Heart failure

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 Heart Failure

Heart failure (HF) is the inability of the heart to pump

sufficient blood to meet the needs of the tissues for
oxygen and nutrients.

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 Global burden of heart Failure (HF)

• At 40 years of age, the

lifetime risk of developing
HF
• For both men and women is
1 in 5

• HF incidence approaches
10 per 1000 population
after 65 years of age
 Definition

“Heart failure (HF) is a syndrome

caused by cardiac dysfunction,
generally resulting from myocardial
muscle dysfunction or loss and
characterized by either left or right
ventricular dilation or hypertrophy
or both.”
 Forms of heart failure
Systolic

Diastolic
Low-Output Low output occurs secondary to IHD, hypertension, dilated cardiomyopathy, and valvular
and pericardial disease.
High Output High output occurs in patients with reduced systemic vascular resistance
Acute Acute HF is a sudden reduction in cardiac output

Chronic Chronic HF is observed in patients with dilated cardiomyopathy or multi-valvular heart

disease
Right sided Right sided –Underlying abnormality affects right ventricle
Left Sided Left sided- Underlying abnormality affects left ventricle
 NYHA functional classification
Severity based on symptoms and physical activity
Class I No limitation of physical activity. Ordinary physical activity does not cause
undue fatigue, palpitation, or dyspnoea

Class II Slight limitation of physical activity. Comfortable at rest, but ordinary

physical activity results in fatigue, palpitation, or dyspnoea

Class III Marked limitation of physical activity. Comfortable at rest, but less than
ordinary activity results in fatigue, palpitation, or dyspnoea

Class IV Unable to carry on any physical activity without discomfort.

Symptoms at rest. If any physical activity is undertaken, discomfort is
increased
Stages of Heart Failure

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Evolution of Heart Failure

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 Etiology
• Myocardial dysfunction is most often caused by -
• Coronary Artery Disease (CAD) – 2/3 of patients with systolic dysfunction

• Aggravation of Hypertension - both systolic and diastolic dysfunctions

• Rheumatic, Viral and other forms of Myocarditis

• Valvular Heart Disease

• Infective Endocarditis

• Arrhythmias

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 Etiology
• Other precipitating factors include –
• Anaemia's,
• Systemic Infections,
• Pulmonary Embolism,
• Thyrotoxicosis and Pregnancy
• Physical, Dietary, Fluid, Environmental and Emotional Excesses
• Administration of Drugs - cardiac depressants drugs like corticosteroids, non-
dihydropyridine calcium-channel antagonists, and non steroidal anti-
inflammatory drugs (NSAIDs).
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 Left-sided heart failure
Left ventricle fails as effective pump

Left ventricle cannot eject blood delivered from right heart through pulmonary
circulation

Blood backs up into pulmonary circulation

Increase pressure in pulmonary capillaries forces blood serum out of capillaries into
interstitial spaces and alveoli

Increase respiratory work and decrease gas exchange occur

Left-sided heart failure

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 Left-sided heart failure
Left-sided heart failure

Decrease cardiac output

Tissue hypoxia

Decrease renal perfusion

Activation of Renin-angiotensin-aldosterone System

Increase Na and water retention

Pulmonary congestion and edema

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 Right-sided Heart Failure

Right ventricle fails as effective pump

Right ventricle cannot eject blood returning through vena cava

Blood backs up into systemic circulation

Right-sided Heart Failure

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 Common Clinical Manifestation
Dominant clinical feature Symptoms Signs
Peripheral oedema/ Breathlessness •Peripheral oedema
congestion Tiredness, fatigue •Raised jugular venous pressure
Anorexia •Pulmonary oedema
•Hepatomegaly, ascites
•Fluid overload (congestion)
•Cachexia

Pulmonary oedema Severe breathlessness •Crackles over lungs, effusion

at rest •Tachycardia, tachypnoea

Cardiogenic shock Confusion •Poor peripheral perfusion

(low output syndromes) Weakness •Anuria or oliguria
Cold periphery

High blood pressure Breathlessness •Usually raised BP, left ventricular hypertrophy
(hypertensive heart failure)

