CARDIOVASCULAR SYSTEM

Tissue Perfusion
▪Blood – 5-6 liters
▪↓ Blood volume → ↓ tissue perfusion → hypovolemic shock
▪Heart pump
▪↓ pump → cardiogenic shock
▪Causes: coronary causes, non-coronary, obstructive shock
Veins
▪Vascular (+) loss → VD → ↓BP = distributive/circulatory shock
1. Infection → inflammation → VD → septic shock
2. Allergy → inflammation → VD → anaphylactic shock
3. SCI → inflammation → VD → neurologic shock
BLOOD VESSELS
Arteries
▪resistance vessels = higher pressure; have thick wall
Veins
▪capacitance vessels = lower pressure
Capillaries
▪exchanges vessels – has one layer
▪smallest vessel but has the largest surface area
ARTERIES
Pulses
▪NORMAL – indicates good blood flow
0 – absent
+2 – weak
+2 – normal
+3 – increases
+4 – bounding, may be abnormal
VASCULAR DISORDERS
1. Aneurysm
2. Peripheral vascular diseases – affects the small and medium size arteries
a. Peripheral arterial disease (PAD)
▪Arteriosclerosis obliterans
▪Raynaud’s disease
b. Venous disorders
▪Varicose veins
▪Deep vein thrombosis / Venous thromboembolism
c. Buerger’s disease
ANEURYSM
▪Abnormal dilation or sac formation in the wall of an artery
TYPES
1. Congenital aneurysm
▪Most common location – cerebral vessels
2. Acquired aneurysm
▪Most common location – aorta
ETIOLOGY – atherosclerosis
▪Atheroma, atheromatous plaque
▪Hardening of the wall
▪Starts in childhood
RISK FACTORS
1. Age – the older we get, the higher the risk
▪blood vessels are more prone to injury
2. Family history (genetics)
3. Sedentary lifestyle
 4. Obesity - ↑fat diet, ↑cholesterol
5. Smoking
6. Stress - ↑ HR, ↑ BP → vasoconstriction
▪BP is most important factor to develop atherosclerosis
▪BP – the pressure exerted by the blood against the walls of the blood vessels
▪↑ BP → hardened vessel wall = DISTENTION OF OUTER WALL
SIGNS AND SYMPTOMS
1. Majority of the patients are asymptomatic
2. AAA – pulsating mass in the abdomen
DIAGNOSTIC TEST
1. DEFINITIVE DIAGNOSTIC TEST FOR ALL VASCULAR DISEASES – Angiography, Angiogram
2. Ultrasound
DANGER – RUPTURE
▪Impending sign of rupture – tearing of the wall
▪Dissecting aortic aneurysm
1. Ascending aorta – severe chest pain
2. Thoracic aorta – severe epigastric pain
3. Abdominal aorta – severe low back pain
CLASSIFICATIONS
▪Type A – ascending aorta is involved
▪Type B – descending aorta is involved
▪Type I – both ascending and descending
▪Standford DeBakey Type A
▪Type II – ascending
▪Type III – descending – Type B
MANAGEMENT
1. Type A – surgery ASAP
2. Type B – monitor BP → control BP first then surgery
3. Control risk factors
VASCULAR INSIFFICIENCY = PVD

Arterial insufficiency Venous insufficiency

Leg Pain Severe pain – ischemia Less severe – venous congestion → phlebitis
Nursing Acute pain; ineffective tissue perfusion, (+) claudication Acute pain; ineffective venous circulation
diagnosis
Skin Pale, thinning of hair, cool to touch Dark, cyanotic, pigmented
Pulse Maybe abnormal Normal but difficult to palpate
Edema Without edema With edema
Ulcer Arterial ulcer Venous ulcer
Small but deep with well circumscribed edges, no Larger lesion with irregular border, with several
granulation tissues granulation tissues
Position Dependent - Reverse trendelenburg Elevate the legs

