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Cardiovascular system, Study notes of Cardiology

University of Pangasinan (UP)Cardiology

Study notes about cardiovascular Medsurg

Typology: Study notes

2022/2023

Uploaded on 11/25/2025

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CARDIOLOGY NURSING
CARDIOVASCULAR SYSTEM
→ It is a closed system
• Closed system → once opened → bleeding
→ Responsible for tissue perfusion bringing blood to the
different parts of the body
→ Very vital system of the body
• Reproductive system - the system not vital for
individual survival; but vital for the survival of the
population/reproduction
TISSUE PERFUSION
→ Blood - Normal: 5-6L
• ↓blood volume → ↓tissue perfusion → shock
(hypovolemic shock)
• Shock is a condition characterized by inadequate
tissue perfusion leading to multiorgan dysfunction
→ Heart - pumping blood
• ↓pump → cardiogenic shock
• Causes of Cardiogenic Shock:
1. Coronary causes: MI, CAD and all its
complications
2. Non-coronary causes: Other cardiac
conditions like congenital heart disease,
rheumatic heart disease
3. Obstructive shock: compression at the heart
→ ↓pump
▪ E.g., tension pneumothorax (air goes
inside the lungs → ↑pressure →
compression of the heart → obstructive
shock); occurs suddenly especially with
trauma
▪ Pleural effusion - slowly compresses the
heart → symptomatic to patient; not
suddenly occurs, thus not an obstructive
shock
→ Blood vessels - distribute blood to different parts of the
body
• Arteries - carry oxygenated blood to different parts
of the body except pulmonary artery
• Veins - carry unoxygenated blood back to the heart
except pulmonary vein
• Lined by smooth muscles
o Smooth muscles contract → blood vessels
constrict
o Smooth muscle relax → blood vessels dilate
• Maintains the vascular tone
o Loss of vascular tone → vasodilation → ↓BP →
shock (distributive/circulatory shock)
o Causes of Circulatory Shock:
1. Infection → inflammation → massive
vasodilation → septic shock
2. Allergy → inflammation → massive
vasodilation → anaphylactic shock
3. Spinal cord injury → neurogenic shock
BLOOD VESSELS
Characteristics
Arteries
→ Resistance vessels → higher pressure
inside
• Bleeding: spurting
→ Thickest muscular layer
→ Largest artery: Aorta
Veins
→ Capacitance vessels
• Thinner muscular layer → wider
lumen → lower pressure (less
resistance than the artery)
→ Largest vein: Inferior vena cava (bigger
than aorta)
Capillaries
→ Distributing vessels
→ Called exchange vessels
• Where gasses and nutrients
exchanges
• Made of only 1 layer: Tunica intima
→ Have the largest surface area (occupy
most of the body)
→ The smaller the capillaries → pressure is
being distributed
Arteries
Veins
Capillaries
Function
Send blood
from heart
Send blood to
heart
Material
exchange
with
tissues
Pressure
High
Low
Low
Lumen
Diameter
Narrow
Wide
Extremely
narrow
(one cell
wide)
Wall
Thickness
Thick
Thin
Extremely
thin (single
cell thick)
Wall
Layers
Three:
→ Tunica
Adventitia
→ Tunica
Media
→ Tunica
Intima
Three:
→ Tunica
Adventitia
→ Tunica
Media
→ Tunica
Intima
One
→ Tunica
Intima
Muscle &
Elastic
Fibers
Large amounts
Small amounts
None
Valves
No
Yes
No
Additional Note:
Arteriovenous (AV) Malformation
→ Cause: Idiopathic; Congenital Defect
→ Affects the neurovascular system
→ Occur in the cerebral vessels
→ Abnormal blood vessel → may rupture → bleed → can
cause hemorrhagic stroke
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CARDIOLOGY NURSING

