Lecture 5.2 MJ slides Flashcards
Define heart failure
“Heart cannot generate enough output to meet the metabolic demands of the tissues”
Describe the progression of heart failure
1) A slow and insidious disease
2) Progressive condition with poor prognosis; 50% mortality in 5 years
When may HF be abrupt? Explain
1) May be abrupt in the case of large myocardial infarct or acute valve dysfunction, but this is usually not what people are referring to
2) Often called CHF, congestive heart failure, but term has fallen out of use
-These days “HF” – heart failure
Differentiate between systolic and diastolic HF and give examples of each
1) Systolic Heart Failure refers to inadequate contractile function
-Usually due to coronary artery disease
2) Diastolic Heart Failure refers to inability of heart to relax and fill
-Left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, constrictive pericarditis
If both of systolic and diastolic heart failure effect output, why is heart failure congestive?
1) When heart can’t send out blood there is an increase in end-diastolic ventricular volumes > increased end-diastolic pressures > elevated venous pressures
2) Therefore “forward failure” leads to “backward failure” in the form of venous congestion
Define forward failure and backward failure (in the context of HF)
1) Forward failure = what the heart pumps out
2) Backward failure = how much blood sits in the venous circuit
How does Frank-Starling mechanism regulate HF?
Increased end-diastolic filling volumes dilate the heart > increased cardiac myofiber stretch > these stretched fibers contract more forcibly > increased cardiac output!
(At this point in the disease, the patient has “compensated heart failure” )
What is the downside of the Frank-Starling mechanism? Explain
Leads to increased oxygen requirements of the heart that is already compromised
-In addition is still has to keep supplying oxygen demand of the rest of the body
-The heart can no longer keep up, the patient has “decompensated heart failure”
Left sided HF:
1) Most common cause?
2) Mechanism?
1) Coronary artery disease
2) Diminished systemic perfusion and elevated back-pressures into pulmonary circulation
Left ventricle fails, blood backs up in the lungs
List signs/ Sx of left sided HF
1) Dyspnea on exertion
2) Orthopnea
3) Cardiomegaly
4) Tachycardia
5) Third heart sound S3
6) Rales at lung bases
7) Progressive ventricular dilation
Left sided HF
1) What causes dyspnea on exertion?
2) What does orthopnea do?
1) Congestion in the lungs
Poor perfusion to tissues
2) Increases surface area of effused lung
Supine position also increases venous return from lower extremities and elevates the diaphragm
Left sided HF
1) Why is there an S3?
2) Why are there rales at the lung bases?
1) Blood falls into the LV with excess residual fluid
Like it’s falling into a “splashy cave”
2) Opening of edematous pulmonary alveoli
Explain progressive ventricular dilation in left sided HF
Leads to papillary muscles displaced outward > mitral regurgitation > chronic dilation of left atrium > atrial fibrillation: irregularly irregular heart-beat
Explain decreased output to systemic circulation in left sided HF
1) Decreased renal perfusion
2) Renin-angiotensin-aldosterone axis increasing intravascular volume
3) This exacerbates the problem
What is the most common cause of right-sided HF? Explain
Left-sided heart failure: pressure increase in the pulmonary circulation produces increased burden on right side of heart
List some causes of isolated right-sided HF
1) Disease of lung parenchyma and/or lung vasculature; cor pulmonale
2) Pulmonic or tricuspid valve disease
3) Congenital heart diseases with left-to-right shunt
What heart changes occur during right-sided HF?
Right ventricle and atrium hypertrophied and dilated
Describe the 2 main S/Sx of right sided HF
1) Portal venous congestion
-Elevated pressure in portal vein and its tributaries
-Hepatic and splenic enlargement
2) Peripheral edema (esp. lower extremities)
(Pure right-sided HF does not generally cause respiratory symptoms directly)
Which shunts are more common, LtR or RtL?
Left to right
Congenital heart disease:
Give 3 examples of left to right shunts (hint: more common, non-cyanotic)
1) Atrial septal defects (ASDs)
2) Ventricular septal defects (VSDs)
3) Patent ductus arteriosus (PDA)
-yes, left-to-right because of pressure
-PDAs are livable
Congenital heart disease: Give 2 examples of right-to-left shunts (cyanotic)
1) Tetralogy of Fallot
2) Transposition of the great arteries (TGA)
Congenital heart disease: What type of shunt is cyanotic?
Right to left
Give an example of an obstructive cause of congestive heart disease
Coarctation of aorta
List the Three Major Groups of congenital heart disease
1) Left-to-right shunts (most common; non-cyanotic)
2) Right-to-left shunts (cyanotic)
3) Obstructions
1) What is the most common congenital heart defect at birth?
