Systolic Dysfunction:: Types of Heart Failure

HEART FAILURE
Clinical syndromes:
 Systolic dysfunction:
LVSD: due to ischemic heart disease, HTN, valvular heart disease

RVSD: 20 to LVSD, pulmonary HTN, RV infarction, RV cardiomyopathy, congenital heart disease
 Diastolic dysfunction:
This syndrome has the clinical features of HF, but there is preserved LV ejection fraction above 45-50%
and abnormal LV relaxation.
Also, there’s stiffness of LV wall and decreased compliance of LV  impaired diastolic filling of LV, and
thus decreased CO.
Types of Heart Failure:

1. High output vs. Low Output
2. Systolic vs. Diastolic
3. Right sided vs. Left sided (or biventricular)
4. Forward Failure vs. Backward Failure
Signs and Symptoms:
Signs:
Symptoms:
- Cardiomegaly
 Exertional dyspnea
- 3rd and 4th heart sounds
 Orthopnea
- Elevated JVP
 PND
- Tachycardia
 Fatigue
- Hypotension
- Bilateral basal crackles
- Pleural effusion
- Peripheral ankle edema
- Ascites
- Tender hepatomegaly
PATHOPHYSIOLOGY OF HF
In response to the hemodynamic changes that occur with HF, compensatory responses occur in order to
maintain CO and peripheral perfusion. With prolonged HF, these mechanisms are overwhelmed.
1. Venous return (preload)

In intact heart: myocardial failure leads to a decrease in the volume of blood ejected with each
heart beat, and an increase in the volume of blood remaining after systole. This increased
diastolic volume stretches the myocardial fibres and, as Starling’s law of the heart (p. 671)
would suggest, myocardial contraction is restored.
Severe myocardial dysfunction: cardiac output can be maintained only by a large increase in
venous pressure and/or marked sinus tachycardia.
 The increased venous pressure contributes to the development of dyspnoea, owing to
the accumulation of interstitial and alveolar fluid, and to the occurrence of hepatic
enlargement, ascites and dependent oedema, due to increased systemic venous
pressure.
 However, the cardiac output at rest may not be much depressed, but myocardial and
haemodynamic reserve is so compromised that a normal increase in cardiac output
cannot be produced by exercise.
 In very severe heart failure, the cardiac output at rest is depressed, despite high venous
pressures. The inadequate cardiac output is redistributed to maintain perfusion of vital
organs, such as the heart, brain and kidneys, at the expense of the skin and muscle
2. Outflow resistance (afterload)

This is the load or resistance against which the ventricle contracts. It is formed by:
Pulmonary and systemic resistance
Physical characteristics of the vessel walls
The volume of blood that is ejected.
An increase in afterload decreases the cardiac output. This results in a further increase of end-
diastolic volume and dilatation of the ventricle itself, which further exacerbates the problem of
afterload: (Laplace’s Law)
3. Myocardial contractility (inotropic state)

CO is maintained in early HF by activation of sym’c nervous system (activated by baroreceptors)
as a compensatory mechanism. It provides inotropic support, maintaining CO.
However, with chronic sym’c activation, bad stuff happens: because there will be further
neurohumoral activation and then myocyte apoptosis. This now is compensated by
downregulation of B- receptors.
Note: hypoxia is a myocardial depressant/ negative inotrpe as is deceases MC contractility.
4. Neurohormonal and sympathetic system activation: Na and H2O retention:

Reduced cardiac output also leads to renal hypoperfusion, activating the RAAS and enhancing
salt and water retention, which further increases venous pressure.
The retention of sodium is in part compensated by the action of circulating atrial natriuretic
peptides and antidiuretic hormone. Retention of salt and water and their accumulation in the
interstitium produces many of the physical signs of heart failure.
5. Ventricular remodeling in HF:

LV remodeling describes the alteration in ventricular size, shape and function due to mechanical
and neurohormonal factors in clinical conditions such as: MI, cardiomyopathy, HTN, valvular
heart diseases.
Its hallmarks include hypertrophy, loss of myocytes and increased interstitial fibrosis.
Remodelling continues for months after the initial insult, and the eventual change in the shape
of the ventricle becomes responsible for significant impairment of overall function of the heart
as a pump.
Note: In cardiomyopathy, remodeling occurs WITHOUS ischemic injury or MI.
Changes in myocardial gene expression:

Human myosin is composed of: 1 pair of heavy chains
2 pairs of light chains
Heavy chains: α and β isoforms. Α- atria; β- ventricles.

In other animals, pressure overload causes a shift from α to β in the atria and this decreases
atrial contractility, but reduces energy demands. But in human ventricles, this shift isn’t very
significant since β already predominates.
Other genes affected in HF: those encoding Na+/K+ATPase, Ca2+-ATPase and β1-adrenoceptors.
Natriuretic peptides (ANP, BNP and C-type

 Atrial natriuretic peptide (ANP) is released from atrial myocytes in response to stretch.
ANP induces diuresis, natriuresis, vasodilatation and suppression of the renin-
angiotensin system. Levels of circulating ANP are increased in congestive cardiac
failure and correlate with functional class
 Brain natriuretic peptide (BNP) (so called because it was first discovered in brain) is
predominantly secreted by the ventricles, and has an action similar to that of ANP but
greater diagnostic and prognostic value
 C-type peptide, which is limited to vascular endothelium and the central nervous
system, has similar effects to those of ANP and BNP
BNP is released from the ventricles in response to
ventricular volume expansion and pressure overload.
• BNP levels 150 pg/mL correlate strongly with
the presence of decompensated CHF.
• BNP may be useful in differentiating between
dyspnea caused by CHF and COPD.
• N-terminal pro-BNP (NTproBNP) is a newer assay
with similar predictive value as BNP. The normal
range for this value depends on the age of the patient,
but a NT-proBNP 300 virtually excludes
the diagnosis of HF.
Kerley B lines are short horizontal lines near periphery of the