CARDIOVASCULAR SYSTEM

→ It is a closed system

  • Closed system → once opened → bleeding → Responsible for tissue perfusion bringing blood to the different parts of the body → Very vital system of the body
  • Reproductive system - the system not vital for individual survival; but vital for the survival of the population/reproduction TISSUE PERFUSION → Blood - Normal: 5-6L
  • ↓blood volume → ↓tissue perfusion → shock (hypovolemic shock)
  • Shock is a condition characterized by inadequate tissue perfusion leading to multiorgan dysfunction → Heart - pumping blood
  • ↓pump → cardiogenic shock
  • Causes of Cardiogenic Shock:
  1. Coronary causes: MI, CAD and all its complications
  2. Non-coronary causes: Other cardiac conditions like congenital heart disease, rheumatic heart disease
  3. Obstructive shock: compression at the heart → ↓pump ▪ E.g., tension pneumothorax (air goes inside the lungs → ↑pressure → compression of the heart → obstructive shock); occurs suddenly especially with trauma ▪ Pleural effusion - slowly compresses the heart → symptomatic to patient; not suddenly occurs, thus not an obstructive shock → Blood vessels - distribute blood to different parts of the body
  • Arteries - carry oxygenated blood to different parts of the body except pulmonary artery
  • Veins - carry unoxygenated blood back to the heart except pulmonary vein
  • Lined by smooth muscles o Smooth muscles contract → blood vessels constrict o Smooth muscle relax → blood vessels dilate
  • Maintains the vascular tone o Loss of vascular tone → vasodilation → ↓BP → shock (distributive/circulatory shock ) o Causes of Circulatory Shock:
  1. Infection → inflammation → massive vasodilation → septic shock
  2. Allergy → inflammation → massive vasodilation → anaphylactic shock
  3. Spinal cord injury → neurogenic shock BLOOD VESSELS Characteristics Arteries → Resistance vessels → higher pressure inside
  • Bleeding: spurting → Thickest muscular layer → Largest artery: Aorta Veins → Capacitance vessels
  • Thinner muscular layer → wider lumen → lower pressure (less resistance than the artery) → Largest vein: Inferior vena cava (bigger than aorta) Capillaries → Distributing vessels → Called exchange vessels
  • Where gasses and nutrients exchanges
  • Made of only 1 layer: Tunica intima → Have the largest surface area (occupy most of the body) → The smaller the capillaries → pressure is being distributed Arteries Veins Capillaries Function Send blood from heart Send blood to heart Material exchange with tissues Pressure High Low Low Lumen Diameter Narrow^ Wide Extremely narrow (one cell wide) Wall Thickness Thick Thin Extremely thin (single cell thick) Wall Layers Three: → Tunica Adventitia → Tunica Media → Tunica Intima Three: → Tunica Adventitia → Tunica Media → Tunica Intima One → Tunica Intima Muscle & Elastic Fibers Large amounts Small amounts None Valves No Yes No Additional Note: Arteriovenous (AV) Malformation → Cause : Idiopathic; Congenital Defect → Affects the neurovascular system → Occur in the cerebral vessels → Abnormal blood vessel → may rupture → bleed → can cause hemorrhagic stroke

Walls of an Artery and Vein → Tunica intima - inner layer → Tunica media - smooth muscle layer → Tunica externa - outer layer; wall Arteries → Create pulses → Assessing pulses, assess the arterial function → Grading:

