Clinical Ex Phys Exam 4

Front 1

The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body's tissues. May be the final and most severe manifestation of nearly every form of cardiac disease.

Back 1

Congestive Heart failure

Front 2

Three things that have led to a decline in coronary artery disease mortality from 1970-95

Back 2

Improved survival after MI due to things such as PTCA, stent, clot-busters; Effective secondary prevention such as aspirin and statins; Progress in primary prevention (controlling risk factors)

Front 3

The study of the causes, typically it is used to mean the study of the causes of a disorder.

Back 3

Etiology

Front 4

A narrowing which restricts red blood from moving from the left ventricle into the aorta

Back 4

Aortic stenosis

Front 5

A disease, deformity, or deficiency existing at the time of birth

Back 5

Congenital

Front 6

More common type of heart failure in which there is reduced contractility, reduced ejection fraction (<40%). It is most commonly caused by CAD with subsequent MI, but may also be caused by dilated cardiomyopathy, hypertension, or chronic valvular heart disease

Back 6

Systolic heart failure

Front 7

Less common type of heart failure in which there is abnormal diastolic relaxation of the ventricles, reduced end-diastolic volume. Most commonly caused by hypertrophy with LV hypertrophy, but may be caused by hypertrophic cardiomyopathy or chronic valvular heart disease

Back 7

Diastolic heart failure

Front 8

A disease of the myocardium (heart muscle) that causes the heart cavity to become stretched and enlarged, and the pumping capacity of the heart is reduced.

Back 8

Dilated cardiomyopathy

Front 9

Umbrella term for diseases involving the valves of the heart.

Back 9

Chronic valvular heart disease

Front 10

Disease in which the heart muscle becomes so thick that it can interfere with its proper functioning

Back 10

Hypertrophic cardiomyopathy

Front 11

A law that states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume). The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully

Back 11

Frank-Starling law

Front 12

A blood disorder consisting of an increase in the volume of circulating blood. Can be caused by a low Frank-Starling curve

Back 12

Hypervolemia

Front 13

A manifestation of acute coronary heart failure in which there is fluid accumulation in the lungs caused by elevated LA and LV pressure.

Back 13

Pulmonary edema

Front 14

Compensatory mechanisms of a heart with congestive heart failure in order to maintain cardiac output and systemic arterial blood pressure.

Back 14

Ventricular hypertrophy, sympathetic activation, neurohormonal activation

Front 15

Receptors in the heart that increase heart rate and increase contractility

Back 15

Beta 1 adrenergic

Front 16

Receptors in vascular smooth muscle cell that lead to arterial vasocontriction and venoconstriction in order to maintain BP and increase preload

Back 16

Alpha-1 adrenergic

Front 17

Mechanism that increases peripheral vasculature resistance to maintain blood pressure

Back 17

Arterial vasoconstriction

Front 18

Mechanism that leads to increased venous return and increased preload

Back 18

Venoconstriction

Front 19

Hormone that aids in sodium and water retention in the kidney, affecting BP

Back 19

Aldosterone

Front 20

Polypeptide that increases peripheral vasoconstriction, blood plasma volume, and sodium and water retention in the kidney. It increases aldosterone production. Can stimulate ventricular hypertrophy

Back 20

Angiotensin II

Front 21

Hormone released from the posterior pituitary in response to a fall in blood volume (cardiac output) that acts on the kidney to retain water, leading to an increased plasma volume

Back 21

Antidiuretic hormone (ADH)

Front 22

Hormone released by the juxtaglomerular cells that catalyzes angiotensiogen to angiotensin I

Back 22

Renin

Front 23

Enzyme that converts angiotensin I to angiotensin II

Back 23

Angiotensin converting enzyme (ACE)

Front 24

Acute CHF Pharmacotherapy that increases water excretion and diuresis

Back 24

Diuretics

Front 25

Drugs such as captopril and ramipril that cause vasodilation via the prevention of Ang II formation, thereby increasing water and Na+ retention and decreasing hypertrophy and ventricular remodeling

Back 25

ACE inhibitors

Front 26

CHF pharmacology that is a positive inotrope (increases contractility) and a negative chronotrope (decreases conduction through the AV node, thereby decreasing HR). Example is digoxin

Back 26

Digitalis

Front 27

CHF pharmacology that reduces preload and dilates coronary arterioles

Back 27

Nitrates

Front 28

Chronic CHF pharmacology, such as coumadin, that prevent the blood from clotting

Back 28

Anti-coagulent

Front 29

Chronic CHF pharmacology that reduces negative effects of sympathetic overactivation. They are only used in stable compensated CHF and they have been shown to decrease mortality. Examples are matoprolol, carvediolol

Back 29

Beta-blockers

Front 30

Troubled breathing or difficulty breathing

Back 30

Dyspnea

Front 31

The inability to breathe well unless one is sitting up or standing erect. It is a symptom of LV failure in CHF

Back 31

Orthopnea

Front 32

sudden, severe shortness of breath at night that awakens a person from sleep, often with coughing and wheezing. It is most closely associated with congestive LV heart failure

Back 32

Paroxysmal Nocturnal dyspnea

Front 33

Swelling of tissues, usually the lower limbs, due to accumulation of tissues. It is a symptom of Congestive RV heart failure

Back 33

Peripheral edema

Front 34

Group of heart disorders which involves structural abnormality of the myocardium. It often leads to heart failure and comes in the types: dilated, hypertrophic, and restrictive.

