CARDIOVASCULAR NURSING

DR. ELENITA C. MANRIQUE – ARREGLO

CARDIOVASCULAR SYSTEM
TISSUE PERFUSION
Shock: inadequate tissue perfusion

Blood 5-6L= ↓BV →↓tissue perfusion = hypovolemic shock

Heart Pumping = ↓ pumping ability → ↓ tissue perfusion = cardiogenic shock
Causes: 1. Coronary causes: CAD, MI
2. Non-Coronary causes: RHD, Obstructive shock
Blood vessels Distribute blood
→ Arteries: oxygenated blood (except pulmonary artery)
→ Vein: unoxygenated (except pulmonary vein)
→ Smooth muscles: vascular tone
→ Smooth muscle: contract; Blood vessels: constrict

(x) Vascular tone → vasodilate (BV) → ↓BP = distributive/circulatory shock

Causes: 1. Infection → inflammation → vasodilation = septic shock
2. Allergy → inflammation →vasodilation = anaphylactic shock
3. Spinal cord injury → inflammation → vasodilation = neurogenic shock

Components of Blood vessels

a. Arteries distributing vessels; resistance vessels= ↑pressure (thick smooth muscle)
b. Veins distributing vessels; capacitance vessels= (thin walls): wider lumen
c. Capillaries exchange vessels; very thin wall; only 1 layer; no smooth muscle

NOTE: Arterio-venous (AV) Malformation (absence of capillaries)

→ Usually seen in cerebral vessel

a. Arteries
Parts: Tunica intima - inner
Tunica media - mid
Tunica externa - outer

NOTE: Largest → Artery → Aorta

→ Vein → Inferior vena cava

Pulses
→ Grading
0 absent
+1 weak
+2 normal
+3 ↑
+4 Bounding, maybe abnormal
VASCULAR DISORDERS

SUMMARY
1. Aneurysm
2. Peripheral Vascular Disease: small and medium sized arteries and veins
a. Peripheral Arterial Disease (PAD)
→ Arteriosclerosis obliterans (ASO)
→ Raynaud’s disease
b. Venous disease
→ Varicose veins
→ DVT = VTE = venous thromboembolism
3. Buerger’s disease: thromboangitis obliterans (TAO) – inflammation and thrombus
formation in small and medium sized arteries and veins

NOTE: Most definitive diagnostic (Vascular diseases): Angiography

→ If allergic to dye: Antihistamine: night before (oral); morning (parenteral)
→ Local anesthesia

1. ANEURYSM → abnormal dilation and sac formation in the wall of an artery

a. Congenital: cerebral circulation (Hemorrhagic stroke)
b. Acquired: aorta (common); etio: atherosclerosis
Risk factor = Age

Aortic Aneurysm
Etiology: Atherosclerosis
→ Atheromatous plaque = deposition of fats, etc.
→ Sclerosis = hardening
Risk factor: 1. Age
2. Family history
3. Lifestyle – sedentary
4. Smoking
5. Stress
6. Alcohol
7. DM
8. HPN (Most risk factor for rupture: uncontrolled HPN)
→ Blood pressure: pressure exerted by the blood against
the walls of the blood vessels

a. Ascending → Ascending aortic aneurysm

b. Descending → Thoracic aortic aneurysm; or
→ Abdominal aortic aneurysm

S/Sx Asymptomatic
Except: AAA = pulsating mass in the abdomen (thin & elderly)

** Rupture → Bleed → Shock (Hypovolemic shock)

 Dissecting aortic aneurysm
→ tearing of the wall = impending sign of rupture
BEQ Difference of type A and B? Saccular Aneurysm
Type A = ascending aorta Fusiform Aneurysm
Type 1: Ascending and Descending Ruptured Aneurysm
Type 2: Ascending only
Type B = descending aorta

S/Sx Ascending dissecting aortic aneurysm = chest pain (severe)

Dissecting thoracic aortic aneurysm = severe epigastric pain
Dissecting abdominal aortic aneurysm = severe low back pain

Dx Angiography – most definitive but invasive, done by cardiac

catheterization under local anesthesia
Ultrasound: Doppler/duplex ultrasound (PVD)