PERIPHERAL VASCULAR DISEASES

▪Arteriosclerosis – forming in small vessels → arterioles
▪Atherosclerosis – forming in larger vessels
ARTERIOSCLEROSIS OBLITERANS
ETIOLOGY – Unknown
RISK FACTORS
▪60 years old and above
▪Sedentary lifestyle, smoking, alcohol, HPN, obesity
GENDER: Men
EXTREMITIES – lower extremities
SIGN AND SYMPTOMS – Leg pain, claudication
NURSING DIAGNOSIS
1. Ineffective peripheral tissue perfusion
2. Acute pain
3. Risk for impaired skin integrity
4. Risk for infection
5. Risk for shock
MANAGEMENT
1. Position legs – dependent
2. Avoid trauma especially in the lower extremities
3. Skin care
4. Manage risk factor
5. Pain reliever – NSAIDS
6. Vasodilators are rarely given
7. Amputation
RAYNAUD’S DISEASE – Blue, red, white disease
▪Reversible
▪Arteriolar vasospasm → blue
▪Severe vasospasm → white
▪Reversible → increase blood flow → red
▪White – lack of blood flow
▪Blue – vessels dilate to keep blood in tissues
▪Red – blood flow returns
ETIOLOGY – unknown
RISK FACTORS – exposure to cold temperature
GENDER – women
EXTREMITIES – more common in upper extremities but also affects lower extremities
SIGNS AND SYMPTOMS
▪Numbness and tingling sensation
▪Raynaud’s phenomenon
▪Etiology – known cause
1. Rheumatoid arthritis
2. SLE
3. Scleroderma
CREST syndrome
Calcinosis – position of calcium in soft tissues
Raynaud’s phenomenon
Esophageal dysmotility
Syndactyly
Telangiectasia (abnormal vein formation)
▪Treat the symptoms not the disease
MANAGEMENT
1. Avoid exposure to cold temperature
2. Always wear gloves/boots
3. Avoid smoking
4. Avoid stress
5. Control BP
6. Skin care
7. Avoid trauma
8. Vasodilators are given as ordered – Dilitiazem
9. Amputation
10. No warm/hot compress – may cause INJURY – Dependent intervention
VARICOSE VEINS
▪Abnormal dilatation and torteous formation in the superficial veins of the lower extremities
ETIOLOGY – incompetent valves
RISK FACTORS – prolonged standing/sitting, crossing of legs, obesity, pregnancy
SIGNS AND SYMPTOMS
 Pain – venous congestion and phlebitis
MANAGEMENT
1. Prevention
2. Manage
a. Medical – Schlerotherapy
▪Not applicable in large veins
b. Surgical – Vein stripping and ligation
DEEP VEIN THROMBOSIS
ETIOLOGY – unknown
RISK FACTORS
▪Immobilization
▪Virchow’s triad = Thrombus
1. Stasis = stagnation
2. Hypercoagulable
3. Endothelial injury
SIGNS AND SYMPTOMS
▪Thrombophlebitis
▪Phlebothrombosis – asymptomatic
▪Homan’s Sign (+) – do not repeat the test
▪EMBOLUS → pulmonary embolism (Dyspnea, tachypnea, chest pain)
1. Atelectasis of the lungs
2. Pulmonary hypertension → right sided heart failure
MANAGEMENT
1. Prevention
2. Immobilize – complete bed rest
3. Heparin – parenteral
4. Pain reliever – NSAIDS
5. Surgery -
6. Thrombolytic – Urokinase, Streptokinase, Alteplase
▪To dissolve the thrombus
7. (TED) Thrombo-embolic deterent hose = 6 months as ordered
8. Remove at HS, then wear again the morning
9. Anticoagulant – Warfarin
BEURGER’S DISEASE – THROMBOANGITIS OBLITERANS
▪Irreversible
▪Only in smokers
▪Gets worse the more you smoke
▪Causes poor circulation in feet and hands
▪ Thrombus and inflammation = arteries and veins
ETIOLOGY – unknown
RISK FACTOR
▪Smoking
▪Young adult men
▪Stress
SIGNS AND SYMPTOMS
1. Leg pain and claudication
MANAGEMENT
1. Stop smoking and avoid tobacco products
2. Avoid trauma
3. Skin care
4. Pain reliever – NSAIDS
5. Vasodilators are rarely given
6. Amputation
HEART
▪Muscular tissue
▪Contractility
▪Conductivity
▪Rhythmicity
▪Automaticity
▪Excitability
▪Average systemic pressure – 110/70
▪Pulmonary pressure – 25/9 – needs cardiac catheterization
▪Closure of the valve will produce heart sounds
HEART SOUNDS
S1 (lub) – closure of the aortic valves
▪Tricuspid and mitral
S2 (dub) – closure of the semi-lunar valves
▪Aortic and pulmonic
S3 (ventricular gallop) – rapid ventricular filling
▪Heard if there is an enlargement of the heart
S4 (atrial gallop) – atrial systole
▪Enlargement of the atria
MURMUR – sign of defective valves
▪Increase turbulence in the flow of blood through the heart
ASSESSMENT
1. Aortic valve – 2nd ICS right parasternal area
2. Pulmonic valve – 2nd ICS left parasternal area
3. Tricuspid valve – 4th ICS left parasternal area
4. Mitral valve – 5th ICS (between 5th and 6th) left mid clavicular line
VALVULAR DISEASES
▪Valvular insufficiency – inability of the valves to close completely/regurgitation
▪↓ CO of left ventricle → heart failure
▪Valvular stenosis – inability of the valves to open completely
▪↓ CO of left ventricle
1. Congenital disorder
