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Cardio (DAY 1)
doc arreglo
• Cardiovascular – responsible for 1ssue perfusion
o Blood: carries oxygen
§ 5 to 6 liters of blood
§ If the blood volume has decrease, 1ssue perfusion also decreases
§ Shock it is the inadequate 1ssue perfusion
• Can lead to mul1ple organ dysfunc1on
• Decreased blood volume – HYPOVOLEMIC SHOCK
o Heart: pumps the blood
§ decrease pumping of the heart = decreased 1ssue perfusion
§ shock involving the heart – CARDIOGENIC SHOCK
• causes of cardiogenic shock
o Coronary causes: MI and CAD
o Non-coronary causes: all cardiac diseases except for
myocardial infarcLon (MI)
o ObstrucLve shock – the heart is compressed. Ex:
pneumothorax
o Blood vessels: distribute blood.
§ Artery: carries oxygenated blood except for pulmonary artery
§ Veins: carries unoxygenated blood except for pulmonary veins
§ Capillaries: for gas exchange
§ Vascular tone: the lining of the blood vessels is made up of smooth muscles
(constricts and dilates) à blood is pushed to different parts of the body
• loss of vascular tone à blood vessels vasodilate (massive
vasodila1on) à blood is note distributed properly à BP goes down
à DISTRIBUTIVE SHOCK or CIRCULATORY SHOCK
o causes of distribuLve shock
§ infec1on à inflamma1on à vasodila1on. à SEPTIC
SHOCK
§ allergy à inflamma1on à vasodila1on à
ANAPHYLACTIC SHOCK
§ spinal cord injury à inflamma1on occurs and loss
of SNS à severe dila1on à NEUROGENIC SHOCK
(peculiar type of shock = no SNS compensa1on thus
bradycardia occurs.
o PaLent in a shock: Priority
§ Refer to physician
§ Give oxygen
§ PosiLon the paLent à modified Trendelenburg.
• Trendelenburg – is contraindicated because the diaphragm is
compressed à the respira1on is compromised this is not prac1ce
in the hospital already for the adverse effects it can cause.
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• Modified Trendelenburg – the diaphragm is no longer compressed

o In obstruc1ve shock, posi1oning the client can make the
circula1on beLer
o Blood vessels
§ Arteries
• Aka resistance vessels because it has a very high blood pressure à
d/t thick smooth muscle in the artery
• Assess bleeding coming from artery: spur1ng.
• Largest artery: Aorta
§ Veins
• Aka capacitance vessels d/t larger lumen and thin smooth muscles
• Largest vein: inferior vena cava à larger than aorta
• Assess bleeding coming from vein: Oozing.
§ Capillaries
• aka exchange vessels
• this is where gas exchange happen.
• with the greatest surface area; they occupy most of the body parts
• circulatory system
o a closed system connected to the capillaries
§ if the blood vessels is punctured à bleeding à decreased BP à
hemorrhagic shock
o blood vessels wall
§ tunica inLma – capillaries only have the tunica in1ma
§ tunica media – made up of smooth muscles
• arteries have thicker smooth muscles
• arteries create pulses
§ tunica externa – external layer
o arteries
§ pulses
• assessing pulses to know the arterial func1on
o 0 – absent
o +1 – weak
o +2 – normal
o +3 – increased
o +4 – bounding which may be abnormal
• Good pulses is equal to good blood flow
• Pulses can be used to assess if a pa1ent will undergo amputa1ons
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• Vascular disorders
o Outline:
§ Vascular disease à (1) arterial disorders, (2) venous disorders, and (3) both
• Arterial disorders
o Aneurysm
o Arterial insufficiency
§ Arteriosclerosis obliterans (ASO)
§ Raynaud’s disease
• Venous disorders
o Varicose veins
o Deep thrombosis/Venous thromboembolism
• Both
o Buergers disease/ thromboagi1s obliterans
o Aneurysm
§ Is a localized sac or dila1on formed at a weak point in the wall of the artery.
§ Types of aneurysms: most common forms of aneurysm are saccular and
fusiform.
• Saccular – projects from one side of the heart
• Fusiform – en1re arterial segments become dilated
o one sided vessels are only dilated and affected à SACCULAR
à not treated à en1re arterial segments dilates à
FUSIFORM
o basically both are just connected type of aneurysm.
• Ruptured
o Congenital aneurysm
§ Common site: cerebral vessels à cerebral aneurysm
o Acquired aneurysm
§ Has cause
§ Common site: aorta à aor1c aneurysm (can also be
congenital)
§ Elderly are commonly affected by acquired
§ AorLc aneurysm
• ELology
o Presence of atherosclerosis (atheroma: atheromatous
plaque)
o Atherosclerosis does not happen in aor1c arc (very fast
blood flow); commonly in the ascending and descending
aorta
§ StarLng age: younger children
• Monitor children’s BP at 3 years old with
appropriate cuff
§ Plaque: fats deposits, cholesterol, Nico1ne (tar)
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• calcium deposits make the blood vessels

harder à SCLEROSIS
o high blood pressure
§ most important risk factor for an aneurysm
§ blood pressure is the pressure exerted by the blood
against the wall of the blood vessels
§ the blood vessels should be elasLc and stretchable.
§ with hardening, the blood vessels are no longer
flexible/no linger distends à abnormal dila1on and
sac forma1on à ANEURYSM
o types of aorLc aneurysms:
§ ascending aor1c aneurysm
§ descending aorLc aneurysm (most common type)
• thoracic aor1c aneurysm
• abdominal aor1c aneurysm has signs and
symptoms:
1. pulsa1ng mass in the abdomen
2. Bruit by ausculta1on
3. Thrill normally can be felt in young age
and thin people
• Thoracic aorLc aneurysm
o 70% are causes by atherosclerosis
o Known to the dissec1ng aneurysm since there is a tear in the
thoracic area.
o Risk factors
§ Gender: men
§ Age: 50 years and 70 years old above
o Are associated with high morbidity and mortality rate
o Clinical manifestaLon
§ Can be ASYMPTOMATIC.
§ Pain is most prominent symptom
• May occur when pa1ent is in supine posi1on
for too long.
§ Dyspnea
• result of pressure of the aneurysm sac
against trachea, main bronchus, or the lung
itself;
o signs and symptoms:
§ cough
§ stridor
§ hoarseness
§ aphonia or complete loss of
voice
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§ Dysphagia
o Medical management
§ Beta blockers – controlling the blood pressure and
correc1ng risk factors are helpful
• Drug involved:
o Atenolol
o Metoprolol
o Carvedilol
§ Angiotensin’s receptor blocks (ARBs)
• Drug involved:
o Losartan
o Valsartan
o Irbesartan
§ Blood pressure should be maintained
• It is important to control the blood pressure
in pa1ent with dissec1ng aneurysm.
o Normal:
§ Systolic: 90 to 120 mmHg – to
maintain the arterial pressure
of 65 to 75 mmHg. Using the
beta-blockers
o Surgical management
§ Endovascular grag
• These endovascular graXs are inserted into
the thoracic aorta via various vascular access
routes, usually the brachial or femoral artery
§ Cerebrospinal fluid drainage
• Abdominal aorLc aneurysm
o most common causes is atherosclerosis
o it expands and con1nuously enlarges if not treated, it is
likely to rupture. It depends also to the size of the aneurysm.
§ At least 5.5cm – the standard treatment has been
open repair of the aneurysm.
o risk factor:
§ gender: male
§ race: white or Caucasian
§ age: older than 65 years old
§ HTN
o most of these aneurysm occur below the renal arteries
which are know to be as infrarenal aneurysm à untreated
à rupture à DEATH
o clinical manifestaLons
§ if associated with thrombus
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• emboli due to the occluded major vessels or

