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Cardiovascular > SM 138 Heart Failure Pathophysiology > Flashcards

SM 138 Heart Failure Pathophysiology Flashcards

1
Q

Define Heart Failure?

A

Heart Failure is a syndrome where the heart: cannot produce enough CO to meet metabolic demands of the body AND/OR can only produce enough CO at the expense of increased cardiac filling pressures

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2
Q

What is a syndrome?

A

A collection of symptoms with varied underlying causes

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3
Q

How does HF relate to other CV diseases?

A

HF is the end result of most CV diseases, including IHD, HTN +/- Diabetes, Valvular Heart Disease, and Arrhythmias

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4
Q

How can HF have a renal basis?

A

HF can arise from too much Na and fluid retention in the Kidneys

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5
Q

Compare forward failure to backward failure in HF?

A

Forward failure refers to a failure to supply the heart whereas backward failure refers to a failure of the heart to pump enough blood to the body

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6
Q

Describe the epidemiology of HF?

A

30 - 35% 5 year survival after hospitalization for HF, very low

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7
Q

Why is the prevalence of HF rising?

A

Rising rates of HTN, Diabetes, and Obesity as well as better treatment of ACS and effective treatments but no cures for HF lead to increased HF prevalence

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8
Q

What type of dysfunction is commonly attributed to HFrEF?

A

Systolic dysfunction

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9
Q

What type of dysfunction is commonly attributed to HFpEF?

A

Diastolic dysfunction

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10
Q

What can cause systolic dysfunction in HF?

A

Impaired contractility and elevated afterload

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11
Q

What can impair contractility in HF and what type of HF does it cause?

A

MI, Mitral and Aortic Regurg, and Dilated cardiomyopathies can impair contractility = HPrEF

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12
Q

What can increase afterload in HF and what type of HF does it cause?

A

Aortic Stenosis and Uncontrolled HTN can increase afterload = HPrEF

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13
Q

How does decreasing contractility in HPrEF change the PV loop?

A

Decreased contractility lowers the slope of the CO line, leading to a greater ESV. Volume begins to accumulate in the ventricle, shifting to a higher point on the lower volume curve, increasing EDV and raising pressure

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14
Q

How does increasing afterload change the PV loop?

A

Increased afterload forces the ventricle to reach a higher pressure before contraction, leaving less energy to contract and causing increased ESV; blood will accumulate in the ventricle to raise EDV, and pressure in the ventricle increases

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15
Q

What is cachexia?

A

Muscle wasting due to insufficient blood supply to the body

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16
Q

How does HFrEF present?

A

Fatigue, dyspnea, exercise intolerance, hypotension, cardiac cachexia

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17
Q

What can impair diastolic filling in HF?

A

LV hypertrophy, restrictive cardiomyopathy, and fibrosis

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18
Q

How does impaired diastolic filling lead to HFpEF?

A

Impaired diastolic filling leads to decreased compliance, which shifts the diastolic pressure-volume curve on the PV loop up, leading to a mostly preserved EF but less SV due to lower EDV and higher pressures in the ventricle

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19
Q

How does increased LV filling pressure present in HF?

A

Pulmonary venous congestion that causes dyspnea, ortopnea, and PND as well as pulmonary rales

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20
Q

How does increased RV filling pressure present in HF?

A

Systemic venous congestion that causes leg swelling and bloating, as well as increased JVP

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21
Q

What causes increased filling pressures?

A

Impaired LV/RV relaxation, reduced LV/RV compliance, and fluid overload

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22
Q

How does systolic/contractile dysfunction relate to systolic HF?

A

Contractile dysfunction can manifest as decreased EF in systolic HF, but it can also be asymptomatic; contractile dysfunction =/= systolic HF

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23
Q

What is systolic HF?

A

Systolic dysfunction + signs/symptoms of HF

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24
Q

How does diastolic dysfunction relate to diastolic HF?

A

Diastolic dysfunction implies impaired relaxation or non-compliant ventricles, which may manifest as increased filling pressures; however, it can also be asymptomatic so diastolic dysfunction =/= diastolic HF

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25
Q

What is diastolic HF?

A

Diastolic dysfunction + signs/symptoms of HF

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26
Q

What is the definition of HFrEF in terms of EF?

A

EF < 40-45%

27
Q

What is the definition of HFpEF in terms of EF?

A

EF > 45-50%

28
Q

Why is “systolic HF” misleading?

A

Many patients with systolic HF have systolic and diastolic dysfunction

29
Q

Why is “diastolic HF” misleading?

A

Many patients with diastolic HF have abnormalities in systolic function despite normal EF

30
Q

Does the Frank-Starling relationship hold in HF?