2. Acquired RHD, endocarditis, Kawasaki
MITRAL VALVE PROLAPSE
ETIOLOGY - unknown
▪Ballooning or bulging of the mitral valve onto the left atrium
▪Produces SYSTOLIC CLICK/MITRAL CLICK
RISK FACTORS
1. Females
2. Family history
3. Stress
SIGNS AND SYMPTOMS
1. Tachycardia
2. Palpitation
3. Easy fatigability
4. Chest pain
5. Syncope – biglang nahihilo
6. Complications
▪Mitral regurgitation
▪Dysrhythmias → cardiogenic shock (non-coronary)
DIAGNOSTIC TEST – MOST DEFENITIVE
▪ 2D ECHO
MANAGEMENT
1. Valculoplasty
2. Valvular replacement
3. Support cardiac function
▪Provide rest
▪Avoid stress
 ▪Avoid infection
4. Management and prevent complications
▪Heart failure
▪Cardiogenic shock (non-coronary)
INFLAMMATORY HEART DISEASE
1. Epicardium
2. Myocardium
3. Endocardium
PERICARDITIS
▪Inflammation of the pericardial sac
ETIOLOGY
1. Infection
2. Trauma to the chest
3. SLE – autoimmune disease of the connective tissue
4. MI induced pericarditis (dressler’s syndrome)
5. Malignancy
6. Idiopathic
SIGNS AND SYMPTOMS
1. Most prominent symptom – CHEST PAIN – Worst: deep inspiration, supine or turning
Relief: Sitting or leaning position (orthopneic position)
▪MI pain: constant
2. Most prominent sign – FRICTION RUB
▪Auscultate at the 4th ICS parasternal area
▪Creaky, leathery, scratching sound heard best at the end of expiration or when
patient is sitting or leading forward
DIAGNOSTIC TEST
1. 2D echo – most definitive test
2. Chest x-ray
3. CBC – ↑ WBC
4. Elevated ESR – systemic inflammation
5. Culture and sensitivity test
6. Coronary Angiography – MI
7. Anti-nuclear antibody test (ANA test) – (+) with patients with immune disorders
8. Biopsy/Cytology – fluids
MANAGEMENT
1. Position – upright
2. Pain reliever – NSAIDS
3. Anti-inflammatory – Steroids
4. Manage the cause
5. Prevent and manage complications
▪Pericardial effusion (constrictive pericarditis)
▪Cardiac tamponade – sign of obstructive shock – NO POSITION THAT CAN CORRECT
BECK’S TRIAD
1. ↓ BP – hypotension
2. ↑ venous pressure – distended neck veins
3. Muffled or distant heart sound
▪Reverse if the procedure is effective, re asses/re evaluate
▪Pericardial Effusion – fluid is accumulation in the pericardial sac (maiipit ang heart)
▪Management
1. Pericardiotomy – para hindi na mag accumulate ang fluid
2. Pericardiectomy – remove pericardium
▪Possibility of development of dysrhythmia
3. Pericardiocentesis
▪Semi fowler’s – space in between
▪X-ray guided
▪Ultrasound guided – approximate the amount of fluid
 ▪ECG guided connected to the needle – during the procedure
▪5 inches needle
ENDOCARDITIS
▪Inflammation of the endocardium
▪Bacterial endocarditis = infective endocarditis
▪GAHBS, staph, pneumococci
RISK FACTORS
1. Has already an existing cardiac disease
2. Immunocompromised
3. Invasive procedure or surgery
▪Bacteria → enters the heart = BACTEREMIA
▪Systemic inflammation → fever, weakness, fatigue, malaise, headache
EMBOLIZATION
▪Microthrombi = vegetations
▪RV → pulmonary embolism
▪IV → embolic stroke
▪Retinal vessels → Roth’s spots (retina)
▪Hemorrhages with pale center
▪Osler’s node – painful nodules on finger pads and toes
▪Janeway lesions – painless macules on palms and soles
▪Splinter – brownish streaks in fingernails and toenails
▪Anemia
Fever and fatigue
Roth Spots (retinal hemorrhage)
Osler’s node: painful, reddish, tender
Murmur changes
Janeway Lesion: painless, reddish, non-tender
Anemia (clubbing)
Nail hemorrhage (splinter)
Emboli, ecchymosis
DIAGNOSTIC TEST
1. Culture and sensitivity
2. CBC
3. ESR
4. 2D ECHO
NURSING MANAGEMENT
1. Manage fever
2. Assess for changes in murmur every shift
3. Monitor vital signs
4. Support cardiac function
MEDICAL MANAGEMENT
1. Prevention – prophylaxis
▪Penicillin, if allergic give → erythromycin/azithromycin
▪Antipyretic
▪Antibacterial drug
▪Support cardiac function
▪Manage heart failure
▪Prevent shock
CARDIOMYPATHY
▪A disease of the cardiac muscle
ETIOLOGY
Types
1. Dilated – significant dilatation of the cardiac muscle diffused necrosis of the
myocardium
 RF: Alcohol, pregnancy, viral infection
▪There is no cure other than heart transplant
▪Contraindicated – calcium channel blockers
2. Hypertrophic – significant thickness of the myocardium especially the interventricular septum
▪Sudden death
▪RF: Family history
▪Contraindicated – Digoxin
3. Restrictive – ventricles become rigid
▪RF: Family history
4. Arrhythmogenic right ventricular – scarring (tumigas) of the right ventricle
▪RF: Family history
DIAGNOSTIC TEST
▪2D echo cardiography
HYPERTENSION

