Overview of Cardiovascular System

What valves open during diastole and close in systole?

atrioventricular valves (tricuspid, mitral); prevents backflow into atria

What valves open during systole and close in diastole?

semilunar valves (pulmonic, aortic); prevents backflow into ventricle

Right Coronary Artery (RCA)

Supplies right atrium&ventricle, SA node, AV node; occlusion → decreased conduction (bradycardia, heart block)

Posterior Descending Artery (PDA)

Feeds posterior/inferior heart; comes from RCA (right dominant)

Left Main Coronary Artery

Splits into LAD and circumflex; supplies majority of LV (widowmaker)

Left Anterior Descending Artery (LAD)

Feeds anterior wall, left ventricle, septum; occlusion = most deadly MI

Collateral circulation

Vessel branching/backflow that compensates for gradual (NOT ACUTE) occlusion

Cardiac electrophysiology pathway

SA → AV → Bundle of His → R/L bundle branches → Purkinje fibers

SA node

Primary pacemaker (60-100); right atrium, fed by RCA (occlusion = 40-60 BPM)

AV node

Delays signal to allow time for ventricular filling

Lower electrophysiological pathway

Slower rates descending electric pathway —- SA 60-100 → AV 40-60 → ventricle 30-40

Atrial Depolarization

SA fires → atria depolarizes → P wave → atrial systole pushes remaining blood into ventricles (final 15-25% of blood)

Ventricular Depolarization

AV → His → Purkinje → ventricles depolarize and contract (QRS) semilunar opens and AV closes (S1)

Ventricular Repolarization

Ventricles repolarize → T wave ; semilunar close (S2)

Cardiac biomarkers for MI

Troponin I/T (most specific), ↑ CK-MB, ↑ Myoglobin

BUN/Creatinine

Higher than normal indicates low CO → poor renal perfusion (bad kidneys)

Coagulation labs

aPTT (heparin); PT/INR (warfarin)

B-type natriuretic peptide (BNP)

Hormone released by ventricles when stretched from high BP or volume (>100 indicates HF, >600-900 is moderate-severe)

Homocysteine

High levels indicates damaged arteries, increased CAD/stroke risk (<12 optimal, 12-15 borderline, >15 high risk)

Ambulatory ECG (Holter/Patch Monitor)

Worn 24hrs-14 days to capture intermittent arrhythmias while walking

Right heart cath

Access via vein (femoral/jugular) to measure pressure and oxygen in right side of heart (due to venous access) and lungs to measure O2 and diagnose pulmonary HTN

Left heart cath

Access via artery (femoral/radial) to evaluate systemic circulation and coronary arteries to detect blockages and guide interventions (PCI, stent, CABG)

Coronary Artery Bypass Graft (CABG)

Surgery using a vessel graft (saphenous) to bypass blocked coronary arteries and restore blood flow to the heart for CAD

Angioplasty (PCTA)

Balloon inserted into narrowed artery to open it, often with a stent to keep it open

Coronary Atherosclerosis

Fat deposits narrow coronary arteries → ischemia/MI → chest pain, SOB, jaw/arm pain, epigastric distress

Angina Pectoris

Reduced blood flow → myocardial ischemia → chest pain/pressure, radiates to neck/jaw/arm, SOB, nausea, diaphoresis; triggered by exertion, stress, cold, heavy meals

Stable Angina

Predictable chest pain with exertion, relieved by rest or nitroglycerin; sometimes O2

Unstable Angina

Chest pain worsens, may occur at rest, not relieved by rest or nitro

Angina Pectoris treatment

Stop activity, semi-Fowlers, O2, nitrogen, beta blockers, CCB, anticoagulants, possible PCI

Myocardial Infarction

Plaque rupture → complete coronary blockage → irreversible death of heart muscle; not relieved by rest/nitro

MONA

Morphine, oxygen, nitroglycerin (vasodilator, can’t give with low BP), aspirin

Mitral Regurgitation

Incomplete mitral closure → blood backflows into LV to LA → LV dilation → pulmonary congestion and possible systolic HF (fatigue, palpitations)

