Presentation about cardiovascular Disorders.

1. Prepared by:
Ms. Jennifer Iguico Magpayo
Cardiovascular Disorders

2. HYPERTENSION

3.  Hypertension is not only a disorder but a significant risk
factor to many diseases and complications. In
particular, hypertension contributes to cardiovascular
morbidity and mortality due to heart failure, rupture of
aortic aneurysms and aortic dissection. In presence of
other diseases like diabetes and other cardiovascular
conditions like ischemic heart disease, hypertension
aggravates the condition. Regardless of whether
hypertension contributes directly to the etiology or
increases risk of cardiovascular mortality, systemic
arterial hypertension has to be controlled.

4. REGULATION OF ARTERIAL BLOOD
PRESSURE
 ARTERIAL BLOOD PRESSURE- is the pressure
exerted by blood against the wall of the arteries.
 2 FACTORS DETERMINE ABP
1. CARDIAC OUTPUT – the amount of blood that
the heart ejects each minute.
2. TOTAL PERIPHERAL RESISTANCE – the
resistance that the blood encounters as it is
being pumped through the peripheral
circulation. This reflects the tone of the
resistance vessels and the viscosity of the blood.

6. REGULATION OF ARTERIAL BLOOD
PRESSURE
BP = CO x TPR

7.  The body maintains blood pressure
by adjusting CO when TPR is
increased; and adjust TPR to
compensate changes in CO.

8. Normally, blood pressure is regulated
through the interplay of four factors:
1. CARDIOVASCULAR COMPONENT
 AUTOREGULATION or the innate ability of the
cardiovascular system to adjust flow of blood in
relation to pressure changes by vasoconstriction or
vasodilatation.
 Heart adapts to changing volumes of venous
return by altering stroke volume
 Changes in blood volume through fluid shifts from
capillary to tissues

9. 2. NEURAL REFLEXES mediated by
baroreceptors and chemoreceptors;
responsible for short term regulation
 Baroreceptors are stretched receptors located in
the carotid sinus and aortic arch.
 Chemoreceptors located in carotid and aortic
bodies; sensitive to chemical stimuli such as
changes in oxygen, carbon dioxide, and
hydrogen ion content in the blood; whenever
arterial pressure drops below a critical level,
chemoreceptors are stimulated because of the
accompanying hypoxia or hypercapnea.

10. 3. HORMONAL MECHANISMS
 Renin-angiotensin mechanism
 Aldosterone secretion – promotes renal tubular
absorption of sodium directly, and water
indirectly, resulting in increase in plasma and
extracellular blood volume leading to increase
cardiac output and arterial blood pressure.

12.  Renal Component by regulating sodium
and water secretion in the kidney tubules
and through the renin- angiotensin-
aldosterone (RAA) mechanism

13. Hypertension
 - refers to systemic arterial hypertension.
It means high blood pressure. Because
blood pressure varies with age, gender
and other factors, definition of
hypertension becomes an important issue.
Thus, hypertension is defined as
sustained elevation in mean arterial
pressure.

14. DEFINITIONS OF HYPERTENSION
 “ … SYSTOLIC BLOOD PRESSURE (SBP) of 140
mmHg or greater, diastolic blood pressure (DBP)
of 90 mmHg or greater, or taking
antihypertensive medication.”
-JOINT NATIONAL COMMITTEE ON PREVENTION,
DETECTION, EVALUATION AND TREATMENT OF
HIGH BLOOD PRESSURE (JNC VI), 1997
 “… sustained SBP of 140 mmHg or greater and
sustained DBP of 90 mmHg or more based on
measurements done during at least 2 visits taken
at least 1 week apart.”
-Philippine Clinical Practice Guidelines on the
Detection and Management of Hypertension

15. CLASSIFICATION OF
HYPERTENSION
 According to Severity
 * Optimal blood pressure
with respect to cardiovascular
risk is below 120/80 mmHg.
However, unusually low
readings should be evaluated
for clinical significance.
 # Based on the average of
two or more readings taken
each of two or more visits
after an initial Screening.
CATEGORY SYSTOLIC
(mmHg)
DIASTOLIC
(mmHg)
Optimal * < 120 And <80
Normal <130 And <85
High-Normal 130-139 And 85-89
Hypertension #
Stage 1 140-159 Or 90-99
Stage 2 160-179 Or 100-109
Stage 3 ≥ 180 Or ≥110

16. According to etiology
1. ESSENTIAL HYPERTENSION
– refers to hypertension with no known medical disorder responsible
for their high blood pressure. Also known as primary hypertension
and idiopathic hypertension.
– There are several working hypotheses for essential
hypertension.
a. Autoregulatory Hypothesis
- High cardiac output states are associated with hypertension.
High CO causes vessels to constrict through autoregulation
resulting in diminished blood flow to tissues and increased TPR.
In other words, HPN occurs as a compensatory response for high
output states like hyperthyroidism and hypermetabolic states.