smaller distal occlusion.
• Cyanosis or moLling of the toes (trash toes)
small cholesterol, platelets or fibrin emboli
may lodge in the interosseous or digital
arteries.
• Signs of impeding rupture
o Sever back or abdominal pain may be
intermi]ent or persistent
§ Abdominal pain may be
localized in middle or lower
abdomen to the leX of the
midline.
o Persistent low back pain caused by
the pressure of the aneurysm on the
lumbar nerves.
§ Leaking or rupturing constant
or intense back pain
o Decreased blood pressure
o Decreased hematocrit
• Retroperitoneal rupture
o Hematoma in the scrotum, perineum,
flank or penis.
• Rupture of the vena cava
o Results in higher arterial blood
entering the low-pressure venous
system.
o Diagnos1c tests
§ Duplex ultrasonography or CTA – used to determine
the size, length, and loca1on of the aneurysm.
o Management
§ Pharmacologic therapy
• An1hypertensive agent
o Diure1cs
o Beta-blockers
o ACE inhibitors
o ARBs
o Calcium channel blockers
§ Surgical management
• Endovascular aor1c repair
o Mainstay of therapy of the
abdominal aor1c aneurysm
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o Involves the transluminal placement

and aLachment of a sutureless aor1c
grag.
o It can performed under local or
regional anesthesia
o May be performed if the pa1ent’s
abdominal aorta and iliac arteries are
not extremely tortuous, small,
calcified, or filled with thrombi.
§ Nursing management
• Before the surgery
o Assess the total func1onal capacity of
all organ system.
o Monitor for the vital signs of the
pa1ent ensure no problem at the
blood pressure and heart rate.
• Who had endovascular repair
o Lie supine for 6 hours
o Elevated head up to 45 degrees ager
2 hours
o Use of bedpan or urinal while on bed
rest
o Vital signs and doppler assessment of
the peripheral pulses performed
every 15 minutes and then
progressively longer intervals if the
pa1ent’s status remains stable
o Access site is assess when vital signs
and pulses are monitored
o Assess for bleeding and hematoma
forma1on
o Watch out for embolism
§ skin changes of the lower
extremity, lumbar area, or
bu]ocks that might indicate
signs of embolism
§ Aneurysm ruptures
• Most dangerous complica1on
• Internal bleeding
• Associated with arteriosclerosis,
• Nsg. Dx
o Risk for inadequate 1ssue perfusion
• Impending sign of rupture:
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o Dissec1ng aor1c aneurysm

§ Dissec1on – tearing resul1ng to pain
• Asc AA – severe chest pain
• Des AA – severe epigastric pain
• Abd AA – severe lower back pin
§ Nsg. Dx
• Acute pain
• Risk factors:
o Age: older = higher risk
o Family history
o AtheroscleroLc gene – has increased risk of 3 1mes than
those without it.
• Lifestyle
o Sedentary life
o Smoking
o Alcohol
o Stress
o Obesity
o High fat and high cholesterol diet
o Diabetes mellitus
o Hypertension
• DissecLng aorLc aneurysm
o Dissec1ng = tearing results to pain
§ Asc AA: severe chest pain
§ Des AA: severe epigastric pain
§ Can s1ll survive
o Nsg. Dx: acute pain
• Types of AorLc DissecLon
o Type A: Ascending aneurysm
§ Type 1 and 2: Ascending aneurysm
• Type 1: ascending and descending aneurysm
• Type 2: ascending aneurysm
o Type B AKA type 3: descending aneurysm
• Diagnos1c test
o Angiography
§ Ask for history of iodine (shellfish) allergy
§ If allergic: the procedure will s1ll con1nue
§ Invasive procedure
o Ultrasound
§ Non-invasive procedure
§ Doppler or duplex ultrasound
• 2-D echo (ascending aorta)
• Abdominal UTZ (descending aorta)
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• Management
o Admit the pa1ent
§ Type A: ascending à surgery ward
• High risk of rupture (has high risk than the
surgery)
§ Type B: Medical ward
• To control BP first prior to surgery
o Monitor blood pressure.
§ Most important role of nurses in AA
o Surgery
§ Stent
§ Repair aneurysm to make it stable.
o Most important health teaching post-surgery
§ Live a healthy lifestyle/manage the risk factors
(AVOID RF)

o Vascular insufficiency (PVD)

arterial insufficiency Venous insufficiency
Leg pain Claudica1on Venous conges1on
and phlebutus
Skin Pale, thinning of air Dark, cyano1c
pigmented
Pulses May be abnormal Normal but difficult to
palpate
Presence of No edema Edema is present
edema
ulcer Arterial ulcer Venous ulcer
Management PosiLon: reversed PosiLon: elevate
Trendelenburg
May have CHF
PosiLon: high fowler
Note:
• More common in the lower extremi1es
• The blood flow of the artery in the lower extremity is downward
• If low blood flow it causes ischemia to happen then results to
leg pain

• Vascular diseases
o Arteriosclerosis obliterans (ASO)
§ Most commonly affec1ng lower extremi1es
§ Hardening of the vessels and plaque deposits
§ Irreversible
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§ELology: idiopathic
§Risk factors
• Age
• Smoking
• Obesity
• Diet
• Family history
§ Gender: most prominent among men than women
§ ExtremiLes: Lower extremi1es > Upper extremi1es
§ Signs and symptoms:
• Leg pain
• Claudica1on
• Thinning of air
• Cool to touch
§ Nursing diagnoses:
• Acute pain
• Ineffec1ve peripheral 1ssue perfusion
• Risk for shoch
§ Management
• Posi1oning: reverse Trendelenburg
• Pain reliever: NSAIDs
• Vasodilators are rarely given
• Manage risk factors
• Avoid trauma
• Skin care
• Wound care
• Preven1on infec1on
• Amputa1on
• Rehabilita1on ager amputa1on
• Live a healthy lifestyle
o Raynaud’s disease
§ Upper extremi1es
§ Reversible
§ A disease characterized by arteriolar vasospasm
§ E1ology: idiopathic
§ Risk factors
• Young women than men
• Smoking
• Stress
• Hypertension
• Exposure to cold temperatures: coldness of an aircon can trigger an
a]ack
§ Extremi1es: upper extremi1es
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§ Signs and symptoms.

