markers located in the heart muscle breakdown and are released during heart damage

They are seen in blood within certain times frames of a heart attack or also called MI:◦ Myoglobin- within 1 hour ◦ Creatine-kinase MB ( CK-MB)- within 4-8 Hours◦ Troponin I- within 3 hours◦ Troponin T- within 3 hours

If a patient enters with chest pain and ECG changes that show a ST elevation. You may need to review lab results called…

A) coag panel B) serum cardiac ma

rkers C) UA and culture D) CBC with diff

The earliest blood test that may show cardiac damage would be

A) troponin I B) troponin T C) myoglobin D) CK- MB

Let’s move on to compensation

Microsoftclipart,2008

Move on to Compensation

Chest pain indicates a cardiac problem rather than a clotting problem. A coag panel determines a clotting time

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This test takes a long time to peak in the blood, a cardiac problem is urgent ,need information in minutes

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Compensatory Mechanisms

OK we know the cause of the problem now to the next part of the problem..

In the beginning of shock, the tissues are not receiving enough oxygen because there is less blood flow to the organs

How does the body try to restore blood flow to the major organs?

Kidney

The kidney plays a big role in the function of the blood pressure

Special enzymes are secreted to help the blood pressure from going too high or too low. This is important in cardiogenic shock.

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Blood Pressure

Remember the heart is not pumping normally, so the blood vessels are not working properly and the blood pressure decreases .

An enzyme called Renin is secreted from the kidney

Renin secretion sets a pathway into motion

Vasoconstriction is a result of this pathway

And Vasoconstriction causes a slight rise in the blood pressure

Renin

BP

First the blood pressure falls

Second, Renin is released from the kidneys

Renin reacts with the protein, Angiotensinogen

Angiotensin I is formed

Angiotensin Converting Enzyme (ACE) from the lungs converts…

Angiotensin II is a product of the conversion and causes…

Vasoconstriction, Move on to see how aldosterone impacts this picture

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Aldosterone flips on the switch for the sodium and potassium pump.

Then what happens?

Alpha and beta adrenergic receptors Body

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Where are the alpha and beta receptors that cause vasoconstriction and cause excitation?

Click on alpha or beta to match the affected organ

alpha alpha

beta beta

eyes

Blood vessel

heart lungs

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What organ is involved with renin secretion?

A. heart B. lungs C. kidney D. brain

The body compensates for decreased tissue perfusion by :

A. Decreasing the heart rate

B. Vasoconstriction C. Vasodilation D. Decreasing the

blood pressureMove on to inflammation

Move on to inflammation

The lungs do host the angiotensin converting enzyme but does not secrete renin

The brain is not involved directly with renin secretion

The heart does not secrete renin

Leukocytes are alerted !! Cytokines are released!!

Living cells in the tissue are injured without oxygen

This cardiac event is preventing oxygen from getting to the tissues

Cytokines are released

Alert Injury !!

Sheffield,2008

Cytokine

A cytokine is an inflammatory mediator that communicates with other cells important to the inflammatory response

Some bind to the cell surface receptors and trigger release of more cytokines and nitric oxide (NO)

Nitric oxide is a strong vasodilator

Attention all neutrophils,I need assistance at this

point of injury !

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TNFGenetic connection in survival

Tumor Necrosis Factor ( TNF) is an inflammatory mediator and one of the cytokines in the inflammatory process

People that have a genetic TNF-2 allele, may survive cardiogenic shock at a better rate than patients without the allele or people with TNF 1 allele

Interestingly enough the opposite has been observed in patients with septic shock

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Leukocytes Action Endothelium Action

Leukocytes make integrins

Integrins help leukocytes bind to the endothelium

Just as leukocytes are making integrins

The endothelium is making integrin receptors and selectins

The cytokines will activate the integrins to attach to the receptors

What is happening?Picture the cytokine action and leukocyte effect

The endothelium has the leukocytes sticking to it

Cytokines are releasing nitric oxide causing vasodilation

Sticky endothelium and pooling of blood products

Pooling of blood and slowing of blood flow through the capillaries

Increased permeability and leaking of fluid into interstitial space

Platelets and leukocytes stick and clog up the endothelial wall

Leukocytes Platelets

Interstitial leakage

The end result of the inflammatory response in cardiogenic shock is:

A) leaky vessels B) decreased oxygen

to the major organs C) Cytokine

secretion D) Endothelium

Changes www.getbodysmart.com,2008

Your answer is part of the inflammatory response but it’s earlier in the events of the total result to the body

Move on to patient care

May develop hours after the initial MI is detected

Who is at risk for cardiogenic shock?