  • 0 - absent
  • +1 - weak
  • +2 - normal
  • +3 - increased
  • +4 - bounding → Normal pulses → good blood flow → good circulation VASCULAR DISORDERS → Diseases of the blood vessels → Invasive Diagnostic test: Angiography (definitive)
  • Done by cardiac catheterization (use of dye) → Non-Invasive Diagnostic Test: Ultrasound (Doppler/Duplex)
  • Non-invasive but definitive ANEURYSM → Arterial problem → Abnormal dilation and sac formation in the wall of an artery → Causes:
  • Congenital Aneurysm - present at birth o Common location: Cerebral vessels o Most common cause of hemorrhagic stroke in young people
  • Acquired Aneurysm - developed o Common location: Aorta → Types of Aneurysm:
  • Saccular Aneurysm
  • Fusiform Aneurysm
  • Ruptured Aneurysm o Most common type of aneurysm that causes death eventually o Shock: hypovolemic shock Aortic Aneurysm → Etiology: Atherosclerosis
  • Athero → Atheromatous plaque
  • Sclerosis → Hardening → Fatty deposits in the ascending or descending aorta → hardening d/t calcium deposition
  • Fatty deposits may start from childhood o Fat will not dissolve in children especially if they have sedentary and unhealthy lifestyle
  • Bad cholesterol (LDL), nicotine and tar can be fatty deposits → Risk factors:
  1. Age: the blood vessels becomes less elastic when we grow older (>60)
  2. Family history
  3. Sedentary lifestyle
  4. Smoking
  5. Alcohol
  6. Stress
  7. Diabetes Mellitus
  8. Obesity
  9. Hypertension: most important risk factor o Blood pressure: pressure exerted by the blood against the walls → vessel distends → hardened blood vessel → cannot distend → d/t continuous pressure by the blood → distends the outer wall of the blood vessel → aneurysm of the aorta o Ascending Aorta o Descending Aorta ▪ Thoracic aortic aneurysm ▪ Abdominal aortic aneurysm (AAA) → Signs and Symptoms: asymptomatic
  • AAA: pulsating mass in the abdomen o Thrill can be palpated in thinner clients (elderly) → Complication: rupture → bleed → hypovolemic shock → death → Sign of impending rupture
  • Dissecting aortic aneurysm ( napunit ) - tearing of the wall
  • Important RF: uncontrolled hypertension → Type A: ascending aorta is involved
  • Type I: ascending and descending
  • Type II: ascending only → Type B: descending aorta is involved
  • Type III: descending only
  • No edema → Nursing diagnosis: ineffective peripheral tissue perfusion → Management:
  1. Position the legs dependently
  2. Manage risk factors: o Weight reduction o Avoid stress o Smoking cessation o Avoid alcohol o Exercise regularly o Control BP, sugar
  3. Avoid trauma (wound will not heal)
  4. Skin care
  5. Pain reliever (NSAIDs)
  6. Vasodilators are rarely given (dilate the normal vessels only) o The doctor will assess the effectivity first before giving vasodilators
  7. Amputation Raynaud’s Disease → Condition characterized by arteriolar vasospasm (smooth muscle contract → blood vessels dilate) → AKA “Blue White Red Disease” → Reversible → Etiology: idiopathic → Risk factors:
  • Exposure to cold temperature
  • Smoking
  • Stress
  • Hypertension → More common in women → Upper extremities are commonly affected than lower extremities → Signs and Symptoms:
  • Vasospasm → blue (cyanosis) o Severe vasospasm → white
  • Pain
  • Paresthesia (numbness and tingling sensation) o Reversible → vasodilation → increased blood flow → red → Nursing diagnosis:
  • Ineffective peripheral tissue perfusion
  • Disturbed sensory perception
  • Risk for injury
  • Impaired skin integrity
  • Risk for infection → Management:
  1. Avoid exposure to cold temperature o Warm or heat application is prohibited d/t burn injury (destruction of small blood vessels)
  2. Always wear gloves and boots (especially if living in a cold weather)
  3. Keep the heat in the environment up
  4. Avoid smoking
  5. Avoid stress
  6. Control BP
  7. Pain relievers (NSAIDs)
  8. Vasodilators are given as ordered (Diltiazem) d/t vasospasm o Monitor BP
  9. Skin care
  10. Avoid trauma
  11. Amputation → Raynaud’s Phenomenon - etiology is known; S/SX of raynaud’s disease are seen in different diseases such as:
  • Rheumatoid Arthritis
  • Systemic Lupus Erythematosus
  • Scleroderma - hardening of the skin (chest, hands); exhibits CREST syndrome o Difficult to treat d/t unknown cause o CREST syndrome - collection of signs and symptoms ▪ Calcinosis - deposition of calcium in soft tissues → hardening of the skin ▪ Raynaud’s phenomenon ▪ Esophageal dysmotility - no movement of esophagus (d/t calcium deposits → hardening) ❖ Possible of GI, nutrition problem ❖ Risk for aspiration ▪ Syndactyly - fusion of hands and fingers (creases and lines are nawawala; weblike) ▪ Telangiectasia - abnormal vein formation in the skin o Affects young adult women (18-25)
  • The disease is being treated in Raynaud’s phenomenon Additional Notes: → Atherosclerosis
  • Affects big vessels → Frostbites happen when there is exposure to extremely cold temperatures (can happen to anyone) while raynaud’s occur with just a slight drop of temperature Test Taking Strategies: → “Always” - usually wrong → Do not memorize questions and answers, understand them! - Doc. Arreglo ✨ VENOUS INSUFFICIENCY Varicose Veins → Involves superficial veins of the lower extremities → Abnormal dilation and tortuous formation of the superficial veins of the lower extremity (kulot kulot)
  • ↑pressure → distention → Irreversible → Valves direct the flow of blood up → Cause: Incompetent valves (destruction of valves) → Risk factors:
  • Prolonged standing
  • Prolonged sitting
  • Prolonged crossing of legs (impediment in the flow of blood)
  • Obesity
  • Pregnancy (enlarging uterus impedes the upward flow of blood) → Signs and Symptoms:
  • Leg pain d/t venous congestion and phlebitis o Injury to the wall → inflammation → phlebitis
  • Edema
  • Skin - dark, pigmented, cyanotic → Nursing Diagnosis:
  • Ineffective venous circulation
  • Acute pain
  • Risk for impaired skin integrity
  • Impaired skin integrity → Management:
  1. Prevention

▪ Avoid prolonged standing, sitting, crossing of legs ▪ Weight reduction ▪ Exercise ▪ Compression stockings → to increase the muscle tone → compress blood vessels → direct the flow of blood upward

