University of the East

RAMON MAGSAYSAY MEMORIAL MEDICAL CENTER

64 Aurora Boulevard, Barangay Dona Imelda, Quezon City, Philippines
College of Nursing
NCM 106

Cardiac Failure
An Emergency Approach
A Written Output for Teach Back Session
Submitted by:
Baguisa, Celine
Crisostomo, Camille
Duran, Darrie
Gonzales, John Paul

Submitted to:
Ms. Janelle P. Castro RN, MAN

CLINICAL CASE:
John Arnold, 80 years old, was admitted to the hospital after visiting his primary physician with
complaints of having experienced general malaise for 3-4 days, shortness of breath, and abdominal pain.
Initial assessment revealed bibasilar crackles, an audible S3, and tachycardia. Mr. Arnold also informed the
nurse of occasional epigastric pain, which he attributed to ulcer acting up.

PATHOPHYSIOLOGY:

Emergency Congestive Heart Failure

Modifiable

Non-Modifiable

Presence of Co-Morbidities
(DM, HTN and CAD)

Coronary Arteries is blocked by plaque

Blood supply to the myocardium is impaired

Myocardium receives subtle amount of oxygen from

the blood

Cardiac cells switches to anaerobic metabolism to

compensate for the reduced oxygen

Age (80 years old)

Gender (Male)

Nitroglycerine

Cardiac muscles are damaged due to the anaerobic metabolism.

Heart loose cardiac muscles to pump blood.

ECG result of Left Bundle Block

Initial
decrease of
BP

#3 Nursing Diagnosis:
Atrioventicular dissociation
Decreased Cardiac Output

RAAS
Activation

Na & H20
retention

The heart compensates by increasing the myocardial

contractility of the lefttricle
BP: 190/100
Dobutamine
HR: 123 bpm
The left ventricle increases its muscle mass in response
to the overwork and straining.
The change of pressure in the pulmonary capillaries
causes H20 to diffuse to the lungs
As the muscle mass increases, the space for the blood
in the left ventricle decreases

Pulmonary Edema

Left Ventricle loses its ability to generate enough

Crackles and wheezes

pressure to eject blood to the systemic circulation

Blood flow is congested in the pulmonary capillaries.

Pressure is altered.

#2 Nursing Diagnosis:
Excess Fluid Volume

Flurosemide

O2 and CO2 cannot exchange properly

#1 Nursing Diagnosis:
Impaired Gas exchange
Difficulty of Breathing

ASSESSMENT DATA:
History:
Diabetes for more than 30 years, peptic ulcer, and hypertension and coronaryartery diseases.

Subjective Cues:
General malaise for 3 to 4 days, shortness of breath an abdominal. Patient stated his weight had increases approximately 3kg
(6lb) during the last 3 days

Objective Cues:
Bibasilar crackles, an audible S3 and tachycardia. cold and clammy. diaphoretic, gasping for air with jugular venous
distention. Bilateral crackles were present with an expiratory wheeze. Audible crackles were also heard with respirations. Urinary
output had been scant since admission
BP: 150/72

Respiration: 24-32/min

HR: 102-123 bpm and irregular

Temp: 37.3 ( 99.2 F)

Upon Admission
Laboratory Results:

Normal

Analysis

Urine : Yellow and cloudy

Color Yellow (light/pale to dark/deep

Normal

amber) Clarity/turbidity Clear or cloudy

Na+ : 40 mmol/L

135-145 mmol/L

Hyponatremia

K+ : 4.2 mmol

3.5-5.3 mmol/L

Normal

Hgb: 11.8 g/dl

13.5 to 17.5 g/dl

Decrease tissue perfusion

Hct :36.2

37-47

Low availability of oxygen. COPD

AST( SGOT) :134 U/L

0 - 42 U/L

Liver damage or injury from different types of

diseases or conditions

BUN : 17 mg/dl

7-20 mg/dL

Normal

Glucose: 332 mg/ dl

Below 11.1 mmol/l Below 200 mg/dl

An abnormal result on the random blood glucose

test may mean diabetes

LDH: 705 U/L

140 U/L

Tissue and cellular damage

CK : 587 U/L

52-336 U/L

High amounts of CK are released into the blood

when there is muscle damage

Laboratory Results
At CCU after 30 mins.