17. b. Renal Salt retention model
- pressure natriuresis which means as
blood pressure increases, kidneys
secrete more sodium and water to
reduce blood volume and hence blood
pressure. This model proposes that this
capability of kidney to regulate blood
pressure through pressure natriuresis is
defective in hypertensive individuals.

18. c. Sodium Transport Hypothesis
- this hypotheis proposes that
hypertensive individuals have a genetic
defect that prevents normal renal sodium
excretion.

19. 2. SECONDARY HYPERTENSION
 - refers to hypertension with
identifiable cause. In other words, HPN
is literally secondary to other medical
disorders. The most common causes
include kidney diseases, endocrine
disorders, pheochromocytoma, coarctation
of the aorta and acute brain lesions. Fluid
overload, drugs and foods, organ
dysfunction, tumors and pregnancy can
also include hypertension.

20.  CARDIOVASCULAR COMPLICATIONS
- include left ventricular hypertrophy,
ischemic heart disease and acute
heart failure.

21. CORONARY ARTERY DISEASE
 CORONARY ATHEROSCLEROSIS
- Abnormal accumulation of lipid or fatty
substance and fibrous tissue in vessel wall.
These substances create blockage or narrow the
vessel in a way that reduces blood flow to
myocardium.
- Involves repetitious inflammatory response to
arterial wall injury and an alteration in the
biophysical and biochemical properties of the
arterial walls.

22. PATHOPHYSIOLOGY
 Deposition of small amounts of lipid material
“fatty streaks” in the intima.
 Accumulation of lipid, especially cholesterol-
rich beta lipoprotein in intima and inner media
 Fibrous encapsulation of the lesions creating
fibrous plaques
 Development of atheromas or complex
atherosclerotic plaques consisting of lipid,
fibrous tissue, collagen, calcium, cellular
debris, and capillaries.
 Degenerative changes in arterial wall.

23. ASSOCIATED RISK FACTORS:
 Modifiable:
- use of tobacco
- Hypertension
- Elevated lipid levels
- Lifestyle
- DM

24.  Non-modifiable:
- family history of premature CVD (1st
degree relative with CVD at age 55 or
younger in women and age 65 or younger
in women
- Age (More than 45 y/o in male and more
than 55 y/o in female)
- Sex
- Race

25. SIGNS AND SYMPTOMS
 Chest pain (angina pectoris) brought
about by myocardial ischemia usually
mild to severe retrosternal pain
 Nausea and vomiting
 Dizziness and syncope
 Diaphoresis & cool and clammy skin
 Apprehension or a sense of impending
doom

26. MANAGEMENT EDUCATION GUIDELINES TO
DECREASE RISK FOR CORONARY ARTERY
DISEASE
 Daily management of hypertension. Take
medication at regular basis.
 Stop smoking immediately. Smoking reduces
available O2 to the heart and can precipitate
angina. Smoking increases HR and BP.
 Avoid passive smoke. Two hours of passive
smoke decreases O2 to heart, increases HR
and BP.
 Plan a regular exercise under medical
supervision.

27.  If overweight, lose weight. Seek help
from professional.
 Follow a healthy heart diet. Reduce
cholesterol and increase fiber diet.
 Reduce stress.
 Allow adequate time for rest and
relaxation.

28. ANGINA PECTORIS
 A symptomatic paroxysmal pain or
pressure sensation associated with
transient myocardial ischemia lasting no
more than 5-15 minutes

29. CARDIAC STRESSORS
CAUSING ANGINA
– Reduced blood flow to cardiac cells resulting
from coronary blood vessel obstruction
– Reduced O2 carrying capacity of blood
– Increased O2 need of the heart in high CO
conditions

30. FACTORS ASSOCIATED WITH
ANGINA PECTORIS
 Physical exertion
– Which can precipitate an attack by increasing myocardial O2
demand.
 Exposure to cold
– Which can cause vasoconstriction & an elevated BP which
increases O2 demand.
 Eating heavy meal
– Which can increase the blood flow to the mesenteric area for
digestion, thereby reducing the blood supply available to the
heart
 Emotional stress
– Causing release of adrenaline and increase BP which may
accelerate the HR and increase myocardial workload.