  1. Medical Management: Sclerotherapy: hardening of blood vessels ▪ Done in skin clinics ▪ Chemicals/ lasers are used; with sessions ▪ Chemicals (white) are injected making the blood vessel hard → lessen discoloration of the skin (match color of the skin) ▪ Blood flows to collateral veins
  2. Surgical Management: vein stripping and ligation ▪ Blood flows to collateral veins Deep Vein Thrombosis – AKA Venous Thromboembolism (VTE) → Deep veins surrounded by big muscles of the leg → valves → Thrombus: an abnormal clot (not dissolved) → Thrombophlebitis
  • Thrombus + inflammation → pain, redness, swelling, heat → Phlebothrombosis
  • Thrombus only, no inflammation → asymptomatic
  • Assessment: o Homan’s sign: dorsiflexion of the foot causes pain in calf muscles ▪ Not reliable ▪ If (+): do not repeat the test (repetition may dislodge the thrombus → embolus) ❖ Dangerous complication: pulmonary embolism (IVC → RA → RV → PA → Lungs → sudden death) ➢ Pulmonary hypertension → Collapse of the lungs ❖ Signs of Pulmonary Embolism: ➢ Dyspnea ➢ Tachypnea (shallow breathing) ➢ Chest pain ❖ Management:
  1. Elevate HOB (semi-fowler’s)
  2. Oxygenation
  3. Refer o Severe obstruction = sudden onset of leg pain (a possible sign of DVT) → VTE to emphasize its dangerous complication → embolus → Etiology: Idiopathic → Risk Factors:
  • Immobilization (muscles are not contracting) o Contraction of big muscles → valves → compress blood vessels → upward flow of blood → Virchow’s Triad = THROMBUS FORMATION
  1. Stasis/stagnation (Slow blood flow)
  2. Hypercoagulability (easy to form clot)
  3. Endothelial injury (intima is lined with endothelial lining o Any of the situations may lead to thrombus formation (E.g., stasis + hypercoagulability)
  • Susceptible (patients with viscous blood): o Bedridden o Comatose o Paralyze o Post operative o DM o Taking contraceptive pills (estrogen increases the viscosity of the blood) - Patients with PCOS → Management:
  1. Prevention - very important AH! o Mobilize! o Elevate the legs o Compression stockings/Antiembolic stockings ▪ Brunner: TED Hose (Thromboembolic Deterrent Hose)
  2. Manage DVT o Complete bed rest without bathroom privileges (immobilize the patient) ▪ Possible dislodge of thrombus with movement → embolus o Anti-coagulant (heparin) o NSAIDs o Surgery - endovascular surgery o Thrombolytic therapy ▪ Purpose: To dissolve the thrombus ▪ Urokinase, Streptokinase, Alteplase (USA)

→ Mitral valve: 5th intercostal space (between 5th and 6th) left midclavicular line

  • The point of maximum impulse (PMI)
  • Apical pulse (apex)
  • Closure of the mitral valve (S1) VALVULAR HEART DISEASES → Non-coronary cardiogenic shock can occur Valvular Insufficiency Valvular Stenosis Inability of the valves to close completely → backflow → regurgitation Inability of the valves to open completely ( narrowing ) → ↓cardiac output → cardiogenic shock (non- coronary) → heart failure → Etiology:
  • Congenital o TOF: pulmonic stenosis
  • Acquired o Rheumatic fever → RHD o Endocarditis → valvular defects → Presence of murmur → Compensatory mechanism: enlargement of the heart (cardiomegaly) → allows strong contraction → ↑cardiac output
  • Cardiomegaly is irreversible (response to a pathologic condition)
  • Physiologic cardiomegaly o Occurs d/t strenuous activities → the heart compensates to increase cardiac output o Normal to Athletes ▪ HR is low when asleep ▪ Cardiac endurance
  • As long as the heart is compensating, the cardiac output is normal
  • The heart will start to fail once it cannot compensate anymore Mitral Valve Prolapse → Bulging/ballooning of the mitral valve onto the left atrium → Etiology: Unknown → Risk factors:
  • Congenital
  • Family history
  • Common on females; young adult
  • Stress → When it closes → mitral click/systolic click is heard at the APEX → Signs and Symptoms:
  • Chest pain
  • Palpitations (feeling of heart beating)
  • Easy fatigability
  • Syncope ( pass out ) → Management: Avoid caffeine or any stimulants; give beta blockers to manage palpitations → Complications:
  • Mitral regurgitations
  • (+) Murmurs
  • (+) Dysrhythmia → Definitive Diagnosis: 2D Echocardiography → It the heart cannot compensate anymore; it will eventually fail Management for Valvular Disorders:
  1. Valvuloplasty (repair)
  2. Valvular replacement (a mechanical valve or fibrous valve)
  3. Support cardiac function: Independent Intervention
  • Provide rest
  • Avoid stress - increases the demand for oxygen
  • Avoid infection - increases the demand for oxygen
  1. Manage heart failure Valvular Repair → Cardiac catheterization → Balloon catheter → inflation → compress the valve → removed LAYERS OF THE HEART