Patient 65 years or older

High blood pressure Diabetes Obesity Those who smoke Hyperdyslipidemia

Frequency◦ 8.6% of patients with a

ST elevation MI

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What will you see, hear and feel from the patient?

Chest Pain

Suggests a myocardial infarct

Defining symptoms Assessment

Minimally you will see:◦Cool extremities◦Decreased urine

output ◦And most

importantly a low blood pressure with systolic <90 mmHg

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Signs and symptoms

Produce these signs and symptoms:

◦ Rapid pulse◦ Narrow pulse pressure◦ Distended neck veins

Right ventricular failure◦ Arrhythmias◦ Decreased mentation◦ Dyspnea◦ Elevated respiratory rate◦ Inspiratory crackles,

wheezing Left ventricular failure

◦ Absent bowel soundsMicrosoftclipart,2008

Mr. CP is a 55 year old man that enters the emergency room complaining of cramping abdominal pain and chest pressure as well as nausea. He is cool and clammy to the touch. He states he cannot remember his phone number and he feels scared about this feeling of pain in chest.

The main defining symptoms of a cardiac injury and possibly cardiogenic shock would include:

A) chest pain B) chest pain, cool

and clammy skin C) confusion D) chest pain and

confusion

Move on to lab values

Move on to lab values

These are signs and symptoms but there are two issues that this patient complains of pinpoint cardiac problems

Chest pain is the main cardinal sign of a cardiac problem and this patient also exhibited something else

Lab Values Assessment

Elevated myocardial tissue markers◦ Elevated myocardial

bands of creatinine phophokinase( MK-CPK)

◦ Elevated Troponin I◦ Elevated BNP-Brain

Natriuretic Peptide Arterial Blood Gases

◦ Decreased PaO2

C Reactive Protein Hemodynamic values Microsoftclipart,2008

What will the physician order?

Narcotics IV fluids Arterial Line Central Line Electrolyte replacement

◦ K+, Calcium, Mg+ ECG, Cardiac monitor

◦ Cardioversion◦ Pacing

Possible Diuretics Antidysrhythmic drugs Vasodilators Narcotics Procedures

Microsoftclipart,2008

Immediate revascularization is necessary to restore oxygen to the heart muscle and then support oxygen delivery to the rest of the body

Intra-Aortic Balloon Pump (IABP) used as a bridge until revascular efforts are completed

Coronary Artery Bypass Graft (CABG) Percutaneous Coronary Intervention (PCI)

Mr. CP is a 55 year old man that enters the emergency room complaining of cramping abdominal pain and chest pressure as well as nausea. He is cool and clammy to the touch. He states he cannot remember his phone number and he feels scared about this feeling of pain in chest.

You take his vital signs and determine that his blood pressure is 80/50 and his heart rate is 96. While you call the physician and other staff to assist you with this patient…

What will you expect the physician to order immediately:

A) Blood cultures

B) ECG, IV fluids, Oxygen support

C ) Antihistamine

D) Abdominal x- rays

Go to next case study

The suspected shock is cardiogenic with the hallmark sign of chest pain, life saving measures need to start after the initial assessment

Go to next case study

Remember that chest pain and symptoms of decreased cardiac output would need interventions that would increase vasodilation and increase oxygen

Let’s rethink that response

Let’s try to see the whole picture using the nursing process…

Problem What you know so far…

Chester Pain is your patient returning from the cardiac cath lab until the cardiac surgical team arrives. The cardiologist noticed several blockages but he was unable to advance the guide wire.

The cardiothoracic team is coming in to perform an emergency bypass surgery. In the meantime..

You will need to monitor and intervene on the cardiac unit until the surgical team arrives…

Chester’s B/P is 80/50, pulse is 115. He is also diaphoretic, weak pulses, low urine output, mild confusion and some agitation

Medical Procedures for Monitoring Purposes

The cardiologist placed an Intra arterial balloon pump for increased myocardial perfusion.

He also placed pulmonary arterial catheter and arterial line.

