HF Sprowls

What is the incidence of HF in the US?

• ~6.5 million ppl over age of 20 have HF & is expected to exceed 8 million by 2030

• ~960,000 new cases each year!

• Roughly 50 of ppl who develop HF die w/in 5 years of diagnosis

• Women have a higher mortality rate due to HF relative to men

• Estimated that 1 in 8 deaths have HF as a contributing cause

What is heart failure (HF)?

Defined as heart’s inability, particularly the ventricles, to pump enough blood to meet body’s metabolic demands

What can HF be caused by?

Any disorder affects heart’s ability to either receive/pump blood

What are the multiple pathologies that can accelerate process (even though naturally heart becomes weaker as we age)?

• Atherosclerosis

• Dyslipidemia

• Diabetes

• Myocardial infarction

• Thyroid disorders

• Chronic HTN

• Mitral stenosis

  • All these alter force to overcome due to decreased diameter

What is left heart failure (LHF)?

Decreased ability of left ventricle to either contract (systole) or fill (diastolic)

What is right heart failure (RHF)?

Decreased ability of right ventricle to either contract (systolic) or fill (diastolic)

What is high output heart failure?

Characterized by increased cardiac output, but low systemic vascular resistance (dilations of blood vessels)

What is the pathophysiology related to LHF?

• Occurs when left ventricle cannot pump blood efficiently enough to supply body’s metabolic demand

• Can lead to a buildup of fluid in lungs & other devastating complications

• Compensatory effects for decreased cardiac output lead to changes in size, shape, & structure of myocytes, called cardiac remodeling

What is systolic LHF?

• Caused by decreased contractility of left ventricle

• Damage to myocardium is primary cause of decreased contractility:

  • Myocardial infarction

  • Dilated cardiomyopathy

  • Myocarditis (less common but it happens!)

• Afterload → HF is an inability to overcome afterload

• Ventricular cardiomyocyte death → impaired contractile force

What does decreased contractility of systolic LHF lead to?

Decreased left ventricular ejection fraction (LVEF) called heart failure w/ a reduced ejection fraction (HFrEF)

• Typically <40% (ejection fraction is 40% of volume in ventricle)

• Left ventricle becomes dilated, or enlarged, causing increased volume of blood contained w/in

What is diastolic LHF?

• Caused by decreased ability of left ventricle to fill appropriately

• Conditions that impart systemic vascular resistance commonly lead to diastolic LHF:

  • HTN

  • Aortic stenosis

  • Hypertrophic cardiomyopathy

• Hypertrophy → decreased ventricular volume, but preserved ejection fraction (HFpEF)

  • Smaller total volume, but exiting fractional volume is about the same

What does the inability to overcome pressure needed to push blood throughout (afterload) body cause?

Hypertrophy of left ventricle, narrowing volume w/in

What happens even though stroke volume may be decreased in diastolic LHF?

LVEF in these pts is normal, or preserved, & termed heart failure w/ a preserved ejection fraction (HFpEF)

• Typically >50%

What are the complications that result left heart failure (LHF)?

• Pulmonary congestion

• Cardiogenic shock

What is pulmonary congestion?

• Decreased ability of heart to eject blood causes a buildup in heart that can translate backwards leading to pulmonary congestion & increased pulmonary capillary wedge pressure (PCWP)

• End result of this fluid buildup in lungs leading to pulmonary edema making it hard to breath, particularly when exercising or lying down

• Can lead to hypoxia (inadequate oxygen supply to tissue) if pulmonary edema becomes severe

What is cardiogenic shock?

• Decreased CO, caused by LHF causes decreased systemic perfusion, leading to organ malperfusion

• Extremities may present as cold & pale, w/ mottling (marbled patches of purple, red, blue discoloration indicating ineffective oxygen supply)

• Can lead to encephalopathy, TIA/CVA, myocardial infarction, acute kidney injury, acute mesenteric ischemia, & buildup of lactate (lactic acidosis)

What is the pathophysiology related to RHF commonly caused by?

Inability of right ventricle to appropriately efficiently pump blood whether by contraction/volume

What is systolic RHF?

• Caused by decreased contractility of right ventricle

  • Really only caused by MI of right ventricle myocardium, but plausible damage to myocardium for any reason can also be etiology of RHF

• Decreased contractility leads to decreased right ventricular ejection fraction (RVEF)

• Cardiomyocyte death → decreased contractility → decreased RVEF

What is diastolic RHF?

• Caused by decreased ability of right ventricle to fill appropriately

• Conditions that impart an increase in pulmonary vascular resistance commonly lead to diastolic RHF:

  • Pulmonary HTN

  • Pulmonary embolism

  • Lung disease (COPD, emphysema)

  • LHF → most common cause of RHF!

What is the inability to overcome pressure needed to push blood (pulmonary afterload) into lungs cause?

• Hypertrophy of right ventricle, narrowing volume w/in

• While stroke volume may be decreased, RVEF in pts is normal, or preserved

• RV hypertrophy → decreased RV volume

What are complications that result right heart failure (LFH)?

• Main, overwhelmingly, most detrimental complication is increased central venous pressure or pressure experienced in large veins (superior & inferior vena cava) & right atrium

• Increased CVP presents in 2 ways:

  • Pitting, lower extremity edema

  • Jugular vein stenosis (distention)

• As blood is continually backed up particularly from liver, emptying into inferior vena cava, liver can be become congested & lead to liver failure

• Portal vein HTN can lead to capillary leak of mesenteric vessels resulting in fluid buildup in peritoneum, or ascites

• While uncommon, it is possible that extreme dilation of right ventricle can cause a septal shift where right ventricle becomes so enlarged it collapses volumetric space of left ventricle

What is the pathophysiology rated to high output heart failure (HOHF)?

• HOHF is caused by extreme vasodilation of systemic vasculature (mainly caused by sepsis)

• B/c of vasodilation, total peripheral resistance is going to drop, lowering BP, causing body to compensate by activating SNS in effort to raise BP

• In heart specifically, this is going to increase HR & SV

• This will increase CO, but is insufficient to overcome minimal TPR, & will be a constant downward spiral of body trying to increase its CO

What are the compensatory mechanisms that lead to worsening HF?

• Baroreceptors are activated due to low MAP activating SNS, & signals to vasomotor center & cardio acceleratory center, causing increased HR, SV, & vasoconstriction

• Decreased CO leads to decreased pressure sensed by JG cells of kidney, & initiates the RAAS

• Atrial stretch causes release of ANP (& other NPs) from left atrium, which is going to try to inhibit actions of ATI-II in attempt to offset RAAS activation but eventually fails

• Reduces contractile efficacy & ejection fraction, further lowering CO, re-triggering neuro-hormonal signaling

• Persistent activation leads to cardiac wall fibrosis & hypertrophy

What happens to SNS with decreased cardiac output?

Increased SNS

→ Increased TPR

→ Increased preload & afterload

→ Ventricular remodeling

• Beta-blocker would block increased TPR

What happens to renin with decreased cardiac output?

Increased renin

→ Increased ATI

→ Increased ATII by ACE

→ Increased aldosterone (ADH)

→ Increased Na+/H2O

→ Edema & increased SV

→ Increased Preload

→ Ventricular remodeling

• ACEi & ARB would block increased ATII

• Neprilsyn would inhibit ANP, inhibiting increased ATII

• Aldosterone antagonist would block increased ADH

• Diuretic would decrease edema