→ Endocardium - inner most layer

  • Inflammation of the endocardium - endocarditis → Myocardium - middle layer
  • Inflammation of the myocardium - myocarditis; common in children; caused by coxsackie virus → Epicardium - outer most layer
  • Inflammation of the epicardium - pericarditis
  • AKA visceral pericardium → Parietal pericardium - protective layer → Pericardial sac → Pericardial fluid - it decreases when ventricles contract PERICARDITIS → Inflammation of the pericardial sac → Etiology:
  • Idiopathic
  • Infection
  • Trauma to the chest
  • Malignancy (sign of metastasis)
  • Systemic Lupus Erythematosus (SLE)
  • MI-induced pericarditis (Dressler’s syndrome) → Sign and Symptom
  • Chest pain - most prominent clinical manifestation/symptom - subjective cue o Pericarditis chest pain - pain worsens with deep inspiration, lying down, or turning and relieved by sitting or leaning forward (Orthopneic/tripod position) o MI chest pain - constant (not affected by breathing or movement of the chest)
  • Friction rub (most common sign - objective cue) o Swelling → ↑pressure when the ventricles contract → friction rub o Friction rub: assessed by auscultation at the 4th intercostal space left parasternal area (bell of the stethoscope) o Creaky, leathery, scratchy sound o Sound heard best at the end of expiration and when the patient is sitting or leaning forward → Nursing Diagnosis: Acute pain related to inflammation of the pericardial sac → Intervention:
  • Position: orthopneic (priority) - to relieve pain; lessens irritation to the wall → Diagnostic Tests
  • 2D echocardiography (most definitive)- seen by the eyes
  • Chest X ray (2nd option to 2D echo) - heart, sac, distention
  • CBC - increased WBC → infection
  • Elevated Erythrocyte Sedimentation Rate (ESR) - systemic inflammation
  • Culture and sensitivity → infection
  • Coronary angiography
  • AntiNuclear Antibody (ANA) Test - suggestive test for SLE; for autoimmune diseases o If (+): the cause of pericarditis is SLE
  • Biopsy (if cancer is the cause) → Management
  • Orthopneic Position (tripod/leaning forward) - priority; independent
  • Pain reliever - NSAIDS
  • Anti-inflammatory drugs - steroids
  • Manage the cause
  • Prevent and manage complications: o Pericardial effusion o Cardiac tamponade
  • Pericardiotomy - opening of the pericardium → stent is placed to allow drainage of fluid into the pericardial cavity (reabsorbed by the lymphatics → systemic circulation) o Done when there is recurrent pericardial effusion
  • Pericardiectomy - removal of the pericardial sac (to prevent compression of the heart) o Complication: dysrhythmias → Complications:
  • Pericardial Effusion - accumulation of fluid in the pericardial sac (>20 ml) o Normal fluid: 15-20 ml o Constrictive pericarditis o Can lead to cardiac tamponade o Pericardiocentesis - Remove the fluid from the pericardium ▪ Done by the doctor ▪ The nurse assists the doctor ❖ Position - semi fowler’s ▪ X-ray and ultrasound guided to avoid puncturing the lungs (done before the procedure) ▪ ECG guided - done during pericardiocentesis ❖ The needle is connected to the ECG to prevent puncturing of the heart
  • Cardiac Tamponade - life-threatening (leading to shock) characterized by the inability of the heart to pump d/t excessive fluid in the pericardium (emergency; can lead to cardiogenic obstructive shock) o Manifestations (Beck’s Triad): ▪ ↓BP d/t ↓cardiac output ▪ ↑jugular vein pressure → distended neck veins ▪ Muffled/ distant heart sounds
  1. Antipyretic - for fever
  2. Analgesic - for pain
  3. Antibiotic as ordered
  4. Support cardiac function
  5. Manage heart failure
  6. Prevent shock (septic/cardiogenic) CARDIOMYOPATHY (CDM) → Non coronary disease → Disease of the cardiac muscle → Etiology: Idiopathic → Cannot given CCB: cannot contract anymore → → Types of Cardiomyopathy
  7. Dilated Cardiomyopathy: Most common type o Significant dilatation w/o hypertrophy o Diffused necrosis of the cardiac muscle (cell death) o Risk factors: ▪ Viral infection ▪ Pregnancy ▪ Alcoholism
  8. Hypertrophic Cardiomyopathy o Significant thickness of the myocardium (esp.: interventricular septum) → resulting to reduced size of the chamber → opening of the aorta is obstructed → no blood flow → sudden death o Risk factor: Family history
  9. Restrictive Cardiomyopathy o Ventricles becomes rigid o Risk factor: Family history
  10. Arrhythmogenic Right Ventricular Cardiomyopathy o Fibrosis of the right ventricle o Risk factor: Family history → Irreversible → heart failure → Cure: heart transplant BLOOD PRESSURE → Classification of blood pressure for adults 18 years old and above → What we consider as normal BP = 110/ → For elderly, expected to be higher >120/> BP CLASSIFICATION (^) PRESSURESYSTOLIC^ DIASTOLIC PRESSURE Normal <120 < Prehypertension <120- 139 80 - 89 Stage 1 140 - 159 90 - 99 Stage 2 (patient is already at risk for complications) =/>160 =/> Source: American Society of Hypertension & International Society of Hypertension (Caucasians) Source: American Heart Association, 2017 (Lifestyle Modifications - Elevated BP) → Etiology:
  • Primary: Idiopathic/Essential HPN/Familial HPN o Hypertension is a disease
  • Secondary: there are known causes such as DM, Kidney Diseases, Pheochromocytoma o Hypertension is a sign of a disease o Could be a sign factor for PAD, MI, etc., o No cure for hypertension; but can be managed and control → Clinical Manifestations:
  • Asymptomatic o NDx: Knowledge Deficit, Non-Compliance, Ineffective Health Maintenance
  • Headache (upon waking up in the morning) o NDx: Acute pain r/t headache
  • Dizziness o NDx: Risk for fall/Injury
  • Blurred Vision o NDx: Disturbed Sensory Perception, Visual o Risk for injury/fall
  • Epistaxis o Risk for ineffective airway clearance r/t clot formation, Risk for Aspiration → Independent Interventions:
  • Diet: Low-salt, low-fat. Low-cholesterol, low sugar o Include the family in the diet therapy o Ask the patient regarding food that he likes (allowed only)