• Pain
• Ineffec1ve 1ssue perfusion
§ Pathophysiology
• Cold temperature à arteriolar vasospasm à ini1al cyano1c
finger1ps d/t vasospasm à severe vasospasm white color fingers
à numbness and 1ngling sensa1ons
• Reversible à vasodila1on à increased blood flow red à thus
results to blue-white-red disease
§ Nursing diagnoses
• Disturbed sensory percep1on (paresthesia > pain)
§ Management
• Avoid exposure to cold temperature
o Always wear gloves and boots: for pa1ents living in cold
temperature
• Increase the temperature of the environment
o Use heater
• Avoid smoking
• Avoid stress
• Control BP
• Avoid trauma
• Skin care
• vasodilators are given as ordered
o normal vessels are being dilated by the vasodilators à
vessels of Raynaud’s disease is normal
• wound care

o Raynaud’s phenomenon
§ the signs and symptoms of Raynaud’s disease are seen in another disease
§ causes:
• rheumatoid arthriLs
o autoimmune disease of the synovial joints; first affects the
hands
• systemic lupus erythematosus
o autoimmune disease of the connec1ve 1ssues
• scleroderma
o hardening of the skin; also, an autoimmune disease; RARE
o skin in the hands – loss of palmar creases à syndactyly
o skin in the face – loss of facial lines
o skin of the chest and back
o Crest syndrome:
§ Calcinosis – deposi1on of calcium in sog 1ssue
§ Raynaud’s phenomenon
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§ Esophageal dysmoLlity
• Calcium is deposi1ng in the esophagus à
dysphagia à nutri1onal problem.
§ Syndactyly – fusion of the creases in the palms
§ Telangiectasia – abnormal vessels forma1on in the
skin
• Venous insufficiency
o Varicose veins
§ Superficial vein
§ Abnormal dila1on and tortuous forma1on of the superficial veins of the
lower extremi1es
§ ELology.
• Presence of incompetent valves (irreversible)
• Blood flow in the lower extremi1es: upwards (against the gavity)
o Valves help the blood to go up
§ Risk factors
• Prolonged standing
• Prolong sipng
• Prolong crossing of legs
• Obesity
• Pregnancy – enlarging uterus compresses the vein in the lower
extremity à blood flow slows down à increase venous conges1on
causes veins to dilate
§ Nurses’ diagnoses
• Acute vein à venous conges1on and phlebi1s
• Ineffec1ve venous circula1on
• Disturbed body image
§ Management
• Preven1on of varicose veins:
o Avoid
§ Prolong standing
§ Prolong sipng
§ Prolong crossing of legs
§ Obesity (weight reduc1on)
o Elevate legs
o Compression stockings
• Sclerotherapy
o Injec1on of sclerosing substance (hardens the vein à
straightens the vein à lighten the color)
o The blood flow will be redirected to collateral vessels
o For small varicose veins
• Veins stripping’s and liga1on
o Removal of vein for larger varicose veins
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• Early ambula1on post-surgery

o To redirect the blood flow to collateral vessels
o Deep vein thrombosis (DVT) AKA venous thromboembolism
§ Thrombus: an abnormal clot that is not dissolving on its own
§ Pathophysiology
• Blood flow going upward à muscles will pump the veins for the
blood to upward.
§ ELology: idiopathic
§ Risk factors:
• Immobiliza1on – most important
o Bedridden, paralyze, comatose pa1ent
o Immobiliza1on à blood flow slows down à
STASIS/stagna1on of blood à blood becomes
hypercoagulable (prone to clot forma1on) à venous
conges1on à endothelial injury àinflamma1on à
thrombophlebi1s à pain, swelling, redness; heat
• Smoking
• Oral contracep1on
• Diabetes mellitus
§ Virchow’s triad
• Stasis of the blood
• Hypercoagulable
• Endothelial injury
§ Phlebothrombosis
• Has no inflamma1on but has stasis of the blood
• Hypercoagulable
§ No signs and symptoms because of no inflamma1on
• Symptoms arise with sudden onset of pain
• Manipulate pa1ent for Homan’s sign
o (+) Homan’s sign: dorsiflex then pain in the calf
§ Do not repeat the test to avoid dislodging the
thrombus à embolism (pulmonary embolism)
o Management for pulmonary embolism
§ Elevate the head of the bed (semi-fowler’s)
§ Give oxygen
§ Refer to MD
o Pulmonary embolism can cause
§ Atelectasis
§ Pulmonary hypertension à right sided heart failure
§ PE in the pulmonary artery à sudden death
§ Signs and symptoms
• Swelling
• Warmth
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• Pain or tenderness
• Redness
• Pallor
§ Management
• Preven1on
o Mobilize the legs
o Elevate the legs
o Compression stockings keep muscles contracted à blood
flow upward
• Complete bed rest without bathroom privileges
• Heparin IV
• Pain reliever: NSAIDs
• ThrombolyLc drugs to dissolve the thrombus
o Within 3 days from the onset of symptoms
o Adverse effect: Bleeding
o Example:
§ U-urokinase
§ S-streptokinase
§ A-alteplase
• TED hose (customized) – as ordered
o Wear 6 months (depends on the case)
o Removed when the pa1ents lie down à upon lying down,
elevate legs wear upon waking up
• Warfarin
o Oral an1coagulant
o Follow-up monthly to prevent another occurrence
• Surgery
o Filter to prevent the thrombus dislodging
• Post-surgery health teaching
o Early ambula1on
o Manage risk factors
o Live a healthy lifestyle
• Buerger’s disease (AKA thromboangiGs obliterans)
o ELology: idiopathic
o Risk factors
§ Smoking
§ Young adult men
§ stress
o Signs and symptoms (involves arteries and veins)
§ Leg pain
§ Claudica1on
§ Dark skin
§ Edema
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o IntervenLons
§ Stop smoking and avoid all forms of tobacco products
§ Avoid stress
§ Avoid trauma
§ Pain reliver: NSAIDs
§ Skin care
§ Wound care
§ Vasodilators are rarely given
• Heart
o Hallow muscular organ
o Middle medias1num
o Muscular 1ssue
§ Contrac1lity
§ Conduc1vity
§ Rhythmicity
§ Automa1city
§ Excitability
o Pathophysiology:
§ RA receives unoxygenated blood from the Upper extremity (via SVC), lower
extremity (via IVC), and from the heart (via coronary sinus) → Tricuspid
(AV) valve → RV to the lungs via pulmonary artery (only artery that carries
unoxygenated blood)
§ Pulmonic (SL) valve: to the lungs (pulmonary circula1on) for blood to be
oxygenated via the pulmonary vein (only vein that carries oxygenated
blood) to the LA → Bicuspid/Mitral (SL) valve to the LV
§ LV to the Aorta via Aor1c (SL) valve to the systemic circula1on
o Blood pressure
§ Systemic circula1on pressure: 110/70 mmHg
§ Pulmonary pressure: 25/9 mmHg
o Primary organ affected by HPN: heart
§ ↑ BP → ↑ Heart workload
o Heart has a good compensa1on mechanism
§ Normally: heart enlarges itself à Cardiomegaly as a compensa1on
§ Cardiomegaly can be normal among athletes d/t strenuous ac1vity which
increases their cardiac endurance
o Valve: prevent backflow of the blood
o 4 heart sounds
§ S1 (lub) – closing of the AV valve
§ S2 (dub) – closing of the SL valve
§ S3: rapid ventricular filling (blood from atria to ventricle)
• Inaudible
• If heard, the heart have enlarged
• Sound:
o Lub dub dub à ventricular gallop
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• Ex: CHF or ventricular regurgita1on

