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MEDICAL SURGICAL NURSING

CARDIOVASCULAR DISORDERS
Assoc. Prof. I. S. TIONKO

CARDIAC DISORDER

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

INTERVENTIONS

Sinus Node slows because of stimulation


of the parasympathetic fibers (vagal
nerve).

ECG:
Ventricular and Atrial Rate: <60 in Adult,
Ventricular and Atrial Rhythm: Regular,
QRS Shape and Duration: Usually normal,
but maybe regularly abnormal, P Wave:
Normal and consistent shape, always in front
of the QRS, PR Interval: Consistent interval
between 0.12-0.20 s, P:QRS- 1:1

If the decrease in HR results from


stimulation of the vagus nerve, such as
bearing down during defecation or
vomiting, attempts are made to prevent
further vagal stimulation

The sympathetic fibers are stimulated


thereby, speed up excitation of the SA
Node

ECG:
Ventricular and Atrial Rate: >100bpm in
Adult, Ventricular and Atrial Rhythm:
Irregular, QRS Shape and Duration: Usually
normal, but maybe regularly abnormal, P
Wave: Normal and consistent shape, always
in front of the QRS but maybe buried in the
preceding T Wave PR Interval: Consistent
interval between 0.12-0.20 s, P:QRS- 1:1

Treat the underlying cause (fever, shock,


Fluid and Electrolyte disturbances)

An Irregularity in rhythm which is related


to respiratory exchange occurs when the
SA Node creates an impulse at an
irregular rhythm

ECG:
Ventricular and Atrial Rate: 60-100bpm in
Adult, Ventricular an
d Atrial Rhythm: Irregular, QRS Shape and
Duration: Usually normal, but maybe
regularly abnormal, P Wave: Normal and
consistent shape, always in front of the QRS,
PR Interval: Consistent interval between
0.12-0.20 s, P:QRS- 1:1

Sinus arrhythmia does not cause any


significant hemodynamic effect and
usually is not treated

MEDICATIONS

I. DYSRYTHMIAS
-

are disorders of the formation


and/or conduction of the electrical
impulses within the heart.
These
disorders can cause disturbances of the
hearts rate, rhythm, or both.

A. SINUS DYSRYTHMIAS
A.1 Sinus Bradycardia
- when the sinus node creates
an impulse at a slower-thannormal rate

A.2 Sinus Tachycardia


- occurs when the sinus node
creates an impulse at a fasterthan-normal rate.

A.3 Sinus Arrythmia


-occurs when the sinus node
creates an impulse at an
irregular rhythm; the rate
usually
increases
with
inspiration and decreases with
expiration.
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Atropine Sulfate 0.5-1.0 mg/IVP


to block vagal stimulation
Isoproterenol 1mg/500 mL D5W
to stimulate sympathetic
response
Pacemaker (transcutaneous
pacing)

Digitalis Administration
Calcium Channel Blockers
Beta Blockers

No medications given.

B. ATRIAL DYSRYTHMIAS
B.1 Premature Atrial Complex
(PAC)
- An ectopic beat that
originates in the atria and is
discharged at a rate faster
than that of SA Node

B.2 Atrial Flutter


- ectopic atrial focus captures
the heart rhythm and
discharges impulses at a rate
between 200-400 times per
minute

B.3 Atrial Fibrillation


- is a dysrhythmia that is
caused by the rapid and
chaotic firing of atrial impulses
by a multitude of foci

*ISTIONKO/USTCON/O5

Occurs when an electrical impulse


starts in the atrium before the next
normal impulse of the sinus node.

Occurs in the atrium and crates impulses


at an atrial rate bet. 250-400 times per
minute. Because the atrial rate is faster
than the AV Node can conduct, not all
atrial impulses are conducted into the
ventricle, causing a therapeutic block at
the AV Node