After a short time

BP: 190/ 100

BP 140/90

HR: 123/ bpm

HR 109 bpm

Respirations: 42/ min

Respirations: 24/

Normal Values

Analysis

Systolic (PASP). 15 -

Increased pulmonary artery pressure may indicate:,

30 mmHg. Diastolic

pulmonary edema, left ventricular failure.

min
PAP: 50/22 mm Hg

PAP: 30/10 mm Hg

(PADP). 8 - 15
mmHg
PCWP :24 mm Hg

PAWP: 12 mm Hg

4-12 mmHg

High PCWP may indicate left ventricle failure, mitral

valve pathology, cardiac insufficiency, cardiac
compression post hemorrhage

CO :4.64 L/ min

CO : 5.5 L/ min

4.0 - 8.0 l/min

Normal

CVP:19 cm H2o

CVP: 8 cm H2o

2-8 cm H20

High CVP values reflect overhydration, increased

venous return or right sided cardiac failure.

SVR : 1810 dyne/s/cm-5

SVR : 1340

800-1200

An increased SVR can be caused by vasoconstrictors

dyne/s/cm-5

dynes/sec/cm5

CI: 2.34 L/ min/ m2

CI: 2.8 L/ min/ m2

2.5 - 4.0 l/min/m2

Normal

Ph7.46 *

Ph 7.43*

7.357.45

pH is elevated (more alkaline, higher pH) with some

pulmonary disease , Some degrees of congestive
heart failure.
Decreased tissue perfusion

PaCO2: 31 mm Hg

PaCO2: 36 mm Hg

3545mmHg

Decreased paCO2 is caused by:

Hyperventilation ,Hypoxia

PaO2: 80 mm Hg

PaO2: 89 mm Hg

80100mmHg

Normal

Sa02: 96%

Sa02: 98 %

95-100 %

Normal

HCO3 : 24 mmol

HCO3:

2226mmol/L

Normal

Diagnostic Exam Results

*CXR: Mild congestive heart failure superimposed on COPD and chronic pulmonary parenchyma changes
*ECG: Sins rhythm with left bundle branch block, long QT interval

THERAPEUTIC REGIMEN:
The immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs.

Course in the Ward

Upon Admission

High fowlers position

o Allows for better chest expansion, thereby improving pulmonary capacity.

Oxygen Therapy 4L/min

o increases the amount of oxygen delivered to the body's tissues
o alleviates signs of hypoxia

Transferred to Cardiac Care Unit

Furosemide (Lasix) 100mg, IV

o Reduces the amount of blood volume in circulation results in less workload of the heart.
o reduce the swelling (edema) and water buildup in the lungs (congestion)

Atropine Sulfate, 0.5 mg, IV

o Blocks the effect of the vagus nerve on the heart.

o Slows heart rate (HR: 102-123bpm)

o decreases bronchial secretions

Dobutamine (Dobutrex) 1g/250 NS at 5 ug/kg/min

o Increases cardiac output to increase perfusion and preserve end-organ
o Reduces pulmonary congestion

7.5 transvenous pacing catheter in right subclavian vein

o provides electrical stimulation to a heart that is compromised by disturbances in the conduction system, resulting in
hemodynamic instability

After a short time

Dobutamine drip was increases to 10 ug/kg/min.

Nitrogylcerin (Tridil) 50mg/250 ml NS

o Enlarges the small arteries or arterioles, which relieve the systolic workload of the left ventricle. Therefore, the heart
has to work less to pump blood through the arteries.
o Lowers blood pressure (From 190/100 to 140/90)

Additional 200 mg of Furosemide (Lasix), IV

The Next 4 Days

All drips, temporary pacing catheter and foley catheter were removed.

Transferred to Medical-Surgical Floor

Treatment:
o Digoxin (Lanoxin) 0.125 mg daily

Slows and strengthens heart contractions, enabling the heart to pump more blood with each beat.

o Furosemide (Lasix) 160 mg PO, BID

Reduces excessive accumulation of fluid and/or swelling (edema) of the body

o Captopril (Capoten) 25 mg Q6H

indicated for the treatment of hypertension.

in combination with diuretics and digitalis.

o Potassium Supplement Q6H

Replacement of loss electrolytes while taking diuretics

NURSING PRIORITIES:

#1 Nursing Diagnosis
ASSESSMENT
Subjective:

DIAGNOSIS
Impaired Gas

PLANNING
Goal:

INTERVENTIONS
Independent:

EVALUATION
After 2 hours of

I experienced shortness of

Exchange related

After 2 hours of

Monitored vital signs.

nursing interventions,

breath for 3-4 days. As

to accumulation

nursing

Monitored for rate,

the patient was able

interventions, the

rhythm, and effort of

to demonstrate

patient will

respirations.