o Modify the diet

  • Exercise: increase the use of glucose in the cell → increase blood flow → burn fats, lower cholesterol, increase cardio endurance
  • Avoid stress: adrenal gland → release cortisol/ catecholamines
  • Avoid smoking d/t vasoconstriction
  • Avoid alcohol → increases cardiac workload, increased HR
  • Restrict caffeine → palpitation, tachycardia
  • Relaxation techniques: Decreases cardiac workload o DBE o Music o Yoga o Massage/Spa o Aromatherapy → Dependent Interventions: o Drug therapy - hypertensive drugs o Secondary cause o Increased SNS = increases BP o Block SNS = decrease BP to normal o To decrease SNS ▪ Alpha 1 Antagonists ❖ Blood vessels = vasodilators ❖ Prazosin ❖ Doxazosin ❖ Terazosin ❖ Prevent activities that may aggravate hypertension: hot shower (dilates vessels) ▪ Alpha 2 agonist ❖ CNS = decreases norepinephrine flow → decrease sympathetic effect → decrease BP ❖ Clonidine (Catapres) ❖ Methyldopa (Aldomet) ❖ Both are called centrally acting antihypertensive drugs ▪ Beta blockers ❖ Beta1 - heart → decrease heart ❖ Beta2 blockers → lungs → bronchoconstriction ➢ B1 and B2 blockers - non cardioselective ❖ Propranolol - b1 and b2 blockers (non- cardioselective) ❖ Metoprolol - b1 blockers (cardioselective) o Renin-Angiotensin-Aldosterone-System (RAAS) ▪ ACE Inhibitors ❖ Captopril ❖ Quinapril ❖ Enalapril ❖ SE: cough ▪ Angiotensin II Receptor Blockers ❖ Losartan - given after meals → cause GI toxicity ❖ Candesartan ❖ Telmisartan ▪ Diuretics ❖ Thiazide diuretics - hydrochlorothiazide; does not cause too much water loss ❖ Furosemide can cause tremendous loss of fluid and electrolytes, dehydration ▪ Vasodilators ❖ Direct Acting Vasodilators ➢ Directly relax the smooth muscles of the blood vessels ➢ Hydralazine ➢ Nitrates - NTG, Isosorbide, Nitroprusside ❖ Indirect Acting Vasodilators ❖ Calcium channel blockers - Decrease the flow of calcium → relax smooth muscles → dilate blood vessels ➢ Nifedipine ➢ Amlodipine ➢ Felodipine ➢ Diltiazem (long acting CCB) ➢ Verapamil (long acting CCB) CORONARY ARTERY DISEASE (ISCHEMIC HEART DISEASE) → Coronary arteries - blood supply of the heart
  • Come from the first branches of the ascending aorta
  • Left coronary artery - supply the anterior and lateral wall
  • right coronary artery - supply the inferior and posterior wall → The heart receives blood during diastole (relaxation) → Acute coronary syndrome - having s/sx of CAD → Etiology: idiopathic → Risk factors
  • Atherosclerosis: Fatty deposits → presence of calcium deposition in the blood vessels hardens it → injury formation → clot formation → decreased oxygen supply to the heart → ischemia → chest pain
  • Age - elderly (atypical - not common) o Confusion o Shortness of breath o Epigastric pain
  • Family history o Atherosclerotic (AS) gene (increases the risk three times than those without the gene)
  • Past health history
  • Common in males than reproductive females (presence of estrogen) o Estrogen has a cardioprotective effect → produces more good cholesterol o But when menopausal phase, men and women have equal chances Angina → Chest pain d/t ischemia → Types of Angina
  1. Stable Angina - d/t increased cardiac workload; reversible ▪ Predictable type of angina - anticipate that it will happen to the patient
  2. Unstable Angina/Pre-infarction Angina - d/t severe atherosclerosis → decreased oxygen supply ▪ Can happen even if the patient is resting
  3. Variant Angina/Prinzmetal Angina - decreasing oxygen supply d/t coronary vasospasm