Right heart failure Breathlessness •Evidence of right ventricular dysfunction

Fatigue •Raised jugular venous pressure, peripheral oedema,
hepatomegaly
 Clinical Manifestation
Left Heart Failure
• Persistent cough • Dyspnea on exertion
• Pink, frothy sputum • Paroxysmal nocturnal dyspnea
• Adventitious breaths sounds- • Orthopnea
• crackles • Fatigue, generalized weakness
• Tachycardia • Oliguria
• Tachypnea • Altered digestion
• Noisy, labored breathing • Dizziness, lightheadedness, confusion,
• Dry cough restlessness, anxiety

• Cyanosis (late)
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 Clinical Manifestation
Right Heart Failure
• Tachycardia • Weight gain
• Jugular venous distension • Anasarca (generalized edema)
• Dependent edema (Pedal, sacral) • Fluid accumulation in body cavities
• Swelling of fingers and hands • Ascites
• Pleural effusion
• Hepatomegaly, tenderness in right
• Pericardial effusion
upper quadrant
• Increased abdominal girth
• Splenomegaly
• Anorexia, nausea
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 Diagnostic test
• The diagnosis of CHF rests primarily on presenting manifestations and pertinent
data from client’s health history. Diagnostic studies assist in determining
underlying cause and degree of heart failure. The various diagnostic tests are -
• Chest radiograph (CXR)
• Laboratory blood tests
• Electrocardiogram (ECG)
• Echocardiography (ECHO)
• Cardiac catheterization
• Others- such as serum electrolytes, blood urea nitrogen (BUN), complete blood count
(CBC) and routine urine analysis.

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 Diagnostic test
• Echocardiography-two-dimensional with Doppler flow studies—may show
ventricular hypertrophy, dilation of chambers, and abnormal wall motion. Makes
definitive diagnosis of type of heart failure (systolic or diastolic).
• ECG (resting and exercise)—may show ventricular hypertrophy and ischemia.
• Chest X-ray may show cardiomegaly, pleural effusion, and vascular congestion.
• Cardiac catheterization—to rule out CAD.
• Right-sided heart catheterization—to measure pulmonary pressure and left ventricular
function.

• ABG studies may show hypoxemia due to pulmonary vascular congestion.

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 Diagnostic test
• Human B-type natriuretic peptide (BNP, Nterminal prohormone brain
NP, or proBNP).
• As volume and pressure in the cardiac chambers rise, cardiac cells produce
and release more BNP. This test aids in the diagnosis of heart failure.

• A level greater than 100ng/mL is diagnostic for heart failure. In addition, the
higher the BNP, the more severe the heart failure.

• BNP is used in emergency departments to quickly diagnose and start

treatment.

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 Initial evaluation of patients with
Heart Failure

Initial Evaluation of Patients with a Diagnosis of HF

• Assess clinical severity of HF by history and physical examination
• Assess cardiac structure and function
• Determine the etiology of HF
• Evaluate for coronary disease and myocardial ischemia
• Evaluate the risk of life-threatening arrhythmia
• Identify any exacerbating factors for HF
• Identify barriers to adherence

Heart Failure Society of America. 2010 Comprehensive Heart Failure Practice Guidelines. Journal of Cardiac Failure.2010;16(6): e1-194.
 Initial evaluation of patients with
heart failure
• Require careful assessment for the presence of
symptoms of HF and, depending on their
Patients at Risk for HF underlying risk, may warrant noninvasive
evaluation of cardiac structure and function

• Evaluation focuses on interpretation of signs and

Patients Suspected of symptoms that have led to the consideration of
Having HF this diagnosis

• Aims to identify the etiology, assess symptom

Patients With Established
nature and severity, determine functional
HF impairment, and establish a prognosis

Heart Failure Society of America. 2010 Comprehensive Heart Failure Practice Guidelines. Journal of Cardiac Failure.2010;16(6): e1-194.
 Management

Goals Of Management

The main goal in the management of CHF is to improve

ventricular pump performance and reduce myocardial
workload.