Mgt 1. Type A dissecting aortic aneurysm = surgery ward

→ priority is surgery : Risk of rupture is higher
2. Type B dissecting aortic aneurysm = medical ward
→ control BP first then surgery
3. Anti-HPN drugs as ordered
4. Manage Risk Factors

VASCULAR INSUFFICIENCY
→ PVD = small and medium sized arteries and veins (upper and lower extremities)
LE > UE
ARTERIAL INSUFFICIENCY VENOUS INSUFICIENCY
(Oxygenated; Blood flow downward) (Deoxygenated; blood flow upward)

Leg pain (ischemia) + CLAUDICATION Leg pain (venous congestion = ↑ pressure

inside the vein → injury in the vein =
PHLEBITIS

Skin – pale, thinning of hair, cool to touch Skin - dark, cyanotic, pigmented

Pulses – may be abnormal (artery) Pulses – normal but difficult to palpate

→ No edema → due to/with edema

Arterial ulcer: small but deep with well Venous ulcer: larger lesions with irregular
circumscribed edge, no or little granulation borders, several granulation tissues
tissues surrounded by dark skin

ARTERIAL INSUFFICIENCY VENOUS INSUFFICIENCY

Position the legs = dependent Position the legs = elevated
→ Reverse trendelenburg
2. VASCULAR DISEASES
Diagnostic tests Angiography
Ultrasound (vascular scan)

a. Peripheral Arterial Disease (PAD)

i. Arteriosclerosis obliterans (ASO) → hardening of wall of arterioles (lower ext.)

Etiology idiopathic
Risk factors Age (60 and above), smoking, alcohol, ↑ fat, ↑cholesterol,
sedentary
Gender men (than women)
Extremities lower extremities
S/SX leg pain + claudication, pale, cool to touch, thinning of
hair
Nursing diagnoses Acute/chronic pain, ineffective peripheral tissue perfusion,
risk for impaired skin integrity, impaired skin integrity, risk
for infection, and risk for shock (septic)
Management 1. Position the bed: dependent
2. Avoid Trauma
3. Skin care
4. Avoid smoking, stress, alcohol
5. Diet: ↓fat, ↓cholesterol
6. Exercise
7. Weight reduction
8. Pain reliever – NSAIDS
9. Vasodilators are rarely given
→ long acting CCB (Diltiazem)
10. Amputation (for gangrene)
11. Prevent shock

ii. Raynaud’s disease → vasospasm of arterioles (s/m sized arteries) (upper ext.)
(aka blue-white-red disease)
Etiology Idiopathic
Risk factors Exposure to cold temperature, smoking, stress, HPN, DM
Gender women (than men); young adult
Extremities upper extremities > lower extremities
S/SX Pain, numbness, tingling sensation, abnormal pulses
Nursing diagnoses Acute/chronic pain, ineffective peripheral tissue perfusion,
risk for impaired skin integrity, impaired skin integrity, risk
for infection, and risk for shock (septic)
Management 1. Avoid exposure to cold temperature
2. Always wear gloves and boots
3. Keep the temp of the environment warm
4. Avoid smoking, stress, trauma
5. Control BP, DM
6. Pain reliever – NSAIDs
7. Vasodilators are given as ordered
→ Diltiazem (monitor before and after BP)
NOTE: Raynaud’s phenomenon → has known cause
Etiology: 1. Rheumatoid arthritis
2. SLE
3. Scleroderma = CREST syndrome
C-alcinosis → deposition of calcium in soft tissues
R-eynaud’s phenomenon
E-sophageal dysmotility
S-yndactyly → fusion of fingers
T-elangiectasia → abnormal vein formation (skin)

b. Venous insufficiency → more common lower extremities

i. Varicose veins - superficial veins
ii. Deep vein thrombosis – Venous thromboembolism VTE
→ Thrombophlebitis
→ Phlebothrombosis