American Heart Association (2017), JNC 7

ETIOLOGY
1. Primary – idiopathic → essential/familial hypertension = HPN is a disease
2. Secondary → known causes = HPN is a sign of a disease
▪cause: DM, renal disease, pheochromocytoma
▪Catecholamines = epi/norepi
▪Hypertension is a RISK FACTOR
▪How to diagnose?
▪Check for BP
SIGNS AND SYMPTOMS
1. Asymptomatic – Majority of patients has no signs and symptoms
▪Ndx: Knowledge deficit, non-compliance, ineffective health maintenance, risk
diagnosis
2. Headache, dizziness, blurred vision
▪Ndx: Acute pain r/t headache, risk for injury/fall, impaired vision, disturbed sensory
perception
3. Epistaxis
▪Ndx: Ineffective airway clearance
INDEPENDENT INTERVENTION
1. Diet - ↓ salt, ↓ fat, ↓ low cholesterol and sugar
▪Include the family
▪Allowed foods
2. Exercise – DM → ↑ the use of glucose, improve blood flow, burn fats, lower cholesterol,
reduce weight
3. Avoid stress
4. Avoid smoking – vasoconstriction
5. Avoid alcohol – increase cardiac workload, increase heart rate
6. Restrict caffeine
7. Relaxation techniques – ↓ cardiac workload
▪Deep breathing exercises, aroma therapy, guided imagery, music therapy
DEPENDENT INTERVENTION
1. Drug therapy – anti hypertensive drugs
▪Secondary cause
▪↑ SNS = ↑ BP
▪Block SNS = ↓ BP to normal
TO DECREASE SNS
1. Alpha 1 antagonist → vasodilation → decrease BP (vasodilators)
▪Prazosin, Terazosin
▪Do not take warm shower → causes vasodilation
2. Alpha 2 antagonist (CNS) – decrease NE flow → decrease sympathetic response
▪Clonidine (catapres), methyldopa (aldomet)
▪Centrally acting anti HPN drugs
3. Beta blockers → heart beats more slowly and with less force
▪Propanolol, Metropolol, Atenolol, Nevibolol
▪Cardio selective – B1 ONLY
R-A-A-S