Chester has a foley catheter in place

Microsoft clipart,2008

Monitoring Equipment

Monitor for changes in ◦ Level of consciousness◦ Heart rate◦ Blood pressure◦ ( Low B/P can lead to

further organ damage)◦ SpO2◦ Breath sounds◦ Urine output◦ Pain and anxiety

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Assessment Intervention and Evaluation Critical Thinking

Administer medications◦ Adjust per lab and monitor

interpretation• Diuretics• Vasopressors ( lo B/P)

Dobutamine, S>80 Dopamine , S<80 Norepinephrine• Vasodilators

Nitroglycerin

Oxygenation◦ Possible monitor of mechanical

ventilation

Is there fluid overload ?

Should I adjust the IV fluids?

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Assess fluid overload by labs and these signs and symptoms:◦ Frothy secretions◦ Decreased oxygen

saturation◦ Crackles

Values that are important:◦ Decreased B/P◦ Narrow pulse pressure◦ Cardiac index < 2.1

l/min/m2◦ Pulmonary artery wedge

pressure > 20mmHG( normal is 8-12 mmHg)◦ Central venous pressure( normal is 2-6 mm Hg.)

ASSESS Interpret and Intervene

He is somewhat short of breath, mild chest pain and anxious about surgery.

His lung sounds reveal slight crackles in the bases

His wedge pressure is 22, CVP is 12 and his urine output is still low

You reassure the patient that his family is aware of the situation . The cardiac team is here and he is going in for surgery in 15 min.

You start a dobutamine drip at 5 mcg/min/kg IV and dopamine 5 mcg/min/kg IV. Plus he still on a heparin drip.

You give him 1 mg morphine IV for pain and anxiety.

Evaluation Further treatment

The cardiac team arrives You give report that

Chester is less anxious,pain free at this time

He still has increased urine output but it is still low. You have not increased his amount of fluid per hour.

He still has crackles in his lungs

Further labs are drawn and the cardiac enzymes are still elevated, the BUN and creat are elevated

You send Chester off to the operating room where he has a successful by pass of 4 arteries.

You later learn that he went home 5 days later.

Monitoring and correcting low blood pressure with vasopressors is important to :

A) prevent organ damage

B) Keep patients comfortable

C) correct breathing problems

D) increase the oxygenation

Fluid overload may be characterized by:

A) pain B) decreased blood

pressure, low urine output

C) Lung assessment that includes crackles, low B/P ,low urine output

D) hypertension with wide pulse pressure

Last slide

This is a good answer. All of the organs have to function for the best patient outcome.

Breathing will not improve from vasopressors. The action of the medication will increase the blood pressure and return oxygen perfusion to the tissues

Oxygenation may improve from better tissue perfusion to the organs so this isn’t the total outcome

Pain is not affected by vasopressors or increasing the blood pressure

You need assessment skills plus the medical information to intervene properly

Last slide

The blood pressure and urine output may be a problem of a result of organ damage or increased heart damage

Sorry Not the answer

Pain is indicative of an advancing cardiac event

Sorry Not the answer

Hypertension and wide pulse pressure is the opposite of what the body would do during fluid overload in this case

Sorry Not the answer

You are finished!!

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Appolini, O., Dupont, E., Vandercruys, M., Andrien, M., Duchateau, J., & Vincent, J. (2004). Association between the TNF-2 Allele and a Better Survival in Cardiogenic shock . Chest, 125(6),

2232-2237. Brandler, E., & Sinert, R. (2008, Apr. 2). eMedicine - Shock,

Cardiogenic : Article by Ethan S Brandler. Retrieved Apr. 14, 2008, from http://www.emedicine.com/emerg

Feldman, H., & Rey, M. (n.d.). Learning EKG interpretation. Retrieved Apr. 11, 2008, from students.med.nyu.edu/erclub/ekghome.html.

Morton, P., Fontaine, D., Hudak, C., & Gallo, B. (2005). Critical Care Nursing : A holistic approach, 8th edition. Philadelphia, PA: Lippincott,Williams & Wilkins.

Mower -Wade, D., Bartley, M., & Chiari-Allwein, J. (2000). Shock Do you know how to respond?. Nursing 2000, 30(10), 34-39.

Sheffield, S. (2008, Apr. 14). GetBodySmart: Interactive Tutorials and Quizzes On Human Anatomy and Physiology. Retrieved Apr.

14, 2008, from http://www.getbodysmart.com. Weil, M. (n.d.). Shock: Shock and fluid resuscitation: Merck Manual

Professional . Retrieved Apr. 14, 2008, from http://www.merck.com/mmpe/print/sec06/ch067/ch067b.html.