o Resumption of sexual intercourse after MI: if can tolerate 1-2 flights of stairs without chest pain ▪ Health teaching/Instructions: ❖ Patient should be passive ❖ Partner should be active ❖ NTG should be at bedside ➢ If pain is still felt, bitin is real; shower na lang po → The most common complication of MI = dysrhythmia, premature ventricular complex/contraction (PVC)

  • Significant number of PVCs: 6 or more per minute
  • Administer antiarrhythmic drug as ordered
  • Can lead to ventricular tachycardia if not treated (defibrillation is done) → Diagnostic tests:
  • Angiography - most definitive
  • ECG Changes o Zone of infarction – ST elevation: early sign of acute MI o Zone of injury – ST depression: sign of myocardial injury o Ischemic area – inverted T wave: sign of myocardial ischemia o Sign of scar – pathologic Q wave/inverted Q wave: old/late sign of MI ▪ Can happen silently
  • Cardiac enzymes/serum cardiac markers (confirmatory test) - released by injured cells o Most specific enzyme: CKMB o Most reliable, sensitive, important: Troponin (elevated for 3 weeks) o 4 - 6 hours from the onset of pain o Troponin elevating earlier than CKMB o First to be elevated is myoglobin (suggestive; 2 hours before elevation) ▪ LDH and CPK are elevated as well (6 hours before elevation) CARDIAC BIOMARKERS TROPONIN I TROPONIN T CK-MB (CREATININE KINASE-MB) Exclusively seen in cardiac muscle (most reliable) Seen in cardiac and skeletal muscle Most reliable before Release^3 - 6 hours after injury 3 - 6 hours after injury 4 - 6 hours after injury Elevation 5 - 10 days after injury 5 - 14 days after injury 2 - 3 days after injury → 2 Types of Myocardial Infarction
  • STEMI
  • NSTEMI o Atypical sign (elderly) → Management:
  1. Pain control is priority - morphine as ordered (during acute attack) o Increase high fiber diet (causes constipation) o Check for respiratory depression
  2. Oxygenation
  3. Drug therapy o Thrombolytic Drug ▪ Dissolve thrombus ▪ Urokinase, Streptokinase, Alteplase (USA) o Antithrombotic Drugs ▪ Anti-platelet (blood thinners); aspirin, clopidogrel ▪ Anticoagulant - warfarin, heparin
  4. Manage risk factors
  5. Drugs to support cardiac function o NTG o Isosorbide o Beta blockers o Calcium channel blockers
  6. PTCA
  7. CABG (coronary artery bypass graft)
  • Peripheral vessels - Saphenous veins are attached to the heart
  • Central vessels are not used as a graft (e.g., subclavian, common carotid, femoral) HEART FAILURE → Inability of the heart to pump effectively → Cardiac decompensation (failed to compensate) → Causes:
  • Cardiac causes
  • Non-cardiac causes - COPD (most common; causes RSHF) Types: → Left sided Heart Failure - the left ventricle fails
  • Most common
  • If the left side fails, right side will follow

o Increased pressure in the the lungs → difficulty of the RV to pump blood → decreased cardiac output