31. SIGNS AND SYMPTOMS
 Chest pain
– Duration: 5-15 minutes
– Location: Substernal or retrosternal which
radiates to the neck, jaw, shoulder and inner
aspects of the upper arm usually left arm
– Description of pain: tightness, heaviness,
choking, strangling sensation, crushing
– Related factors: 5 E’s
– Relief: rest; nitroglycerin, O2

32.  pallor
 Diaphoresis
 Dyspnea
 Faintness
 Palpitation
 Dizziness
 Digestive disturbance due to vagal stimulation
- Not all chest pain is angina. There are other conditions
that can be mistaken for angina such as peptic ulcer,
epigastric reflux, musculoskeletal disorders, extreme
emotion, and hyperventilation.

33. TYPES OF ANGINA
 Classic/ Effort/ Exertional/ Stable
– Associated with atherosclerotic disease of
the coronary artery. Occurs when metabolic
needs of myocardium exceed the ability of
the occluded coronary artery to deliver
adequate blood flow.
– Pain is usually precipitated by increase
demand of heart such as exertion, emotional
stress, and exposure to cold.
– Relieved by rest, nitroglycerin.

34.  Variant/ Rest/ Prinzmetal
- Caused by spasm of coronary artery resulting
to “vasospastic angina”
- Occurs during rest or with minimal exercise
- Frequently nocturnal associated with REM
sleep
- Dysrhythmia is often present when pain is
severe
- With reversible ST segment elevation

35.  Unstable/ Pre infarction/ Crescendo/
Intermittent coronary syndrome
- An accelerated form of angina where pain is
characterized by a changing pattern.
- Begins and appear more frequently, last longer
and occur at rest, pain last more than 15
minutes but less than 30 minutes.

36.  Silent ischemia
- Occurs without complain of anginal pain.
Caused by impaired blood flow due to effect of
coronary atherosclerosis or vasospasm.
- Affects 3 population:
– People who are asymptomatic without other
evidence of coronary heart disease.
– People with angina who also have episodes of silent
ischemia
– Even people who had MI and continue to have
episodes of silent ischemia.

37. DIAGNOSIS
1. ECG
2. CRP (C-reactive protein)
Is a marker for inflammation of vascular
endothelium. Increased level of CRP is
associated with increased coronary artery
calcification and risk of an acute
cardiovascular event in healthy individuals.
3. Increased level of homocysteine.

38. MEDICAL MANAGEMENT
 PTCA ( Percutaneous Transluminal Coronary
Angioplasty)
– Mechanical dilatation of coronary vessel wall by compressing
the atheromatous plaque
– It is recommended for client with single vessel coronary
disease
– A specially designed balloon-tipped catheter is inserted under
fluoroscopy and advanced to the site of coronary obstruction.
– Inflation of the balloon and the catheter tip compresses and
splints the atherosclerotic plaque on the intimal layer of the
vessel. Stretching and partial disruption of the medial and
adventitial layers of the arterial wall also occurs which results
to increase vessel diameter.

41.  Intravascular stenting
- Biologic stenting is produced through
coagulation of collagen, elastin, and other
tissues in the vessel wall by laser,
photocoagulation or radiofrequency induced
heat.
- Prosthetic intravascular cylindric stents
maintain good luminal geometry after balloon
deflation and withdrawal.
- Intravenous stenting is done to prevent
restenosis after PTCA.

42. SURGICAL MANAGEMENT
 CORONARY ARTERY BYPASS GRAFT (CABG)
- Reduces angina and improves activity tolerane.
- It is recommended for one or more branches of coronary
arteries exist.
- Main purpose is myocardial revascularization.
- Commonly used grafts are the saphenous vein from the
leg and left internal mammary artery (LIMA) from the
chest.
- With saphenous vein bypass graft, one end of the vein
segment is anastomosed to the ascending aorta and the
other end is attached beyond the site of vessel
obstruction. Thus a vascular conduit is created to shunt
blood around the lesion to the myocardium at risk.

