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Patho > Cardiology deck 2 > Flashcards

Cardiology deck 2 Flashcards

1
Q

What creates the myocardial stretch?

A

end-diastolic volume and the muscle fibers

The muscle fibers reach a certain length at a certain speed, and these factors will determine the force of contraction. The principle is similar to when you stretch a rubber band. The more you stretch a rubber band the more forceful the snap when released.

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2
Q

What is the limit to the Frank-Starling law

A

beyond a certain point the muscle fibers will lose contractile ability. Overstretching over time will eventually cause the rubber band to lose elasticity; when stretched and released, it will barely snap

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3
Q

Laplace’s law

A

explain factors influencing afterload, which is a pressure that is opposite to preload. In Laplace’s law, wall stress (i.e., tension) is due to pressure in the ventricle and the radius (i.e., diameter), which is inversely related to wall thickness. In other words, the wall stress is influenced by pressure, diameter, and wall thickness.

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4
Q

In Laplace’s law….Wall stress affects metabolic demands, and the higher the wall stress the __________________

A

greater the metabolic demand.

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5
Q

When the ventricle wall thickness increases……

A

the opposite happens, and like a bodybuilder’s big muscle, the heart does not have to contract as hard.

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6
Q

increasing radius or pressure ______ wall stress

A

increases

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7
Q

increasing wall thickness _______ wall stress

A

decreases

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8
Q

baroreceptors sense drops in blood pressure, causing the heart rate to ______, vessels to _____, and the contractility to _______ to maintain perfusion.

A

Increase, constrict, increase

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9
Q

baroreceptors sense increase in blood pressure, causing the heart rate to ______, vessels to _____, and the contractility to _______ to maintain perfusion.

A

decrease, vasodilate, decrease

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10
Q

How does aging affect baroreceptors

A

Aging causes changes to these receptors that make them less effective and leads to a slower response.

When an elderly person changes position from sitting to standing, the receptors do not respond as quickly (i.e., blood pressure does not rise) and hypotensive signs such as dizziness or blurred vision occur. This response is termed postural hypotension.

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11
Q

ADH, also known as vasopressin,

A

increases water reabsorption in the kidney, which increases blood volume. Additionally, ADH is a vasoconstrictor, which increases SVR.

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12
Q

When is the renin–angiotensin–aldosterone system (RAAS) activated?

A

renal blood flow is decreased,

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13
Q

How does the renin–angiotensin–aldosterone system (RAAS) work?

A

When renal blood flow decreases ->renin is released from the kidneys ->activates angiotensin I ->converts to angiotensin II (a vasoconstrictor) through the actions of angiotensin-converting enzyme in the lungs ->aldosterone secretion is stimulated ->Aldosterone (from the adrenal cortex) increases the reabsorption of Na+ and Cl- in the kidneys ->Na+ attracts water, which, like ADH, increases blood volume

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14
Q

what does the renin–angiotensin–aldosterone system (RAAS) do in a hypotensive state?

A

this mechanism raises blood pressure and maintains the blood supply to vital organs

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15
Q

renin–angiotensin–aldosterone system (RAAS) do in a hypertensive state?

A

inappropriately activated because of reduced blood flow (vasoconstriction) to the kidneys, further contributing to the hypertension.

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16
Q

natriuretic hormones (e.g., atrial natriuretic peptide) cause _____ of Na+, Cl-, and water.

A

loss

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17
Q

what is the lymphatic system

A

an extensive network of vessels and glands that returns excess fluid (about 3 liters per day) in body tissue to the circulatory system and works with the immune system

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18
Q

What does Interstitial fluid provide for the cells?

A

Interstitial fluid surrounds cells and provides a medium through which nutrients, gases, and wastes can diffuse between the capillaries and the cells.

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19
Q

What is included in the lymphatic system?

A

lymph nodes, the spleen, the thymus, the bone marrow, and tonsils

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20
Q

What is the primary function of the lymphatic system

A

immune response

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21
Q

What happens as the lymph passes through the nodes,

A

he fibers filter out bacteria, viruses, and cellular debris. Numerous macrophages line the channels to phagocytize microorganisms and other material.

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22
Q

What is the rate at which lymph is produced

A

the rate at which it is removed.

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23
Q

What are some examples of lymph produced exceeds the capacity of the system.

A

burns can cause extensive damage to capillaries, causing them to leak fluid into the tissues. This flooding results in excessive fluid in the tissue, or edema. Fluid can also leak into the tissues as a result of lymphatic vessels becoming occluded, often because of infection.

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24
Q

Valvular disorders cause

A

disruption of normal blood flow through the heart.

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25
Q

How is Valvular heart disease diagnosed?

A

a history and physical examination and evaluation with an echocardiogram.

valuate causes or consequences of the valve disease and can include heart catheterization, chest X-rays, EKG, or MRI.

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26
Q

Valvular heart disease management

A

geared toward the actual or potential consequences of the valve disease such as heart failure, cardiomyopathy, and symptomatology.