i. Varicose veins
Etiology incompetent valves
→ Stasis= stagnation of blood
→ Abnormal dilation and torteous formation of the
superficial veins of the lower extremities
Risk factors Prolong standing/sitting, pregnancy, crossing of legs
S/Sx pain, dark, pigmented, cyanotic, (+) edema, pulses are
normal but difficult to palpate
Nursing diagnosis Acute/chronic pain, ineffective venous circulation, risk for
impaired skin integrity, risk for shock (septic)
Interventions 1. Prevention
→ avoid prolonged standing, crossing of legs,
obesity, wear compression stocking
→ Medical Mgt: sclerotherapy
→ Surgery: vein stripping and ligation

ii. DVT
Etiology Idiopathic
Risk factors Immobilization (bedridden, postop, stroke), oral
contraceptive (↑ viscosity of blood), DM, HPN
Virchow’s triad = thrombus
1. Stasis= stagnation of blood
2. Hypercoagulable
3. + endothelial injury
S/SX Phlebothrombosis= asymptomatic; some may manifest
sudden onset of leg pain
Homan’s sign- dorsiflex foot and pain is felt in calf muscle
(not reliable)
(+) Homan sign = DO NOT REPEAT THE TEST
→ Pulmonary embolism (dyspnea, tachypnea, chest pain)
Mgt: elevate HOB (semi-fowler), o2 then refer
 Thrombophlebitis= redness, warm, pain, swelling
Interventions: 1. Prevention
→ mobilize the leg/ ROM, TED hose
(Thromboembolic deferent) hose
2. CBR – immobilize
3. Heparin IV – to prevent further thrombus formation
4. Pain relievers – NSAIDs
5. Surgical mgt: endovascular surgery
6. Thrombolytic drug – dissolve the thrombus
→ Urokinase, Strptokinase, Altaplase
7. TED hose – 6 mos. As ordered
8. Anticoagulant – oral warfarin = to prevent thrombus
formation

3. BUERGER’S DISEASE (lower extremities)

Aka THROMBOANGITIS OBLITERANS
→ inflammation & thrombus formation in the small and medium sized arteries and veins
→ Only in smokers
→ Causes poor circulation in feet and hands
→ May lead to tissue death and amputation
→ gets worse the more you smoke

Etiology Idiopathic
Risk factors Smoking, men, young adult, stress
S/SX Leg pain and claudication, dark skin, cyanotic, pigmented, edema,
vascular ulcers
Interventions 1. Avoid smoking – ALL tobacco products
2. Avoid trauma, stress
3. Pain reliever – NSAIDs
4. Vasodilators are rarely given
5. Avoid complications
6. Amputation as needed

HEART → ―heart circulation‖

→Muscular tissue
1. Contractility
2. Conductivity
3. Rhythmicity
4. Automaticity
5. Excitability

AV valves close →S1= lub

SL valves close →S2= dub
S3 → rapid ventricular filling (CHF: lub dub dub = ventricular gallop)
S4 → atrial systole (enlargement of the atria; atrial gallop = lub lub dub)

**Valvular defects = +murmurs

VALVES
Assessment (SL) Aortic valve 2nd ICS right parasternal
(SL) Pulmonic valve 2nd ICS left parasternal
(AV) Tricuspid valve 4th ICS left parasternal area
(AV) Mitral valve 5th ICS (between 5th & 6th) ICS; left mid clavicular line
→ Apical pulse – point of maximum impulse (PMI)

(+) murmurs → ↑ turbulence in the flow of blood through the heart

VALVULAR DISEASES
1. Valvular insufficiency inability of the valve to close completely (valvular
regurgitation)
2. Valvular stenosis inability of the valves to open completely (narrowing)
→ ↑ turbulence
Etiology 1. Congenital
2. Acquired
Rheumatic fever → RHD
Endocarditis
Kawasaki’s disease

Cardiomegaly = pathologic/ physiologic response

3. Mitral valve prolapse bulging or ballooning of the mitral valve onto the left
atrium
→ Systolic click/mitral click (heard at apex)
Etiology Idiopathic
Risk factor Congenital, female, young adult, family history
S/Sx chest pain, palpitation, easy fatigability, tacjycadia,
syncnope (fainting)
Diagnostics 2d echo
Complications 1. Mitral regurgitation
2. Dysrhythmias
**cargiogenic shock (non-coronary)
Interventions 1. Beta blockers (olol)
2. Support cardiac function
3. Avoid caffeine, infection
4. Provide rest