§ S4: due to atrial systole (atrial contrac1on)
• Inaudible
• If heard, the atria is enlarged, has high atrial pressure
• Sound:
o lub, lub dub à atrial gallop (abnormal)
• Ex. Cardiac hypertrophy, disease or injury to the ventricular wall
• Valves (APTM 2245)
o Assessment: bell of the stethoscope
o AorLc valve
§ 2nd ICS right parasternal
§ S2 heart sound because semilunar valves
o Pulmonic valve
§ 2nd ICS leg parasternal.
§ S2 heart sound
o Tricuspid valve
§ 4th leg parasternal
§ S1 heart sound
o Mitral valve
§ 5th leg MCL
§ S1 heart sound
§ PMI – apex (apical pulse)
§ Loudest
• Murmur: sound created by increased turbulence in the flow of
blood inside the heart
o Heard in valvular damage à blood back flows

• Valvular diseases
o Valvular Insufficiency
§ Known as the valvular regurgitaLon.
§ Not enough func1on of the valve à inability of the valve to close
completely.
§ Blood back flows
§ ManifestaLons:
• Has murmur
• Decreased cardiac output.
• Non-coronary cause of cardiogenic shock
o Valvular stenosis
§ Stenosis or known as narrowing then blood does not flow smoothly
§ Inability of the valve to open completely.
§ ManifestaLons:
• Has murmur
• Decreased cardiac output
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• Non-coronary cause of cardiogenic shock

o Mitral valve prolapse
§ Ballooning or bulging of the mitral valve on to the leg atrium
§ Systolic click/mitral click: heard every 1me mitral valve closes; heard in the
5th leg MCL (apex)
o Causes of valvular diseases
§ Congenital:
§ Acquired: rheuma1c heart disease, endocardi1s, Kawasaki disease
o Risk factors
§ Women than men
§ Stress
§ Family history
o Signs and symptoms
§ Palpita1on à avoid caffeine.
§ Tachycardia
§ Chest pain
§ Fa1gue
§ Syncope
o Nursing diagnosis
§ Fa1gue
§ Ac1vity intolerance
§ Pain
§ Risk for injury
o ComplicaLons
§ Dysrhythmias
§ Mitral regurgita1ons

o DiagnosLc test:
§ 2D echocardiography
• UTZ of the heart
• Allowed for pregnant and children
• No prepara1on needed
o Management for valvular disease
§ Provide rest
§ Avoid stress
§ Support cardiac func1on
§ Repair the valve
§ Valvular replacement
§ Manage heart failure
§ Prevent and manage shock
o Surgical management
§ Valvuloplasty
• Catheter with balloon – to prevent valvular dila1on
Cute si dims J

• Suture valve
§ Valvular replacement
• Mechanical valve to replace aor1c valve
• Fibrous replacement: newer methid
• Layers of the heart
o Endocardium – inner lining
o Myocardium – myocardi1s is d/t coxsackievirus
o Epicardium AKA visceral pericardium
o Parietal pericardium - envelops visceral pericardium
§ Between visceral and parietal pericardium, there is a fluid to decrease the
fric1on in each contrac1on

Cardio (DAY 2)
doc arreglo
• Inflammatory in the heart
o PericardiLs – constric1ve pericardi1s
§ ELology:
• Infec1on due to open heart surgery
• Chest trauma
• SLE – autoimmune disease of the connec1ve 1ssue
o ALacks the ehart and pericardium
• MI-induced percardi1s (dressler’s syndrome)
• Malignancy (secondary) – metastasis in cancer
• Idiopathic
o If idiopathic: pericardiotomy – places a stent to prevent fluid
accumula1on
§ If not effec1ve, pericardiotomy à risk for
dysrhythmias
§ Signs and symptoms
• Redness, swelling, heat, and inflamma1on of the sac → heart is
compressed
§ SubjecLve: chest pain – most prominent symptom
• Rule out heart aLack
• MI pain: constant à not affected by breathing of the chest
• Pericardi1s pain”.
o Worsens with deep inspira1on, lying down, or turning
o Relieved by sipng or leaning (orthopneic/tripod posi1on) à
chest well is moved away from pericardium à less
irrita1on.
o Objec1ve: (+) Fric1on rub: auscultate in the 4th leg ICS
(Tricuspid valve) → creaky, leathery, scratching sound, heard
best at the end of expira1on (lung is collapsed) and when
pa1ent is in orthopneic posi1on
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§DiagnosLcs tests
• 2D echocardiography
• Chest x-ray
• CBC: high WBC
• ESR: (+) ESR systemic inflamma1on
• Depending on the cause:
o Culture and sensi1vity: blood is cultured.
o Coronary angiography
o Biopsy
o ANA test: an1-nuclear an1body test
§ Management
• Independent: orthopneic posi1on
• Pain reliever: NSAIDs
• AnL-inflammatory drugs: steroids
• Manage the cause
o If the infec1on, abx
o MI, treat MI
o Cancer, treat cancer
o SLE, treat SLE
• Prevent and manage the complicaLons
o Pericardial effusion: accumula1on of fluids in the
pericardial effusion
§ Pericardiocentesis – aspira1ng fluid from pericardial
effusion
• MD will do; RN will assist
• Posi1on: semifowlers positon
• Chest X-ray – to know the placement
• Ultrasound – to know how many fluids to
remove
• During procedure, the needle is connected
to the ECG à heart is normal = ECG should
be normal à if the needle touches the heart
à abnormal ECG à withdraw the needle
and aspirate the fluid again
o Cardiac tamponade – high amount of fluids in the
pericardium compresses the heart à LOW BP à the blood
backflows to the RA à JVD (neck vein disten1on)
o Pericardiocentesis
§ BP normalizes.
§ Heart sounds can now be heard.
§ Neck veins flaLens
§ Instant relief
o EndocardiLs – inflamma1on of the endocardium
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§ ELology:
• Two types
o Infec1ve: bacteria most common cause, known as the
infec1ve endocardi1s, and most common bacteria is
strep/staphylococcus
o Non-infec1ve
• Risk factors
o Exis1ng cardiac disorder the pa1ent becomes at risk.
§ RHD, CHD, VHD, and A.fib
o Immunocompromise state low immune system which
makes the pa1ent easily get infected.
§ Low immune system à decreased WBC
§ Extremes of ages
§ Chemotherapy pa1ents
§ HIV pa1ents
o Invasive procedure or surgery these when pa1ent is cut
open and bleeding occurs which predispose the pa1ent.
§ Cardiac catheteriza1on
§ Endoscopy
§ Surgery involves opening of blood vessels
o Poor hygiene and low socioeconomic status
• Pathophysiology
o Part I: when bacteria enter the blood vessels and
proliferates.
§ Pa1ent with valvular heart disease à has slow blood
flow in the leg side of the heart à dental extrac1on
à rupture of blood vessels à streptococcus enters
the blood vessels à which makes the pa1ent
immunocompromised à bacteria proliferate à
BACTERMIA.
o Part 2: signs and symptoms of fever, chest pain, fa1gue,
chills, weakness, and joint pains.
§ Bacteria goes to the heart à leg atrium has slow
blood flow à decreased CO à bacteria enter
endocardium (systemic inflamma1on) prominent
signs of symptoms is fever, chest pain, fa1gue, chills,
weakness, and joint pains.
• Note: fever or no fever pa1ent are s1ll prone
to endocardi1s which are more relevant
among geriatric pa1ents.
• Nursing diagnosis:
o Hypothermia
o Pain
o Risk for injury
Cute si dims J

