Cardiac Cycle: Definitions & Equations

•  Systole = isovolumic ventricular contraction & ejection

•  Diastole = isovolumic ventricular relaxation & filling

•  Cardiac output = stroke volume × heart rate

→ volume of blood pumped by each ventricle per minute

Figure 16-1. Frank–Starling relationship.

•  Stroke volume = amount of blood pumped out of each ventricle with each contraction

•  Cardiac reserve = difference between cardiac output at rest & the max volume of blood the heart is capable of pumping per minute

•  Preload = volume of blood in ventricle before systole, used to estimate left ventricular end diastolic volume (LVEDP)

•  Starling’s law = contractility depends on muscle fiber length

•  Afterload = resistance to ejection of blood by each ventricle

•  Coronary perfusion pressure (CPP) = aortic diastolic BP – LVEDP

•  Left ventricular wall tension → Law of Laplace: T = p × r/(2 × t) where T = wall tension, p = pressure, r = radius, t = wall thickness

•  Fick equation:

Cardiac output (C.O.) = O₂ consumption/([arterial O_{2 content}] – [venous O_{2 content}])

COMMON DISEASE STATES AFFECTING THE HEART

Determinants of Myocardial Perfusion

Supply: CPP, HR, PaO₂, coronary artery diameter

Demand: Myocardial O₂ consumption, HR, LV wall tension, contractility, conduction, relaxation

Hypertension (HTN)

•  Definition: >140/90 or 130/80 in high-risk pts

•  Essential HTN (1° HTN)—no definable cause (95% of pts)

•  2° HTN: Iatrogenic (meds), renal, aortic coarctation, pheochromocytoma, adrenocortical hormone excess, thyroid hormone abnormal, estrogen therapy, Cushing’s disease

•  Consequences of HTN

• Organ damage: Ventricular hypertrophy, systolic dysfunction, CAD, stroke, abd aortic aneurysm, aortic dissection

• Hypertensive crises: HTN encephalopathy—headache, blurred vision, confusion, somnolence, coma

•  Treatment: Diuretics, sympatholytic agents (β-blockers/α-2 agonists/α-1 antagonists), vasodilators, (Ca-channel blockers, ACE inhibitors, ARBs), nitrates

•  Anesthetic considerations

• Monitoring: BP cuff vs. arterial line as indicated

• Goal: Keep BP within 20% of baseline

Valvular Disease

Mitral Stenosis

Causes: Rheumatic fever, congenital stenosis

Pathophysiology

•  ↑ LA pressure → pulmonary edema, LV hypertrophy

•  Atrial fibrillation may result from LA dilation, LA thrombus from stasis of flow

•  Develop pulmonary HTN

•  Atrial kick provides 40% of LV filling

•  Stroke volume is fixed

Clinical feature

•  High-pitched “opening snap” followed by low-frequency diastolic rumble

Classification

•  Mild = valve area of ≤2 cm²; critical = valve area ≤1 cm²

Treatment

•  Medical therapy; balloon mitral valvuloplasty; open mitral commissurotomy; mitral valve replacement

Anesthetic management

•  Maintain sinus rhythm (atrial kick provides 40% vent filling)

•  Maintain preload & SV to avoid drop in SVR

•  Maintain normal HR (to allow time for filling)

•  Prevent ↑ in PVR (avoid hypoxia, hypercarbia, acidosis)

Mitral Regurgitation

Causes: Myxomatous disease (mitral valve prolapse [MVP]), ischemic heart dz, heart failure, annular dilation, endocarditis, rheumatic heart dz, hypertrophic cardiomyopathy (SAM), myocardial infarction (necrotic papillary muscle, ruptured chordae)

Pathophysiology

•  Severity determined by

• Systolic pressure gradient between LV and LA

• Systemic vascular resistance opposing forward LV blood flow

• Left atrial compliance

• Duration of regurgitation with each systole

•  Regurgitant fraction = volume of MR/total LV stroke volume (>0.6 = severe)

•  Acute MR: ↑ pulmonary pressure & pulmonary congestion

•  Chronic MR: ↑ LA size & compliance

Clinical features

•  Apical holosystolic murmur radiating to axilla

Treatment

•  Medical therapy; mitral valve repair/replacement

Anesthetic management

•  Maintain HR normal or high

•  Avoid myocardial depression

•  Avoid ↑ SVR (can worsen regurgitation)