DIAGNOSTIC TESTS 2D echo

INTERVENTIONS: 1. Valvular repair = valvuloplasty
2. Valvular replacement
3. Support cardiac function
4. Provide rest
5. Avoid stress
6. Avoid infection
 Valve stenosis
→ Narrow valve
Valve Dilation
→ Catheter
→ Balloon
Valvuloplasty
Valvular replacement

LAYERS OF THE HEART

1. PERICARDITIS → inflammation of pericardial sac → chest pain

ETIOLOGY 1. Infection
2. Trauma
3. SLE
4. MI – induced
5. Malignancy
6. Idiopathic
RISK FACTORS 1. Infection
2. Trauma
3. SLE
4. MI – induced
5. Malignancy
6. Idiopathic
S/SX chest pain – pain that worsens with deep inspiration lying down
or turning and relieved by sitting or leaning forward (orthopneic
position)
Prominent sign – friction rub (auscultate @ 4th ICS left
parasternal area = hear a scratching, leathery, creaky sound
heard best at the end of expiration and when patient is sitting or
leaning forward
NSG. DIAGNOSIS Acute pain related to inflammation of the pericardial sac
→ priority intervention = position
 Dx 1. 2D echo
2. Chest xray
3. Elevated ESR (Erythrocyte Sedimentation Rate) = systemic
inflammation
4. Elevated WBC – leukocytes
5. Infection – culture and sensitivity
6. SLE- anti nuclear antibody test (ANA)
7. Malignancy – Biopsy
8. MI – coronary angiography

MANAGEMENT 1. Pain relief

a. position
b. pain relief – NSAIDs
2. Anti-inflammatory drugs – steroids
3. Manage the cause
a. Infection – anti-infective drugs
b. SLE
c. MI
d. Malignancy
4. Prevent and manage complications
a. Pericardial effusion – accumulation of fluid in the
pericardial sac (constrictive pericarditis)
b. Cardiac tamponade – life threatening complication →
obstructive shock

COMPLICATIONS OF PERICARDITIS
A. Pericardial effusion accumulation of fluid in the pericardial sac (constrictive
pericarditis)
→ Aspirate fluid from the pericardial sac
= pericardiocentesis
→ Position during the procedure= semi fowlers
→ x-ray guided, ultrasound guided, ECG guided
(connected to needle during procedure)

B. Cardiac tamponade life threatening complication → obstructive shock

Beck triad – triad of cardiac tamponade
1. Dec BP
2. Inc venous pressure (distended neck veins)
jugular vein distention
3. Muffled heart sounds – distant heart sounds

NOTE: MI pain = constant not affected by breathing or movement of the chest

2. ENDOCARDITIS – inflammation of the endocardium

ETIOLOGY bacteria: infective endocarditis
GABHS, staph, pneumococci → enters blood → multiplication of
bacteria in the blood → enters heart → lungs → back to heart →
bacteria stays
C. Manifestation Systemic inflammation → fever intermittent, leukocytosis,
fatigue, weakness, malaise, elevated ESR

→ microthrombi = vegetation
Left ventricle dislodge - thrombus —> embolus —> Brain
(embolic stroke)
Right ventricle dislodge thrombus —> embolus —> lungs
(pulmonary embolism)

Risk factor 1. Already has an existing cardiac disease

2. immunocompromised
3. invasive procedure or surgery S/Sx Pericarditis FROMJANE
Fever
*** Septic shock or cardiogenic shock Roths spot
Oslers nodes
S/Sx due to embolization/inflammation Murmur
Roth’s spot (Retina) Janeway lesions
Hemorrhanges with pale centers Anemia
Osler’s nodes – painful nodules in finger pads and toes Nail changes
Janeway lesion – painless macules on palms and soles Ecchymosis/ embolization
Splinter hemorrhages – brownish streaks and toenails
→ anemia
→ worsening of valvular defects = changes in murmurs