2) What happens to most of these? Explain
1) VSDs (42%)
2) Most VSDs close spontaneously in childhood
Incidence in adults less than that of ASDs
Ventricular septal defects (VSDs):
1) What does it result in? What do 70% occur with?
2) Differentiate between small and large VSDs
1) Left-to-right shunt; 70% occur with other cardiac malformations
2) Surgical correction required for large lesions
Differentiate between small and large VSDs
1) Small VSDs: asymptomatic and more noisy
2) Large VSDs: severe left-to-right shunt, may lead to Eisenmenger syndrome (?) , with cyanosis and CHF; earlier, more often than with ASDs
1) Are ASDs or VSDs more common?
2) Which are less likely to close spontaneously? What does this imply?
3) What shunt do ASDs cause? What are the Sx?
4) What may ASDs lead to?
1) ASDs less common than VSDs (10% of CHD)
2) ASDs; they are the most common congenital heart defects to first be diagnosed in adults
3) Left-to-right shunt; asymptomatic in most people
4) Eisenmenger Syndrome
Atrial Septal Defects (ASDs):
1) Surgical repair prevents what?
2) What are the most common locations?
1) Surgical repair prevents irreversible pulmonary changes and heart failure
2) Ostium secundum (90%) near the foramen Ovalle
then ostium premium (5%) lowest part of atrial septum
Patent Ductus Arteriosus (PDA):
1) What is it during fetal development?
2) What happens after birth?
1) Ductus arteriosus permits blood to flow from pulmonary artery to aorta, bypassing lungs during fetal development
2) PDA will reverse flow and travel from aorta to pulmonary artery
Patent Ductus Arteriosus (PDA): what are the differences in Sx between small and large PDAs
Small PDA: asymptomatic
Large PDA: left-to-right shunt; may lead to Eisenmenger syndrome, with cyanosis and CHF
PDA:
1) Does it typically close after birth?
2) What is the condition “PDA”?
3) What % of cases are isolated?
4) What does it sound like?
1) Closes spontaneously by day 1-2 of life
2) Duct fails to close (7% of CHD)
3) 90%
4) Audible as “machinery-like” murmurs
Our body’s prostaglandins keep open the ductus arteriosus for a few days after birth. What does this imply?
Giving NSAID, which inhibits cyclooxygenase and therefore prostaglandin is given to induce closure
Indomethacin is used to do this
The ductus may be intentionally kept open in some congenital heart disease by giving what? Give an example
Prostaglandins, in particular Prostaglandin E
Tetralogy of Fallot
1) Large VSD
2) Aorta overrides left and right ventricles
3) Pulmonary artery stenosis
4) Right ventricular hypertrophy
(Can develop Right-to-left shunt through the VSD)
Tetralogy of Fallot:
1) What can Tetralogy of Fallot develop?
2) What is it the most common cause of?
3) What are some Sx?
4) Can pts survive without Tx?
1) Right-to-left shunt
2) Cyanotic congenital heart disease; right-to-left shunt (5% of all CHD)
3) Cyanosis, clubbing of fingertips, polycythemia, paradoxical emboli
4) Even untreated, some patients survive into adult life
Tetralogy of Fallot:
1) What is the severity?
2) Can it be treated?
3) What are some things to note abt this Dx?
1) Clinical severity depends on degree of RV outflow obstruction
2) Surgical correction possible in most cases
3) “TET spells”; prostaglandin E
Transposition of the Great Arteries (TGA):
1) What is it?
2) What is the outcome?
3) Can people live with this?
1) Aorta arises from right ventricle; pulmonary artery arises from left ventricle
Atrium-to-ventricle connections are normal
2) Separation of systemic and pulmonary circulations
3) Incompatible with life unless there is a big shunt (VSD)
True or false: Even with a stable shunt, most uncorrected TGA patients will die within first few months of life, so corrective surgery usually performed within first few weeks of life
True
Coarctation of the Aorta:
1) Define. Who is more affected?
2) What are some Sx?
3) What does severity depend on?
1) Narrowing of the aorta
Males affected twice as often as females
2) Cyanosis and/or low blood pressure in lower extremities
3) Degree of coarctation
What are the 2 main kinds of cortication of the aorta? Describe
1) Preductal (“Infantile”): leads to early symptoms and cyanosis, particularly in lower half of body
2) Postductal (“Adult”): usually asymptomatic
Myocardial Infarction (MI):
1) What is it?
2) How common?
3) What does the freq. increase with?
4) What can salvage myocardium?
1) Necrosis of heart muscle resulting from ischemia; “Heart attack”
2) 1.5 million people in U.S. each year (one-third die)
3) Frequency of MI increases with age
4) Prompt reperfusion
MI: What are most caused by? Describe how
Acute coronary artery thrombosis:
1) sudden plaque disruption
2) platelets adhere
3) coagulation cascade activated
4) thrombus occludes lumen within minutes
5) irreversible injury/cell death in 20-40 minutes
Myocardial Infarction (MI):
1) Laboratory evaluation of MI is based on measuring what? When?