  • Signs and Symptoms: o Pulmonary edema ▪ Increased pressure → leaked fluids o Paroxysmal nocturnal dyspnea (earliest manifestation) ▪ Sudden occurrence of dyspnea at night o Orthopnea o Progressive cough o Dyspnea o (+) Crackles/Rales on auscultation
  • Nursing diagnosis: o Ineffective airway clearance o Ineffective breathing pattern o Impaired gas exchange o Decreased cardiac output o Ineffective tissue perfusion → Right sided Heart Failure (congestive heart failure) - the right ventricle fails
  • Signs and Symptoms: o Systemic edema: Bipedal edema o Ascites o Hepatomegaly o Splenomegaly o Weight gain o Enlarged heart ▪ Heart sound: (+) ventricular gallop (lub dub dub) - S3 sound
  • Nursing diagnosis: Fluid volume excess New York Heart Association (NYHA) Classification of Heart Failure → Class I - risk for activity intolerance → Class II - activity intolerance → Class III - decreased cardiac output Diagnostic test → 2D Echocardiography: most definitive → Chest X ray → Brain/Beta Type (BNP)
  • Natriuretic Peptide - protein released by the ventricles in response to congestion
  • Normal: <100 pcg/mL o CHF: >400 pcg/mL (>800 pcg/mL)
  • When pulmonary edema is present, there is an elevated BNP o Cardiac cause (CHF) - extremely elevated;

400 pcg/ml o Pulmonary cause (ARDS) - elevated; 300 pcg/ml Management: depends on the nursing diagnosis Ineffective Airway Clearance - Airway and Breathing Problems → Position the patient- high fowler’s → Administer oxygen → IV line → Furosemide (40 mg IV stat) → Catheterize the patient → Monitor I and O accurately → Monitor vital signs Fluid volume excess → Restrict water (1-1.5L) → Restrict sodium → Monitor intake and output → Monitor vital signs → Weigh the patient daily (same time, clothes, weighing scale) → Oral diuretics

  • Furosemide (potassium wasting → hypokalemia )
  • Spironolactone (adjunct diuretic; potassium sparing → hyperkalemia) → Monitor serum potassium levels (N: 3.5-5.5 meq/L) Decreased Cardiac Output r/t inability of the heart to pump effectively → To increase cardiac output → Goals:
  • To decrease cardiac workload
  • To improve cardiac contractility → To decrease cardiac workload:
  • Support cardiac function o Provide rest o Avoid stress o Avoid infection
  • Drugs that will decrease cardiac function o ACE inhibitors - peripheral vasodilation → low BP → decreased cardiac workload; e.g., captopril o Angiotensin II receptor blockers - vasodilator; e.g., losartan o Beta blockers - decrease heart rate → decrease workload; e.g., metoprolol (cardioselective) o Calcium channel blocker - peripheral vasodilators → low BP → decreased cardiac workload; e.g., diltiazem, verapamil (long- acting vasodilators) → To improve cardiac contractility
  • Cardiotonic Drugs o Sympathomimetic → enhances sympathetic effect → increase contractility and HR; e.g., dobutamine, dopamine ▪ Given via infusion pump to prevent arrhythmias ▪ (+) inotropic effect = increase contractility ▪ (+) chronotropic effect = increase HR ▪ Adrenergic agonists o Cardiac Glycosides; e.g., digoxin, digitalis ▪ (+) inotropic effect = increasing calcium release in the cardiac cell → increase cardiac contractility ❖ (X) combine with CCB - digoxin release calcium, CCB blocks calcium ▪ (-) chronotropic effect = decrease HR ❖ Slowing down repolarization → slow down potassium efflux → decreased HR ▪ Nursing consideration: ❖ Monitor HR ➢ Do not give drug if HR is < ❖ Monitor ECG ➢ It affects repolarization ❖ Monitor potassium level ➢ Hypokalemia increase digoxin toxicity ➢ Watchfulk: thera ❖ Do not combine with CCB ❖ Do not combine with amiodarone (antiarrhythmic drug) ➢ Have same action with digoxin → heart may stop ❖ Maintain therapeutic level: 0.5-2. ng/mL ❖ Monitor s/sx of toxicity ➢ Hallmark: visual disturbances ➢ Bradycardia ➢ Lack of appetite ➢ ECG changes ➢ Nausea and vomiting