Diagnostics Test 1. Culture and sensitivity

2. CBC – Inc WBC, dec RBC
3. Erythrocyte sedimentation rate = elevated
4. 2D echo
5. CXR

MANAGEMENT Nursing management

1. Manage fever
2. Assess for change in murmurs – every shift
3. Monitor vital signs
4. Support cardiac function
a. provided rest periods
b. avoid stress
c. avoid infection
5. assess for possible complications: shock (septic, cardiogenic)

Medical management
1. prevention = prophylaxis
→ Antibiotic prior to any invasive procedure or surgery
(penicillin/erythromycin)
a. Valvular heart disases – except MVP unless it
already has mitral regurgitation
b. congenital heart disease
c. Rheumatic heart disease
 2. Antipyretic
3. Antibiotic
4. Drugs to support cardiac function
5. prevent and manage complications
a. heart failure
b. shock

3. CARDIOMYOPATHY → disease of the cardiac muscle

Etiology idiopathic
Types of CDM 1. Dilated CDM – most common type
Risk factor: viral infection, alcohol, pregnancy
→ significant dilation of cardiac muscles without
hypertrophy
→ diffused necrosis of myocardium
2. Hypertrophic CDM – significant thickness of the myocardium
especially the interventricular septum
Risk factor: Family history
3. Restrictive CDM – ventricles become rigid = dec BP
Risk factor: Family hx
4. Arrhythmogenic right ventricular CDM – scarring of the
right ventricle → right sided heart failure
Risk factor: Family hx

Diagnostics 2D echo
Contraindicated contact sports, strenuous activities
Management Heart Transplant
→ No known cure except heart transplant

BLOOD PRESSURE
→ Classification of blood pressure for adults 18 years old and above
1. Hypertension
Etiology Primary- idiopathic – essential HPN/familial HPN
(HPN is a disease)
Secondary- known causes
= DM, renal disease, pheochromocytoma = tumor of adrenal
medulla
→ ↑ release of chatecholamines – epi, nepi
HPN is a sign of the disease

Risk factor modifiable

C. manifestations Asymptomatic
 Headache
 Dizziness
 Blurred vision
 Epistaxis

Nursing diagnosis 1. Knowledge deficit

2. Non compliance
3. Ineffective health maintenance
→ risk diagnosis
4. Acute pain related to head ache
5. risk for fall
6. Impaired vision
7. Disturbed sensory perception, visual

Independent interventions (Cardiac diseases)

1. Diet – low salt, low fat, low cholesterol (must be good cholesterol,
unsaturated fat), low sugar
2. Exercise – inc use of glucose by the cell: improves circulation, dec fats,
cholesterol, reduce weight
3. Avoid stress – most active gland = adrenal glands = cortex – cortisol/medulla
= catecholamines = epi/norepi
4. Avoid smoking = vasoconstriction
5. Avoid alcohol inc HR = inc cardiac workload
6. Restrict caffeine inc HR/palpitation
7. Relaxation techniques = decrease cardiac workload
→ Deep breathing exercises
→ Guided imagery

Dependent intervention
1. Drug therapy – Antihypertensive drugs

Antihypertensive drugs
Secondary cause
 Increase SNS = ↑ BP
 Block SNS = ↓ BP to normal
 To decrease SNS
1. Alpha 1 antagonists (vasodilators)
Prazosin
Doxazosin
Terazosin

2. Alpha 2 agonists (CNS- dec NE flow → dec SNS)

Clonidine (Catapress)
Methyldopa

3. Beta blockers B1-heart – dec HR , B2-lungs – bronchoconstrinct

Propranolol non selective
Metoprolol cardioselective

R–A–A–S
RENIN (kidney) → ANGIOTENSIONOGEN + (renin) = ANGIOTENSIN I + ACE (lungs) = coverts
to ANGIOTENSIN II →
1. RECEPTORS (Blood vessels) → VASOCONSTRICTION
2. ALDOSTERONE (Adrenal gland) → ↑Na retention →↑H20 retention → HYPERVOLEMIA