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Approaches for managing heart failure

1.
Lifestyle
considerations

Approaches

2.
3.
Pharmaco-
Surgical
therapeutic
 Lifestyle considerations
• HF society of America
recommend the following with
respect to diet and nutrition :
• Dietary instruction regarding
sodium intake
• Specific attention on nutritional
management of patients with
advanced HF
• Documentation of the type and
dose of natural products
Heart Failure Society of America. 2010 Comprehensive Heart Failure Practice Guidelines. Journal of Cardiac Failure.2010;16(6): e1-194.
 Lifestyle considerations
• HF society of America
recommend the following
with respect to exercise:
• Undergo exercise testing to
determine suitability for
exercise training
• understanding of exercise
expectations and to increase
exercise duration

Heart Failure Society of America. 2010 Comprehensive Heart Failure Practice Guidelines. Journal of Cardiac Failure.2010;16(6): e1-194.
 Pharmacotherapy of heart failure

Pharmaco-therapy of heart failure

Positive
ACE inhibitors Diuretics β-blockers Antiarrhythmics
Inotropes

Ridha M, et al. Pharmacotherapy of systolic heart failure. Bulletin of Kuwait Institue of Medical Specialization. 2004;3:65-72.
 Management
General

• Positioning- the client is placed in a high fowler’s position to

reduce pulmonary venous congestion and ease dyspnea.
Oxygen Administration

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 Management
• Consider intubation if:
» O2 saturation cannot be kept >90% on supp. O2
» PaO2 cannot be kept >60 or on supp. O2
» Patient displays signs of worsening cerebral hypoxia
» PaCO2 progressively increases
» Patient becoming exhausted

• Monitor ECG
» Hypoxia, increased heart wall tension leads to dysrhythmias

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 Drug Therapy
NITROGLYCERIN
• Nitrate therapy before IV is started
• Reduces preload/afterload
• Improves coronary artery perfusion

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 Drug Therapy
FUROSEMIDE (LASIX)
• 0.5 - 1 mg/kg slow IV, Patients already on furosemide may have
tolerance Increase dose to 2X daily oral dose

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 Drug Therapy
MORPHINE SULFATE
• 2 mg IV push slowly
• Peripheral vasodilation leads to - Decreased preload & afterload
• Decreased venous return leads to - Decreased cardiac work load
& O2 demand
• Decreased anxiety - Decreased release of catecholamines
• Monitor Ventilations and BP - Systolic BP should be > 90 - 100
mm Hg
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 Drug Therapy
DOBUTAMINE

• 2 - 20 mcg/kg/min

• Increases contractility
• Increases level of cardiac output

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 Drug Therapy
BRONCHODILATORS

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 Management
• if the BP is too low (BP < 65 mm Hg)
• norepinephrine, 0.5 - 30 mcg/min IV infusion

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 Nursing Process
Assessment
• History
• Sleep disturbances
• ADL ability
• Client’s understanding of disease
• treatment
• desire to adhere to treatment regimen
• Coping skills
 Nursing Process
Physical Assessment • Temperature

• Lungs • Edema

• Auscultate for crackles and wheezes • Sacrum, back, fingers, and hands for
• Heart edema
• Auscultate • Liver (enlarged)
• Heart rate and rhythm • Intake and output if hospitalized
• Sensorium • Weight
• Level of consciousness
• Less oxygen getting to brain
• Lower extremities
• Color
 shock

A physiological state characterized by a significant, systemic

reduction in tissue perfusion, resulting in decreased tissue
oxygen delivery and insufficient removal of cellular metabolic
products, resulting in tissue injury.
 Types of Shock
• In 1972 Hinshaw and Cox suggested the following classification which is still
used today. It uses Four Types Of Shock,
1. Hypovolemic Shock,
2. Cardiogenic Shock,
3. Distributive Shock,
a) Septic Shock,
b) Anaphylactic Shock,
c) Neurogenic Shock,

4. Obstructive Shock,
5. Endocrine Shock, (Recently a 5th form of shock has been introduced)
 Cardiogenic Shock = Pump Failure
• This type of shock is caused by the failure of the heart to pump
effectively.