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27
Q

What are the Two types of alterations r/t valvular heart disease

A

stenosis and regurgitation.

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28
Q

__________ and __________valve disease are more common due to the higher pressures and workload on the left side of the heart.

A

Aortic and mitral

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29
Q

Atresia

A

lack of the valve opening

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30
Q

What happens to the workload of the heart when you have valvular atresia?

A

Pressures in the overfilled chambers increase to pump against the resistance of the stenosed valve. Because the heart (specifically the chamber) is working harder, hypertrophy of the chamber develops. Hypertrophy and increased workload escalate the heart’s oxygen demands, but the decreased cardiac output resulting from the stenosis makes it difficult to meet these increased demands. The cardiac output ultimately decreases, leading to clinical deterioration. Other heart disorders such as cardiomyopathy and heart failure can develop

31
Q

one of the most common valvular diseases in the United States

A

Aortic stenosis

32
Q

Regurgitation

A

also called insufficiency or incompetence, occurs when the valve leaflets do not completely close, so blood continuously leaks. Additionally, heart valves normally allow blood to flow in one direction; incompetent valves, however, allow blood to flow in both directions. This regurgitation of blood increases the amount of blood that must be pumped and, in turn, increases the cardiac workload. The increased workload contributes to hypertrophy developing in the affected chambers. Additionally, the increased blood volume in the heart causes the chambers to dilate to accommodate the larger volume.

33
Q

What can cause Valvular disorders

A

congenital defects, infections, endocarditis, rheumatic fever, hypertension, myocardial infarction, cardiomyopathy, and heart failure.

34
Q

What valvular problems are associated with Marfan syndrome

A

aortic and mitral valve can become regurgitant.

35
Q

Mitral Valve Prolapse

A

common valve disorder and is the most common cause of mitral regurgitation
causes the valve leaflets to billow into the left ventricle or flail and prolapse into the left atrium during systole

36
Q

Treatment for Aortic stenosis or regurgitation

A

can be medically managed, but most patients will ultimately need valve repair or replacement

37
Q

Treatment for Mitral stenosis and regurgitation

A

can be treated medically first, but there are circumstances when repair or replacement is necessary urgently (e.g., acute mitral regurgitation caused by an MI or chest trauma).

38
Q

valvotomy

A

technique involves percutaneously introducing a catheter with a balloon that goes through the stenotic valve and is inflated to clear the calcifications

39
Q

Cardiomyopathies

A

disease of the heart muscle that can lead to several types of structural (e.g., hypertrophy) and functional (e.g., systolic/diastolic dysfunction) changes. The structural and functional changes in cardiomyopathy can cause heart failure.

40
Q

cardiomyopathies are classified into three groups

A

dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy

41
Q

Cardiomyopathy Classification

MOGE(S) stands for:

A

M morphofunctional phenotype

O organ involvement

G genetic or family inheritance pattern

E etiologic description

S functional status.

42
Q

Key heart changes with Dilated Cardiomyopathy

A

Dilated hypertrophied ventricles but normal wall thickness

systolic dysfunction

43
Q

Key heart changes with hypertrophic cardiomyopathy (HCM)

A

Hypertrophied thick walled ventricle (usually interventricular septum)
Diastolic dysfunction

44
Q

Key heart changes with Restrictive Cardiomyopathy

A

Rigid ventricle walls but normal wall thickness

Diastolic dysfunction

45
Q

Complications of Cardiomyopathy

A

Atrial fibrillation
Ventricular Tachyarrhythmias
heart failure

46
Q

What is heart failure

A

condition in which the heart has a problem with ventricular filling or ejection, which then leads to a decreased cardiac output and inadequate perfusion

47
Q

most common risk factors of heart failure

A

hypertension, metabolic syndrome, diabetes mellitus, and atherosclerotic disease

48
Q

One of the top causes of death from cardiovascular disease

A

Heart failure with a 50% death rate usually occurring within 5 years of diagnosis

49
Q

Heart failure incidence increases dramatically after the age of

A

65

50
Q

two preferred categorizations for heart failure (for left sided heart disease)

A

heart failure with reduced EF (HFrEF) for systolic dysfunction and heart failure with preserved EF (HFpEF) for diastolic dysfunction

51
Q

Right-sided heart failure is a result of

A

right ventricle impairment and is most often a consequence of left-sided heart failure

52
Q

cor pulmonale

A

Right ventricle impairment can also occur with pulmonary diseases that cause pulmonary hypertension
The term cor pulmonale is generally not used when the right-side dysfunction is due to left-sided heart failure.

53
Q

The most common causes of either type of heart failure are

A

coronary artery disease and hypertension

Other common risks more frequently seen in patients with HFpEF are diabetes, obesity, coronary artery disease, and dyslipidemia.

54
Q

compensatory mechanisms are activated in times of decreased cardiac output

A

catecholamine release (epinephrine and norepinephrine) ->stimulates SNS->vasoconstriction ->, increases heart rate, contractility->antidiuretic hormone secretion

With SNS stimulation and decreasing cardiac output, renal perfusion decreases, which activates RAAS.