o Risk for infec1on

o Risk for sep1c shock or cardiogenic
shock
o Part 3 these are the vegeta1on
§ VegetaLon bacterial adherence to damaged
endothelium and microthrombi there will be small
bleeding and it ac1vates the platelets to form a cloth
and stop the bleeding à ac1vates clopng
mechanism fibrin covers the bacteria à WBC cannot
kill bacteria it is because fibrin + bacteria =
THROMBUS that covers the bacteria à Vegeta1on:
thrombus, bacteria, platelets, and WBC à it will
result to dislodged vegeta1on à EMBOLIZATION (LV
– cerebral embolism and RV – pulmonary embolism)
à small blood vessels of the UE and LE ruptures the
micro blood vessels in the hand and feet à splinter
hemorrhages (bleeding under the nails)
• FROTHS SPOTS: these are white centered
re1nal hemorrhages found in the eyes
• OSLERS NODES: painful nodes on finger pads
and toes
• JANEWAY LESION: painless macules
• VALVE DEFECT: murmur
• Signs and symptoms
o Fever
o Roths spots
o Osler nodes
o Murmur
o Janeway Lesions
o Anemia
o Nail-bed hemorrhage
o Emboli
• DiagnosLc tests
o Culture and sensi1vity – to detect the bacterial infec1on.
o CBC – high or low WBC, low RBC, low HgB, High ESR
(systemic inflamma1on)
o 2-D Echo – to visualize if there is vegeta1on

• Management:
o Nursing management no doctors involved these are
independent interven1ons, no drug therapy.
§ Manage fever.
Cute si dims J

§ Assess for murmur/assess for changes in murmur to

know if there is deteriora1on.
§ Monitor the following:
• Vital signs
• Intake and output
• Signs and symptoms of heart failure
• Signs and symptoms of sep1c and
cardiogenic shock
§ Provide rests it will help alleviate possible HF.
§ Avoid stress.
o Medical management dependent interven1on these are as
ordered medica1on.
§ Preven1on
• Prophylaxis an1bio1cs
o An1bio1cs before any invasice
procedure for at risk pa1ents (RHD,
CHD, VHD, etc.)
o Excep1on:
§ Mitral valves prolapse, no
need for prophylaxis.
o Penicillin V/G – narrow spectrum
§ Amoxicillin broad spectrum
good for strep
§ Ampicillin broad spectrum
§ Cloxacillin broad spectrum
o Erythromycin – if allergic to penicillin
• An1pyre1c
• An1bio1cs
• Support cardiac func1on
• Prevent and Manage heart failure
• Prevent and manage shock
o Cardiomyopathy (CDM)
§ Disease of the cardiac muscles which is idiopathic the only management is
heart transplant.
§ 4 types of cardiomyopathies
• Dilated CDM
o Most common type of CDM
o There is significant dila1on of the myocardium or stretch of
the myocardium without hypertrophy, no enlargement.
o Risk factors
§ Viral infec1on
§ Alcoholism
§ Pregnancy induced CDM.
Cute si dims J

• Hypertrophic CDM
o Significant thickness of the myocardium especially the
interventricular septum then there is decrease size of the
chamber and during contrac1on aorta is compressed which
results to no blood flow à SUDDEN DEATH.
o Risk factors
§ Family history
• RestricLve CDM
o Ventricles becomes rigid can also have sudden death it is
because of hardened ventricles with idiopathic cause.
o Risk factors
§ Family history
• Arrhythmogenic right ventricular CDM
o Fibrosis or scarring of the right ventricle then right ventricles
fails because of these scarring which may result to leX
ventricles will also fail.
o Risk factors
§ Family history

§ ELology: Idiopathic
§ Risk factors
• Viral infec1on
• Alcoholism
• Pregnancy-induced CDM
• Family history
§ DiagnosLcs test: 2D echocardiography
§ Management:
• Avoid strenuous ac1vity.
• Provide rest
Cute si dims J

• Avoid stress.
• Support cardiac func1on.
• Manage heart failure.
• Heart transplant
o No cure for CDM à only heart transplant
o Source: Human (brain dead)

§ Blood pressure: classifica1on of blood pressure for adults 18 years old and
above.
BP classificaLon Systolic pressure Diastolic pressure
Normal <120 <80 average: 110/70
Prehypertension <120 – 139 80-89
Stage 1 140 – 159 90-99
Stage 2 ≥160 ≥100

• Hypertension
o HPN – elevated blood pressure
o Type:
§ Primary HPN
Cute si dims J

•
Idiopathic
•
Risk factors:
o Family history
o Age
o Obesity
§ Secondary
• Has known causes.
o Example:
§ DM
§ renal disease
§ pheochromocytoma (tumor of the adrenal medulla)
à increased SNS à high BP
• secondary hypertension is a sign of a disease
• hypertension is also a risk factor (modifiable)
o can cause stroke, aneurysm
• Hypertension called the silent killer
o Major is asymptoma1c à pa1ents generally do not care
un1l symptoms arises.
o NO SIGNS AND SYMPTOMS à Nsg Dx: Risk diagnosis
o ELology:
§ Primary HPN
§ Secondary HPN
o Clinical manifestaLons
§ AsymptomaLc
• Nsg Dx: Risk diagnosis
• Knowledge deficit
• Non-compliance – pt not taking medica1on.
• Ineffec1ve health maintenance – pt not exercising.
§ If with signs and symptoms:
• Headache (occipital pain) – acute pain r/t headache
• Dizziness – risk for fall or injury
• Blurred vision – impaired vision
• Epistaxis – risk for ineffec1ve airway clearance r/t clot or risk for
aspira1on
o Diagnos(c test:
§ Sphygmomanometer – measures BP
§ 180/100 mmHg à consult MD (HPN crisis)
§ Elder with HPN
• With maintenance an1hypertensive drug. give another dose of the
maintenance drug.
o Monitor BP before and ager
o Do not tell the BP to the pa1ent to avoid eleva1ng BP.
Cute si dims J