There is a rapid, disorganized and


uncoordinated twitching of atrial
musculature

ECG:
Ventricular and Atrial Rate: Depends on
the underlying cause, Ventricular and Atrial
Rhythm: Irregular due to early P Waves,
creating a PP interval that is shorter than the
others. This is sometimes followed by a
longer-than-normal PP interval, but one that
is less than twice the normal PP interval.
This type of interval is called a
NONCOMPENSATORY PHASE QRS Shape
and Duration: The QRS that follows the
early P wave is usually normal, but it maybe
abnormal. It maybe absent (blocked PAC) , P
Wave: An early and diff. P wave may be
seen in the Y-wave, other P waves in the
strip are consistent, PR Interval: The early P
wave ahs a shorter-than normal PR Interval,
bur still between 0.12-0.20 s interval
between 0.12-0.20 s, P:QRS- 1:1
ECG:
Ventricular and Atrial Rate: 250-400 (atrial
rate), 75-150 (ventricular rate) , Ventricular
and Atrial Rhythm: Atrial rhythm is regular,
but the ventricular rhythm is usually irregular
bec. of a change in AV conduction, QRS
Shape and Duration: Usually normal, but
maybe regularly abnormal, P Wave: Saw
toothed shape. These waves are referred as
F waves, PR Interval: multiple F waves
maybe difficult to determine the PR interval,
P:QRS- 2:1. 3:1, 4:1
ECG:
Ventricular and Atrial Rate: Atrial rate:300600, VR: 120-200 in untreated fibrillation,
Ventricular and Atrial Rhythm: Normal,
QRS Shape and Duration: Usually normal,
but maybe regularly abnormal, P Wave: No
discernible P waves; irregular undulating
waves are seen and are referred as F or
fibrillatory waves, PR Interval: Cant be
measured, P:QRS- many:1

If PACs are insufficient, no treatment.


If it increases in frequency (>6/min),
Quinidine or Calcium Channel
Blocker maybe necessary

Proper monitoring.

Depends on its cause and duration


and the patient symptoms, age and
co-morbidities
Cardioversion

Digitalis preparation or digoxin


Quinidine
Calcium Channel Blockers
Bete-adrenergic Blockers
IV adenosine
Cardioversion

Digitalis if uncontrolled fibrillation


Quinidine
Beta adrenergic blockers

C. VENTRICULAR
DYSRYTHMIAS
C.1. Premature Ventricular
Contraction (PVC)
- dysrhythmia that is produced
by an ectopic beat originating
in a ventricle and being
discharged at a rate faster
than that of the next normally
occurring beat.

C.2 Ventricular Tachycardia


- is a life threatening
dysrhytmia that originates
from an irritable focus within
the ventricle.
- it is an effective rhythm for
maintaining cardiac output.

C.3 Ventricular Fibrillation


-a dysrhythmia that is
characterized by the random
and chaotic discharging of
impulses within the ventricle at
rates that exceed 300 beats
per minute.

Premature Ventricular Contractions


Ventricular Fibrillations Cardiac
Standstill/Arrest Dysrythmias
CO Cardiac Irritability
Myocardial Perfusion Dysrythmia

Originates form an irritable focus within


the ventricle. It is an ineffective rhythm
for maintaining CO

Characterized by random and chaotic


discharging of impulses within the
ventricle at rates exceed 300 bpm.

-characterized by absent QRS


complexes, although the P waves my be
apparent for a short duration in two
-commonly called flatline,
-No heartbeat, no palpable different leads.

C.4. Ventricular Asystole


(Flatline)
pulse, no respiration
*ISTIONKO/USTCON/O5

1. Lidocaine/IVP, drip
Initial bolus dose: 75-100 mg
then 50-100 mg within 10-15
min, as needed
Continuous IV drip is D5W, 4:1
concentration
2. Procainamide: IV drip bolus dose:
300 mg
3. Bretylium: continuous infusion if
Lidocaine and procainamide
are ineffective

ECG:
Ventricular and Atrial Rate: Depends on
the underlying rhythm, Ventricular and
Atrial Rhythm: Irregular due to early QRS,
creating one RR interval thats shorter than
the others. PP interval may be regular,
indicating that the PVC did not depolarize the
sinus node, QRS Shape and Duration:
Duration is 0.12 s or longer, bizarre shape
and abnormal, P Wave: Visibility of P wave
depends on the timing of the PVC; may be
absent or in front of QRS. If the P wave
follows the QRS, the shape of the P wave
may be different, PR Interval: If the P wave
is in front of the QRS, the PR interval is less
than 0.12 s, P:QRS- 0:1, 1:1
ECG:
Ventricular and Atrial Rate: Atrial rate:
depends on the underlying cause , VR: 100200, Ventricular and Atrial Rhythm:
Usually regular, QRS Shape and Duration:
Duration is 0.12 s or more, P Wave: difficult
to detect, PR Interval: Very Irregular ,
P:QRS- Difficult to determine

Defibrillation if no pulse and


unconscious
Cardioversion if conscious

ECG:
Ventricular Rate: >300 bpm, Ventricular
Rhythm: Extremely irregular, QRS Shape
and Duration: Duration is 0.12 s or more,:
Irregular,
undulating
waves
without
recognizable QRS complex

Immediate DEFIBRILLATION: 200-400


watt/sec (J)

ECG:
Absent QRS complex, P waves maybe
apparent for short duration

CPR and E services are necessary


Transcutaneous pacing

Lidocaine: bolus dose; followed by a


continuous IV drip from 1-4 mg/min

Epinephrine
Na HCO3 to relieve lactic acidosis
which causes unsuccessful
defibrillation

Epinephrine: bolus, 3-5 minutes


interval

CARDIAC DISORDER

PATHOPHYSIOLOGY

II. CORONARY ARTERY DISEASE


-most common is atherosclerosis, which
is an abnormal accumulation of lipid, or
fatty substances and fibrous tissue in
the vessel of the wall.
These
substances create blockages or narrow
the vessel in a way that reduces blood
flow to the myocardium.