• This can be due to damage to the heart muscle, most often

from a large Myocardial infarction.

• Other causes of cardiogenic shock include Arrhythmias,

Cardiomyopathy, Congestive heart failure (CHF), Contusio
cordis or cardiac valve problems.
 Cardiogenic Shock

Due to Myocardial
SNS: Increased Heart’s INCREASED CARDIAC
damage, Cardiac
Pumping WORKLOAD
Insufficiency

Decreased SYSTEMIC
DECREASED
Inadequate Tissue AND CORONARY
MYOCARDIAL
Perfusion Circulation / Circulated
PERFUSION
Blood Volume

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• Jugular venous distension .

• Increases CVP ( In right sided heart failure).

• Pulmonary edema , crackles in lungs. (In left sided heart

failure).

• Decreased blood pressure.

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 Diagnostic Studies
• History Collection,
• Physical Examination,
• ECG 12 Leads,
• Continuous Cardiac Monitoring,
• X-Ray Chart,
• Haemodynamic Monitoring,
• Continuous pulse Oximetry,
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 Cardiogenic Shock
• Nursing Management

• Prevention of cardiogenic shock

• Enhance oxygen supply

• Monitoring hemodynamic status

• Administering medications, IV fluids

• Ensure safety and comfort

Shock

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 Shock Is……..

Simply stated, shock results from

inadequate perfusion of the body’s cells

with oxygenated blood.

 Introduction
• Shock is a serious, life-threatening medical emergency and one of the
most common causes of death for critically ill people.

• Shock leads to insufficient blood flow which reaches the body tissues.
As the blood carries oxygen and nutrients around the body

• The process of blood entering the tissues is called perfusion, so when

perfusion is not occurring properly this is called a hypo perfusion.

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 Definition

Shock is defined as inadequate tissue perfusion, inadequate tissue

perfusion can be caused by various disease that result in
decreased oxygenation at the cellular level.

Inadequate oxygenation leads to abnormal physiological state in

which these abnormal physiological state in which these is
inadequate cellular metabolism.

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 Stages of Shock

Non-
progressive or Progressive or
Irreversible
initial intermediate
stage
compensatory stage
stage
 Stage of Shock
There are Four Stages of shock. As it is a complex and continuous
condition there is No sudden transition from one stage to the next.

1) INITIAL STAGE,

2) COMPENSATORY (Compensating) STAGE,

3) PROGRESSIVE (Decompensating) STAGE,

4) REFRACTORY (Irreversible) STAGE,

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 Initial Stage

During this stage………. The hypoperfusional state Cellular Hypoxia,

The cells perform anaerobic Mitochondria being unable to

Lack of oxygen and atp
respiration. produce ATP.

These compounds getting

This causes a build-up of lactic Which results in systemic
removed by the liver requires
and pyruvic acid metabolic acidosis.
oxygen, which is absent.

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 Intermediate Stage
• This stage is characterised by the body employing physiological mechanisms, including
neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition.

The person will begin to

As a result of the hyperventilate in order attempt to raise the pH
acidosis, to rid the body of of the blood.
carbon dioxide (CO2).

Causes
predominately
The Baroreceptors in The release of The
vasoconstriction with
the arteries detect adrenaline and combined
a mild increase in
the resulting noradrenaline. effect results
heart rate,
hypotension, AND in an
AND increase in
Renin-angiotensin blood
vasopressin is
axis is activated pressure.
released to conserve
fluid via the kidneys.
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 Progressive (Decompensating) Stage

• When the cause of the crisis not successfully treated, the shock
will proceed to the progressive stage and the compensatory
mechanism begin to fail.