•Without maintenance an1hypertensive drug, calm down the

pa1ent and refer to the MD.
o Give pineapple juice and/or garlic cloves if the placebo
effect can calm down the pa1ent.
o Independent IntervenLon (applicable to other cardiac diseases)
§ Diet: low salt, low fat, low cholesterol, and low sugar
§ Exercise
• In DM pt. – it will increase the use of glucose by the cell.
• In cardiovascular – it will improve the circula1on, weight reduc1on,
decrease fats and cholesterol.
o 30mins/day, 3x a week
§ Avoid
• Stress – adrenal gland à secretes cor1sol and catecholamines.
o Cor1sol: it causes the following.
§ High sugar
§ High HCl
§ Water reten1on
§ Low WBS
o Catecholamines:
§ Increase SNS à high HR and BP
• Smoking – vasoconstric1ons à Increase HR and BP
• Restricts caffeine and avoid alcohol increase HR = increase cardiac
workload
§ RelaxaLon technique
• Deep breathing exercise when inhala1on occurs it expands the
lungs and improve the circula1on.
• Decrease cardiac workload.
• Guided imagery
• Music therapy
• Massage
• Medita1on
• Aromatherapy
• Yoga
• Sex
o Dependent intervenLon
§ Drug therapy: an1hypertensive drugs
§ Increased BP à lowers BP (normal)
• Pheochromocyoma (Secondary casues) à increases SNS =
Increases BP à with an1hypertensive drugs à block SNS =
decreases BP to normal
§ To decrease SNS.
1. Alpha-1 Antagonist: vasodila1on
a. Prozasim
Cute si dims J

b. Doxacosin
c. Terazosin
i. Avoid prolonged standing and warm shower aXer A-
1
2. Alpha-2 Agonist CNS à decrease NE flow à decrease SNS
a. Clonidine – catapres
b. Methyldopa -- Aldomet
i. S/E: drowsiness so it should be given at night, do not
drive and operate machine
3. Beta blockers – heart: vasodila1on it will slow down heart rate which will
lower the BP but it can also result to bradycardia, Lungs:
bronchoconstrictor.
a. Propranolol
b. Metoprolol
c. Long ac1ng CCB:
i. Dil1azem
ii. Verapamil
4. RAAS.

a. ACE inhibitors – vasodilators

i. Such as:
1. Captopril
2. Quinapril
3. Enalapril
ii. S/E: cough
iii. AcLon: enzymes
b. Angiotensin II receptor Blockers (ARB )
i. Such as
1. Losartan
2. Candesartan
3. Telmisartan
ii. S/E: GI toxicity à with meals or ager meals
iii. AcLon: receptors
c. DiureLcs to decrease blood volume
i. DOC: thiazide Diure1cs: hydrochlorothiazide
Cute si dims J

1. Can be combined with other

an1hypertensive drugs
ii. Loop diure1cs can be but not as maintenance à
too much loss of water and electrolytes
iii. Ac1on of the diure1cs: kidneys
iv. Give diure1cs in the morning to avoid disturbance
of sleep.
d. Vasodilators all vasodilators will case HEADACHE
i. Ac1on: blood vessels
ii. Direct acLng: Directly relax the smooth muscles
1. Hydralazine
a. apresoline
2. Nitrates sensi1ve to light and heat used for
angina pa1ent.
a. Nitroglycerine
b. Isosorbide nitrate
c. Nitroprusside
3. S/E: hypotension
iii. Indirect acLng: do not directly relax the smooth
muscles but decrease the release of the calcium.
1. Calcium channel blockers
a. It decreases calcium in the smooth
muscles
b. Nifedipine
c. Amlodipine
d. Felodipine
e. Long ac1ng CCB:
i. Dil1azem
ii. Verapamil
• Coronary artery disease also known as the ischemic heart disease
o Disorder of the coronary arteries from the ascending aorta – first branches of asc
aorta; coronary arteries provide blood supply to the heart and oxygen.
1. Lef CA: It will supply blood to the anterior or lateral wall.
a. Leg anterior descending (LAD) branch, most common affected by
MI.
b. Circumflex branch
2. Right CA: supplies the posterior and inferior wall of the heart.
a. Posterior interventricular branch
b. Marginal branch
o Heart receives blood during diastole (relaxa1on)
§ Dangerous if pt have high diastolic pressure.
• !40/100 mmHg – high diastolic pressure compromises blood flow
of the coronary muscles
o Venous drainage: it drains unoxygenated blood and brings to the right atrium
Cute si dims J

§ Great cardiac vein

§ Middle cardiac vein
o ELology:
§ Idiopathic
§ Atherosclerosis à thrombus forma1on then result to ischemia to the heart
• Pain: most prominent manifesta1on to ischemia
o Angina – chest pain d/t ischemia
o Risk factors
§ Age (commonly to elderly which is atypical manifesta1on)
• Atypical symptoms: no chest pain but s1ll can have MI
o Confusion but may have heart a]ack.
o SOB but may have heart a]ack
o Epigastric pain but may have heart a]ack.
§ Gender: common among men than reproduc1ve women
• Estrogen has a cardioprotec1ve effect for women à estrogen
produces good cholesterol (it has more protein than lipids and will
not par1cipate in atherosclerosis, increase HDL it lowers the LDL.)
• Women in menopausal age: the incidence becomes equal with men
because of the loss or decreased of estrogen.
§ Family history/past health history
• Past CAD/MI there is higher chance of re-occurrence of the CAD.
• Angina pectoris VS myocardial infarcLon
DescripLon Angina pectoris Myocardial infarcLon
Problem Imbalance between ↓oxygen Ischemia and necrosis of
supply and ↑cardiac workload cardiac cells
Irreversibility Reversible Irreversible
Timing Less than 15 minutes More than 30 minutes
Relieving • Rest No relieving factors
factors • Nitroglycerine

• Assessment of chest pain (angina Vs. MI)

o P – posi1on/loca1on: chest pain
o P – provoca1on (precipita1ng factor) – what happened before the chest pain
o Q – quality
§ Pain is constant; unaffected by breathing or movement of rh chest
§ Quality must be descrip1ve.
o R – radia1ng
§ Leg arm, shoulder, neck, jaw
§ In MI, the radia1on may be present or not
o R – relieving factors
§ Angina: rest and NTG
§ MI: none
o S – severity
Cute si dims J

§ Pain scale
o T – Timing
§ Angina: less than 15 minutes
§ MI: more than 30 minutes

