Lecture 5.2 MJ slides

Question 1

Define heart failure

Answer 1

“Heart cannot generate enough output to meet the metabolic demands of the tissues”

Question 2

Describe the progression of heart failure

Answer 2

1) A slow and insidious disease
2) Progressive condition with poor prognosis; 50% mortality in 5 years

Question 3

When may HF be abrupt? Explain

Answer 3

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

Question 4

Differentiate between systolic and diastolic HF and give examples of each

Answer 4

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

Question 5

If both of systolic and diastolic heart failure effect output, why is heart failure congestive?

Answer 5

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

Question 6

Define forward failure and backward failure (in the context of HF)

Answer 6

1) Forward failure = what the heart pumps out
2) Backward failure = how much blood sits in the venous circuit

Question 7

How does Frank-Starling mechanism regulate HF?

Answer 7

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” )

Question 8

What is the downside of the Frank-Starling mechanism? Explain

Answer 8

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”

Question 9

Left sided HF:
1) Most common cause?
2) Mechanism?

Answer 9

1) Coronary artery disease
2) Diminished systemic perfusion and elevated back-pressures into pulmonary circulation
Left ventricle fails, blood backs up in the lungs

Question 10

List signs/ Sx of left sided HF

Answer 10

1) Dyspnea on exertion
2) Orthopnea
3) Cardiomegaly
4) Tachycardia
5) Third heart sound S3
6) Rales at lung bases
7) Progressive ventricular dilation

Question 11

Left sided HF
1) What causes dyspnea on exertion?
2) What does orthopnea do?

Answer 11

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

Question 12

Left sided HF
1) Why is there an S3?
2) Why are there rales at the lung bases?

Answer 12

1) Blood falls into the LV with excess residual fluid
Like it’s falling into a “splashy cave”
2) Opening of edematous pulmonary alveoli

Question 13

Explain progressive ventricular dilation in left sided HF

Answer 13

Leads to papillary muscles displaced outward > mitral regurgitation > chronic dilation of left atrium > atrial fibrillation: irregularly irregular heart-beat

Question 14

Explain decreased output to systemic circulation in left sided HF

Answer 14

1) Decreased renal perfusion
2) Renin-angiotensin-aldosterone axis  increasing intravascular volume
3) This exacerbates the problem

Question 15

What is the most common cause of right-sided HF? Explain

Answer 15

Left-sided heart failure: pressure increase in the pulmonary circulation produces increased burden on right side of heart

Question 16

List some causes of isolated right-sided HF

Answer 16

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

Question 17

What heart changes occur during right-sided HF?

Answer 17

Right ventricle and atrium hypertrophied and dilated

Question 18

Describe the 2 main S/Sx of right sided HF

Answer 18

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)

Question 19

Which shunts are more common, LtR or RtL?

Answer 19

Left to right

Question 20

Congenital heart disease:
Give 3 examples of left to right shunts (hint: more common, non-cyanotic)

Answer 20

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

Question 21

Congenital heart disease: Give 2 examples of right-to-left shunts (cyanotic)

Answer 21

1) Tetralogy of Fallot
2) Transposition of the great arteries (TGA)

Question 22

Congenital heart disease: What type of shunt is cyanotic?

Answer 22

Right to left

Question 23

Give an example of an obstructive cause of congestive heart disease

Answer 23

Coarctation of aorta

Question 24

List the Three Major Groups of congenital heart disease

Answer 24

1) Left-to-right shunts (most common; non-cyanotic)
2) Right-to-left shunts (cyanotic)
3) Obstructions

Question 25

1) What is the most common congenital heart defect at birth? 2) What happens to most of these? Explain

Answer 25

1) VSDs (42%) 2) Most VSDs close spontaneously in childhood Incidence in adults less than that of ASDs

Question 26

Ventricular septal defects (VSDs): 1) What does it result in? What do 70% occur with? 2) Differentiate between small and large VSDs

Answer 26

1) Left-to-right shunt; 70% occur with other cardiac malformations 2) Surgical correction required for large lesions

Question 27

Differentiate between small and large VSDs

Answer 27

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

Question 28

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?

Answer 28

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

Question 29

Atrial Septal Defects (ASDs): 1) Surgical repair prevents what? 2) What are the most common locations?

Answer 29

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

Question 30

Patent Ductus Arteriosus (PDA): 1) What is it during fetal development? 2) What happens after birth?

Answer 30

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

Question 31

Patent Ductus Arteriosus (PDA): what are the differences in Sx between small and large PDAs

Answer 31

Small PDA: asymptomatic Large PDA: left-to-right shunt; may lead to Eisenmenger syndrome, with cyanosis and CHF

Question 32

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?