improved ventilation,

Monitoredcolor of skin,

adequate oxygenation

improve ventilation,

mucus membranes, and

of tissues by ABGs,

adequate

nail beds.

and absence of

verbalized by the patient.

of fluid in the
lungs secondary

Objectives:

to pulmonary

Respiratory Rate =

edema as

24-32 breaths/min

evidenced by

Arterial pH = 7.46

dyspnea

demonstrate

oxygenation of

Monitored ABGs.

symptoms respiratory

PaCO2 = 31mm Hg

tissues by ABGs, and

Positioned patient in High

distress as evidenced

Bibasilarcrackles

absence of

Fowlers position.

by RR of 24

with an expiratory

symptoms

Encouraged frequent

breaths/min and

wheeze

respiratory distress

position changes.

PaCO2 of 36 mm Hg.

Crackles also heard

Encouraged deep

in expiration

breathing exercises

Sweating heavily /

(Pursed lip breathing).

diaphoresis

Use of accessory
muscles (Trapezius
Muscles) during

Encouraged adequate
rest periods.

Dependent:

inspiratrion

Administeredoxygen
therapy as ordered (4
Lpm)

Administered
medications such as
Atropine Sulfate 0.5 mg,
IV.

Suction secretions as
needed.

Collaborative:

Referred to pulmonary
rehabilitation.

Consulted to respiratory
therapist physician.

Referred to laboratory for

assessment of ABGs.

#2 Nursing Diagnosis
ASSESSMENT
Objectives:

Weight gain of

Excess Fluid
Volume related to

3kg in 3 days

accumulation of

duration (79

fluid in the

PLANNING
Goal:

Independent:

interventions, the

nursing

Monitored intake and

patient was able to

output.

verbalize understanding

Positioned patient in High

of causative factors and

Fowlers position.

demonstrate behaviors

Encouraged frequent

to resolve excess fluid

position changes.

volume.

interventions, the
patient will

Shortness of

pulmonary edema

verbalize

as evidenced by

understanding of

difficulty of

weight gain of 3kg

causative factors

breathing

in 3 days duration

and demonstrate

Bibasilar

(79 kg)

behaviors to

crackles

resolve excess fluid

Blood Pressure

volume.

Encouraged adequate rest

periods.

Maintained the rate of IV

infusions carefully.

Provided health teaching

about the current condition.

Respiratory
Rate = 24-32
breaths/min

After 2 hours of nursing

Monitored vital signs.

Hg

EVALUATION

lungssecondary to

= 150/72 mm

INTERVENTIONS

After 2 hours of

kg).

breath /

DIAGNOSIS

Dependent:

Administered oxygen

mmol/L

therapy as ordered (4 Lpm).

Na = 40

Administered medications

Presence of S3

such as Furosemide (Lasix)

sound

100 mg, IV.

Use of
accessory
muscles

Collaborative:

monitoring of sodium.

(Trapezius
Muscles)
during
inspiratrion

Referred to laboratory for

Consulted dietitian as
needed.

#3 Nursing Diagnosis
ASSESSMENT
Subjective:
I experienced
shortness of breath for
3-4 days. As
verbalized by the
patient.

Objectives:

ECG result of
Left Bundle
Block
Atrioventicular
dissociation
Bibasilar

DIAGNOSIS
Decreased
Cardiac Output
related to altered
contractility as
evidenced by ECG
result of Left
Bundle Block
Atrioventicular
dissociation

PLANNING
Goal:
After 2 hours of

INTERVENTIONS
Independent:

nursing

blood pressure and pulse.

the patient was able to

interventions, the

Monitored

report decreased

patient will report

Encouraged rest and assisted

episodes of dyspnea

decreased

with activities.

episodes of

Provided quiet environment.

dyspnea.

Monitored oxygen saturation

and ABGs.

Positioned patient in High

Fowlers position.

Encouraged changing position

slowly and dangling of legs

Blood Pressure

before standing.

= 150/72 mm

Respiratory
Rate = 24-32

After 2 hours of

Monitored vital signs especially nursing interventions,

crackles

Hg

EVALUATION

Dependent:

Administered oxygen therapy

as ordered (4 Lpm)

breaths/min

Heart Rate =

Administered medications such

as:
Nitroglycerin (Tridil 50

102-123
beats/min

mg/250mL NS)
Atropine Sulfate 0.5

Presence of S3

mg, IV

sound

Dobutamine (Dobutrex)
1g

Collaborative:

Collaborated with significant

others on acitivity restriction
of the patient.