4. ACE INHIBITORS
Captopril, Quinapril, Enalapril

5. ANGIOTENSIN II RECEPTOR BLOCKERS

Losartan, Candesartan, Telmisartan

6. DIURETICS
Thiazide diuretics – Hydrochlorthiazide

7. VASODILATORS
DIRECT ACTING VASODILATORS – directly relax the smooth muscles of
the blood vessels
Hydralazine
Nitrates
INDIRECT ACTING VASODILATORS – dec the release of Ca in the smooth
muscle of the BV
Calcium channel blockers
Nifedipine
Amlodipine
Felodipine
Diltiazem
Verapamil

CORONARY ARTERY DISEASE Acute coronary syndrome/Ischemic Heart Disease

→ Coronary arteries – blood supply of the heart
1. Left coronary artery – arterior and lateral wall of the heart
a. left anterior descending branch – most common affected
b. circumflex branch
 2. Right coronart artery – inferior and posterior wall of the heart
a. posterior interventricular br
b. marginal branch

** the heart receives oxygenated blood during diastole

160/90
140/110 = ↑ diastolic pressure compromises blood flow to the heart muscles

→ Venous drainage
1. great cardiac vein
2. middle cardiac vein

Etiology idiopathic
Risk factor atherosclerosis

Risk factor: 1. Age = elderly (atypical-uncommon): confusion, shortness of

breath, epigastric pain
2. Past health history
3. Family history – gene for MI = ASgene = increase risk 3x

NOTE: Chest pain due to ischemia = angina

1. Angina pectoris - Imbalance between oxygen supply ↓ and cardiac workload↑

→ Reversible
→ Timing – less than 15 min
→ Relieving factors : Rest
→ Nitroglycerine

Types of angina 1. Stable angina = predictable angina;

→ inc cardiac workload → rest
2. Unstable angina – preinfarction angina – severe atherosclerosis
3. Prinzmetal angina – coronary vasospasm
4. Intractable angina – severe chest pain
(+) Levine sign
5. Silent ischemia

2. Myocardial infarction - Ischemia and necrosis of cardiac cells

→ Irreversible
→ Timing – more than 30 min
→ No relieving factors

ASSESSMENT PQRST assessment

Position/location-chest/substernal pain
Quality- constant, heaviness, crushing pain, stabbing pain
Radiation – left arm, shoulder, neck
Relieving factor
AP = rest/ nitroglycerine
MI = none
 S-everity = pain scale
T-iming
AP <15 mon
MI >30 min

Angina pectoris
Nursing diagnosis Ineffective myocardial tissue perfusion - priority
Acute pain
Anxiety – restlessness = inc the need for more demand
Ineffective health maintenance
Noncompliance – knowledge deficit

Priority intervention (depends on types of angina)

Stable angina – independent = rest (semi-fowlers)
Unstable angina – severe atherosclerosis dependent
Prinzmetal angina (variant) – coronary vasospasm
dependent
***Dependent > NTG first then o2 admin

Diagnostic tests 1. Angiography

2. Blood test (suggestive only)
→ Elevated homocysteine level
→ Elevated c reactive protein
3. ECG = during the pain
→ < 15 mins
→ T wave inversion – myocardial ischemia

Management 1. Rest
2. O2 administration
3. Manage risks factors
4. Drug therapy
a. Nitroglycerine
Acute attack = SL = fast onset of action
Chronic angina = NTG patch – 24 hours
→ coronary vasodilator – inc o2 supply
→ peripheral vasodilator – ↓ BP – ↓ cardiac
workload
b. Isosorbide Nitrate – slow onset of action
c. Beta blockers = metropolol – ↓ HR – ↓ cardiac
workload
d. CCB = peripheral vasodilation – ↓ BP – ↓ cardiac
workload ex diltiazem, verapamil
5. Surgery = percutaneous transluminal coronary
angioplasty

Medical management: 1. Nitroglycerine

2. Isosorbide nirate
3. Beta blockers
 4. Calcium channel blockers
5. Ranolazine

Myocardial infarction
Nursing diagnosis Acute pain – pain control is priority; pain – restless →
↑ O2 demand → necrosis
Dependent - morphine
Ineffective myocardial tissue perfusion
Anxiety
Risk for dysrhythmias PVCs= premature ventricular
complex = 6 or more/min
→may lead to vtach
Risk for cardiogenic shock
Risk for decrease cardiac output