43. NURSING MANAGEMENT IN
CABG
1. Promote comfort
 Relieve pain
 Nitroglycerin is the drug of choice to relieve pain
from ischemic attack
2. Promote tissue perfusion
– Instruct the client to avoid over fatigue
– Stop activity immediately in the presence of chest pain,
dyspnea, light headedness or faintness which indicates low
tissue perfusion

44. 3. Promote activity and rest
 Encourage slower activity or shorter periods of activity
with more rest periods. Avoid over exertion.
 Plan for regular activity programs
 Take nitroglycerin before exercise
 Increase extent of exercise gradually

45. 4. Facilitate learning
 Promote a positive attitude and active participation of
the client and family to encourage compliance.
5. Promote relief of anxiety and feeling of
well being
 Facilitate reduction in the client’s level of anxety
 Advise the client to minimize emotional outbursts,
worry and tension
 Encourage to maintain an optimistic outlook to help
relieve the work of the heart.

46. MEDICAL MANAGEMENT
1. NITROGLYCERIN
 Effects:
 Direct relaxing effect on vascular smooth muscle, resulting
in generalized vasodilation.
 Decrease peripheral resistance, decrease systolic pressure,
produce venous pooling, decrease preload.
 Coronary vasodilation, redistributes myocardial blood flow
more efficiently
 Routes: Sublingual (under the tongue or cheek
[buccal pouch]), spray, topical agent, IV
administration.

47. Nursing Interventions:
 Assume sitting or supine position when taking the drug.
To prevent orthostatic hypotension.
 Take maximum of 3 doses at five minutes interval.
 Gradual change of position to prevent orthostatic
hypotension.
 If taken sublingual, the medication causes burning or
stinging sensation under the tongue.
 Sublingual routes produces onset of action within 1-2
minutes, duration of action is 30 minutes.
 Offer sips of water before giving sublingual nitrates;
dryness of the mouth may inhibit drug absorption.

48.  Instruct patient to avoid drinking alcohol, to avoid
hypotension, weakness and faintness.
 Advise client to always bring 3 tabs in his pocket.
 Store nitroglycerin in cool, dry place, use dark/amber-
colored, air tight container; may be destroyed by heat,
light or moisture.
 Change stock of nitroglycerin every 6 months.
 Observe for side effects: headache, flushed face,
dizziness, faintness, tachycardia; these are common on
the first doses of medication. Do not discontinue the
drug.
 Transderm – nitropatch is applied once a day, usually in
the morning. Rotation of skin sites is necessary, usually
on the chest wall.
 Evaluate effectiveness: relief of pain.

49. 2. BETA-ADRENERGIC BLOCKING
AGENTS (Propanolol, Metoprolol,
Atenolol)
 Effects:
- Reduce myocardial O2 consumption by
blocking the β-adrenergic sympathetic
stimulation to the heart. The result is
decrease HR, hypotension, reduced
myocardial contractility.

50. Nursing Interventions
 Side effects and possible contraindications:
hypotension, bradycardia, advanced AV block,
decompensated heart failure.
 If given IV, ECG, BP & HR are monitored closely
after the administration of the medication.
 Assess PR before administration of the drug;
withhold if bradycardia is present.
 Administer with food to prevent GI upset.

51.  Do not administer propanolol to clients with
asthma. It causes bronchoconstriction.
 Do not stop taking them abruptly, angina may
worsen and MI may develop.
 Do not administer propanolol to clients with DM.
It causes hypoglycemia.
 Give with extreme caution in clients with heart
failure.
 Observe for side effects: nausea and vomiting,
mental depression, mild diarrhea, fatigue and
impotence, worsening of hyperlipidemia.

52. 3. CALCIUM CHANNEL BLOCKERS
(verapamil, Amlodipine, Diltiazem,
Felodipine)
 Effects:
- Inhibit Calcium ion transportation into
myocardial cells to depress inotropic and
chronotropic activity, decrease myocardial
workload.
- Reduces coronary vasospasm
- It has vasodilating effect.

53.  Side effects:
- AV block
- Bradycardia
- Constipation
- Gastric distress

54. NURSING INTERVENTIONS
 Assess HR and BP
 Monitor hepatic and renal function
 Administer 1 hour before or 2 hours after
meals. Food delays absorption and
decrease plasma level of the drug.

