Intro to Heart Failure Flashcards Preview

Cardiovascular Block > Intro to Heart Failure > Flashcards

Flashcards in Intro to Heart Failure Deck (21)

NYHA Classification System

Class I
Asymptomatic on ordinary physical activity
VO2 max > 20 ml/min/kg (normal = 30-40 ml/min/kg)

Class II
Symptomatic on ordinary physical activity (slight physical limitation)
VO2 max = 16-20 ml/min/kg

Class III
Symptomatic on less than ordinary physical activity (marked physical limitation)
VO2 max = 10-15 ml/min/kg

Class IV
Symptomatic at rest or unable to perform any activity (severe physical limitation)
VO2 max


Heart Failure Stages

Stage A
Patient at risk for developing HF; no structural defects or symptoms (may have CAD, HTN, family history of HF)

Stage B
Structural disease (e.g., LVH, LV dilation, valve disease, past MI); no symptoms

Stage C
Structural disease with current or prior symptoms

Stage D
Structural disease and marked symptoms at rest despite medical therapy; may require special intervention (e.g., transplant; mechanical assist)


Signs and Symptoms of Low CO

Decreased memory/mentation
Cool Extremities
Narrow pulse pressure
Oliguria - low urine output due to decreased GFR


R vs. L Heart Failure Signs and Symptoms

R heart failure = increased RA pressure (leg swelling, abdominal bloating, nausea, RUQ pain, LE edema, ascites, tender/enlarged liver, elevated JVP)

L heart failure = increased PCWP (dyspnea, orthopnea, PND, positional cough, rales, S3 gallop, CXR with pulmonary congestion)


Cardiac Excitation-Contraction Coupling

Cells depolarize the Ca2+ runs through T tubules and then go to dihydropyidine receptors (trigger and subtype of the L type Ca2+ channels) and Ca2+ is released from SR and then causes contraction and once reuptake through SR relaxation occurs but also can have Ca2+ exit the cell through the Na/Ca exchanger (not as much)

Circuit pump: phopholamban is associated with circuit pump and inhibits it; in cases of high cAMP and PKA activity it becomes phosphorylated, the phospholamban drops away and the circuit can go to at a higher rate which increases the ability to relax and Ca2+ reuptake


Cardiac Excitation-Contraction Coupling in Heart Failure

Pathologic changes: high sympathetic activity continuously

Lose t tubules and L type Ca2+ channels (DHPR) when Ca2+ comes through you get less trigger signal leading to Ca2+ transient and amplitude and reduced contraction and reduced reuptake because phospholamban doesn’t get phosphorylated as much so impaired relaxation, an important part of heart failure

Efflux becomes greater (upregulation of Na/Ca exchangers and over time it depletes SR Ca stores = bad


Normal Ca2+ Levels vs. HF

Normal heart; high peaks of Ca2+ and low toughs of Ca2+; good contraction and relaxation

Failing heart: low peaks and troughs and impaired contraction and relaxation and increased diastolic tension and prolongs relaxation time

Ca2+ entry = trigger signal (Ca2+ induced Ca2+ release) = reduced
SR Ca2+ release is reduced
Ca2+ binding to TN-C is reduced
Myosin ATPase and SERCA pump activity becomes impaired because reduction of phospholamban
Ca2+ extrusion from the cell is impaired because more activity of efflux


Inotropy vs. Lusitropy

Inotropy Increases by
Increased Ca2+ entry into cell
Increased Ca2+ release by SR
Decreased Ca2+ transport out of the cell

Lusitropy (relaxation) depends on SERCA activity to re-sequester Ca2+ into SR


Vascular Smooth Muscle Contraction

Increased Ca causes increased contraction

Increased Ca2+ intracellular caused by increased Ca2+ into channels

Ca2+-calmodulin complex activates myosin light chain kinase to cause contraction by MLC phosphorylation

VSM: key difference is increase cAMP causes relaxation via inhibition of MLCK, which in cardiomyocytes if increased cAMP you will increase contraction/inotropy


Alpha vs. Beta Agonists: IP3 and cAMP

Alpha 1 = IP3 connection = vasoconstriction

Beta 1 and 2 = cAMP; dilation in vascular smooth muscle, and constriction in cardiac muscle

Inotropy is enhanced by increased cAMP and IP3, but IP3 to a lesser extent

Increase in cAMP, decrease in IP3, and increase in cGMP (NO production) = dilation of vasculature