lung near the costophrenic
angles, and indicate pulmonary congestion secondary to dilation
of
pulmonary lymphatic vessels
Echo tells about EF: Patients with systolic

dysfunction (EF 40%)
should be distinguished from patients with
preserved left ventricular function
(EF 40%).
COMPLICATIONS OF HF:
1. Renal failure:
Due to renal hypoperfusion. Exacerbated by diuretics, ACE inhibitors and ARB’s.
2. Hypokalemia: Due to-

 therapy with K-losing diuretics
 Hyperaldosteronism: caused by RAAS and impaired aldosterone metabolism because of
hepatic congestion.
3. Hyperkalemia:
 Drugs that promote renal resorption of K (esp when used in combo with ACE inhibitors
or ARB’s and mineralocorticoid antags.
4. Hyponatremia: Feature of severe HF.

 Diuretic therapy
 High ADH secretion  inappropriate H2O retention
 Failure of membrane ion pump
5. Impaired liver function:

 Hepatic venous congestion
 Poor arterial perfusion  mild jaundice, abn LFT’s, decreased synthesis of clotting
factors.
6. Thromboembolism: DVT and PE

 Low CO and immobility
 A. fib or A. flutter  emboli
7. Atrial and ventricular arrhythmias:

 Electrolyte changes: ↓K and ↓Mg
 Underlying cardiac disease
 Pro-arrhythmic effects of sympathetic activation
Ventricular arrhythmia  sudden death

MANAGEMENT OF HF
Goals of mng:
 relieving symptoms
 prevention and control of disease leading to cardiac dysfunction and heart failure
 retarding disease progression
 improving quality and length of life.
Diuretics:
Promote renal excretion of Na and H2O by blocking tubular reabsorption of sodium and chloride. Note:
diuretics improve dyspnea and exercise tolerance, not mortality. Serum electrolytes and renal function
must be monitored regularly (risk of hypokalaemia and hypomagnesaemia).
- Loop diuretics: furosemide, bumetanide
Give to pts with fluid overload
- Thiazide diuretics: bendroflumethiazide, hydrochlorothiazid
Angiotensin converting enzyme inhibitors (ACEI):
Captopril, Enalapril, Ramipril
Benefits pts. With asymptomatic HF post M and improve survival in patients in all functional classes
(NYHA I-IV). They interrupts the vicious circle of neurohumoral activation
Prevents conversion of angiotensin I to angiotensin II. This prevents: - peripheral vasoconstriction
- activation of the sympathetic nervous system
Adverse effects: - salt and water retention due to aldosterone release
- RAAS activation by diuretic therapy
Cough
Hypotension
Hyperkalemia
Renal dysfunction
Angiotensin II Receptor Blockers (ARB’s)
Candesartan, Valsartan, Losartan
Second line therapy in pts. Who don’t tolerate ACEI’s. They block the action of angiotensin II on the
heart, peripheral vasculature and kidney. The effects are similar to ACEI’s, but they’re better tolerated
but have the same serious side effects: hyperK+ and renal dysfunction.
B- adrenoceptor Blockers:
Bisoprolol, Carvedilol, Nebivolol
They block the action of epinephrine  decreases heart rate and contraction. When given in small doses
they are beneficial. In standard doses, B- blockers precipitate acute- on – chronic HF.
Aldosterone Antagonists
Spironolactone, Eplerenone
Remember aldosterone causes Na and H2O retention, aldosterone antags inhibit this. However, also
remember there are non-ACE pathways, and mortality can be attributed to this.?
Cardiac glycosides
Digoxin: inhibits the Na/K ATPase pump, which results in a small increase in IC sodium. This alters the
driving force for the sodium- calcium exchanger, leading to less Ca being removed from the cell 
increased IC calcium (stored in sarcoplasmic reticulum). Upon release of the stored calcium contractile
force of the heart is increased. Digoxin can cause arrhythmias.
Vasodilators and Nitrates
The combination of hydralazine and nitrates reduces afterload and pre-load and is used in patients
intolerant of ACEI or ARB’s
Inotropics and Vasopressors
Intravenous inotropes and vasopressor agents are used in patients with chronic heart failure who are
not responding to oral medication.
Surgical therapy
Implantable defibrillators
Coronary artery bypass
Heart transplant

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HEART FAILURE

LVSD: due to ischemic heart disease, HTN, valvular heart disease

Types of Heart Failure:

1. Venous return (preload)

2. Outflow resistance (afterload)

3. Myocardial contractility (inotropic state)

Note: hypoxia is a myocardial depressant/ negative inotrpe as is deceases MC contractility.

4. Neurohormonal and sympathetic system activation: Na and H2O retention:

5. Ventricular remodeling in HF:

Changes in myocardial gene expression:

Heavy chains: α and β isoforms. Α- atria; β- ventricles.

Natriuretic peptides (ANP, BNP and C-type

Kerley B lines are short horizontal lines near periphery of the

Echo tells about EF: Patients with systolic

2. Hypokalemia: Due to-

4. Hyponatremia: Feature of severe HF.

5. Impaired liver function:

6. Thromboembolism: DVT and PE

7. Atrial and ventricular arrhythmias:

Ventricular arrhythmia  sudden death

Angiotensin converting enzyme inhibitors (ACEI):

Captopril, Enalapril, Ramipril

Angiotensin II Receptor Blockers (ARB’s)

Candesartan, Valsartan, Losartan

Bisoprolol, Carvedilol, Nebivolol

Vasodilators and Nitrates

Inotropics and Vasopressors

Coronary artery bypass

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