Back 34

Cardiomyopathy

Front 35

A disease of the myocardium (heart muscle) that causes the heart cavity to become stretched and enlarged, making the myocardium thinner and the pumping capacity of the heart is reduced. It can occur due to MI, ischemia, infection, chemo, or toxicity from drugs/alcohol. Most common cardiomyopathy

Back 35

Dilated cardiomyopathy

Front 36

Congenital (familial) disease in which the myocardium of the heart is enlarged to the point that it interferes with normal heart functioning. It results from a genetic mutation of myosin heavy chain gene. Increases risk of sudden death (esp during exercise)

Back 36

Hypertrophic cardiomyopathy

Front 37

Condition in which the myocardium stiffens, preventing adequate heart function and decreasing blood flow. It is caused by fibrosis (formation of excessive fibrous connective tissue) of the myocardium. It is the least common type of cardiomyopathy

Back 37

Dilated Cardiomyopathy

Front 38

A mechanical device that is used to partially or completely replace the function of a failing heart. It takes blood from the LV, passes it through a pump and then to the aorta. They are often considered a "bridge to heart transplantation" because they are given to those who are waiting for a transplant

Back 38

Left Ventricular Assist Device (LVAD)

Front 39

Survival "threshold" found by one study. It is the Peak VO2 in which subjects above this value showed a significantly higher survival rate than their counterparts who had a lower VO2 peak below this

Back 39

14 ml/kg*min

Front 40

There [is/ is not] a correlation between LV ejection fraction and exercise duration. There [is| is not] a correlation between peak VO2 and ejection fraction.

Back 40

Is not; is not

Front 41

Mechanism of exercise intolerance in individuals with CHF. Individuals with this have a decreased peak cardiac output and therefore a decreased peak oxygen consumption.

Back 41

Impaired diastolic function

Front 42

Mechanism of exercise intolerance in individuals with CHF in which there is a shift away from %Type I fibers towards type IIa and IIb/x, decrease in muscle girth, infiltration of fat and fluid to muscle tissue, reduction in muscle strength and endurance, and a "cardiac cachexia" syndrome in which there is muscle and bone wasting

Back 42

Skeletal muscle myopathy (Atrophy)

Front 43

Mechanism of exercise intolerance in individuals with CHF in which there is a decrease in oxidative enzyme activity (eg. citrate synthase), an increase in glycolytic enzymes (eg. LDH), a decrease in size and # of mitochondria, a rapid depletion of muscle PC, and a rapid fall in muscle PH

Back 43

Skeletal muscle myopathy (Decrease in metabolic capacity)

Front 44

Mechanism of exercise intolerance in individuals with CHF in which there is either a sympathetic nervous system overactivation (NE concentrations rise much higher in people with CHF than in healthy people) or RAAS overactivation.

Back 44

Neurohormonal activation

Front 45

Norepinephrine levels rise [faster| slower] in individuals with CHF.

Back 45

Faster

Front 46

Mechanism of exercise intolerance in individuals with CHF in which there is an increased sympathetic activation to peripheral vasculature or impaired endothelial function. Ex: individuals with CHF have been found to have lower calf blood flow after plethysmography than individuals without CHF

Back 46

Impaired muscle blood flow due to vasodilatory capacity

Front 47

Exercise training in CHF patients has been shown to [increase|decrease] Ang II, Aldosterone, and Vasopressin (ADH) levels at rest.

Back 47

Decrease

Front 48

$37 million, NIH-sponsored multicenter randomized controlled exercise clinical tria with over 3000 patients in 50 US and canadian hospitals that investigated the outcomes of exercise training in subjects with heart failure

Back 48

Heart Failure and A Controlled Trial Investigating Outcomes of Exercise Training (HF ACTION) Clinical Trial

Front 49

Therapy to help prevent rejection of transplanted organs

Back 49

Immunosuppressive therapy

Front 50

Immunosuppressive drug that decreases neutrophils. Has sidde effects of hypertension and kidney failure

Back 50

Cyclosporine

Front 51

Immunosuppressive glucocorticoid steroid drug that serves as an anti-inflammatory and has side effects of muscle atrophy, osteoporosis, fat redistribution, and mood swings

Back 51

Prednisone

Front 52

Cardiac output changes in response to exercise are similar in transplant patients and control patients. This is due to an increase in ____ as opposed to an increase in _____ which does not change much in transplant patients during exercise.

Back 52

Stroke volume; heart rate

Front 53

Norepi levels increase [faster\slower] in response to exercise in heart transplant patients than in control subjects

Back 53

faster

Front 54

Affecting the timing or rate of heart contraction. Positive means HR increases, negative means HR decreases

Back 54

Chronotropic

Front 55

Effect of a substance that affects the contractility of the heart. Positive improves contractility while negative worsens contractility

Back 55

Inotropic

Front 56

What three things lead to a decreased peak cardiac output and therefore exercise intolerance in heart transplant recipients (HTR)?

Back 56

Impaired chronotropic response to exercise, reduced maximal HR during exercise, and impaired EDV and reduced SV

Front 57

Resistance exercise elicits myofibrillar shifts from type __ to type __ is transplant recipients.

Back 57

II to I

Front 58

Volume of blood in a ventricle after filling (diastole)

Back 58

End Diastolic Volume

Front 59

The length of the sarcomeres of the cardiac muscle cells prior to systole

Back 59

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