• The prolonged Vasoconstriction will also cause the vital organs

to be compromised due to Reduced perfusion.

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 Refractory (Irreversible) Stage

the vital the shock can

At this stage, organs have no longer be
failed reversed.

Death will Brain damage

occur and cell death
immediately. have occurred.

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 Hypovolemic Shock=insufficient volume
• This is the most common type of shock and based on
insufficient circulating volume.

• Its primary cause is loss of fluid from the circulation from either
an internal or external source.

• An internal source may be hemorrhage. External causes may

include extensive Bleeding, High Output Fistulae or Severe
burns.
 Distributive Shock = Low Resistance
• Also known as Vasogenic shock
• As in hypovolemic shock there is an insufficient intravascular volume
of blood.
• dilation of blood vessels which diminishes Systemic vascular
resistance.
• Types of Distributive shock
• Septic Shock,
• Anaphylactic Shock,
• Neurogenic Shock,
 Septic Shock
• This is caused by an overwhelming infection leading to
vasodilation, such as

• by Gram negative and positive bacteria

• release an endotoxin which produces adverse biochemical,

immunological and occasionally neurological effects which are
harmful to the body.
 Anaphylactic Shock

• Caused by a severe anaphylactic reaction to an allergen,

antigen, drug or foreign protein causing the release of
histamine which causes widespread vasodilation, leading
to hypotension and increased capillary permeability.
 Neurogenic shock
• Neurogenic shock is the rarest form of shock. It is caused by
trauma to the spinal cord resulting in the sudden loss of
autonomic and motor reflexes below the injury level.

• Without stimulation by sympathetic nervous system the vessel

walls relax in uncontrolled manner, resulting in a sudden
decrease in peripheral vascular resistance, leading to
vasodilation and hypotension.
 Obstructive Shock
• In this situation the flow of blood is obstructed which impedes circulation and can
result in circulatory arrest. Several conditions result in this form of shock.
• Cardiac Tamponade in which blood in the pericardium prevents inflow of blood
into the heart (venous return). Constrictive pericarditis, in which the pericardium
shrinks and hardens, is similar in presentation.
• Tension Pneumothorax. Through increased intrathoracic pressure, blood flow to
the heart is prevented (venous return).
• Massive Pulmonary Embolism is the result of a thromboembolic incident in the
blood vessels of the lungs and hinders the return of blood to the heart.
• Aortic Stenosis hinders circulation by obstructing the ventricular outflow tract.

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 Endocrine Shock
• Based on endocrine disturbances.

• Hypothyroidism, in critically ill patients, reduces cardiac output

and can lead to hypotension and respiratory insufficiency.

• Thyrotoxicosis may induce a reversible cardiomyopathy.

• Acute adrenal insufficiency is frequently the result of

discontinuing corticosteroid treatment without tapering the
dosage.
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 Hypovolemic Shock
Hemorrhage or other fluid
loss decreased intra
vascular volume

Decreased Cardiac Output

Decreased Tissue
Perfusion

Compensatory Mechanism
are Activated
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 Hypovolemic Shock
Compensatory Mechanism
are Activated

-
Epinephrine and Renin Angiotensin
Nor-Epinephrine Aldosterone System
Stimulation activated

ADH released

Increased Heart rate Intracellular fluid

and Systemic Vascular shift to Intravascular
Resistance Space

Increased Blood Volume

Increased Cardiac Output

Compensatory
Mechanism Fails
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 Hypovolemic Shock
Compensatory
Mechanism Fails

Decreased Cardiac Output

Decreased Blood Pressure

Decreased Perfusion of
Vital Organ

Multi System Organ Failure

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 Anaphylactic Shock
Antigen re-Exposure