•  Initiate prophylaxis against endocarditis

•  PA catheter v waves increase as regurgitant fraction increases

Aortic Stenosis

Causes: Bicuspid AV, senile degenerative disease, rheumatic fever

Risk factors: Male gender, hypercholesterolemia, smoking

Pathophysiology

•  Blood flow across valve is obstructed during systole

•  Concentric LV hypertrophy

•  Dependence on atrial kick to fill stiff ventricle

•  Stroke volume is fixed

•  Compression of subendocardial vessels → ischemia

Symptoms & severity

•  Angina—median survival 5 yrs

•  Syncope—median survival 3 yrs

•  Congestive heart failure—median survival 2 yrs

Clinical features

•  Harsh, holosystolic, crescendo–decrescendo murmur

Classification

•  Mild = valve area <2.5 cm², moderate = 0.7–1.2 cm², critical <0.7 cm²

Treatment

•  Percutaneous balloon valvuloplasty, percutaneuous, transapical, or open aortic valve replacement

Anesthetic management

•  Maintain sinus rhythm (atrial kick provides 40% of preload)

•  Maintain HR slow to normal (allow time for ventricular filling)

•  Avoid ↓ SVR (will ↓ CO because of fixed SV)

→ because of this, severe AS is a relative contraindication to spinal anesthesia

•  Initiate prophylaxis against endocarditis

•  Avoid myocardial depression as stroke volume is fixed

•  Consider arterial line placement for severe AS

•  Consider percutaneous pacing capability in case of cardiac arrest (chest compressions usually ineffective)

Aortic Regurgitation (AR)

Causes: Leaflet abnormalities (rheumatic heart dz, endocarditis, bicuspid valve), dilation of aortic root (aortic aneurysm/dissection, Marfan syndrome, syphilis, cystic medial necrosis)

Pathophysiology

•  Acute = surgical emergency—sudden ↑ LV diastolic pressure rise backs up to pulm circulation causing pulm congestion, acute pulm HTN, & edema

•  Chronic—LV compensates with dilation & hypertrophy → heart failure

Clinical features

•  Bounding pulses

•  Austin Flint murmur—turbulent flow across mitral valve during diastole due to AR jet

Treatment

•  Asymptomatic—nifedipine, ACE inhibitor, diuretics

•  Symptomatic—aortic valve replacement

Anesthetic management

•  Maintain sinus rhythm

•  Maintain normal to high normal heart rate

•  Avoid ↑ SVR (will worsen regurgitant fraction)

•  Avoid myocardial depression

•  Initiate prophylaxis against endocarditis

•  Consider vasodilators (nitroprusside) to ↓ afterload

Pulmonic Stenosis

Causes: Congenital deformity, carcinoid heart disease

Classification

•  Mild: Pressure gradient <40 mm Hg, moderate 40–80 mm Hg, severe >80 mm Hg

Treatment

•  Balloon valvuloplasty; valve replacement

Pulmonic Regurgitation

Causes: Annular dilation 2° enlarged pulm artery in pulm HTN, congenital/carcinoid heart dz

Tricuspid Stenosis

Causes: Congenital, rheumatic heart dz, right atrial tumor, endocarditis

Tricuspid Regurgitation

Causes: Congenital, endocarditis, carcinoid heart dz, secondary event from mitral valve or left-sided heart dz

Hypertrophic Cardiomyopathy (HCM)

Causes: Genetic, mixed, acquired

Pathophysiology

•  LV outflow obstruction (asymmetrical hypertrophic septum interferes with LV ejection)

•  LVH & RA enlargement, ↑ myocardial O₂ consumption

→ subendocardial ischemia

Clinical features

•  Mitral regurgitation from SAM (systolic anterior motion of anterior mitral leaflet)

•  ↑ risk of sudden death

Anesthetic management

•  Maintain slow HR (to allow for ventricular filling)

•  Maintain sinus rhythm

•  Maintain low to normal contractility (can cause/exacerbate SAM)

•  Maintain preload & afterload

•  Treatments include β-blockers, verapamil, pacing, ICD, surgical myectomy

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