ANGINA PECTORIS
-

clinical
syndrome
usually
characterized
by
episodes
or
paroxysms of pain or pressure in the
anterior chest. The cause is usually
insufficient coronary blood flow.

CAD begins as fatty streaks, lipids that


are deposited in the
intima of the arterial wall.
Although,
they are
thought to be the
precursors
of
atherosclerosis,
fatty
streaks are common
even
in
childhood.
Moreover, not all develop
into more advanced
lesions. The reason why
fatty streaks continue to
develop is unknown,
although genetic and
environment factors are
involved. The continued
development of CAD
involves an inflammatory
response. T lymphocytes
and monocytes infiltrate
the area to ingest the
lipids and then die; this
causes smooth muscle
cells within the vessel to
proliferate an die; this
causes smooth muscle
cells within the vessel to
proliferate and from a
fibrous cap over the
dead fatty core. These
deposits
called
atheromas or plaques,
protrude into the lumen
of the vessel, narrowing
it and obstructing blood
flow. If the fibrous cap of
the plaque is thick and
the lipid pool remains
relatively stable, it can
resist the stress from

ASSESSMENT FINDINGS

Angina Pectoris

Myocardial Ischemia (acute onset of


chest pain)

Heart Failure

ECG abnormalities

High levels of cardiac enzymes

INTERVENTIONS

Controlling Cholesterol

MEDICATIONS

3Hydroxy-3methylglutaryl

Abnormalities

coenzyme A (HMG-CoA)

CABG

reductase inhibitors or statins

Dietary Measures

block cholesterol synthesis, lower

Regulating Physical Activity

LDL and triglyceride levels, and

Promoting cessation of tobacco use

increase HDL levels.

Dysrythmias

Nicotinic acids decrease


lipoprotein synthesis, lower LDL and
triglyceride

Fibric Acid or fibrates decrease


synthesis of cholesterol

CAD is believed to result from


inflammation of the arterial endothelium.
C-reactive protein (CRP) is a marker for
inflammation of vascular endothelium.
High blood levels of CRP have been

Treatment
1. Percutaneous Transluminal
Coronary Angioplasty
2. Percutaneous Transluminal
Revascularization (PTMR)

Vasodilators (Nitrates)
Beta- adrenergic blockers
Calcium channel blockers
Platelet Aggregation Inhibitors
Anticoagulants

*ISTIONKO/USTCON/O5

blood flow and vessel


movement. If the cap is
thin, the lipid core may
grow causing it to rupture
and hemorrhage into the
plaque,
allowing
a
thrombus to develop.
The thrombus may
obstruct blood flow,
leading
to
sudden
cardiac death or an cute
MI which is the death of
heart tissue.

Atherosclerosis, hypertension, DM,


thromboangitis obliterans,
polycythemia vera, aortic regurgitation
coronary tissue perfusion
myocardial oxygenation anaerobic
metabolism lactic acid
production (lactic acidosis) angina

MYOCARDIAL INFARCTION
formation of localized necrotic
areas within the myocardium.
Prolonged ischemia lasting more
than 35 45 minutes produces
irreversible cellular damage and
necrosis of the myocardium

Several factors are associated with


anginal pain:
1. physical exertion which can
precipitate an attack by
myocardial o2 demand
2. Exposure to cold which can
cause vasoconstriction and an
elevated BP with O2
demand
3. Eating a heavy meal which
blood flow to the mesenteric
area for digestion, thereby
reducing the blood supply
available to the heart muscle
4. Stress which increases the
sympathetic response

associated with increased coronary


artery calcification and risk of an acute
cardiovascular event in seemingly
healthy individuals. There is interest in
using CRP blood levels as an additional
risk factor for cardiovascular disease in
clinical use and research.
An elevated blood level of homocysteine,
an amino acid, has also been proposed
as an independent risk factor for
cardiovascular disease.
However,
studies have not supported the
relationship between mild to moderate
elevations of homocysteine and
atherosclerosis. No study has yet
shown that reducing homocysteine
levels reduces the risk for CAD.

3.
4.

