Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular Exam I > Cardiac Specializations, Aging, CHF, Congenital Heart Dz, Ischemic Heart Dz > Flashcards

Cardiac Specializations, Aging, CHF, Congenital Heart Dz, Ischemic Heart Dz Flashcards

1
Q

Atrial myocytes have storage granules that contain ANP which promotes arterial vasodilation and stimulates natriuresis and diuresis, which is beneficial in the setting of ___ and ____

A

HTN; CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Due to their thin structure, heart valves derive most of their nourishment via _____; normal leaflets and cusps’ vessels are limited to the ____ portions

A

Diffusion; proximal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 general types of damage that occur in valves

A

Collagen —> mitral prolapse

Nodular calcification —> calcific aortic stenosis

Fibrotic thickening —> rheumatic heart dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

During ventricular diastole, closure of the ____ valve leads to _____

A

Aortic; blood flow to myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe cardiac stem cells

A

Bone marrow derived precursors and stem cells are present in the myocardium but only replace about 1% each year — thus no significant recovery in zone of necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effects of aging on myocardium and chambers of the heart

A

Increased LV chamber size, increased left atrial cavity size, sigmoid shaped ventricular sepum

Increased epicardial fat

Myocardium changes include lipofuscin, basophilic degeneration, and possible amyloid deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effect of aging on heart valves

A

Aortic and mitral valves undergo annular calcification

Fibrous thickening

Mitral leaflets buckle towards left atrium —> increased left atrium size

Lambl excrescences = small filiform processes that form on closure lines of aortic and mitral valves, probably resulting from organization of small thrombi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Vascular changes that occur with aging

A

Coronary atherosclerosis

Stiffening and dilation of the aorta, elastic fragmentation and collagen accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

____ occurs when the heart is unable to pump blood at a rate to meet peripheral demand, OR can only do so with increased filling pressure

May result from loss of myocardial contractile function (systolic dysfunction) or loss of ability to fill the ventricles during diastole (diastolic dysfunction)

A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiac myocytes become hypertrophic in the setting of sustained pressure or volume overload (such as in ____ or _____), or in the setting of sustained ____ signals (such as beta-adrenergic stim)

A

Systemic HTN; aortic stenosis

Trophic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In the setting of ______ overload hypertrophy, myocytes become thicker and the LV increases in thickness concentrically

In the setting of _____ overload hypertrophy, myocytes elongate and ventricular dilation is seen

A

Pressure

Volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypertrophy of myocytes isn’t accompanied by a matching increase in blood supply despite increased energy demand — thus what is a major complication of cardiac hypertrophy?

A

Ischemia-related decompensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Left sided heart failure can be systolic or diastolic; it is most commonly a result of what conditions?

A

Myocardial ischemia

HTN

Left-sided valve dz

Primary myocardial dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical effects of left sided heart failure? What causes them?

A

Clinical effects include paroxysmal nocturnal dyspnea, elevated pulmonary capillary wedge pressure, pulmonary congestion (cough, crackles, wheezes, blood-tinged sputum, tachypnea), restlessness, confusion, orthopnea, tachycardia, exertional dyspnea, fatigue, cyanosis

These occur d/t decreased tissue perfusion and congestion in pulmonary circ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Left-sided heart failure is characterized by left ventricular hypertrophy. Left ventricular dysfunction leads to left atrial dilation, resulting in what potential complications?

A

Atrial fibrillation, stasis, thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The decreased ejection fraction associated with left sided heart failure may result in what complications concerning the kidneys?

A

Decreased EF —> decreased glomerular perfusion —> renin release —> increased volume

Prerenal azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Histologic finding with left-sided heart failure

A

Heart failure cells = hemosiderin-laden macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Advanced CHF may lead to decreased cerebral perfusion —> ____ ____

A

Hypoxic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Most common cause of right sided heart failure

A

Left sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Isolated right sided heart failure may result from what conditions?

A

Anything that causes pulmonary HTN — parenchymal lung dz, primary pulmonary HTN, or pulmonary vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical features of right-sided heart failure

A

In primary right sided failure, pulmonary congestion is minimal

The venous system is markedly congested, leading to:
Liver congestion (nutmeg liver)

Splenic congestion (splenomegaly)

Effusions involving peritoneal, pleural, and pericardial spaces

Edema, especially in dependent areas (e.g., ankles)

Renal congestion

Other Symptoms: fatigue, distended jugular vv, anorexia and complaints of GI distress, weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Sporadic genetic abnormalities are the major known causes of congenital heart disease. What are the major examples?