Mitral Stenosis

Narrowed mitral valve → reduced LA to LV flow → LA enlargement → pulmonary congestion and right heart strain → dyspnea, fatigue, palpitations, orthopnea

Aortic Valve Regurgitation

Blood backflows from aorta to LV during diastole → LV dilation (eccentric) → widened PP, DOE, angina, syncope, orthopnea

Aortic Valve Stenosis

Narrow aortic valve → LV → aorta obstruction → LV dilation (concentric) → possible HF, DOE, angina, syncope, orthopnea

Concentric hypertrophy

Walls get thicker (smaller size, muscular) to compensate for work put in heart

Eccentric hypertrophy

Walls stretches outward to compensate for larger volume load

Treatment for Valvular Disorders

Assess complications (HF, dysarrhythmias, syncope), daily weights, elevate HOB to ease breathing, plan activities

Commissurotomy/balloon valvuloplasty

Separates fused valve leaflets using finger or blade for stenosis

Annuloplasty

Tightens or reinforces valve annulus (ring) to improve closure and prevent regurgitation

Chordoplasty

Adjusts chordae tendineae (length/tension) to optimize valve opening and closing

Types of Valve Replacements

Mechanical (lifelong coagulants needed!!), bio prosthesis, homograft, autografts

Rheumatic Endocarditis

Post-group A streptococcus → immune system damages valves → mitral valve (stenosis/regurg), cardiomegaly, pericarditis, HF

Myocarditis

Heart muscle inflammation (viral) → necrosis, dilation → cardiomyopathy/HF; BACTERIAL in endocarditis

Pericarditis

Pericardial inflammation → effusion → can cause cardiac tamponade

Nursing Considerations for Infectious Heart Disease

-Monitor hemodynamics and arrhythmias

-Infection control

-NSAIDs/colchicine for pericarditis

-AVOID NSAIDs in myocarditis if viral

Heart failure (HF)

Inability of a pump to keep up with metabolic demand (not volume, but issue of function)

Left Sided HF

Pulmonary congestion → dyspnea, orthopnea, crackles, pink/frothy sputum, pulmonary edema

Right Sided HF

Systemic congestion → peripheral edema, JVD, hepatomegaly, ascites, fatigue, weakness

Congestive Heart Failure (CHF)

Often both sides failing; combined symptoms of left and right sided HF

Nursing management for Heart Failure

-Reduce fluid volume (preload) w/ diuretics

-Reduce afterload w/ vasodilators (e.g., ccbs)

-Reduce cardiac work (-lol)

-Increase pump effectiveness w/ digoxin

Nursing diagnoses for Heart Failure

Activity tolerance r/t decreased CO (encourage 30-45 min of exercise), fluid volume excess

Positive inotropes

Increases heart contractility → increases CO for weak heart (e.g., digoxin, dobutamine, milrinone)

Negative inotropes

Decreases heart contractility → decreases workload (HTN, angina, arrhythmias); (e.g., atenolol, clonidine)

Primary HTN

No identifiable cause (due to genetics + lifestyle); 90-95% of cases; develops w/ diabetes, obesity, smoking, poor diet, alcohol, FMHx

Secondary HTN

HTN due to identifiable cause (5-10%) such as CKD, renal artery stenosis, pregnancy, PAD, hyperaldosteronism

When to suspect secondary HTN

Sudden/severe HTN, BP stagnant despite >3 meds, age <30, signs of target organ damage ta diagnosis

HTN medications

If lifestyle changes insufficient or if BP >140/90, take thiazide, ACE inhibitors, ARBs, CCBs, and beta blockers

HTN nursing management

Evaluate target organ damage (heart, kidneys, brain, eyes), educate on adherence and side fx

Hypertensive Crisis

>180 systolic and/or >120 diastolic BP with evidence of target organ damage

Hypertensive Crisis management

Goal is rapid, but controlled BP reduction (20-25% in first hour); exceptions would be ischemic stroke or aortic dissection (perfusioon)

Hypertensive Urgency

>180/120 BP with no target organ damage; gradual BP reduction with labetalol, captopril, clonidine