Answer 32

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

Question 33

Our body’s prostaglandins keep open the ductus arteriosus for a few days after birth. What does this imply?

Answer 33

Giving NSAID, which inhibits cyclooxygenase and therefore prostaglandin is given to induce closure Indomethacin is used to do this

Question 34

The ductus may be intentionally kept open in some congenital heart disease by giving what? Give an example

Answer 34

Prostaglandins, in particular Prostaglandin E

Question 35

Tetralogy of Fallot

Answer 35

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)

Question 36

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?

Answer 36

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

Question 37

Tetralogy of Fallot: 1) What is the severity? 2) Can it be treated? 3) What are some things to note abt this Dx?

Answer 37

1) Clinical severity depends on degree of RV outflow obstruction 2) Surgical correction possible in most cases 3) “TET spells”; prostaglandin E

Question 38

Transposition of the Great Arteries (TGA): 1) What is it? 2) What is the outcome? 3) Can people live with this?

Answer 38

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)

Question 39

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

Answer 39

True

Question 40

Coarctation of the Aorta: 1) Define. Who is more affected? 2) What are some Sx? 3) What does severity depend on?

Answer 40

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

Question 41

What are the 2 main kinds of cortication of the aorta? Describe

Answer 41

1) Preductal (“Infantile”): leads to early symptoms and cyanosis, particularly in lower half of body 2) Postductal (“Adult”): usually asymptomatic

Question 42

Myocardial Infarction (MI): 1) What is it? 2) How common? 3) What does the freq. increase with? 4) What can salvage myocardium?

Answer 42

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

Question 43

MI: What are most caused by? Describe how

Answer 43

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

Question 44

Myocardial Infarction (MI): 1) Laboratory evaluation of MI is based on measuring what? When? 2) How long do these values last?

Answer 44

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

Question 45

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

Answer 45

1) Total creatine kinase (CK) and a myocardial-specific isoform (CK-MB) may also be ordered 2) 2-4 hours; 72 hours

Question 46

Heart Failure: Hypertrophy Explain pressure overload states (4 steps)

Answer 46

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

Question 47

Heart Failure: Hypertrophy Explain volume overload states (4 steps)

Answer 47

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

Question 48

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?

Answer 48

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

Question 49

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?

Answer 49

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

Question 50

Calcific Aortic Stenosis: 1) What are the Sx? 2) What is the mortality?

Answer 50

1) Angina, HF, or fainting 2) 50% mortality within two years of HF inception if not treated by surgery

Question 51

Mitral Valve Prolapse: 1) What is this? 2) What causes it? 3) Is it common? Explain

Answer 51

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

Question 52

Mitral Valve Prolapse: 1) What causes it? 2) What are the Sx? 3) What does auscultation reveal?

Answer 52

1) Pathogenesis unknown 2) Most patients asymptomatic 3) Auscultation reveals midsystolic click

Question 53

Rheumatic Valvular Disease: 1) What causes it? Define this

Answer 53

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

Question 54

Rheumatic Valvular Disease: 1) Where is it important to consider? 2) What does it cause?

Answer 54

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

Question 55

Very briefly describe what dilated cardiomyopathy looks like

Answer 55

1) Enlarged 2-3X 2) Flabby 3) Dilation of all chambers

Question 56

Very briefly describe what restrictive cardiomyopathy looks like

Answer 56

1) Atria dilated 2) Ventricles not dilated, but wall is stiffer (hardest to Tx)

Question 57

Very briefly describe what hypertrophic cardiomyopathy looks like

Answer 57

1) Hypertrophy, no ventricular dilation 2) Thickened ventricular septum

Question 58

Pericardial Disease: 1) What is it? What type of rub? 2) What may it cause?

Answer 58

1) Pericarditis; atypical chest pain, not related to exertion, often worse on reclining -Prominent friction rub 2) Cardiac tamponade

Question 59

Pericarditis: List and describe the 2 main kinds

Answer 59

1) Secondary, usual: acute MI, cardiac surgery, irradiation, pneumonia, uremia 2) Primary, very rare: mainly infection by viruses

Question 60

Pericardial Effusions: what are the 3 different kinds and their common causes?

Answer 60

1) Serous: CHF, hypoalbuminemia 2) Serosanguinous: blunt chest trauma, malignancy, ruptured MI, aortic dissection 3) Chylous: mediastinal lymphatic obstruction

Question 61

Valvular Heart Disease: 1) Outcome depends on what? 2) Explain

Answer 61

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