• Angina Pectoris
o Types of anginas
1. Stable angina – one of its causes is increased the cardiac workload.
2. Unstable angina – decreases O2 due to severe atherosclerosis (pre-
infarc1on)
3. Prinzmetal – decreases O2 due to coronary v-spasm but it is irreversible.
4. Intractable angina – severe excrucia1ng pain; no objec1ve sign except
LEVINES SIGN
5. Silent ischemia – pa1ent may have MI without feeling anything or without
signs and symptoms.
o Nursing diagnosis
§ Ineffec1ve myocardial 1ssue perfusion
§ Acute pain
§ Anxiety r/t fear of unknown
• Dangerous d/t physical symptoms
o Increased O2 demand, increased cardiac workload à pt
becomes restless.
§ Ineffec1ve health maintenance
§ Non-compliance
• Knowledge deficit
o Priority intervenLon
§ Stable angina
• Rest
• Posi1on: semi-fowlers posi1on
§ Unstable angina
• Nitroglycerine first then oxygen
o AcLon: dilate the coronary arteries first before giving
oxygen priority nursing management
o Priority nursing management: OXYGEN
o DiagnosLc test
§ Angiography – most defini1ve diagnos1c test for all cardiovascular
diseases
• invasive procedure
• local anesthesia is used for cardiac catheteriza1on.
• assess for shellfish allergy.
§ Blood test (not defini1ve but suggest test only)
§ ECG
• Non-invasive defini1ve test
Cute si dims J

•
T-wave inversion – sign of myocardial ischemia
•
Best 1me to take ECG: during the pain which is less than 15 minutes;
when there is no longer pain then altera1on will not be seen.
o Medical management for angina (SUMMARY)
§ Rest
§ Manage risk factors.
§ Oxygen therapy
§ Drug therapy
• Nitroglycerine
o a type of nitrate
o medical management: stool soXener
o NGT:
§ Coronary vasodilators à increases O2
§ Peripheral vasodilators à low BP à low cardiac
workload
o nurses should monitor the BP before and aXer
o acute a]ack: given sublingual for fast ac1on for about 3-5
minutes.
§ Un1l 3 doses only (1 dose every 5 minutes)
§ Call 911 aXer 2nd dose.
• S1ll go with the EMT even if the angina is
gone in 2nd dose à con1nuity of care.
o S/E: headaches
o Low BP before giving an1-angina drugs: do not give but
rather posi1on the pa1ent to modified Trendelenburg in
which the pa1ent may be in shock, then give O2 aXerwards
refer to the physician.
• Isosorbide nitrate
o Coronary vasodilators
o Peripheral vasodilators
o Slow onset of ac1on and it is not for acute a]ack.
o Only given when pa1ents need to be maintained with
nitrate.
• Beta-blockers
o Low bp à low cardiac workload
o S/E: bradycardia
• Calcium channel blockers
o Long term: dil1azem and verapamil à peripheral
vasodilator à low bp à low cardiac output
• Ranolazine
o New medica1on
o Ac1on
Cute si dims J

§ Electrical ac1vity of the heart (depolariza1on and

repolariza1on)
§ Decreased lac1c acid produc1on.
• Percutaneous transluminal coronary angioplasty
o Done by cardiac catheteriza1on.
o Local anesthesia are used and pt. may be awake
o Contraindica1on: straining (less blood flowing to the
coronary arteries)
o Process:
§ Stent is placed via arm or thigh un1l catheter
reaches coronary vessels.
§ Balloon inflates to the place the stent to keep the
blood vessels open.
§ Balloon deflates but the stent will be leX in place.
• Nursing management:
o High fiber diet
o Increased water intake unless
contraindicated.
• Myocardial infarcLon
o Nursing diagnosis
§ Acute pain
• Primary medical management: PAIN CONTROL
• No independent interven1on can relieve the pain of the pa1ent.
• Dependent: morphine
o Addic1ve
o Cause cons1pa1on, respirator depression, and drug
tolerance
• Priority nursing management: OXYGENATION
§ Ineffec1ve myocardial 1ssue perfusion
• Priority: oxygen
§ Anxiety
• r/t fear of death
• most common complica1on of MI: dysrhythmias (premature
ventricular contrac1on)
o PVC: 6 or more per minute
§ Give an1arrhythmic drug as ordered because it has
already been an1cipated
§ In not given, PVC (premature ventricular complex)
will turn in to Vtach → Defibrillate ASAP
§ Risk for dysrhythmias
§ Risk for cardiogenic shock
§ Risk for decrease cardiac output.
§ Sexual dysfunc1on post-MI
Cute si dims J

• Men is sexually ac1ve LIFETIME.

• When do sexual intercourse can resume post-MI: if they can do one
flight of stairs then they can do sexual intercourse.
o Diagnos1c tests:
§ Angiography – most defini1ve
§ EC – during pain (more than 30 minutes)

o EKG indicaLon heart ahacks

§ Zone of infarc1on: area of necrosis
• In ECG, ST segment eleva1on which is an early sign of acute MI
§ Zone of injury: surrounding the zone of infarc1on
• ST depression: sign of myocadiac injury
§ Zone of ischemia: surrounding the zone of injury
• T-wave inversion
§ Presence of pathologic Q wave: indicates even a silent MI
• Scar of MI
• Old sign of MI
• Late sign
o 2 types of MI:
§ STEMI
§ NSTEMI – no ST eleva1on MI; and it is atypical
• Atypical sign à elderly
• To know if there is an MI, do blood test (cardiac enzyme)
• Enzymes from produced by necro1c cells the more cells produced
the higher it is released in the blood, and only produced in the MI
§ Enzyme eleva1on
• CK MB – most specific and most indica1ve of enzyme of MI
o Within 3 hours DEFINITIVE
Cute si dims J

•Troponin – most reliable, sensi1ve, important (protein in the

cardiac muscles) DEFINITIVE
o Within 3 hours
o Released when cardiac muscle dies
o Types
§ Troponin I – prolonged dura1on in the blood
§ Troponin C
§ Troponin T
• CPK – SUGGESTIVE
o Within 3 hours
• LDH – SUGGESTIVE
o Within 6-we hours (an enzyme)
• Myoglobin
o Within 2 hours (a protein)
o Only sugges1ve à elevates also in skeletal injury
o MI management
§ Pain control is priority.
• Morphine is orders
§ OxygenaLon
§ ThrombolyLcs drugs
• Given only to pa1ent who are good candidates (within 30 minutes
to 1hr)
• No bleeding problem
• abort thrombus forma1on à reperfusion
• Drug involved:
o Urokinase
o Streptokinase
o Alteplase
§ AnL-thromboLc drugs à prevent further thrombus forma1on.
• Such as the following:
o An1platelets:
§ Aspirin
§ Clopidogrel
o An1coagulant:
§ Heparin
§ Warfarin
§
o MONA TASS this is only management not prioriza1on
Cute si dims J

o Summary of management: M.I

§ Rest
§ O2 therapy
§ Drug therapy
§ PTCA
§ CABG
§ Manage RF (independent interven1ons)
§ Live a healthy lifestyle.
• Heart failure
o It is a syndrome it is the collec1on of signs and symptoms, but know it is a
complica1on.
o HF: inability of the heart to pump effec1vely.
§ In heart failure, the heart is in cardiac decompensa1on.
o Causes of heart failure
§ Cardiac causes
§ Non-cardiac causes
• COPD à right sided HF
o Types of heart failure
§ Leg sided heart failure leX ventricles fails.
Cute si dims J

• Leg ventricles fails à RV will follow.