Diagnostic tests Angiography ST elevation – early sign of acute MI

2 types of MI 1. STEMI – ST elevation MI

2. NSTEMI – Non ST elevation MI
Atypical symptoms
Confirmatory test – definitive teast
→ Cardiac enzyme elevation
(Cardiac Serum markers)
1. CKMB – most indicative, most specific enzyme
2. Troponin – most reliable, most sensitive, most
important
→ persistent to be elevated for 3 weeks
3. CPK
4. LDH
5. Myoglobin
 Management Pain control is priority
→ MORPHINE AS ORDERED
Oxygenation
Thrombolytic drugs
Urokinase
Streptokinase
Alteplase
Anti – thromobotic drugs
Anti platelet
Anti coagulant

HEART FAILURE
Heart failure – inability of the heart to pump effectively
→ Cardiac decompensation
Causes a. Cardiac causes
b. Non cardiac causes = COPD
Types 1. Left sided heart failure → left ventricle falls
2. Right sided heart failure → right ventricles

a. Left sided heart failure → Pulmonary edema

Pulmonary edema
PND- paroxysmal
Nocturnal dyspnea
Orthopnea
Dyspnea
Progressive cough
(+) crackles (rales)

b. Right sided heart failure → Systemic edema

Bipedal edema
Ascites
Hepatomegaly
Splenomegaly
Weight gain
Fluid volume excess
CHF = ventricular gallop (lub dub dub)

NYHA classification of heart failure

Class 1: No limitation of physical activity
Ordinary physical activity does not cuse undue breathlessness, fatigue,
palpitations
Risk for activity intolerance

Class 2: Slight limitation of physical activity

Confortable at restm but ordinary physical activity results in due breathlessness,
fatigue, palpitations
Activity intolerance
Class 3: Marked limitation of physical activity
Comfortable at rest, bit less than ordinary physical activity results in undue
breathlessness, fatigue, or palpitations
↓ Cardiac output

Class 4: Unable to carry on any physical activity without discomfort. Symptoms at rest
can be present. If any physical activity is undertaken. Discomfort is increased.
Depend on sign and symptom

Nursing diagnoses Ineffective airway clearance

Ineffective breathing pattern
Impaired gas exchange
Fluid volume excess
Decreased cardiac output

Diagnostic Test 1. 2D echo

2. CXR
3. BNP = brain/beta type natriuretic peptide = protein
released by the ventricles in response to congestion
→ >400 pcg/ml (heart failure)
→ Too high (HF)

Interventions Priority - airway and breathing problems

Mgt: airway, breathing
1. Postion- high fowlers position
2. O2 administration
3. IV line
4. Furosemide 40mg IV stat
5. Catheterize
6. Monitor I and O
7. Monitor vs

FVE (Fluid volume excess)

1. Restrict fluid
2. Restrict sodium
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Diuretics
a. Furosemide - hypokalemia
b. Spironactone – hyperkalemia
7. Monitor serum k level

for decreased cardiac output

Goals
To decrease cardiac workload
To improve cardiac contractility
 To decrease cardiac workload
1. Provide rest
2. Avoid stress
3. Avoid infection
4. Drugs to support cardiac function
a. ACE inhibitors ex Captopril – peripheral
vasodilation → dec bp → dec cardiac workload
b. AIIR blockers ex losartan – peripheral
vasodilation
c. Beta blockers – selective – dec HR→ dec cardiac
workload
d, CCB – peripheral vasodialto → dec cardiac
workload = diltiazem, verapamil

To increase cardiac contractility

CARDIOTONIC DRUGS – inc cardiac contractility = (+)
inotropic effect
Sympathomimetic drugs
Cardiac glycosides

SYMPATHOMIMETIC DRUGS
Dobutamine
Dopamine

CARDIAC GLYCOSIDES
Digoxin
Digitalis

DIGOXIN
Increase contractility
– increasing calcium release
Decrease heart rate - slow repolarization