Hypersensitive Antibody
response

Vasoactive mediator
release

Massive Vasodilation Increased Capillary

Permeability

Profound
Hypovolaemia Vascular Collapse

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Anaphylactic Shock
Profound
Hypovolaemia Vascular Collapse

Angio Edema, Uriticaria

Pulmonary Congestion

Airway Obstruction

Respiratory Arrest

Cardiac Arrest

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 Septic Shock
Severe Localized Infection of
Gram Negative Bacilli

Bacterial Invasion of Blood stream

(Septicaemia)

Inflammatory Response

Endotoxins are released into

Circulation

Immune system releases Histamine

and many other Chemical Mediators

Massive Increased Three-Spacing

Vasodilation Capillary Fluids
Permeability

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 Septic Shock

Massive Increased Three-Spacing

Vasodilation Capillary Fluids
Permeability

Inadequate tissue Perfusion

Compensatory mechanism are

activated

Decreased perfusion of Vital Organs

Multiple Organ Failure

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Neurogenic Shock
Spinal Cord Injury, Spinal
Anaesthesia centre Depression

Increased Sympathetic Tone

Arterial and Venous dilation

Arterial/ Venous Blood

pooling

Hypotension

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 Neurogenic Shock
Hypotension

Bradycardia Warm, Dry, Flushed skin

Decreased Perfusion of vital

organs

Multisystem Organ Failure

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 Clinical manifestations
Respiratory
• Rapid, shallow respirations.
system
SYSTEMIC MANIFESTATIONS

• Tachycardia.
Cardiovascular • Weak and thready pulse.
system • Hypotension.
• Pulse pressure- often less than 20 mm hg.

• Decrease in urine output.

Renal system
• Urinary flow of less than o.5 ml / kg /hour .

• Client feel anxious, nervous and irritable.

• Dizziness and postural hypotension.
Neuroendocrine • Apathy and confusion .
system • Decrease in cerebral perfusion pressure ( less than 50 mm of hg).
(CPP = MAP- ICP)
• Coma.
 HYPOVOLEMIC SHOCK CARDIOGENIC SHOCK

• Hypothermia due to decreased

perfusion and evaporation of
sweat.
• Thirst and dry mouth, due to
fluid depletion.
• Fatigue due to inadequate
oxygenation.
• Cold and mottled skin (cutis
marmorata), especially
extremities, due to insufficient
perfusion of the skin.
• Distracted look in the eyes or
staring into space, often with
pupils dilated.
 DISTRIBUTIVE SHOCK

SEPTIC SHOCK ANAPHYLACTIC SHOCK NEUROGENIC SHOCK

• Hypotension, coagulation disorders • Feeling of uneasiness. • Bradycardia

and multisystem organ dysfunction. • Headache due to • hypotension.
• Sepsis is suspected if vasodilation. • Dry skin
• Temperature > 380 c< 36 0 c • Severe dizziness, anxiety,
• Heart rate > 90 beats / min. disorientation.
• Respiratory rate > 20/ minute. • Loss of consciousness.
• WBC count > 12000 cells/ml or < • Feeling of lump in the
4000 cells/ ml . throat, followed by
• Initial stage hoarseness, coughing ,
dyspnea.
• Warm, dry and flushed skin
• Auscultation – diffuse
• Later stage
wheezes and prolonged
• Skin becomes pale, cold , clammy expiratory phase.
and mottled.
• Decreased oxygen
• Crackles and wheezes. saturation level.
• Drowsiness and stupor • Pruritis and urticaria.
progressing to coma.
• Edema of the eyelids, lips or
tongue.
 NURSING MANAGEMENT
AIRWAY & BREATHING MONITORING
 Assess for noisy respirations
 Check for obstructions
 Listen to lung sounds
 Assess respiratory rates
 Evaluate chest wall expansion/bulges/defects
 Restlessness
 NURSING MANAGEMENT

PERFUSION MONITORING:

 Pulse, BP, skin colour, temperature, heart sound,

peripheral pulses, state of hydration and skin perfusion.

