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Lecture 10

PAT 20A/B Lecture Notes - Lecture 10: Anticoagulant, Chest Radiograph, Pulse Oximetry


Department
Pathotherapeutics
Course Code
PAT 20A/B
Professor
Audrey Kenmir
Lecture
10

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(2)PAT20 Fall Week 10 Notes (Heart Failure)
By: Bina Nsimba
Heart Failure
- Heart failure (HF): an abnormal clinical syndrome involving impaired cardiac pumping
and/or filling.
Etiology & Physiology
Hypertension is a major contributing factor for the development of HF, increasing the risk
approximately three-fold.
Diabetes mellitus predisposes an individual to HF regardless of the presence of
concomitant CAD or hypertension.
The etiology is thought to be complex and related in part to microvascular pathology
caused by diabetes.
Other risk factors for the development of HF include cigarette smoking, obesity, and high
serum cholesterol.
HF may be caused by any interference with the normal mechanisms regulating cardiac
output (CO).
CO depends on (1) preload, (2) afterload, (3) myocardial contractility, (4) heart rate (HR),
and (5) metabolic state of the individual.
Any alteration in these factors can lead to decreased ventricular function and the resultant
manifestations of HF.
In general, major causes of HF may be divided into two subgroups: (1) primary causes
and (2) precipitating causes.
Precipitating causes often increase the workload of the ventricles, causing a
decompensated condition that leads to decreased myocardial function.
Pathology of Ventricular Failure
Systolic Heart Failure
Systolic heart failure: (the most common type of HF) results from an inability of
the heart to pump blood.
Systolic heart failure is caused by a defect in the ability of the ventricles to
contract (pump) or by increased afterload or mechanical abnormalities.
The left ventricle (LV) loses its ability to generate enough pressure to eject blood
forward through the high-pressure aorta.
The hallmark of systolic HF is a decrease in the left ventricular ejection fraction
(the fraction or percentage of total amount of blood in the LV that is ejected
during each ventricular contraction).
Normal ejection fraction (EF) is greater than 55% of the ventricular volume.
Systolic HF is caused by impaired contractile function (e.g., MI), increased
afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities
(e.g., valvular heart disease).
Diastolic Heart Failure

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Diastolic heart failure: (often referred to as HF with preserved systolic function) is
an impaired ability of the ventricles to fill during diastole.
Decreased filling of the ventricles will result in decreased stroke volume.
Diastolic HF is characterized by high filling pressures and the resultant venous
engorgement in both the pulmonary and the systemic vascular systems.
The diagnosis of diastolic HF is made on the basis of the presence of pulmonary
congestion, pulmonary hypertension, ventricular hypertrophy, and a normal EF.
Diastolic HF is usually the result of left ventricular hypertrophy from chronic
systemic hypertension, aortic stenosis, or hypertrophic cardiomyopathy.
Diastolic HF is commonly seen in older adults, and predominantly women, as a
result of myocardial fibrosis and hypertension.
However, the majority of patients who are seen with HF and normal systolic
function do not have an identifiable heart disease.
Mixed Systolic & Diastolic Heart Failure
oHF of mixed origin is seen in disease states such as dilated cardiomyopathy.
oDilated cardiomyopathy: a condition in which poor systolic function (weakened
muscle function) is further compromised by dilated left ventricular walls that are
unable to relax effectively.
oThese patients often have extremely poor EF (<35%), high pulmonary pressures,
and biventricular failure (both ventricles may be dilated and have poor filling and
emptying capacity).
oThe patient with HF of any type has low systemic arterial blood pressure (BP),
low CO, and poor renal perfusion.
oPoor exercise tolerance and ventricular dysrhythmias are also common.
oWhether a patient arrives at this point acutely as a result of an MI or chronically
from worsening cardiomyopathy or hypertension, the body's response to this low
CO is to mobilize its compensatory mechanisms to maintain CO and BP.
Figure 37-1 A: Dilated Heart Chambers; B: Hypertrophied Heart Chambers
Compensatory Mechanism

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HF can have an abrupt onset, as with acute MI, or it can be an insidious process resulting
from slow, progressive changes.
The overloaded heart resorts to certain compensatory mechanisms to try to maintain
adequate CO.
Dilation
-
Dilation: an enlargement of the chambers of the heart.
-
It occurs when pressure in the heart chambers (usually the LV) is elevated over
time.
-
The muscle fibres of the heart stretch in response to the volume of blood in the
heart at the end of diastole.
-
The degree of stretch is directly related to the force of the contraction (systole)
(Starling's law).
-
Initially, dilation is an adaptive mechanism to cope with increasing blood volume,
and this increased contraction leads to increased CO and maintenance of arterial
BP and perfusion.
-
Eventually, this mechanism becomes inadequate because the elastic elements of
the muscle fibres are overstretched and can no longer contract effectively, and CO
diminishes.
Hypertrophy
Hypertrophy: an increase in the muscle mass and cardiac wall thickness in
response to the overwork and strain of chronic HF.
It occurs slowly because it takes time for this increased muscle tissue to develop.
Hypertrophy generally follows persistent or chronic dilation and, thus, further
increases the contractile power of the muscle fibres.
This will lead to an increase in CO and maintenance of tissue perfusion.
However, hypertrophic heart muscle has poor contractility, requires more oxygen
to perform work, has poor coronary artery circulation (tissue becomes more easily
ischemic), and is prone to ventricular dysrhythmias.
Sympathetic Nervous System Activation (Least Effective)
SNS stimulation is often the first mechanism triggered in low-CO states.
Because there is inadequate stroke volume and CO, there is increased SNS
activation, resulting in the increased release of epinephrine and norepinephrine.
This results in an increased HR, myocardial contractility, and peripheral vascular
constriction.
Initially, this increase in HR and contractility improves CO.
However, over time, these factors are counterproductive, increasing the
myocardium's need for oxygen and the workload of the already failing heart.
The vasoconstriction causes an immediate increase in preload, which may initially
increase CO.
However, an increase in venous return to the heart, which is already volume-
overloaded, actually worsens ventricular performance.
Neurohormonal Response
As the CO falls, blood flow to the kidneys decreases.
This is sensed by the juxtaglomerular apparatus in the kidney as decreased
volume.
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