• Most common
§ Right sided heart failure right ventricles fails
• Right ventricles fails à LV will follow
• COPD can cause RHF
o LEFT SIDED HEART FAILURE
§ Known Pulmonary edema
§ Unable to pump to systemic circula1on
§ Process:
• Blood in LA cannot go down à increased pressure in the lungs à
fluids in the lungs
§ Signs and symptoms
• Pulmonary edema
• Progressive cough
• Paroxysmal nocturnal dyspnea
• Orthopnea – difficulty breathing in supine positon
• Dyspnea
• crackles/rales
§ Nursing diagnosis
• Ineffec1ve airway clearance
• Ineffec1ve breathing paLern
• Impaired gas exchange
• Fluid volume excess due to the hepatomegaly
• Decreased cardiac output
§ RV is affected à RA à venous circula1on.
o RIGHT SIDED HEART FAILURE
§ Aka conges1ve heart failure
§ Systemic edema
§ Right ventricles fails à leg ventricles follows
§ Process:
• Right ventricles fails à conges1on of peripheral 1ssue + viscera
(outermost layer of the heart) predominates à increased venous
pressure à jugular venous disten1on + increased capillary
hydrosta1c pressure.
§ Signs and symptoms
• Distended neck veins
• Hepatomegaly enlargement of the liver and splenomegaly
enlargement of the spleen
o There is tenderness of the RUQ result from venous
engorgement of the liver. à increased pressure à
disrup1on of the liver func1on
Cute si dims J

o Disrup1on of the liver func1on à increase pressure within

the portal vessels à forces fluids into the abdominal cavity
à ASCITES
• Ascites accumula1on of fluid in the peritoneal cavity
o Increased abdominal girth
o May accompany lower body edema
• Weight gain due to fluid reten1on
• Edema starts from the feet
o Can gradually progress up the legs and 1ght and eventually
into the external genitalia and lower trunk
o Mngt: eleva1on of the legs
• S3 can be heard = ventricular gallop (gallop)
• Anorexia
• Abdominal pain
§ Nursing diagnoses:
• Ineffec1ve airway clearance
• Ineffec1ve breathing paLern
• Impaired gas exchange
• Fluid volume excess due to the
• Decreased cardiac output
• NYHA ClassificaLon of Heart Failure
Class 1 • No limita1on of physical ac1vity
• Ordinary physical ac1vity does not cause undue
breathlessness, fa1gue, or palpita1ons.

Nsg. Dx: risk for ac1vity intolerance

Class 2 • Slight limita1on of physical ac1vity
• Comfortable at rest but ordinary physical ac1vity results in
undue breathlessness, fa1gue, palpita1ons

Nsg. Dx. Decreased ac1vity intolerance

Class 3 • Marked limita1on of physical ac1vity
• Comfortable at rest, but less than ordinary physical ac1vity
results in undue breathlessness, fa1gue, or palpita1ons

Nsg. Dx. Decreased cardiac output

Class 4 • Unable to carry on any physical ac1vity without discomfort.
• Symptoms at rest can be represent
• If any physical ac1vity is undertaken, discomfort is increased

Nsg. Dx.
Ineffec1ve airway clearance
Ineffec1ve breathing pa]ern
Cute si dims J

Impaired gas exchange

Fluid volume excess
Decreased cardiac output
• DiagnosLcs test (all are definiGve test)
o 2D echo
o CXR – heart enlarged and pulmonary conges1on
o Elevated BNP/Beta type natriure1c pep1de – protein releases by the ventricles in
response to pulmonary conges1on
§ Normal: less than 100 picograms per ml
§ CHF: more than 800 picograms per ml
§ ARDS: increased BNP but not as high as CHF
• Nursing IntervenLons: both independent and dependent
o Priority: airway and breathing paLern (done in ER)
§ Posi1on: High-fowlers posi1on à pooling of blood downwards à lesson
pooling of blood in the heart
§ O2
§ IV line – an1cipate giving furosemide 40mg IV stat.
§ CatheterizaLon: monitor I&O
§ Monitor VS
• Circulatory problems occur:
o IntervenLon of FVE
§ Restrict fluids
§ Restrict sodium
§ Monitor I&O
§ Monitor VS
§ Weight pt daily same 1me, clothes, weigh1ng scale
§ Con1nue giving diure1cs (oral)
§ Give furosemide
• K was1ng à cardiac muscles the most sensi1ve cells to potassium
changes à arrhythmia
§ Spironolactone – adjunct diure1c to maintain serum potassium. It is
because changes in the potassium can affect the heart.
• IntervenLons for decreased cardiac output r/t inability of heart to pump.
o Increase the cardiac output à(1) decrease cardiac workload , and (2) improve the
contrac1lity of the heart.
o Goals:
§ To decrease cardiac workload
1. Provide rest
2. Avoid stress
3. Support cardiac func1on
a. Give the following drugs”:
i. ACE inhibitors (captopril) – vasodilators
Cute si dims J

ii. ARBs “sartan” (angiotensin receptor blockers) –

decrease cardiac workload.
iii. Beta-blockers “olol” – decreased HR; decrease
Cardiac workload
iv. CCB “dipine” – vasodilators; decrease BP;
decreased cardiac workload
• To improve the contracLlity of the HEART:
o Cardiotonic drugs: (+) inotropic à increases contrac1lity of the heart
§ SympathomimeLc drugs: s1mulates beta 1 receptors à (+) chronotropic
effect (increase heart rate)
• Dobutamine IV via infusion pump usually in ICU; (+) inotropic effect
• Dopamine IV via infusion pump usually in ICU; (+) chronotropic
effects
§ Cardiac glycosides
• Used upon discharge from hospital à
o (+) inotropic effect (increase calcium release)
o (-) chronotropic effects prolong cardiac repolariza1on of
the heart à slows heart rate
• Contraindicated with calcium channel blockers and beta blockers
(S/E: bradycardia)
o Digoxin – narrow margin of safety; with 0.25mg
§ Nursing consideraLon for digoxin administraLon:
• Monitor HR prior to administra1on do not
give less than 60bpm
• Monitor K level, decreased K can increase
the toxicity
• Monitor ECG
• Maintain therapeu1c level
• Do not combine with CCOB, BB, and
Amiodarone (an1-arrhythmic drug;
func1ons like digoxin → lowers HR)
• Monitor for toxicity
o Bradycardia
o Visual disturbances
o Lack of appe1te
o ECG changes à dysrhythmias
o Nausea and vomi1ng it is a sign of
toxicity
§ If pa1ent has vomited do not
give another dose
§ If the pa1ent has toxicity:
WITHHOLD than refer (only
MD can discon1nue)
Cute si dims J

o an1cipate for the an1dote:

DIGIBIND binds the digoxin and
remove them from the blood.
o Digitalis
• TherapeuLc level: 0.5 – 2.0ng/ml à monitor for toxicity