 Condition of the mucous membrane, sclera & conjunctiva

 Presence of pallor or cyanosis

 Fullness of the neck veins

 NURSING MANAGEMENT
PERFUSION MONITORING cont….

 Determine the adequacy of blood volume before

administration of opioids

 Assess the clients' BP after administration of opioids

 After potentially life threatening problems are treated

then obtain complete vital signs
 NURSING MANAGEMENT
BLOOD PRESSURE MONITORING

 brachial or radial pulse

 Doppler instrument

 Arterial BP ( arterial line)

 NURSING MANAGEMENT
OF SHOCK
TEMPERATURE MONITORING:
 Rectal probe
 Indwelling urinary catheter
 Tympanic temperature
 Swan-Ganz catheter
 Skin temperature
CARDIAC MONITORING
 ECG
 NURSING MANAGEMENT
OF SHOCK
HEMODYNAMIC MONITORING:
 Measurement of CVP

 Peripheral intra-arterial lines are commonly used to measure arterial

BP, MAP, to collect samples for chemical & blood gases

 Pulmonary artery & pulmonary capillary wedge pressure (PCWP)

 Cardiac output

 Assess renal function

 NURSING MANAGEMENT
OF SHOCK
Additional assessments :

 Level of consciousness

 Ability to move extremities

 Sensation in all extremities

 Response to verbal and painful stimuli

 Pupil size & reaction to light

 NURSING MANAGEMENT
OF SHOCK
Additional assessment:-

 Presence of abnormal posturing

 Abdominal distension/rigidity

 Presence of lacerations, contusions, ecchymosis, purpura

 Bone deformities

 Presence of medical alert tags or bracelets

 NURSING MANAGEMENT
NURSING DIAGNOSIS:

 Ineffective tissue perfusion( cerebral, cardiac and systemic)

related to reduced circulating blood volume, fluid deficit or
abnormalities of tone of blood vessels.
 Decreased cardiac output related to decrease venous return
 Deficient fluid volume related to hemorrhage, inadequate
intake
 Impaired gas exchange
 NURSING MANAGEMENT
OF SHOCK
NURSING DIAGNOSIS CONT..
 Impaired breathing pattern
 Ineffective airway clearance related to increased pulmonary
secretions, bronchospasm
 Impaired physical mobility
 Disturbed sensory perceptions
 Imbalanced nutrition
 Self care deficit
 NURSING MANAGEMENT
OF SHOCK
NURSING DIAGNOSIS CONT..

 Disturbed sleep pattern

 Activity intolerance

 Acute pain

 Anxiety

 Impaired skin integrity

 NURSING MANAGEMENT
OF SHOCK
GOALS:

To correct the causative factor if possible

To improve oxygenation

To restore & maintain adequate perfusion

To prevent complications
 Hypovolemic Shock
• Nursing Management

• Prevention of hypovolemic shock

• Proper positioning

• Minimize fluid losses

• Enhance volume replacement

• Ensure safe administration of fluids, medications and documenting .

• Monitor signs of complications

 Anaphylactic Shock
• Prevention of anaphylactic shock
• Note all allergies

• Facilitate ventilation, prepare for CPR

• Enhance volume replacement

• Promote comfort

• Hemodynamic monitoring
 Neurogenic Shock
• Neurogenic Shock

• Prevention of neurogenic shock

• Elevate head bed (30oc) in spinal/epidural anaesthesia

• Immobilization of spinal cord injuries

• Deep Vein Thrombosis prevention

 Septic Shock
• Septic Shock

• Prevention of septic shock

• Multidisciplinary collaboration
• Provide comfort if patient experiences, fever, chills &
shivering
• Monitor blood levels of antibiotic agent, BUN,
creatinine, WBC, serum albumin, daily weight.
 NURSING MANAGEMENT
OF SHOCK
• Multiple Organ Dysfunction Syndrome
• Multidisciplinary collaboration