A

Turner syndrome, trisomies 13, 18, and 21

The single MOST COMMON genetic cause of congenital heart disease is TRISOMY 21 — about 40% of pts with Down syndrome have at least one heart defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe heart defects associated with trisomy 21

A

Usually derived from second heart field (arterioventricular septae) — most commonly defects of the endocardial cushion, including ostium primum, ASDs, AV valve malformations, and VSDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What congenital heart diseases are associated with the Notch pathway?

A

Bicuspid aortic valve (NOTCH1)

Tetralogy of Fallot (JAG1 and NOTCH2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

______ mutations are associated with Marfan syndrome which is associated with ____ defects and aortic aneurysms

A

Fibrillin; valvular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Most common type of congenital cardiac malformation

A

Ventricular septal defect (VSD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Genes associated with the nonsyndromic congenital heart defects

A

ASD or conduction defects (NKX2.5)

ASD or VSD (GATA4)

Tetralogy of fallot (ZFPM2 or NKX2.5)

Note that tetralogy of fallot when associated wtih alagille syndrome is associated with JAG1 or NOTCH2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What type of shunt is considered the most common congenital heart dz?

A

Left-to-right shunts — including ASD, VSD, and PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Of the common congenital left-to-right shunts, the _____ causes increased outflow volume from the RV and pulmonary system, while the ____ and _____ both cause increased pulmonary blood flow and pressure

A

ASD; VSD, PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T/F: Atrial septal defects tend to be rapidly fatal

A

False — ASDs are usually asymptomatic until adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

3 types of atrial septal defects

A

Secundum ASD: 90% of all ASDs — occurs at center of atrial septum; may be multiple or fenestrated

Primum anomaly: 5% of all ASDs — occurs adjacent to AV valves; often associated with AV valve abnormalities and/or VSD

Sinus venosa defects: 5% of all ASDs — occurs near entrance of SVD; can be associated with anomalous pulmonary venous return to the R atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical consequences of congenital left to right shunting

A

Left-to-right shunting causes volume overload on the right side, which may lead to pulmonary HTN, right heart failure, or paradoxical embolization

May be closed surgically with normal survival

33
Q

80% of PFOs close permanently by 2 y/o, in the remaining 20% the flap can open if there is an increase in ____-sided pressure, inducing brief periods of ___-___ shunting, such as with pulmonary HTN, bowel movement, coughing, or sneezing. One of the complications of most concern is the possibility for ________ _______

A

Right; R-L; paradoxical embolus

34
Q

T/F: the majority of VSDs are infundibular (occuring below pulmonary valve or within muscular septum)

A

False - 90% of VSDs are membranous

35
Q

Clinical effects of a VSD

A

Effects depend on size and presence of other heart defects (those that manifest as children are often associated with other heart anomalies)

Many small VSDs close spontaneously

Large VSDs may cause significant shunting, leading to right ventricular hypertrophy and pulmonary HTN which can ultimately reverse flow through the shunt, leading to cyanosis

36
Q

Patent ductus arteriosus may fail to close when infants are ______, and/or have defects associated with increased ______ pressure (such as with VSD)

A

Hypoxic; pulmonary vascular

37
Q

Major clinical findings with patent ductus arteriosus

A

PDA produces harsh, machine-like murmur

Effect is further determined by shunt’s diameter — large shunts can increase pulmonary pressure and eventually shunt reversal and cyanosis

38
Q

Cyanosis early in postnatal life may occur as a result of what cyanotic congenital heart diseases?

A 
Tetralogy of fallot (most common)
Transposition of the great arteries
Persistent truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous connection
39
Q

Clinical presentation of a child with TOF

A

Squatting
Cyanosis
Clubbing
Syncope

[clinical severity depends on degree of subpulmonary stenosis which obstructs the RV outflow tract. Mild stenosis causes L to R shunt. Classic TOF is R to L shunting with cyanosis. Most infants are cyanotic from birth, or soon thereafter]

40
Q

4 cardinal pathologic features of TOF

A

VSD

Obstruction of RV outflow tract

Aorta overrides the VSD

RV hypertrophy (heart is enlarged and “boot-shaped” because of this)

41
Q

Describe prognosis and comorbidities associated with transposition of the great vessels

A

Transposition of the great vessels results in 2 separate circuits and is incompatible with life unless a shunt is present for mixing of blood from the 2 circuits

Approximately 1/3 have a VSD

2/3 have a PFO or PDA

Right ventricule becomes hypertrophic (supports systemic circulation), and the left ventricle atrophies