55. 4. ANTI-PLATELET &
ANTICOAGULANT (ASA,
Dipyridamole, Ticlopidine,
Clopidogrel)
 Effects:
- ASA- prevents platelet activation and
decrease incidence of MI and death in
patient with CAD.

56.  Side effects:
- GI upset and bleeding:
- Intervention- Use H2 blocker to allow continued
aspirin therapy. Do not give ASA with coumadin,
ASA should be given with food, observe for ASA
toxicity: tinnitus
- Plavix and Ticlid are give to patients who are
allergic to aspirin or given in addition to ASA in
patients at high risk for MI.

57. 5. HEPARIN
 Effects:
- Inactivates thrombin and other clotting
factors, inhibiting conversion of
fibrinogen to fibrin, fibrin clotting
formation is prevented.

58. Nursing Interventions:
 The patient receiving heparin is placed on bleeding
precaution which include:
– Applying pressure to the site of any needle puncture for a longer
time than usual.
– Avoiding intramuscular injection.
– Avoiding tissue injury and bruising from trauma or use of
constrictive devices.
 Assess for signs and symptoms of bleeding
 Keep protamine sulfate always available
 If administered Sc, do not aspirate, do not massage, to
prevent hematoma formation.
 Use for a maximum of 2 weeks.

59. 6. COUMADIN
 Effects:
- Inhibits hepatic synthesis of vitamin K
 Nursing interventions:
- Assess for signs and symptoms of bleeding
- Keep Vitamin K always available
- Monitor PT
- Minimize green leafy vegetables in the diet.
These contain Vit K.

60.  DIET: Low sodium, low
cholesterol, high fiber diet. Avoid
saturated fats. White meat and fish are
low in cholesterol.
 ACTIVITY: No restrictions are placed on
activity, within the patient’s limitations.
 OXYGEN ADMINISTRATION: To
increase the amount of O2 delivered to
the myocardium & to decrease pain.

61. MYOCARDIAL INFARCTION
 MYOCARDIAL INFARCTION
- Other name: Heart attack, coronary occlusion.
- If ischemia is prolonged over 30-45 minutes, this
causes irreversible cellular damage and necrosis
of affected myocardium.
- MYOCARDIAL ISCHEMIA- causes imbalance
between myocardial blood supply and demand.
- MYOCARDIAL INFARCTION- is caused by total
obstruction in blood supply to a portion of the
heart muscle.

62. ETIOLOGY
 Thrombosis
 Ulceration and hemorrhage in
atherosclerotic plaque
 Prolonged vasospasm
 Platelet aggregation

63. OTHER CHANGES ASSOCIATED
WITH MYOCARDIAL INFARCTION
 Injured and ischemic cells revert to anaerobic
metabolism causing lactic acid production and severe
angina.
 Necrotic cells release their intracellular contents like
potassium causing alterations in contractility and
possible left ventricular dysfunction.
 Alterations in conduction of impulse resulting in typical
ECG changes.
 Cell death causes inflammation and release of
intracellular proteins and enzymes causing fever,
leukocytosis, increased ESR and elevated serum
enzymes like CPK and LDH.

64. MANIFESTATIONS:
 General Category of Clinical Manifestations:
1. Chest pain
– Duration- more than 15 minutes
– Location- substernal or over precordium
– Characteristic – crushing, severe and prolonged
– Radiation- spreads widely throughout the chest, with
painful disability of the shoulders and hands.
– Relief- Morphine SO4

65.  Anxiety and Apprehension
- Feeling of doom and restlessness, light
headedness which may indicate increase
sympathetic stimulation or a decrease in
contractility and cerebral oxygenation.
- Patient may also deny that anything is wrong.
 Murmur, (+) heart sounds S3 and S4,
increased jugular vein distention seen if
patient with AMI has HF.

66.  Increased BP due to SNS response to decreased BP
due to reduced contractility and impending cardiogenic
shock producing cold, clammy skin, diaphoresis, pallor,
edema.
 Respiratory s/sx: SOB, dyspnea, tachypnea and
crackles if AMI has congestion.
 GI s/sx: vomiting, gas pain around the heart
(indigestion)
 GUT: Oliguria (urine output less than 30 cc/hour)
indicates renal hypoxia due to inadequate renal
perfusion.
 Fever results from destruction of myocardial tissue and
ensuring inflammatory process.

67. DIAGNOSTIC PROCEDURE:
 Definitive diagnosis of AMI requires at
least 2 of the following:
1. history of characteristic chest pain
discomfort
2. evolutionary changes in ECG
3. Elevated cardiac enzymes (elevated CPK-
MB is the most definitive finding in MI
especially in the presence of elevated
levels of LDH.)

69.  ECG CHANGES:
- Pathologic Q wave- signifies infarction
- Elevated ST- signifies injury
- T wave inversion- signifies ischemia

70. COMPLICATIONS OF ACUTE
MYOCARDIAL INFARCTION
 Dysrhythmia (75-90%)
 Heart failure (60%)
 cardiogenic shock (10%) – occurs when the heart
is unable to contract with adequate force to deliver a
CO sufficient to meet normal metabolic needs. It
causes a shock-like state with inadequate perfusion to
tissues. In cardiogenic shock, this is due to failure of
the heart as a pump.
 Rupture of free wall, septum or papillary muscle
(1-5%)
 Other complication- pericarditis which may
occur 2-4 weeks after infarction

71. MANAGEMENT
 M- MORPHINE
 O- OXYGEN
 N- NITROGLYCERIN
 A- ASPIRIN

72. GOAL OF MEDICAL
MANAGEMENT
 Minimize myocardial damage
 Preserve myocardial function
 Prevent complication
 pain relief.

73. PHARMACOLOGIC
MANAGEMENT
 THROMBOLYTIC THERAPY
– Used to dissolve blood and platelet clots allowing
blood to flow through coronary artery again.
– STREPTOKINASE, UROKINASE, & TISSUE
PLASMINOGEN ACTIVATOR (TPA) are examples.
– Administration is most crucial between 3-12 hours
after initial infarction has occurred (when tissue can
still be salvaged and infarction can be prevented)
– Detect for occult bleeding during and after
thrombolytic therapy.
– Assess neurologic status changes which may
indicate GI bleeding or cardiac tamponade.

74.  NARCOTIC ANALGESIC
 MORPHINE SULFATE & MEPERIDINE HCL
(DEMEROL)
- To promote coronary blood supply
- Morphine SO4 is most ideal because it not only
addresses pain but also relieves anxiety and
induces sleep, reducing myocardial workload.
- Demerol is indicated because it does not cause
respiratory depression
- NALOXENE HCL 0.1-0.2 mg is the antidote of
morphine.

75.  ANGIOTENSIN CONVERTING ENZYME
INHIBITORS
- Prevents conversion of angiotensin 1 to
angiotensin II, reduces BP, and kidney
excretes Na and fluid causing reduced O2
demand of the heart
 IV LIDOCAINE
- Maybe given within 24 hours to prevent
dysrhthmia.
 OTHER MEDS SAME AS IN ANGINA

76. SURGICAL MANAGEMENT:
 PTCA
– Must be done within few hours of onset of
MI.
 CABG
- To improve directly circulation to myocardium
& therefore limit infarct size
- To be successful, CABG should be done 4-5
hours after the onset of AMI.
- Not beneficial because most patient develop
AMI outside of hospital.

77. OTHER MANAGEMENT
 OXYGEN THERAPY:
- At 3-5 lpm via nasal cannula for 24-48 hours to correct
mild hypoxemia and relieve pain.
 BED REST:
- To reduce O2 demand of the heart
 DIET:
- Liquid diet for the 1st 24 hours, progressing to soft diet
to avoid constipation, avoid large meals and avoid
caffeine contained in coffee, tea, &cola.
- Low cholesterol, low salt diet.

78. HEART FAILURE
 HEART FAILURE - the heart as a pump is
unable to deliver blood to meet the metabolic
requirements of the tissues.
 The effectiveness of the heart is determined by
the cardiac output, which is the amount of
blood ejected by the heart in a minute. Cardiac
determinants include preload, afterload,
myocardial contractility, heart rate.
 An indicator for the failure of the heart as a
pump is an alteration or decrease in cardiac
output.

79. CAUSES OF HEART FAILURE
 Problems in the heart itself
 Non-cardiac disorders that place undue
demands on the heart

80. DIAGNOSIS OF HEART
FAILURE
 This will depend on the presence of two
conditions:
- History of an underlying condition that can lead
to heart failure
- Signs and symptoms of heart failure based on
history, physical assessment and routine
laboratory tests.
 Diagnosis of heart failure rarely requires use of
non-invasive or invasive tests. The nurse
therefore plays an important role in recognizing
signs and symptoms that may indicate heart
failure.