Intravascular Stenting
Laser therapy

Surgical Management:
1. Coronary Artery Bypass Graft (CABG)
Nursing Interventions:
1. Diet- Low Na, low fat and low
cholesterol, high fiver
2. Avoid saturated fats
3. White meat- chicken without
skin, fish are low in saturated
fats
4. No restrictions are placed on
activity within the patients
limitations

CLINICAL MANIFESTATIONS
Pain described as transient, paroxysmal
substernal or precordial pain. Heaviness
or tightness of the chest, indigestion,
crushing, Radiates down both arms, left
shoulder, jaw, neck and back. Precipitated
by activity or exertion and relieve by rest
or nitroglycerine
Diaphoresis
Dyspnea
Pallor
Faintness
Palpitations
Dizziness
Digestive Disturbance due to vagal
simulation

Pain Crushing, severe, prolonged,


unrelieved by rest or nitroglycerine,
often radiating to one or both arms,
the neck and back - Characterized
by Levines sign
Anxiety and Apprehension
-feeling of doom, restlessness
Shock -systolic pressure below
80mmHg, gray, facial color, lethargy,
cold diaphoresis, peripheral cyanosis,
Tachycardia/ Bradycardia, weak pulse

Medical Management:
1.
Goals
a. Prevention of further tissue
injury and limitation of infarct
size
b. Maximize myocardial tissue
perfusion and reduce
myocardial tissue demands
2.
Supplemental O2 by nasal
cannula. This increases
myocatdial O2 supply and relieves
pain
3.
Cardiac monitoring to detect

Analgesics- Morphine SO4


Thrombolytic Therapy
Anticoagulant
Beta adrenergic blockers
Sedatives

*ISTIONKO/USTCON/O5

*ISTIONKO/USTCON/O5

CARDIAC DISORDER

MI is usually caused by reduce


blood flow in a coronary artery due
to atherosclerosis and occlusion of
an artery by an embolus or
thrombus.
Because
unstable
angina and acute MI are
considered to be the same process.
Other causes of MI include
vasospasm of coronary artery,
oxygen supply and demand for
O2. In each case, a profound
imbalance
exists
between
myocardial supply and demand.

PATHOPHYSIOLOGY

Oliguria -<30 mL/hr

4.

Fever-slight elevation of temp. occurs


within 24 hours and extends 3-7 days
accompanied by leukocytosis and
elevated ESR

5.
6.

Indigestion -gas pains around the


heart, nausea and vomiting
Acute Pulmonary Edema-sense of
suffocation, Dyspnea, orthopnea,
gurgling/ bubbling respiration
ECG changes - MI causes elevation
of ST segment, inversion of T wave
and enlargement of the Q wave
Elevated CK-MB, LDH, AST

ASSESSMENT FINDINGS

dysryhythmias
PTCA may be done to reopen an
occluded artery
Diet: low cholesterol, low salt
Bed rest is usually prescribed for
24-48 hours to o2 demand.
Progressive ambulation is
implemente4ted ASAP, unless
there are complications

Nursing Management
1. Promote oxygenation and
tissue perfusion
2. Promote adequate Cardiac
Output
3. Promote Comfort
4. Provide rest
5. Promote gradual in activity
6. Promote Proper Nutrition and
Elimination
7. Promote Relief of Anxiety and
Feeling of Well-Being
8. Facilitate learning

INTERVENTIONS

MEDICATIONS

III. ACQUIRED VASCULAR


DISEASE
MITRAL VALVE PROLAPSE
- formerly known as mitral prolapse
syndrome, is a deformity that usually
produces no symptoms. Rarely, it
progresses and can result in sudden
death.

IN MVP, a portion of a mitral leaflet


balloons back into the atrium during
systole. Rarely, the ballooning
stretches the leaflet to the point that
the valve doesnt remain closed
during
systole.
Blood
then
regurgitates form the LV back into the
LA

Maybe asymtomatic
fatigue, shortness of breath
light-headedness, dizziness,
syncope, palpitations, chest
pain and anxiety
Physical Examination of the heart
discloses an extra heart sound
referred as mitral click
Symptoms of Heart Failure

Medical Management:
1. Symptomatic
2. Advised to eliminate caffeine
and alcohol
3. Stop smoking
Surgical Intervention
1. Mitral Valve Repair or
Replacement in advanced
stages
Nursing Management:
1. Health education
2. Instruct patients to take the

Calcium Channel Blockers

Beta Adrenergic Blockers

3.

*ISTIONKO/USTCON/O5

4.
5.

MITRAL STENOSIS

AORTIC REGURGITATION
-

is the flow of blood back into the


left ventricle from the aorta during
diastole.
It may be caused by
inflammatory lesions that deform the
leaflets of the aortic valve, preventing
them form completely closing the aortic
valve orifice.

prescribed medications on time


and complete the drug
Tell the patients to avoid
caffeine and alcohol
Encourage the patient to read
drug labels carefully
Explore with the patients
possible diet, activity, sleep
and other lifestyle

Normally, the mitral valve opening is as


wide as the dm. Of 3 fingers. In cases of
marked stenosis, the opening narrows to
the width of a pencil. The LA has great
difficulty moving blood into the ventricle
because of the resistance of the
narrowed orifice; it dilates and
hypertrophies because of BV it holds.
Because there is no valve to protect the
pulmonary veins from the backward flow
of blood from the atrium, the pulmonary
circulation becomes congested. As a
result, the RV must contract against an
abnormally high pulmonary arterial
pressure and is subjected to excessive
strain. Eventually the RV fails.

The pulse is weak and often irregularly


because of atrial fibrillation. A lowpitched, rumbling, diastolic murmur is
heard at the apex. As a result of the
increased blood volume and pressure,
the atrium dilates, hypertrophies, and
becomes electrically unstable, and the
patient experiences atrial dysrythmias.
Echocardiography is used to diagnose
mitral stenosis. ECG and cardiac
catherterization with angiography are
used to determine the severity of the
mitral stenosis.

Medical management
1. Antibiotic prophylaxis therapy
2. Treat CHF

Blood from Aorta LV (diastole) LV


dilates and hypertrophies arteries try
to compensate for the pressure (reflex
vasodilation) peripheral arterioles
relax peripheral resistance and
diastolic BP

A diastolic murmur is heard as a high-pitched,


blowing sound at the third or fourth
intercostals space at the left sternal border.
The pulse pressure is considerably widened
in patients with aortic regurgitation. One
characteristic sign of the disease is the waterhammer pulse, in which the pulse strikes the
papating finger with a quick, sharp stroke and
then suddenly collapses.

Medical Management
1. Antibiotic prophylaxis
2. Treat dysrythmias and HF

Asyymptomatic
forceful heart beat
marked arterial pulsations that are
palpable
exertional Dyspnea
fatigue

Surgical Management:
1. Valvuloplasty
2. Mitral Valve Replacement

Prophylactic Antibiotics

Anticoagulants - Warfarin
(Coumadine)

Nursing Management:
1. Health education
2. Instruct patients to take the
prescribed medications on time
and complete the drug
3. Tell the patients to avoid
caffeine and alcohol
4. Encourage the patient to read
drug labels carefully
5. Explore with the patients
possible diet, activity, sleep
and other lifestyle

Surgical Management:
1. Aortic valvuloplasty
2. Valve Replacement
Nursing Intervention:
1. Health education
2. Instruct patients to take the
prescribed medications on time
and complete the drug
3. Tell the patients to avoid
caffeine and alcohol

Prophylactic Antibiotics

progressive signs of LCHF


diastolic murmur at the 3rd or 4th ICS at
the left sternal border
Wide Pulse Pressure
WATER hammer pulse
Diagnosis confirmed by 8D- Echo, MRI ,
radionuclide imaging and
Cardiac catheterization

*ISTIONKO/USTCON/O5

AORTIC STENOSIS
aortic valve is narrowing of the
orifice between the left ventricle and the
aorta.

Progressive narrowing of the valve


orifice LV obstruction pressure
on LV thickening of the muscle wall
heart muscle hypertrophies Heart
Failure

*ISTIONKO/USTCON/O5

Asymtomatic
exertional Dyspnea
dizziness and syncope
angina pectoris
Low BP
rough-loud systolic murmur is heard in the
aortic area
systolic crescendo-decrescendo murmur
LVH- 12 lead ECG
2D-Echo- diagnose and monitor the
progression
Pressure tracings form the aorta
higher systolic pressure in the LV than
the aorta during systole

4.
5.

Encourage the patient to read


drug labels carefully
Explore with the patients
possible diet, activity, sleep
and other lifestyle

MEDICAL MANAGEMENT
1. Antibiotic prophylaxis to
prevent endocarditis
SURGERY: replacement of aortic valve
Patients who are symptomatic and
are not surgical candidates may
benefit form 1 or 2 balloon
Percutaneous Valvuloplasty

CARDIAC DISORDER
IV. CADIOMYOPATHY
-

is a heart muscle disease


associated with cardiac dysfunction. It
is classified according to the structural
and functional abnormalitites of the
heart muscle.

PATHOPHYSIOLOGY
Stroke Volume SNS and RAA
Systemic Vascular Resistance
Na and water retention workload of
the heart Heart Failure

ASSESSMENT FINDINGS
stable and asymptomatic
signs and symptoms of Heart Failure
PND
orthopnea
fluid retention
peripheral edema
nausea
chest pain
palpitations
dizziness
syncope with exertion
sudden death with HCM
Tachycardia and extra heart sounds
2D Echo and ECG
CXR
Cardiac Cath to rule out coronary artery
disease as a cause
Endomyocardial biopsy

INTERVENTIONS
Medical management:
1. Treat the underlying cause
2. Low Na diet
3. Exercise Rest Regimen
4. Control dysrythmias with
medications
5. If there are symptoms of CHF
limit fluid intake into 2 L/day
6. Pacemaker

MEDICATIONS
Antidysythmic drugs for dysrythmia

Surgical Management
1. Heart Transplantation
2. LVAD
3. Left Ventricular Outflow Tract
Surgery
Nursing Management
1. Improve CO
2. Increase activity tolerance
3. Reduce anxiety
4. Decrease the sense of
powerlessness
5. Promote Self-Care
6. Promote Home and
Community-Based care
7. Continuing Care

V. INFECTIOUS DISEASES OF THE


HEART
PERICARDITIS
- refers to an infection of the
pericardium, the membranous sac
enveloping the heart

*ISTIONKO/USTCON/O5

Underlying Cause: idiopathic, viral and


bacterial
infection,
disorders
of
connective
tissue,
hypersensitivity
states, disorders of adjacent structures,
neoplastic disease, radiation therapy,
trauma, renal failure and uremia, TB
accumulation of fluid in the pericardial
sac pressure on the heart
cardiac tamponade

Pain in the anterior chest, aggravated by


coughing,
yawning,
swallowing,
twisting and turning the torso; relieve
by upright, leaning forward position
Pericardial friction rub
Dyspnea
Fever, sweating, chills
Joint pains
Arrhythmias

Medical and Surgical Management:


1. Determine the cause,
administer therapy and be alert
for cardiac tamponade
2. Pericardiocentesis
3. Pericardictomy
Nursing Management:
1. Elevate HOB. Place pillow on
the overbed table so that the
patient can lan on it
2. Bed rest
3. Administer prescribed

Analgesics
NSAIDS
Cortocosteroids

4.
INFECTIVE ENDOCARDITIS
-

is the infection of the valves and


the endothelium surface of the heart.

The invasion of bacteria produces


vegetative growths on the heart valves,
the endocardial
lining or the
endothelium of a blood vessel that may
embolize the spleen, kidneys, CNS and
lungs

nonspecific and include malaise


weakness, anorexia, athralgia, night
sweats, chills, valvular insufficiency
and intermittent fever for weeks
loud regurgitant murmur

embolization of other vital organs

pharmacotherapy
Assist in pericardiocentesis

Medical and Surgical Management:


Supportive treatment- bed rest
Surgical valve replacement
aortic or mitral valve excision
are required

Antibiotic therapy
Antipyretics

Nursing Management:
Monitor vital signs
Assess signs of organ damage
Administer pharmacotherapy
Instruct activity restrictions,
medications and signs and
symptoms of infection
Emotional support
Coping strategies
If patient received surgical
management, strict post-op
care is observed

MYOCARDITIS
- is an inflammatory process involving
the myocardium. Myocarditis can cause
heart dilation, thrombi on the heart wall,
infiltration of circulating blood cells
around coronary vessels and between
the muscle fibers.

Viral, bacterial, fungal, parasitic,


protozoal infection inflammation in
one small area and spread throughout
the myocardium myocarditis

chest pain
dysrythmias
cardiomegaly
faint heart sounds
gallop rhythm
systolic murmur

Medical and Surgical Management:


Bed rest
Limit sports or strenuous
activities for 6 months
Physical activity is increased
slowly
If develops heart failure
management is essentially the
same
Nursing Management:
Monitor VS
Proper cardiac monitoring
Elastic compression stockings
Passive and active exercises
should be used
Instruct the patient not to take
aspirin, take caution when
taking corticosteroids

Antibiotic therapy
corticosteroids
Antipyretics

CARDIAC DISORDER

PATHOPHYSIOLOGY

VI. COMPICATIONS FROM


HEART DISEASES
CONGESTIVE HEART FAILURE

ASSESSMENT FINDINGS
Left CHF

Heart Damage, Ventricular Overload,


Ventricular Contraction it may lead to
Tachycardia, ,ventricular dilatation.
Myocardial hypertrophy CO
renal perfusion Na retention
osmotic pressure ADH water
absorption edema heart failure

Dyspnea
PND
Orthopnea
Rales /Crackles
Moist cough
wheezing
blood tinged frothy sputum
syncope
fatigue
weakness
anorexia
hypokalemia
clubbing of fingers
polycythemia
S3,S4 sounds, pulsus alternans
PAO, PWCP, LVEDP

Right CHF

CARDIOGENIC SHOCK
(POWER/PUMP FAILURE)

MASSIVE MI Myocardial
Contractility CO Hypoperfusion
(heart, brain , kidney) Tissue Hypoxia
Organ Damage Death

1.
2.
3.
4.

Jugular Vein Engorgement


Hepatomegaly
Splenomegaly
Portal Hpn
Ascites
Peripheral Edema
Jaundice
Hemolytic Anemia
Internal Hemorrhoids
Weight gain
Leg Varicosities
Cardiac cirrhosis
Extra Heart Sounds
Elevated CVP reading

Systolic Blood Pressure


Oliguria
Cod, clammy skin, weak pulse,
cyanosis due to circulatory
insufficiency
mental lethargy, confusion due to
poor cerebral perfusion

INTERVENTIONS

Oxygen therapy
balanced program of activity
and rest
Sodium restricted to prevent
fluid excess

MEDICATIONS

Digitalis Therapy
Diuretic Therapy
Vasodilators

Vasodilators
Inotrophic Agents
Diuretics

Nursing Management

Provide Oxygenation
Provide rest and activity
Decrease anxiety
Facilitate fluid balance
Provide skin care
Promote proper nutrition
Promote elimination
Facilitate learning

If acute pulmonary edema occurs:


High Fowlers position
Morphine Sulfate
Oxygen therapy
Aminophylline
Rapid digitalization
Diuretic therapy
Vasodilators
Dopamine or dobutamine
Monitor serum K

Medical and Nursing Management


1. Perform hemodynamic
monitoring:PAP, PWCP
measurements, Intraarterial BP
2. Administer oxygen therapy
3. Correct Hypovolemia
4. Administer IV fluids as ordered
5. Monitor I and O, LOC,

6.
7.
8.

CARDIAC DISORDER

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

arrhythmias
Provide psychosocial support
Decrease pulmonary edema
Utilize counterpulsation to
decrease ventricular work with
severe shock

INTERVENTIONS

MEDICATIONS

VII. PERIPHERAL VASCULAR


DISORDERS
HYPERTENSION

ARTERIOSCLEROSIS

RISK FACTORS: Family History. Age,


High Salt Intake, Low K intake, Obesity,
Excess Alcohol Consumption, Smoking,
Stress Changes in Arteriolar Bed
Systemic Vascular Resistance
Afterload Blood Flow to Organs
Renal Perfusion, BP, Beta receptor
activation Juxtaglomerular cells
(Hypovolemia and hyponatremia )
Renin Angitensinogen (ACE)
Angiotensin 1 (ACE) Angiotensin II
Arteriolar vasoconstriction
Peripheral Vascular Resistance

The most common direct result of


artherosclerosis include narrowing of the
lumen, obstruction, aneurysm,
ulceration and rupture. Its indirect results
are malnutrition and subsequent fibrosis
of the organs. All actively functioning
tissue cells require an abundant supply
of nutrients and oxygen and are sensitive
to any reduction in the supply of these
nutrients. If such reductions are severe
and permanent, the cell undergoes

headache. The most characteristic


sign
epistaxis
dizziness
tinnitus
unsteadiness
blurred vision
depression
nocturia
retinopathy,papilledema
Maybe asymptomatic

Prevention
a. Primary
Moderation in Na intake,
saturated fats, maintenance of
IBW, maintenance of regular
pattern of exercise, cessation of
cigarette smoking, moderation
in alcohol consumption, stress
reduction
b. Secondary
Control of HPN in high risk
groups

1.

Diuretics
a.
Thiazides
b.
Loop
c.
Potassium sparing
Adrenergic Inhibitors
a.
Beta Adrenergic
Blockers
b.
Centrally acting
alpha blockers
c.
Peripherally acting
Adrenergic
antagonists
d.
Alpha-1 adrenergic
blockers
e.
Vasodilators
f.
ACE Inhibitors
g.
Calcium Channel
Blockers

2.

NURSING INTERVENTIONS:
1. Patient teaching and
counseling
2. Teaching about medication
3. Prevent non-compliance

Intermittent claudication is an
aching, persistent cramplike
squeezing pain that occurs after a
certain amount of exercise of the
affected extremity. It is relieved by
rest
Coldness or cold sensitivity
Color changes
Ulceration and gangrene
Edema
Sexual dysfunction

Primary, Secondary Tertiary


Prevention
Quit smoking
Control serum lipid levels
Skin and foot care
Low fat, low cholesterol
Daily walking program

SURGICAL MANAGEMENT
1. Bypass Graft

Vasodilators
Antihyperlipidemics

*ISTIONKO/USTCON/O5

necrosis and is replaced by fibrous


tissue, which require lesser blood flow.

2.
3.
4.
5.
6.
7.

Endarterectomy
Endovascular Surgery
Balloon angioplasty
Laser angioplasty
Stent
Amputation

NURSING INTERVENTION
1. Promote Tissue Perfusion
2. Maintain Skin Integrity and
Prevent Infection
3. Promote Activity
4. Prevent Injury

PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE

AORTIC ANEURYSM

Atheromatous plaques blood flow


tissue Ischemia tissue hypoxia
necrosis ulceration and gangrene

Hypertension Alteration in integrity of


its wall irreversible. Localized
dilatation of an artery

intermittent Claudication
Coldness or cold sensitivity
Color changes
Ulceration and gangrene
Sexual dysfunction
Impaired arterial pulsation
Edema

pulsatile mass over the abdomen


Low back pain
Lower abdominal pain
Flank pain
Collapse
Shock
Possible complication is rupture,
causing massive internal
hemorrhage, shock and death

MEDICAL MANAGEMENT
Exercise Program combined
with weight reduction and
cessation of tobacco and
alcohol use

Vasodilators
Antihyperlipidemics

Antihypertensives

SURGICAL MANAGEMENT
Bypass Graft
Endarterectomy
Endovascular Surgery
Balloon angioplasty
Laser angioplasty
Stent
Amputation

MEDICAL MANAGEMENT
1. Medications
Surgery:
If greater than 4 cm
Teflon/Dacron/gortex graft may be used
in a surgical repair
NURSING INTERVENTION AFTER
SURGERY:
1. Monitor VS and hemodynamic

measurements, urine output, BUN


creatinine, bowel sounds peripheral
pulses
2. Promote Fluid Volume by checking
excessive drainage, Hgb and Hct
levels

*ISTIONKO/USTCON/O5

RAYNAUDS DISEASE

Cold exposure, stress Digital artery


Contraction/ Spasm Occlusion of
arteries Tissue Ischemia Tissue
Hypoxia Tissue Necrosis Tissue
Ulceration Gangrene

pallor
cyanotic
color sequence: white-blue-red
numbness, tingling and burning
pain

MEDICAL MANAGEMENT
Avoid exposure to cold
Quit smoking
Teach effects of smoking
Teach to avoid exposure to
cold
Discuss importance of
reducing emotional stress
Avoid drugs that causes
vasoconstriction such as pills,
beta blockers and ergotamines

Calcium Channel Blockers


Vasodilators
NSAIDS

NSAID
Non-narcotic analgesic

Anticoagulation therapy
Thrombolytics

Surgery
1. Amputation - Sympathectomy to
relieve vasospastic symptoms

THROMBOPHLEBITIS

Results form venous thrombosis and


inflammation in a superficial vein

DEEP VEIN THROMBOSIS

Venous Stasis, Vessel Wall Injury,


Hypercoagulability of the Blood DVT

pain
tenderness
palpable induration along the
course of vein
no edema

calf pain (+) Homan Sign


edema
tenderness

MEDICAL MANAGEMENT;
Bed rest with leg elevation
Local moist heat application
Compression support
stockings
NURSING INTERVENTIONS:
Prevent venous stasis
Prevent recurrence
Maintain IBW
Alternate standing with sitting
at work or at home
Regular Patterns of exercise

MEDICAL MANAGEMENT:
Minimize intake of green leafy
vegetables

*ISTIONKO/USTCON/O5

VARICOSE VEINS

BUERGERS DISEASE
(Thromboangitis Obliterans)

Congenital absence of valves of the


veins, hereditary weakness of the valves,
prolonged sitting or standing, wearing of
constricting clothing, obesity,
thrombophlebitis, pregnancy, RCHF, liver
cirrhosis effects of gravity on venous
pressure dilated, prominent veins

palpable induartion along the


course of the brain

SURGERY:
Thromboembolectomy
Greenfield vena cava fiber to
prevent pulmonary embolism
NURSING INTERVENTIONS:
Maintaining tissue perfusion
Promote comfort

dilated, purplish, tortuous veins


leg pain
leg edema
heaviness in the legs

Intermittent Claudication
Skin Cyanosis
Pain

1.Analgesics as ordered

Anticoagulants
Calcium Channel Blockers

MEDICAL MANAGEMENT:
Elevation of affected limp for
15-30 min at a time. Average
of 20 min.]
Compression with support
stockings
Sclerotherapy
Early ambulation
SURGERY:
1. Vein ligation and stripping to
relive pain

Diffuse inflammation of the small and


medium arteries then veins

NURSING INTERVENTION
1. Wear elastic stockings during
activities requiring long periods
of standing or during
pregnancy
2. Moderate exercise and elevate
the legs during sitting
3. Proper post-operative care
Medical Management:
1. eliminate smoking
Surgery:
1. Sympathectomy
2. Amputation of ulcerated fingers
and toes
Nursing Management:
1. during activities requiring long
periods of standing or during

2.
3.

pregnancy
Moderate exercise and elevate
the legs during sitting
Proper post-operative care

*ISTIONKO/USTCON/O5

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