Renin, angiotensin, and aldosterone are released, which leads to fluid retention, vasoconstriction, cell hypertrophy, cell death, and myocardial fibrosis. These compensatory mechanisms increase cardiac output in the beginning, but they eventually lead to excessive preload and afterload. The compensatory mechanisms eventually become inadequate to meet the body’s metabolic needs, and excessive myocardial oxygen demand and an increased preload result in decreased contractility and decompensation

55
Q

Left ventricle (LV) remodeling

A

changes in the mass, volume, and shape of the heart and occurs in response to decompensation and injury.

56
Q

Left sided heart failure basic effects

A

decreased cardiac output

pulmonary congestion

57
Q

R sided heart failure basic effects

A

decreased cardiac output

systemic congestion

58
Q

key manifestations of L sided heart failure

A

pulmonary congestion, dyspnea, activity intolerance

59
Q

Key manifestations of R sided heart failure

A

edema and weight gain

60
Q

As L sided heart failure worsens….

A

symptoms start to occur with less activity and even at rest. Orthopnea (shortness of breath when supine) is a late symptom and occurs due to fluid shifts from the peripheral to the central circulation. The fluid shifts occur while in a supine position and results in increased pulmonary pressure. Increased pressure around bronchial vessels and the increased airway resistance causes paroxysmal nocturnal dyspnea. Paroxysmal nocturnal dyspnea symptoms include coughing and wheezing that wake patients up at night. If blood continues to accumulate, pulmonary edema and right-sided heart failure will develop.

61
Q

Right-sided heart failure is a result of

A

ineffective right ventricular contraction

62
Q

When R sided heart failure progresses

A

blood does not move appropriately out of the right ventricle. Blood backs up first in the right atrium, and then the peripheral circulation, causing increased pressures in the peripheral capillary bed. The patient begins to gain weight, as fluid is not excreted by the kidneys. Tissue becomes edematous, as pressures in the capillaries push fluid out of the circulatory system. Most patients have a combination of left- and right-sided heart failure and therefore manifestations will reflect a combination of both.

TABLE 4-3 Clinical Manifestations of Left- and Right-Sided Heart Failure

63
Q

Stage A heart failure

A

At risk

64
Q

Stage B heart Failure

A

structural disease but no symptoms yet.

65
Q

Stage C and D heart failure

A

have clinical heart failure

66
Q

New York Heart Association classes (I–IV)

A

used to evaluate functional capacity symptoms of heart failure with activity. Patients can go back and forth with New York Heart Association classes (i.e., III–II or I–II).

67
Q

heart failure Diagnosis, staging, and class determination are based on

A

a history and physical and diagnostic tests.
echocardiogram -function and causes.

A brain natriuretic peptide (BNP) or N-terminal pro brain natriuretic peptide

A chest X-ray may reveal signs of fluid retention such as pleural effusions and vascular congestion.

Thoracic ultrasonography can be used to evaluate for acute cardiopulmonary respiratory failure, pleural effusion, and pneumothorax.

A 12-lead EKG may expose causes and coexisting disorders that occur with heart failure such as atrial fibrillation and myocardial infarction, but no finding is specific to heart failure.

Other routine labs include urinalysis, CBC, a chemistry profile with calcium and magnesium, lipid panel, liver function, and thyroid-stimulating hormone evaluation. Other additional blood work may be ordered if there is suspicion of certain causes of the heart failure (e.g., HIV, hemochromatosis). With patients who are hospitalized, additional tests may include a troponin test, arterial blood gases, cardiac catheterization, and myocardial biopsy depending on causes and status.

68
Q

Lab that shows a hormone released by the ventricles in response to overstretching

A

brain natriuretic peptide (BNP) or N-terminal pro brain natriuretic peptide

69
Q

lifestyle modifications for heart failure

A

weight reduction, tobacco cessation, reduced salt consumption, fluid restriction, and exercise

70
Q

angiotensin-converting enzyme (ACE) inhibitors

A

stop the renin–angiotensin–aldosterone cycle

71
Q

pharm for HFrEF

A

ACE inhibitors
angiotensin receptor blockers (ARBs), or an angiotensin receptor neprilysin inhibitors (ARNIs)
ARNIs, are a combination of an ARB with an inhibitor of the enzyme neprilysin. Neprilysin causes the breakdown of beneficial natriuretic peptides, which help to maintain fluid homeostasis

72
Q

All patients with heart failure should be on either an

A

ACE, ARB, or ARNI and a selective beta-1–adrenergic blocking agent or an alpha-1, beta-1, beta-2 receptor blocker (to slow the heart rate and thereby increase diastolic filling).

73
Q

type of diuretic for patients in fluid volume overload

A

preferably loop diuretics, which act at the loop of Henle to prevent sodium or chloride reabsorption

74
Q

HFpEF

A

Heart failure with preserved ejection fraction

Patho (10 decks)

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