Heart Failure

General

  • Heart muscles weaken, dilated ventricles swell and can’t pump blood efficiently, heart muscles stiffen due to cardiac and vascular remodeling.

  • Perfusion (cool) - insufficient delivery of oxygenated blood cells shown by fatigue or decreased cognition. Since no blood flow, affected areas are cool to touch

  • Congestion (Wet) - insufficient return of blood to heart causes pooling in veins and leakage.Fluid accumulates as peripheral edema or pulmonary edema (lungs SOB) limiting ability of heart to expand

  • Impaired circulation causes increase in RAAS and sympathetic nervous system straining the heart and causing further damage from attempt to increase circulation and blood pressure

Acute

  • crisis situation from new or exacerbating factors, develop CHF over time

    • body is unable to compensate sufficiently to maintain function

    • goal to prevent immediate death, increase CO and deal with fluid imbalance

Chronic

  • ongoing situation from (CHF) as a result of overwork and injury

    • body can compensate to maintain function, but decreases over time

    • goal protect the heart, decrease CO and damage and deal with fluid imbalance

Acute Decompensated Heart failure

  • immediate emergency

    • goal keep patient alive by addressing underlying causes and surgical intervention

  • decrease fluid accumulation

    • loop diuretics furosemide, bumetanide, torsemide, ethacrynic acid

      • high ceiling high doses big response

    • vaptans conivaptan or tolvaptan → hypernatremia risk

  • lack of hemoperfusion with inotropes IV agents short ½

    • milrinone PDE 3 inhibitor

      • protect and increase cAMP to raise contractility via Ca

    • dopamine or dobutamine sympathomimetics

      • B1 and other receptors to raise cardiac activity

    • nitroglycerin or nitroprusside vasodilators

  • stimulate heart to maintain perfusion

Treatment Goals

  •  Fluid Removal to reduce congestion and edema, since less fluid to pump and less pressure to push against

    • diuretics also some minor vasodilation and cardiac remodeling prevention

      • spironolactone mineralocorticoid receptor antagonist for heart failure

    • SGLT-2 inhibitors good for heart failure due to control of Ca levels, decreased kidney sympathetic activity, increased RBC production and production of mitochondria

  • Increase vasodilation to decrease cardiac workload (more heart room)

    • ACEs/ARBs (anti-RAAS)

    • Vasodilators

    • Brain natriuretic peptide (BNP) compensatory anti-RAAS body system. Increase BNP by inhibiting neprilysin enzyme with sacubitril

      • produced in response to increased BP (ventricular stretching)

  • Slow Heart rate to reduce stress on the heart and give more time for ventricular filling (more efficient)

    • ivabradine blocks HCN channel to slow SA node pacemaker thus more effective in rapid heart rate with no contractility affects

    • beta-blockers

    • digoxin increases vagal (parasympathetic) effects on AV node, but inotropic (stronger contractions) at higher concentrations

  • Cardiac Remodeling protection (harmful structural changes)

    • Anti-RAAS, beta blockers, aldosterone agonists, neprilysin inhibitors, SGLT-2 inhibitors

Neprilysin

  • Synthetic BNP tried, but not effective

  • Neprilysin breaks down BNP, angiotensin II, bradykinin and other peptides

  • increased Neprilysin will decrease BNP (harmful) and decrease angiotensin II (helpful)

  • decreased Neprilysin will increase BNP (helpful) and increase angiotensin II (harmful)

  • co-admin sacubitril with valsartan to counter undesirable angiotensin II increase

    • Entresto ( ARNI) angiotensin receptor/neprilysin inhibitor