A

Yes; Frank-Starling says that with increased stretch/LVEDV/LVEDP, Stroke Volume rises; in HF, the curve shifts downward but increasing venous return can still partially compensate for HF, at the expense of greater pressures

31
Q

Which branch of the nervous system is active in HF?

A

The SNS

32
Q

How does the SNS respond to HF?

A

Decreased CO is detected by decreased stretch of the carotid and aortic baroreceptors, leading to increased sympathetic outflow to increase HR, Contractility, and TPR to preserve BP compensation

33
Q

What role does Renin play in HF?

A

Kidneys secrete Renin in response to decreased plasma volume and salt conc., leading to more fluid retention to raise venous return and CO

34
Q

What are the deleterious effects of Angiotensin II?

A

Abnormal vasoconstriction, ventricular remodeling, endothelial dysfunction

35
Q

What are the effects of ADH/AVP?

A

ADH causes vasoconstriction through V1 receptors to increase TPR as well as increase water retention through V2 receptors to increase Preload

36
Q

What role does ANP play in HF?

A

ANP is released in response to stress on the myocardium, caused by increased fluid volume and filling pressure, and counteracts the effects of SNS, RAAS, and AVP activity

37
Q

How can ANP be used to diagnose HF?

A

ANP is released in response to stress on the heart to lower fluid volume, and elevated ANP indicates worse HF outcomes

38
Q

Do SNS, RAAS, and AVP activation benefit or worsen HF?

A

Initially, they are beneficial and compensatory but overtime they worsen the HF syndrome

39
Q

How can increased sodium and water retention worsen HF?

A

Increased sodium and water retention lead to increased congestion in the heart and lungs

40
Q

How can increased vasoconstriction worsen HF?

A

Increased vasoconstriction leads to increased TPR and decreased CO

41
Q

How can the RAAS system worsen HF?

A

Ang II and Aldosterone promote fibrosis

42
Q

What can cause eccentric remodeling in HF?

A

Volume overload = systolic dysfunction

43
Q

What can cause concentric remodeling in HF?

A

Pressure overload = diastolic dysfunction

44
Q

Why is eccentric remodeling bad in HF?

A

Leads to mitral regurg and systolic dysfunction

45
Q

Why is concentric remodeling bad in HF?

A

Leads to increased stiffness, predisposes ischemia and causes diastolic dysfunction

46
Q

How does the La Place relationship dictate concentric remodeling in HF?

A

Since Tension = Pressure / Radius, to keep Tension constant with rising Pressure from volume overload, Radius must also increase leading to increased ventricular thickness

47
Q

What are the common electromechanical problems in HF?

A

Scar formation, atrial enlargement, and electric remodeling

48
Q

How does scar formation lead to HF?

A

Scar formation promotes focal re-entry = VT

49
Q

How does atrial enlargement lead to HF?

A

Atrial enlargement causes fibrosis which promotes AFib

50
Q

What can cause the heart to begin decompensation?

A

Decompensation refers to the compensatory mechanism becoming maladaptive, and can be induced by sodium intake, infection, uncontrolled HTN

51
Q

Outline the progression of systolic HF?

A

CAD/HTN/Diabetes lead to LV injury; Pathologic remodeling occurs from compensatory SNS stimulation as well as endothelial dysfunction; symptoms such as dyspnea and edema arise from Low EF; proceed to HF and/or death

52
Q

How does left sided HF present?

A

Dyspnea, PND, Fatigue, and pulmonary rales

53
Q

How does right sided HF present?

A

Peripheral edema, elevated JVD, Hepatomegaly

54
Q

What is the staging system for HF?

A

Stages A through D, progresses from high risk to end stage HFrEF

55
Q

What is Stage A HF?

A

High risk for developing HF, such as HTN/DM/CAD

56
Q

What is Stage B HF?

A

Asymptomatic HF that accompanies LV remodeling, such as MI and LV hypertrophy

57
Q

What is Stage C HF?

A

Symptomatic HF such as HFpEF and HFrEF

58
Q

What is Stage D HF?

A

End-stage HF = HFrEF

59
Q

What is the class system for HF?

A

A way of categorizing HF from Class I to IV on the basis of severity of symptoms, ending with symptoms while at rest

60
Q

Which ventricle is more compliant?

A

The RV is highly compliant and needs preload to function

61
Q

Which ventricle is more sensitive to afterload?

A

The RV is more sensitive to afterload, and fails easily against increased afterload

62
Q

What can increase RV afterload?

A

Pulmonic stenosis, lung disease that vasoconstricts, LV failure that leads to pressure backups

63
Q

What is high output cardiac failure?

A

Different than HFpEF and HFrEF, leads to HF due to inability of the heart to sustain a high output in the context of hyperthyroidism and severe anemia

Cardiovascular (25 decks)

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