Systolic vs. Diastolic Dysfunction

Systolic failure where you lose inotropy, it reduces the ESV relationship which tells how much pressure you can have for a given empty volume; lose ability to contract you can only achieve the higher pressures at much higher volumes by increasing overall preload (EDV) and that is the basis of dilation and heart failure; reduced EF

Diastolic failure: untreated HTN and get strong stiff ventricle, it is difficult to fill it out and decreases compliance from stiffness and filling pressures are going to be much greater; preserved EF


Causes of Systolic Dysfunction

Coronary artery disease (ischemia)
Myocardial infarction
Dilated cardiomyopathy (idiopathic, viral, bacterial)
Chronic volume and pressure overload
Cardiogenic shock
Septic shock


Systolic PV Loop

If you lose the slope, you achieve the ESP or empty volume, at much higher volumes; increase in compliance and moves loop to the right; increases ESV, more so than EDS so get decrease in SV = reduces EF

Increase of wedge pressure increases risk for pulmonary edema

Increases wall stress thus increasing myocardial O2 demand


Acute and Chronic Compensation for Increased ESV

ACUTE: increased ESV (due to reduced SV) is added to normal venous return thereby adding to next cycle and get increased EDV

CHRONIC: increased blood volume and decreased venous compliance (venous constriction) - neurohumoral compensation
Ventricular dilation (increased compliance) - anatomic compensation (remodeling)


Chronic Systolic Dysfunction and Ventricular Compliance

Compliance is how much given change in volume affects given change in pressure aka C = change in V / change in P

Stiff ventricle: small increase in volume is going to give big increase pressure

Compliance is inversely related to stiffness
At a given EDV if you have higher compliance and stiffness you have lower EDP

At 120 you have typical EDP of 8-12mmHg, if you increase compliance by ventricular remodeling you get enlargement of ventricle thus increasing EDV and attenuates wedge pressure

If decreasing compliance, then go from normal to stiff ventricle and get elevated EDP for same EDV


Systolic Dysfunction and Afterload

Decreased inotropy reduces velocity of fiber shortening at any given afterload

When inotropy is decreased, decreased afterload can partially restore velocity of fiber shortening and therefore ejection velocity and SV


Causes of Diastolic Dysfunction

Reduced structural compliance:
Ventricular hypertrophy
Restrictive cardiomyopathy
Cardiac tamponade

Reduced functional compliance due to impaired relaxation:
Ischemia/hypoxia (Decreased ATP)
Altered cellular handling of Ca2+


Diastolic Dysfunction and Ventricular Compliance

Diastolic dysfunction causes decrease in compliance meaning have higher pressures for any given EDV

As it becomes stiffer and stiffer it takes more pressure to get the same volume


Diastolic Dysfunction PV Loop

See upshift in overall EDPVR because of reduced compliance so it takes much increased pressure to fill the volume (EDV) and this puts you at greater risk for pulmonary edema or pericardial effusion

Increase in ESV gives you a much increased EDP, which greatly increase your pulmonary capillary wedge pressure (final filling pressure of L ventricle) and ESV may decrease because of decreased afterload and if lower CO then get lower arterial pressure and reduced pressure in aorta and get reduced pressure in ESV

SV will decrease but won’t change EF


Chronic Activation of Sympathetic Innervation

RAAS: increases preload, minimally increases inotropy, and greatly increases overall blood volume

Sympathetic stimulation of kidney: all these signal release of renin to convert Angioteninogen to AI and then ACE converts AI to AII

Long term effects: stimulates hypertrophy of heart and vessels, increases sympathetic drive and arterial pressure

Adrenal cortex: aldosterone release to cause fluid retention via stimulation of AII

Basic effects of RAAS: increasing venous return, blood volume, and arterial pressure

Overtime: cardiac hypertrophy and negative outcomes due to prolonged induction of the system


Opposition to Sympathetic Innvervation

Opposing system: natriuretic system

Sympathetic drive increases RAAS activation = bad for heart failure as it progress, but ANP and BNP opposes it

When myocytes become stretched chronically they release ANP to counteract the effects the of RAAS system; increase GFR to get diuresis and natriuresis and decreases central venous pressure that reduces CO and relaxes systemic arterial system to reduce pressure; also reduces blood volume and preload dependent CO

Reduces renin release therefore reduces conversion of angiotensinogen