4. ACE INHIBITORS – vasodilators

▪Action – enzyme
▪Captopril, Quinapril, Enalapril
5. ANGIOTENSIN II RECEPTOR BLOCKER – vasodilators
▪Action - receptor
▪Losartan, Candesartan, Valsartan
6. DIURETICS
▪Thiazide diuretics – Hydrochlorothiazide (for HPN ONLY)
 ▪Furosemide – may cause dehydration and electrolyte imbalance
7. VASODILATORS
▪Action – smooth muscles of the blood vessels
1. Direct acting vasodilators – directly relax
▪Hydralazine → Apresoline (A/E: Hypotension)
▪Nitrates → isosorbide nitrate, nitroprusside
2. Indirect acting vasodilators – decrease calcium release in the smooth muscles of the
blood vessel
▪Nidefipine, amlodipine,
▪Amlodipine can cause edema – MAX DOSE 10 mg/day
CORONARY ARTERY DISEASE / ISCHEMIC HEART DISEASE
▪Coronary arteries – blood supply of the heart
▪Left CA – supply anterior and lateral wall
▪Right CA – inferior and posterior wall
▪Heart received blood during diastole
ETIOLOGY – unknown
RISK FACTORS
1. Atherosclerosis
2. Age – elderly (atypical symptoms) – not common
▪SOB
▪Confusion
▪Epigastric pain
3. Male > reproductive females – estrogen (cardio protective) including HDL
▪If menopausal = male (equal chances)
4. Family history – AS gene = 3x
5. Past history

ANGINA
1. Stable angina – predictable
▪Increase cardiac workload
2. Unstable angina – pre infarction angina
▪Decrease O2 supply due to severe atherosclerosis
3. Variant/Prinzmental – decreased O2 supply is due to coronary vasospasm
4. Intractable angina – severe excruciating pain → Levine’s sign
5. Silent ischemia – can happen without signs and symptoms
 ANGINA PECTORIS
NURSING INTERVENTIONS
1. Ineffective myocardial tissue perfusion- PRIORITY
2. Acute pain
3. Anxiety → restlessness – increases cardiac workload and O2 demand
4. Ineffective health maintenance
5. Non-compliance
PRIORITY INTERVENTION
1. Stable angina → position: REST, semi-fowler’s
2. Unstable angina and Prinzmental
▪Nitroglycerine first before giving oxygen
DIAGNOSTIC TEST
1. Angiography - Definitive
2. Blood test – suggestive test
▪Elevated homocysteine level
▪Elevated C reactive protein
3. ECG – myocardial ischemia
▪T wave inversion – during the pain
MANAGEMENT
1. Rest
2. Oxygen
3. Manage risk factors
4. Drug therapy (A/E: Hypotension)
A. NTG
▪Coronary vasodilator → ↑ oxygen
▪Peripheral vasodilator → ↓BP → ↓ cardiac workload
▪Acute attack – SL – fast onset of action
B. Patch NTG
▪If chronic angina
C. Isosorbide Nitrate – slow onset of action
▪Given if the condition is stabilized
D. Beta blockers – ↓cardiac workload (Diltiazem, Verapamil)
E. CCB – vasodilators
 F. Ranolazine (NEW) – decrease impulse transmission in the heart muscle
5. Surgery – PTCA (Percutaneous Transluminal coronary angioplasty)
▪Local anesthesia
6. Position to shock → administer oxygen → call the doctor
MYOCARDIAL INFARCTION
NURSING DIAGNOSIS
1. Acute Pain – pain control is priority – DEPENDENT
2. Ineffective myocardial tissue perfusion
3. Anxiety fear of death
4. Risk for dysrhythmias – premature ventricular contraction/complex = 6 or more/minute
▪Patient is transferred to ICU for close monitoring plus anti-dysrhythmia drugs
5. Risk cardiogenic shock
6. Risk for ↓ cardiac output
7. Sexual dysfunction
8. Powerlessness
DIAGNOSTIC TEST
1. Angiography
2. ECG during attack
Early sign – ST elevation
▪ST depression – myocardial injury
▪T wave inversion – ischemia
▪Scar (inverted Q wave) – old sign of MI/late sign of MI