2) How long do these values last?
1) Cardiac troponins; released from cardiac muscle into the blood following an MI
2) Troponins increase within 2-4 hours after MI and remain elevated for a week or two
Myocardial Infarction (MI):
1) What two other tests may be ordered besides troponin?
2) CK-MB increases within____ hours after MI and returns to normal within ____ hours
1) Total creatine kinase (CK) and a myocardial-specific isoform (CK-MB) may also be ordered
2) 2-4 hours; 72 hours
Heart Failure: Hypertrophy
Explain pressure overload states (4 steps)
1) Hypertension; valve stenosis
2) Adaptation occurs > hypertrophy
3) Sarcomeres are added in parallel to long axis of myocytes
4) Muscle grows causing “concentric hypertrophy” > ventricle wall thickens
Heart Failure: Hypertrophy
Explain volume overload states (4 steps)
1) Valve regurgitation; shunts
2) Adaptation occurs > hypertrophy
3) Sarcomeres are added in series with existing ones so that fiber length increases
4) Ventricles dilate instead
Hypertensive Heart Disease:
1) What can it affect?
2) What is Cor pulmonale?
3) When does the heart respond w. myocyte hypertrophy?
4) What increases ventricle wall thickness?
1) Either left or right ventricle
2) Right ventricle is enlargement due to pulmonary hypertension caused by primary lung disorders
3) Increased pressure or volume overload
4) Pressure overload
Calcific Aortic Stenosis:
1) When does it occur? What is it the most common cause of?
2) What are the two ways in which it can occur?
3) What does it result in?
1) Part of aging process
Most common cause of aortic stenosis in U.S.
2) Can occur on normal aortic valve (70-80 years) or congenitally bicuspid aortic valve (40-50 years)
3) Increased LV pressure, LV hypertrophy, and relative ischemia
Calcific Aortic Stenosis:
1) What are the Sx?
2) What is the mortality?
1) Angina, HF, or fainting
2) 50% mortality within two years of HF inception if not treated by surgery
Mitral Valve Prolapse:
1) What is this?
2) What causes it?
3) Is it common? Explain
1) Mitral leaflets are enlarged, rubbery, floppy and prolapse back into left atrium during systole
2) Deposition of myxomatous (mucoid) material within leaflet
3) Common, affects 3% to 5% of adults in U.S.
Affects women seven times greater than men
Mitral Valve Prolapse:
1) What causes it?
2) What are the Sx?
3) What does auscultation reveal?
1) Pathogenesis unknown
2) Most patients asymptomatic
3) Auscultation reveals midsystolic click
Rheumatic Valvular Disease:
1) What causes it? Define this
1) Rheumatic fever: systemic inflammatory disease occurring a few weeks after streptococcal pharyngitis (“strep throat”); children 5-15 years
2) Rhematic fever causes acute rheumatic heart disease (RHD)
3) Incidence has declined in industrialized world
Rheumatic Valvular Disease:
1) Where is it important to consider?
2) What does it cause?
1) Important in developing countries and economically depressed urban areas
2) RHD causes valve deformities, especially scarring and stenosis of the mitral valve, followed by damage to both mitral valve and aortic valve
Very briefly describe what dilated cardiomyopathy looks like
1) Enlarged 2-3X
2) Flabby
3) Dilation of all chambers
Very briefly describe what restrictive cardiomyopathy looks like
1) Atria dilated
2) Ventricles not dilated, but wall is stiffer (hardest to Tx)
Very briefly describe what hypertrophic cardiomyopathy looks like
1) Hypertrophy, no ventricular dilation
2) Thickened ventricular septum
Pericardial Disease:
1) What is it? What type of rub?
2) What may it cause?
1) Pericarditis; atypical chest pain, not related to exertion, often worse on reclining
-Prominent friction rub
2) Cardiac tamponade
Pericarditis: List and describe the 2 main kinds
1) Secondary, usual: acute MI, cardiac surgery, irradiation, pneumonia, uremia
2) Primary, very rare: mainly infection by viruses
Pericardial Effusions: what are the 3 different kinds and their common causes?
1) Serous: CHF, hypoalbuminemia
2) Serosanguinous: blunt chest trauma, malignancy, ruptured MI, aortic dissection
3) Chylous: mediastinal lymphatic obstruction
Valvular Heart Disease:
1) Outcome depends on what?
2) Explain
1) Outcome depends on ability of pericardial sac to stretch, amount of fluid accumulated, and speed of accumulation
2) Slow = asymptomatic
Sudden = fatal cardiac tamponade
