Unit 3 Physiology: Congestive Heart Failure

SALA:
Definition of HF:
- AHA: clinical syndrome that can result from any structural or functional cardiac disorder
that impairs the ability of the ventricle to fill or eject blood
- ESC: clinical symptoms/signs secondary to abnormal ventricular function
Problem:
- 5,000,000 people in the US with heart failure (~half a million new cases a year)
- 300,000 deaths per year
- Incidence has doubled in the past 10 years
- Most common reason for hospital admission in people over 65 (median life expectancy
after hospitalization only 2.4 years)
Etiology:
- Why has HF increased?
o Better treatment for CAD
o Better survival rates after acute MI
o Aging population
o Wider use of ICD (intracardiac defibrillator)
- Can be caused by:
o A primary condition of the heart (ie. CAD, valve disorders, cardiomyopathies)
o Can be secondary to systemic changes that place new demands on the heart
or alter its function (HTN, respiratory or metabolic acidosis, electrolyte imbalance,
cardiac tamponade)
Classifications:
- Systolic (forward) or diastolic (backward) HF
- Right side or left side HF (failure of right ventricle often secondary to left ventricle
dysfunction)
- Acute or chronic HF (based on how it occurred)
- All these types can occur concurrently*
Systolic HF: caused by anything that decreases contractility or overloads the heart
- Decreased Myocardial Contractility:
o Coronary occlusion, pharmacological agents that depress contractility, severe
acidosis, myocarditis
- Afterload Mismatch:
o Malignant HTN, progressive aortic stenosis, pulmonary embolism
- Valvular Disease and Other Forms of Cardiac Overload:
o Valve defects (regurgitation, insufficiency)
o Septal defects
Diastolic HF: anything that alters the relaxation of the heart
- Clinical syndrome characterized by the usual signs and symptoms of heart failure with the
distinguishing features of:
o Preserved ejection fraction (above 50%)
o Abnormal diastolic distensibility, filling pressures (increased), or relaxation
- Caused By:
o Impaired myocardial relaxation
o Increased resistance to ventricular inflow
o Diastolic Ca++ overload: SERCA pump activity decreased (rare)
Clinical Assessment:
- Hallmarks are fatigue and exercise intolerance
o Left Ventricular Dysfunction: leads to congestive lungs and pulmonary edema
o Right Ventricular Dysfunction: leads to systemic venous congestion, peripheral
edema, and ascites
- Respiratory Signs and Symptoms:
o Crackles and wheezes, SOB, orthopnea, non-productive cough
o Pulmonary edema can also lead to increased respirations, use of accessory
respiratory muscles (bulging neck muscles), cyanosis, cold extremities and
diaphoresis
- CV Signs and Symptoms:
o Palpitations, resting tachycardia, 3rd heart sound, low cardiac output, hypotension
 - Other:
o Exaggerated jugular pulse
o Oliguria/anuria (decreased CO and hypotension leads to decreased GFR)

Heart Failure Mechanics:

- Systolic Heart Failure:
o Cardiac function curve is moved down and to the right; this means that the heart
becomes insensitive to changes in preload (ie. decreased preload wont
decrease stroke volume much)
o Left ventricular end systolic pressure volume relationship flattens (Emax is less)
and the heart becomes more sensitive to changes in afterload (ie. small
increases in afterload result in huge decreases in SV)
o For these reasons we treat patients with:
Vasodilators: used to decrease afterload
Decrease in afterload will cause a greater increase in SV than in a
person without heart failure (more sensitive to changes in
afterload)
Decrease in preload due to vaso-/venodilation will not cause
significant decrease in SV (insensitive to changes in preload)
Diuretic: used to decrease blood volume and reduce load on the heart
- Diastolic Heart Failure:
o Due to decreased relaxation and/or decreased ventricular compliance, leading to
increases in ventricular pressure
o The ventricle does not fill enough (does not normally lengthen) during diastole, and
is therefore unable to generate adequate stroke volume
Compensatory Mechanisms: are able to compensate for a period of time, but eventually
lead to self-destructive loop that results in overt cardiac failure
- Adrenergic Compensatory Mechanism:
o Works to increase HR and venous return (preload), in order to increase CO
o Controlled by SNS:
Increase in SS activity causes vasoconstriction which shunts blood away
from nonvital organs to vital organs
- Renal Compensatory Mechanism:
o Works to increase fluid retention, blood volume, and venous return (preload)
o Activation of renin-angiotensin-aldosterone system, decreased GFR, renal arteriolar
constriction, increase Na+ reabsorption
All this occurs despite increases ANP secretion
- Ventricular Remodeling:
o Wall Stress= (PXR)/h
o Eccentric Hypertrophy: due to volume overload (ie. aortic/mitral regurgitation);
sarcomeres replicate in series causing fiber elongation and ventricular
enlargement
o Concentric Hypertrophy: due to increases in wall stress (HTN, aortic stensis);
sarcomeres replicate in parallel leading to increase in ventricular wall thickness
(increase h) in an attempt to increase the force of contraction in order to overcome
increased afterload
Reflex Control in HF:
- Baroreflex is depressed in heart failure condition (especially a loss of the cardiac
component of the baroreflex, although vascular component is also compromised)
o Decreased baroreflex reactivity
o Impaired central integration
o Reduced efferent reponses
- Muscle metaboreflex control of the ventricular contractility is virtually abolished in HF
conditions
o In a normal person, activation of the metaboreflex causes an increase contractility
of the heart
o In a person with HF, activation of the metaboreflex has little to no change in
contractility of the heart
ROSSI: KIDNEY IN HEART FAILURE
Kidneys Role in HF:
- Kidney causes Na+ and water reabsorption (to maintain blood pressure)
- Results in excess body Na+ and water
- Symptoms include: edema, SOB, low plasma [Na+] and low plasma osmolality
Na+ and Water Balance:
- Plasma [Na] does not tell use the Na content of the body; it is directly proportional to
plasma osmolality
o Plasma osmolality ~ 2 x plasma [Na]
- Therefore, the plasma [Na] tells us the amount of water in the body
- The amount of Na+ determines the size of the ECV; assessing the size of ECV allows us to
infer total body Na

Positive Na+ Balance:

- Increase Na+ intake and Na+ excretion does not go up immediately (positive Na+ balance)
- The result is an increase in ECV (body needs to gain water to maintain Na concentration)
and an increase in plasma volume
- Increase in PV causes increase in Pc, decrease c leading to increased filtration and
increased ISV (edema)
- Eventually, urinary excretion of Na+ increases to come into balance (abolish positive Na+
balance state), although this balance will be at a higher concentration of Na+
- Basically:
o Water balance affects plasma [Na]
o Na balance affects the size of the ECV
Normal Response to Increased PV:
- Increased venous return and increased CO Increased BP
o Increased stretch at JG cells Decreased renin Decreased Ang II,
decreased aldosterone
o Increased stretch at aortic arch/carotid sinus Decreased ADH, decreased SNS
activity
- Increased stretch at pulmonary veins and atria Increased ANH
- All this leads to increased urinary excretion of Na+
o Mostly due to a decrease in Na+ reabsorption (GFR and plasma Na+ does not
change)
o If little Na+ is filtered or more Na+ is reabsorbed, then positive Na+ balance
occurs
Hemorrhage:
- Decreased plasma volume Decreased BP
o Decreased ANH
o Increased SNS activity
o Increased ADH
o Increase renin (increased angiotensin II and aldosterone)
- All lead to a decrease in urinary Na+ excretion in an attempt to preserve blood
volume
Heart Failure:
- Decreased CO Decreased BP
o Increased SNS activity
o Increased ADH
o Increased renin (increased angiotensin II and aldosterone)
o Increased stretch of atria (increased PV and venous return) Increase
ANH
Normally, this would cause Na+ and water loss by decreasing SNS activity
and ADH secretion
However, chronic stretch of atria prevents it from performing its inhibition
functions
- All lead to decreased urinary excretion of Na+ (even in the presence of ANH),
decreased urinary excretion of water, increased PV, decreased plasma
osmolality, increased venous return and further increase in right heart pressure
- Treatment:
o Heart transplant
 o Drugs for HF:
Beta blocker (inhibit actions of catecholamines)
ACE inhibitor (block Ang II formation)
Aldosterone antagonist (Spirinolactone)
Diuretics (block Na+ reabsorption at TALH and distal tubule)
Aquaretics (block water reabsorption at collecting duct)
Hyperaldosteronism:
- Usually due to tumor of adrenal gland that releases large quantities of aldosterone
- Increased aldosterone leads to:
o Decreased Na+ excretion (increase ECV) and increased K+ excretion
Causes increased BP, decreased plasma [K+]
- Increased ECV and blood pressure lead to:
o Increased GFR
o Decreased renin and Ang II
o Increased ANH
- All these effects result in excretory rate of Na+ coming to a new baseline (escape from
aldosterone) at the expense of hypertension (blood pressure must go up to compensate)