TYPES OF MI
1. STEMI
2. NSTEMI – atypical sign (elderly)
CARDIAC ENZYMES / SERUM CARDIAC MARKER
▪Most specific, indicative enzyme – CK-MB
▪Most reliable, most sensitive, most important – TROPONIN
Enzyme elevation
1. CK MB isoenzyme
2. Troponin
3. CPK
4. LDH – suggestive
5. Myoglobin – suggestive
MANAGEMENT
▪Pain control is priority
▪MORPHINE AS ORDERED
▪Oxygenation
CORONARY ARTERY BYPASS GRAFT (CABG)
▪Expect a sternal incision, possible arm or leg incision, chest tubes, Foley catheter,
endotracheal tube and IV fluid catheters and mechanical ventilation
▪Major surgery – thoracic surgeon
CONGESTIVE HEART FAILURE
▪Inability of the heart to pump blood effectively
▪Cardiac decompensation
CAUSES
1. Cardiac cause
2. Non-cardiac cause – COPD
TYPES
1. Left sided heart failure - COPD
▪Most common
▪Left ventricle fails
2. Right side heart failure
▪Right ventricle fails
LEFT-SIDED HEART FAILURE
▪Pulmonary edema
▪PND (Paroxysmal nocturnal dyspnea) – earliest sign
▪Progressive cough
▪Crackles/Rales
RIGHT-SIDED HEART FAILURE
▪Systemic edema
▪Bipedal edema
▪Ascites
▪Distended neck veins
▪Splenomegaly
 NYHA Classification of Heart Failure

NURSING DIAGNOSIS
▪INEFFECTIVE AIRWAY CLEARANCE
▪INEFFECTIVE BREATHING PATTERN
▪IMPAIRED GAS EXCHANGE
▪FLUID VOLUME EXCESS
▪DECREASED CARDIAC OUTPUT
DIAGNOSTIC TEST
1. 2D echo
2. Chest X-ray
3. BNP (brain/beta type natriuretic peptide)
▪Protein released by the ventricles in response to congestion
▪Normal: <100 pcg/ml
▪>400 pcg/ml, sometimes >800 pcg/ml
▪The BNP will confirm if the pulmonary edema is of cardiac ORIGIN
BNP
1. Cardiac cause – very HIGH
2. Pulmonary cause – ARDS – Elevated BNP
PRIORITY – Airway and breathing
MANAGEMENT
1. Position – high fowler’s
2. Oxygen administration
3. IV line
4. Furosemide 40 mg IV stat
5. Catheterize patient
6. Monitor I and O
7. Monitor vital signs
MANAGEMENT – Fluid volume excess
1. Restric fluid
2. Restrict sodium
3. Continue monitong I & O
4. Monitor VS
5. Weight pt daily – same clothes, same time, same weighing scale
6. Diuretics
a. Furosemide
b. Spironolactone
7. Monitor Potassium level – 3.5-5 mEq/L
DECREASE CARDIAC OUTPUT – MAIN PROBLEM
1. ↓ Cardiac WL
▪Provide rest
▪Avoid stress
▪Avoid infection
 ▪Manage risk factors
▪Drugs to support cardiac function
1. ACE inhibitors – vasodilators – captopril
2. AII R blocker – Losartan
3. BBs – cardio selective
4. CCBs – vasodilation
2. Improve cardiac contractility
▪CARDIOTONIC DRUGS (+) inotropic effect
▪Sympathomimetic drugs (Adrenergic agonist)
▪Stimulate
▪(+) inotropic - ↑ contractility, (+) chronotropic – ↑ heart rate
▪Dobutamine, dopamine
▪Cardiac glycosides
▪Digoxin
▪Digitalis
DIGOXIN
1. ↑ contractility
2. ↑ Calcium release
3. ↓ HR → slow repolarization
▪A/E – bradycardia
NURSING CONSIDERATIONS
1. Monitor HR prior to administration
2. Do not give drug is HR is <60
3. Monitor serum K level, hypokalemia ↑ digoxin toxicity
4. Maintain therapeutic level 0.5-2.0 ng/ml
5. Do not combine with CCD
6. Do not combine with Amiodarone (slow down repolarization)
7. Monitor s/s of toxicity – go to hospital and check amount of digoxin in blood
▪Bradycardia
▪Halos around lights
▪N&V
▪Lack of appetite
8. ECG
9. If toxicity occurs – withhold medication dose then refer
10. Anticipate antidote – DIGIBIND
11. With DIGIBIND – WOF recurrence s/sx of heart failure