81. SIGNS AND SYMPTOMS
 Signs of compensatory mechanisms
– Tachycardia
– Elevation of blood pressure
– Edema
– Cardiac dilatation and hypertrophy based on PE (displaced
apical pulse), EKG, chest X-ray and echocardiographic studies.
 Shortness of breath, dyspnea, orthopnea, and fatigue
resulting from pulmonary congestion, and increased cardiac
workload.
 Physical examination may also reveal ventricular gallop or
S3, which generally accompanies left ventricular failure.
 Fluid retention and edema
 Elevated central venous pressure based on examination of
the neck for elevated jugular venous pressure, or more
accurately obtained by using a catheter inserted.

82. MANAGEMENT OF HEART
FAILURE
 Improve ventricular pump performance
- Increasing stroke volume and CO
 Reduce myocardial workload by:
- Decreasing preload
- Decreasing afterload
- Regulating HR and correcting arrhythmias
- Correcting other factors such as infection
 Increase myocardial perfusion and oxygenation

83. PHARMACOLOGIC TREATMENT
OF HEART FAILURE
 DIGITALIS
– A cardiac glycoside, is the mainstay of
treatment of heart failure.
– The most common we use locally is digoxin
(Lanoxin)
– Digitalis increases force and velocity of
ventricular contraction (positive inotropic
effect)

84.  CAUTION!
 DIGITALIS may be dangerous. There is very narrow
difference between the therapeutic dose and the toxic dose.
In other words, digitalis toxicity can easily develop. Watch
out for DIGITALIS TOXICITY!
 Identify at risk patients. (elderly pts, those with advanced
heart disease, severe arrhythmias, or acute MI.)
 Monitor for signs and symptoms of digitalis toxicity- take a
full minute heart rate to determine abnormal slowing of the
heart (possible heart block), GI symptoms etc.
 Teach patients and caregivers to recognize digitalis toxicity.

85.  DIURETICS
- Enhance renal excretion of sodium and water, which
reduces circulating blood volume, diminishes
preload, and lessens systemic and pulmonary
congestion.
 Nursing Implications:
- Monitor urine output to evaluate effectiveness of
treatment and to monitor for possible hypovolemia.
- Diuretics should be given in the morning to prevent
disturbing sleep at night.
- Monitor serum electrolytes, particularly potassium level
especially in patients taking digitalis.
- Educate patient and caregivers.

86.  VASODILATORS
- Direct dilation of veins
- Dilation of arterioles
- Combined action on veins and arterioles
- Inhibition of angiotensin converting
enzyme

87.  ANGIOTENSIN CONVERTING ENZYME
(ACE) Inhibitors
- Suppress RAA system thereby blocking
production of the potent vasoconstrictor
angiotensin II.
- This results in increase renal blood flow,
and decrease renal vascular resistance,
which enhances diuresis.

88.  MORPHINE
- The most useful drug for the treatment of pulmonary
edema.
- Primary effect is peripheral vasodilation causing
pooling of blood thereby reducing both venous return
and cardiac workload.
- Allays anxiety associated with severe dyspnea.
- It reduces afterload by decreasing arterial blood
pressure and resistance.
 BETA-ADRENERGIC BLOCKERS
- Recent studies shown that administration of this
medication may result in improved symptomatic and
functional status by slowing the heart rate.

89. OTHER MEDICAL AND
NURSING INTERVENTIONS
 POSITIONING
- High fowler’s position to reduce pulmonary congestion and ease
dyspnea.
- Legs are maintained in dependent position because if legs are
raised, this will increase venous return and further aggaravate
pulmonary congestion.
 BED REST
- The overall pumping demand of the heart is decreased and slows
down heart rate.
 FLUID AND SODIUM RESTRICTION
- To prevent, control or eliminate edema.
 OXYGEN ADMINISTRATION
- May be ordered if the patient is hypoxemic and dyspneic.
Hypoxemia in HF is the result of pulmonary congestion, specifically
VQ mismatch.

90. References
– Edition: Cardiovascular Care Made Incredibly easy
 Second
– Style:
 Softbound
 ISBN 10:
– 0-7817-8824-2
– ISBN 13:
 978-0-7817-8824-3
– Publication Date:
 May, 2008
N261 Cardiovascular Nursing Module
– University of the Philippines Open University