Introduction to CHF

Question 1

Heart failure

Answer 1

-inability for the heart to deliver sufficient blood/oxygen to meet the demands of the peripheral tissues or to do so at abnormally high filling pressures or both

Question 2

Diagnosis of heart failure

Answer 2

a clinical diagnosis
Characterized by signs and symptoms of decreased CO and volume overload
(doesn’t tell why have it!)

Question 3

Cardiomyopathy - what is it, how is it characterized

Answer 3

• disease of heart muscle
• due to a number of causes
• clinically characterized by heart failure (clinical manifestation of heart failure is generally caused by cardiomyopathy)

Question 4

Different types of heart failure

Answer 4

1) Systolic heart failure (aka. hfref-heart failure with reduced ejection fraction)
2) Diastolic heart failure (hfpef)
3) Co-existance of systolic and diastolic (frequent)

Question 5

Systolic heart failure (cause, result)

Answer 5

• poor systolic performance of the heart
• results in decreased CO and increased venous pressures
• typically occurs in association with impaires LV systolic function
• LVEF < 40%

Question 6

Diastolic heart failure (cause, result)

Answer 6

• poor diastolic performance of the heart resulting in decreased CO and increased venous pressures
• may occur in association with preserved LVEF (>40%) or decreased LVEF

Question 7

NYHA Classification of heart failure with 1 year survival rate

Answer 7

Classification based on when get symptoms and correlation to survival

1) Grade 1:
- early HF
- no symptoms with regular exercise or restrictions
- >95% survival
2) Grade 2:
- ordinary activity results in mild symptoms
- comfortable at rests
- 80-90% survival
3) Grade 3:
- advanced hf
- comfortable only at rest
- increased physical restrictions
- 55-65% survival
4) Grade IV
- severe failure
- symptoms at rest
- 5-15%

Question 8

LVEF and mortality rate

Answer 8

• LVEF is not great predictor of mortality
• person with preserved LVEF who has symptoms at rest much greater mortality rate than someone with reduced LVEF who is running a marathon

Question 9

ACC/AHA HF classification

Answer 9

-tool for thinking about when therapy and investigations should be initiated
Stage A:
High risk with no symptoms
Stage B:
Structural heart disease with no symptoms
Stage C:
Structural disease, previous or current symptoms
Stage D:
Refractory symptoms, requiring special intervention

Question 10

Stage A treatment -3

Answer 10

1) Risk factor reduction +Patient and family education

3) Treat hypertension, diabeties, dyslipideia (ACE inhibtor, ARBs in some patients)

Question 11

Stage B treatment

Answer 11

• Ace inhibitors or ARBs in all patients

- beta blockers in selected patients

Question 12

Stage C treatment

Answer 12

1) Ace inhibitors and B-blockers in all patients
2) Dietary Na+ restriction, diuretics, digoxin
3) Cardiac resynchronization if bundle branch block present
4) Revascularization, mitral-valve surgery
5) Multidisciplinary team
6) Aldosterone antagonist

Question 13

Stage D treatment

Answer 13

1) inotropes
2) VAD, transplantation
3) Hospice

Question 14

Causes of decreased SV (4)

Answer 14

1) Low LV preload
2) Impaired LV contractility
3) Back flow
4) High afterload

Question 15

Causes low LV preload (3)

Answer 15

1) Mitral stenosis
2) Pericardial constriction
3) Increased LV wall thickness

Question 16

Causes impaired LV contractility (2)

Answer 16

1) Infarction/ischemia

2) Myocarditis

Question 17

Causes of back flow (2)

Answer 17

1) Regurgitant valves (MR/AR)

2) Shunts

Question 18

Causes of high afterload (2)

Answer 18

1) Hypertension

2) Aortic stenosis

Question 19

Causes of systolic heart failure/cardiomyopathy

Answer 19

1) MI
2) Mitral and aortic regurg
3) Alcohol
4) Thyroid disease
5) Chemotherapy
6) Familial /genetic cardiomyopathy
7) Nutritional deficiencies

Question 20

Causes of diastolic heart failure/cardiomyopathy

Answer 20

1) Myocardial infarction
2) Aortic stenosis
3) Hypertension
4) Infltration disorders
5) Radiation therapy
6) Hypertrophic cardiomyopathy
7) Amyloidosis

Question 21

Remodeling in HF -pathophysiology

Answer 21

1) Decreased forward flow leading to:
- increased ventricular filling pressures (LVEDP)
- progressive ventricular dilation

• Initially these are adaptive mechanisms- to maintain adequate CO
• these become maladaptive later on (i.e. frank starling curve - as LVEDP builds beyond a certain point/ dilates beyond a certain point become maladaptive)
• then see clinical presentation of HP

Question 22

Frank starling curve

a) normal heart
b) heart failure

Answer 22

a) normal heart
- As preload increases stroke volume increases (compensatory)
- eventually increases in preload become decompensatory and stroke volume falls
b)
- heart already failing to begin with
- curve attenuated- not even able to generate same SV and takes lesser amounts of increase in LVEDP before heart begins to fail

Question 23

Mechanism of LV remodeling post infarct

Answer 23

1) Segmental infarction of LV
2) Decrease systolic performance
3) INcreased LVED volume/pressure
4)
a) by Franks starling mechanism SV increases and restores SV
b) increase wall stress
5) Increased wall stress leads to:
a) increase pressure on infarcted part of scar –> applying pressure to a scar = not elastic so wiill expand = more impaired systolic performance
b) non infarcted hypertrophy in response to increased pressure - impaired relaxation and diastolic performance of the heart
6) HEART FAILURE

Question 24

Neurohormonal activation in heart failure

Answer 24

Decreased forward flow associated with:
A) Impaired renal perfusion
1. Activation of renin-angiotensin-aldosterone system (RAAS)
- perceives low CO as low perfusion
-wants to try and restore body volume by activating RAAS
2. Activation of sympathetic nervous system
-increase heart rate to maintain CO
B) Elevated Intra-Cardiac filling pressures
-release ANP and BNP

Question 25

RAAS activation - what does it do (4)

Answer 25

1) Sodium and fluid retention at the level of the kidney
2) Vasoconstriction
3) Myocardial fibrosis
4) SNS activation

Question 26

Consequences of Na+ and fluid retention at level of the kidney by RAAS

Answer 26

1) Increased total body fluid volume
2) Increase intra-cardiac filing pressure
3) Ventricular dilation/remodelling
4) Decrease in CO –> vicious cycle continues
5) Eventually filling pressures transmitted back to lungs and peripheral tissues resulting in congestion and renal edema

Question 27

Consequences of vasoconstriction by RAAS

Answer 27

-vasoconstriction increases afterload
-makes it harder for failing heart to pump
-co decreases and cycle continues
ALSO
-vasoconstriction results in myocyte hypertrophy which contributes to diastolic dysfunction and increased wall stiffness

Question 28

Receptors mediating RAAS function

Answer 28

-AT1 and AT2 receptors
AT1:
-vasoconstriction, cell growth, Na/H2O retention, sympathetic activation
AT2:
-vasodilation, proliferation

-therefore system also has some good effects - is balance between AT1/AT2 that determines whether a patient with HF will have a good or bad response to renin release

Question 29

SNS activation consequences

Answer 29

1) Increased HR
2) Increased contractility
3) Vasoconstriction
4) RAAS activation

Question 30

Consequences of increased HR

Answer 30

-initially compensatory to preserve CO
but
-increased myocardial work and oxygen consumption–> further stressing out myocardium leading to more ischemia
-catecholamines increased risk of arrhythmia (leading to sudden cardiac death)

Question 31

Consequences of increased contractility

Answer 31

• increased myocardial work and O2 consumption –> sressing out myocardium leading to more ischemia
• catecholamines cause beta-receptor downegulation and apoptosis (high levels)

Question 32

Consequences of vasoconstriction

Answer 32

-increased afterload/systemic vascular resistance
-decreased SV –> decrease CO
-myocyte hypertrophy and ensuing associated diastolic dysfunction
(just like RAAS)

Question 33

Treatments for HF targetting neurohormonal activation

Answer 33

1) Angiotensin converting enzyme inhibitors (ACEi)
2) Angiotensin receptor blockers (ARB)
3) Beta blockers

Question 34

Taking HF history:

a) what are symptoms of heart failure (main categories)

Answer 34

1) Symptoms of low CO (2% of patients present with these symptoms)
- fatigue and lethargy
- cool extremities
- confusion
2) Symptoms of volume overload or venous congestion (98% present with these symptoms)
- dyspnea (orthopnea and PND - nocturnal cough)
- angina
- swelling (more common in elderly) and bloating (more common in children- abdominal ascites)

Question 35

Orthopnea

Answer 35

-can’t lie flat in bed at night (sleep with many pillows)

Question 36

Paroxysmal noctural dyspnea

Answer 36

-severe shortness of breath and coughing that occurs at nigh and awakens person from sleep

Question 37

Why get angina during heart failure

Answer 37

As increase LVEDP
1) Subendocardial ischemia
2) Decrease presure graident for blood to flow across coronary arteries (aortic end diastolic pressure - LVEDP)
LVEDP risease and AEDP falls (as CO decreases) so gradient gets smaller

Question 38

Physical exams: sign of HF

Answer 38

1) Signs of low CO
- hypotension
- cool mottled peripheries
2) Signs of volume overload (98%)
- elevated JVP
- extra heart sounds (S3 and S4)
- peripheral edema and ascites
- rales

-these signs very rare to find to begin with so if patient does have them should heighten suspicion that in HF