Introduction to CHF Flashcards
Heart failure
-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
Diagnosis of heart failure
a clinical diagnosis
Characterized by signs and symptoms of decreased CO and volume overload
(doesn’t tell why have it!)
Cardiomyopathy - what is it, how is it characterized
- 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)
Different types of heart failure
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)
Systolic heart failure (cause, result)
- 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%
Diastolic heart failure (cause, result)
- 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
NYHA Classification of heart failure with 1 year survival rate
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%
LVEF and mortality rate
- 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
ACC/AHA HF classification
-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
Stage A treatment -3
1) Risk factor reduction +Patient and family education
3) Treat hypertension, diabeties, dyslipideia (ACE inhibtor, ARBs in some patients)
Stage B treatment
- Ace inhibitors or ARBs in all patients
- beta blockers in selected patients
Stage C treatment
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
Stage D treatment
1) inotropes
2) VAD, transplantation
3) Hospice
Causes of decreased SV (4)
1) Low LV preload
2) Impaired LV contractility
3) Back flow
4) High afterload
Causes low LV preload (3)
1) Mitral stenosis
2) Pericardial constriction
3) Increased LV wall thickness
Causes impaired LV contractility (2)
1) Infarction/ischemia
2) Myocarditis
Causes of back flow (2)
1) Regurgitant valves (MR/AR)
2) Shunts
Causes of high afterload (2)
1) Hypertension
2) Aortic stenosis
Causes of systolic heart failure/cardiomyopathy
1) MI
2) Mitral and aortic regurg
3) Alcohol
4) Thyroid disease
5) Chemotherapy
6) Familial /genetic cardiomyopathy
7) Nutritional deficiencies
Causes of diastolic heart failure/cardiomyopathy
1) Myocardial infarction
2) Aortic stenosis
3) Hypertension
4) Infltration disorders
5) Radiation therapy
6) Hypertrophic cardiomyopathy
7) Amyloidosis
Remodeling in HF -pathophysiology
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
Frank starling curve
a) normal heart
b) heart failure
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
Mechanism of LV remodeling post infarct
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
Neurohormonal activation in heart failure
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
RAAS activation - what does it do (4)
1) Sodium and fluid retention at the level of the kidney
2) Vasoconstriction
3) Myocardial fibrosis
4) SNS activation
Consequences of Na+ and fluid retention at level of the kidney by RAAS
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
Consequences of vasoconstriction by RAAS
-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
Receptors mediating RAAS function
-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
SNS activation consequences
1) Increased HR
2) Increased contractility
3) Vasoconstriction
4) RAAS activation
Consequences of increased HR
-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)
Consequences of increased contractility
- increased myocardial work and O2 consumption –> sressing out myocardium leading to more ischemia
- catecholamines cause beta-receptor downegulation and apoptosis (high levels)
Consequences of vasoconstriction
-increased afterload/systemic vascular resistance
-decreased SV –> decrease CO
-myocyte hypertrophy and ensuing associated diastolic dysfunction
(just like RAAS)
Treatments for HF targetting neurohormonal activation
1) Angiotensin converting enzyme inhibitors (ACEi)
2) Angiotensin receptor blockers (ARB)
3) Beta blockers
Taking HF history:
a) what are symptoms of heart failure (main categories)
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)
Orthopnea
-can’t lie flat in bed at night (sleep with many pillows)
Paroxysmal noctural dyspnea
-severe shortness of breath and coughing that occurs at nigh and awakens person from sleep
Why get angina during heart failure
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
Physical exams: sign of HF
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