Without surgery, pts will die in a few months

42
Q

Differentiate presentation of coarctation of the aorta (narrowing of the aorta) in infants vs. adults

A

Infantile form: generally seen WITH a PDA, manifests at birth; may produce cyanosis in lower half of the body

Adult form: generally seen WITHOUT a PDA; usually asymptomatic but can see hypERtension in UEs and hypOtension in LEs. LEs may also exhibit coldness and claudication; may eventually see concentric LV hypertrophy

[regardless of type, degree of narrowing is variable with variable clinical effect — clinical severity depends on degree of stenosis and patency of ductus arteriosus]

43
Q

What patient populations are at higher risk for coarctation of the aorta?

A

Males > females

Turner syndrome (45,XO)

44
Q

Ischemic heart dz results from insufficient perfusion to meet metabolic demands of the myocardium. Blood to the myocardium is supplied by the coronary arteries, so any disruption of coronary flow may result in ischemia. Ischemia may lead to what complications?

A

Myocardial infarction
Angina pectoris
Chronic IHD with heart failure
Sudden cardiac death

45
Q

Ischemic heart dz is the leading cause of death in the US, and >90% are secondary to _______

A

Atherosclerosis

[associated with chronic vascular occlusion; acute plaque change —> thrombus]

46
Q

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction

A

Angina pectoris

47
Q

3 clinical varians of angina pectoris

A

Stable angina

Prinzmetal variant angina

Unstable (or “crescendo”) angina

48
Q

Describe stable angina variant

A

Stenotic occlusion of coronary artery

“Squeezing” or burning sensation, relieved by rest or vasodilators

Induced by physical activity or stress

49
Q

Describe prinzmetal variant angina

A

Episodic coronary a. spasm, relieved with vasodilators

Unrelated to physical activity, HR, or BP

50
Q

Describe unstable (crescendo) variant angina

A

Frank pain, increasing in frequency, duration, and severity at progressively lower levels of physical activity, eventually even at rest

Usually rupture of atherosclerotic plaque with partial thrombus

~50% may have evidence of myocardial necrosis; ACUTE MI MAY BE IMMINENT

51
Q

In terms of myocardial infarction, age distribution and risk factors mirror those of atherosclerosis in general because nearly 90% of infarcts are caused by an atheromatous plaque. What are some other potential causes of MI?

A

Embolus

Vasospasm

Ischemia secondary to vasculitis, shock, or other hematologic abnormalities

52
Q

Classic presentation of MI

A

Prolonged CP (>30 min) described as crushing, stabbing, squeezing, tightness, radiating down left arm or left jaw

Diaphoresis

Dyspnea

N/V

HOWEVER - up to 25% are asymptomatic

53
Q

The location, size, and features of an acute MI depend on what factors?

A

The site, degree, and rate of occlusion of the artery

Size of the area perfused

Duration of the occlusion

Metabolic and oxygen needs of the area at risk

Extent of collateral blood flow

Presence of arterial spasm

54
Q

Physiologic changes that occur following severe myocardial ischemia

How long until onset of irreversible injury?

A

Onset of ATP depletion within seconds and loss of contractility within 2 minutes; increase in lactic acid

Onset of irreversible injury around 20minute mark; microvascular injury takes about 1 hr

55
Q

T/F: upon occlusion of coronary artery, the area of necrosis begins in the area directly adjacent to the occluded vessel first

A

False — the necrotic area begins in region of endocardium furthest from occluded vessel and extends back toward area of obstruction

56
Q

Most common coronary vessels occluded in acute MI and the subsequent areas of infarction

A

LAD (40-50%) —> apex, LV anterior wall, anterior 2/3 of septum

RCA (30-40%) —> RV free wall, LV posterior wall, posterior 1/3 of septum

LCX (15-20%) —> LV lateral wall

57
Q

What occlusion locations result in transmural infarcts?

A

Permanent occlusion of LAD branch

Permanent occlusion of left circumflex branch

Permanent occlusion of RCA (or its posterior descending branch)

58
Q

What occlusion locations result in non-transmural infarcts?

