Summary
Summary Robbins Basic Pathology - Chapter 11
- Course
- Institution
- Book
Summary Chapter 11 - Heart from Robbins Basic Pathology
[Show more]
Connected book
Book Title:
Author(s):
- Edition:
- ISBN:
- Edition:
More summaries for
-
TEST BANK FOR Robbins Basic Pathology (Robbins Pathology) 10th Edition by Vinay Kumar & Abul K. Abbas , ISBN: 9780323353175 |Chapters 1-24| Guide A+
-
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
-
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
2 reviews
By: Sanjana0511 • 2 year ago
By: oellethy01 • 3 year ago
Seller
Followsachajacobs
Reviews received
Content preview
Chapter 11 – The HeartHeart Failure
Heart failure, often referred to as congestive heart failure (CHF), is the common end point
for many forms of cardiac disease and typically is a progressive condition with a poor
prognosis. CHF occurs when the heart cannot generate sufficient output to meet the
metabolic demands of the tissues (forward failure) or can only do so at higher-than-normal
filling pressures (backward failure). Heart failure may result from systolic or diastolic
disfunction.
Systolic dysfunction
o Inadequate myocardial contractile function
o Consequence of ischemic heart disease or hypertension
Diastolic dysfunction
o Inability of the heart to adequately relax and fill
o Consequence of massive left ventricular hypertrophy, myocardial fibrosis,
amyloid deposition, or constrictive pericarditis.
The cardiovascular system attempts to compensate for the failure through several
homeostatic mechanisms:
The frank starling mechanism
o Compensated heart failure
Dilated ventricle is able to maintain cardiac output
o Decompensated heart failure
With time, the failing muscle is no longer able to propel sufficient
blood to meet the needs of the body
Activation of neurohumoral systems
o Release of norepinephrine
Increase heart rate and contractility
o Activation of renin-angiotensin-aldosterone system
Increase vascular tone
Myocardial structural changes, including augmented muscle mass
o Pressure overload states (hypertension or valvular stenosis)
Concentric hypertrophy ventricular wall thickness increases
without an increase in the size of the chamber
o Volume overload states (valvular regurgitation or shunts)
Heart weight is the best measure of hypertrophy in volume
overloaded hearts
Left-sided HF
The most common causes of left sided cardiac failure are ischemic heart disease, systemic
hypertension, mitral or aortic valve disease and primary disease of the myocardium.
Dyspnea (shortness of breath) on exertion is usually the earliest and most significant
symptom of left-sided heart failure. Other manifestations include an enlarged heart,
tachycardia, third heart sound, and fine rales at the lung base, caused by the opening of
edematous pulmonary alveoli. Subsequent chronic dilation of the left atrium can cause atrial
fibrillation. Treatment is typically focused on correcting the underlying cause.
Right-sided HF
, Right-sided heart failure is usually the consequence of left-sided heart failure, since any
pressure increase in the pulmonary circulation inevitably produces an increased burden on
the right side of the heart. The causes of right sided HF include all those that induce left
sided HF. The major morphological and clinical effects of pure right sided HF differ from
those of left sided HF in that engorgement of the systemic and portal venous systems
typically is pronounced and pulmonary congestion is minimal. Pure right sided HF typically is
not associated with respiratory symptoms. Instead, the clinical manifestations are related to
systemic and portal venous congestions and include hepatic and splenic enlargement,
peripheral edema, pleural effusion, and ascites.
Congenital Heart Disease
Congenital heart disease are abnormalities of the heart or great vessels that are present at
birth. Congenital heart disease most commonly arises from faulty embryogenesis during
gestational weeks 3 through 8, when major cardiovascular structures develop. Of the
accepted etiologic factors, environmental exposures, including congenital rubella infection,
teratogens, and maternal diabetes, and genetic factors are best characterized. The various
structural anomalies in congenital heart disease can be assigned to three major groups
based on their hemodynamic and clinical consequences:
1. Malformation causing a left-to-right shunt
a. Cyanosis and poorly oxygenated blood
2. Malformation causing a right-to-left shunt
a. Increase blood flow, ventricular hypertrophy and right sided HF
3. Malformations causing obstruction
a. Atresia complete obstruction
Malformation associated with left to right shunts
Atrial Septal Defects (ASD) and Patent Foramen Ovale
The patent foramen ovale results from low left sided pressure being able to close the
foramen ovale by the septum primum and septum secundum. The unsealed septa can allow
transient right-to-left blood flow. An ASD is an abnormal fixed opening in the atrial septum
that allows unrestricted blood flow between the atrial chambers. ASDs usually are
asymptomatic until adulthood. ASDs initially cause left-to-right shunts, due to lower pressure
in the pulmonary circulation and the right side of the heart. Over time, chronic volume and
pressure overloads can cause pulmonary hypertension.
Ventricular Septal Defects
Defects in the ventricular septum allow left-to-right shunting and constitute the most
common congenital cardiac anomaly at birth. Most VSDs close spontaneously in childhood.
Small VSDs may be asymptomatic. Larger defects result in chronic left-to-right shunting,
often complicated by pulmonary hypertension and CHF.
Patent Ductus Arteriosus
The ductus arteriosus permits blood to flow from the pulmonary artery to the aorta,
bypassing the unoxygenated lungs. PDAs are high pressure left-to-right shunts that produce
harsh, ‘machinery-like’ murmurs. Small PDA generally causes no symptoms, although larger
defect can lead to Eisenmenger syndrome with cyanosis and congestive heart failure.
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller sachajacobs. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for $4.27. You're not tied to anything after your purchase.
Can Stuvia be trusted?
4.6 stars on Google & Trustpilot (+1000 reviews)
55628 documents were sold in the last 30 days
Founded in 2010, the go-to place to buy study notes for 14 years now