A

Transient/partial obstruction in coronary vessels —> subendocardial infarct

Global hypotension —> circumfirential subendocardial infarct

Small intramural vessel occlusions —> microinfarcts

59
Q

Gross features, light microscope, and electron microscope findings immediately following MI

A

Gross features: none

Light microscope: none

Electron microscope: relaxation of myofibrils, glycogen loss, mitochondrial swelling

60
Q

Gross features, light microscope, and electron microscope findings within 30 minutes—4hours following an MI

A

Gross features: none

Light microscope: usually none; variable waviness of fibers at border

Electron: sarcolemmal disruption, microchondrial amorphous densities

61
Q

Gross features and light microscope findings within 4-12 hours of acute MI

A

Gross features: occasional dark mottling

Light micro: early coagulation necrosis; edema; hemorrhage

62
Q

Gross features and light microscope findings within 12 hours—3 days of acute MI

A

Gross features: dark mottling with yellow-tan infarct center

Light micro: ongoing coagulation necrosis; pyknosis of nuclei, myocyte HYPEREOSINOPHILIA, marginal contraction band necrosis; early neutrophilic infiltrate. Within 1-3 days there is loss of nuclei and striations + brisk interstitial infiltrate of NEUTROPHILS

63
Q

Gross features and light microscope findings within 3-10 days of acute MI

A

Gross features: hyperemic border; central yellow-tan softening. Within 7-10 days becomes maximally yellow-tan and soft with depressed red-tan margins

Light micro: beginning disintigration of dead myofibers with dead neutrophils, early phagocytosis of dead cells by macrophages at infarct border. Within 7-10 days there is well-developed phagocytosis of dead cells and GRANULATION TISSUE appears at margins

64
Q

Gross features and light microscope findings within 10-14 days of acute MI

A

Gross findings: red-gray depressed infarct borders

Light mico: well-established granulation tissue with NEW BLOOD VESSELS and collagen deposition

65
Q

Gross features and light microscope findings within 2-8 weeks of acute MI

A

Gross findings: gray-white scar, progressive from border toward core of infarct

Light micro: increased collagen deposition with decreased cellularity

66
Q

How long does it take for dense collagenous scarring to be complete after acute MI?

A

> 2 months

67
Q

After acute MI, it takes 24+ hours to see _____ necrosis, _____ nuclei, and loss of cross ______

A

Coagulative; pyknotic; striations

68
Q

Areas surrounding necrosis following MI can rupture, causing blood to fill the pericardial sac leading to ____ ____ and further decreased heart function

A

Cardiac tamponade

69
Q

Timeline for PMNs, macrophages, and granulation tissue to form after MI

A

3-4 days = PMNs

7-10 days = macrophages

10 days = granulation tissue

70
Q

Gross findings of hemorrhage and Contraction bands seen on light micro are signs of ____ injury following MI

A

Reperfusion

71
Q

Lab evaluation of an MI consists of measuring the blood levels of proteins that leak out of irreversibly damaged myocytes. The most sensitive and specific biomarkers of myocardial damage are ____ and _____. ______ can also be used

A

cTnT and cTnI; CK-MB

72
Q

T/F: the MB form of creatine kinase (CK-MB) is sensitive but not specific, since it can also be elevated after skeletal muscle injury

A

True

[while MM homodimers are found predominantly in cardiac and skeletal muscle, and BB homodimers in brain, lung, and many other tissues, MB heterodimers are principally localized to cardiac muscle, but there is still some in skeletal muscle, albeit low amounts]

73
Q

Time to elevation, peak, and return to normal of cardiac biomarkers/enzymes following MI

A

Time to elevation of CKMB, cTnT, and cTnI is 3-12 hours

CKMB and cTnI peak at 24 hours

CKMB returns to normal in 48-72 hours

cTnI returns to normal in 5-10 days

cTnT returns to normal in 5-14 days

74
Q

Half of MI deaths occur within 1 hr of onset, and are usually secondary to ________

A

Arrhythmia

[arrhythmia can be a longer-term complication of MI, depending on site and extent of lesion; can result from permanent damage to the conducting system, or from myocardial “irritability” following the infarct]

75
Q

Complications of MI other than arrhythmia

A

Contractile dysfunction

Fibrinous pericarditis

Myocardial rupture

Infarct expansion

Ventricular aneurysm

76
Q

Myocardial rupture is a complication of MI that typically requires a _____ infarct. It occurs 2-4 days post MI, when inflammation and necrosis have weakened the wall. Risk factors include increased age, large transmural anterior MI, first MI, and absence of ____ hypertrophy

A

Transmural; LV

77
Q

Describe process of infarct expansion

A

Muscle necrosis —> weakening, stretching, and thinning of the wall

Mural thrombus is often seen

78
Q

Describe ventricular aneurysm as a complication of MI

A

Late complication of large transmural infarcts with early expansion

Composed of thinned wall of scarred myocardium

Also associated with mural thrombus

Rupture does NOT usually occur

Cardiovascular Exam I (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions