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Cardiopulm Exam 1 > Heart Part 1 > Flashcards

Heart Part 1 Flashcards

1
Q

The myocardium contains atrial myocytes that have storage granules that contain?

A

atrial natriuretic peptide

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2
Q

What does atrial natriuretic peptide promote?

A

arterial vasodilation and stimulates renal salt and water elimination (natriuresis & diuresis) which is beneficial in
the setting of HTN and CHF

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3
Q

What are the 3 types of valvular damage?

A
  1. collagen (mitral prolapse)
  2. nodular calcification (calcific aortic stenosis)
  3. fibrotic thickening (rheumatic heart dz)
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4
Q

What happens to the myocardium and chambers as we age?

A
  • LV cavity/volume is reduced
  • Increased epicardial fat

• Myocardium changes:
- Lipofuscin and basophilic degeneration

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5
Q

What happens to valves as we age?

A
  • Aortic and mitral valves annular CALCIFICATION
  • Fibrous thickening
  • Mitral leaflets buckle towards Lt atrium –> Increased left atrium size
  • LAMBL EXCRESCENCES: small filiform processes form on the
    closure lines of aortic and mitral valves, probably resulting
    from the organization of small thrombi
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6
Q

What vascular changes happen as we age?

A

– Coronary atherosclerosis

– Stiffening of the aorta

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7
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
A

Congestive heart failure (CHF)

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8
Q

How does Congestive heart failure (CHF) occur?

A 
• Loss of myocardial contractile
function (systolic dysfunction)

• Loss of ability to fill the ventricles during diastole (diastolic dysfunction)

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9
Q

How do cardiac myocytes become hypertrophic?

A
  • Sustained pressure or volume overload (systemic HTN or aortic stenosis)
  • Sustained trophic signals (Beta-adrenergic stimulation)
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10
Q

What happens in the setting of PRESSURE overload hypertrophy?

A

Myocytes become thicker, and LV increases thickness concentrically

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11
Q

What happens in the setting of VOLUME overload hypertrophy?

A
  • Myocytes elongate, and ventricular DILATION is seen

* Heart weight best measure of hypertrophy in dilated heart (vs wall thickness)

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12
Q

What is the best measure of hypertrophy in dilated heart?

A

Heart weight

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13
Q

Hypertrophy of myocytes isn’t accompanied by a matching
increase in blood supply, despite increased energy demand which means that the hypertrophied heart is vulnerable to what?

A

the hypertrophied heart is vulnerable to ischemia-related

decompensation

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14
Q

Left-sided heart failure is most commonly a result of?

A
  • Myocardial ischemia
  • Hypertension
  • Left-sided valve Dz
  • Primary myocardial dz
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15
Q

Clinical effects of left-sided heart failure are due to?

A

– Congestion in the pulmonary circulation

– Decreased tissue perfusion

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16
Q

Left-sided Heart Failure:

  • Left ventricular dysfunction leads to ? which leads to ?
  • Pulmonary congestion and edema can cause ?
  • Decreased ejection fraction may result in ? Which stimulates?
  • Advanced CHF may lead to ? which leads to ?
A

• Left ventricular dysfunction leads to left atrial dilation
– This can lead to atrial fibrillation, stasis, thrombus

• Cough, dyspnea, orthopnea, paroxysmal nocturnal
dyspnea

• Decreased ejection fraction may result in decreased glomerular perfusion
– Stimulating release of renin leading to increased volume
– Prerenal azotemia

• Advanced CHF may lead to decreased cerebral perfusion
– Hypoxic encephalopathy

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17
Q

What is the most common cause of right-sided heart failure?

A

Left-side failure ***

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18
Q

Right-Sided Heart failure:

• ISOLATED right-sided failure results from any cause
of? Examples?

A

• Isolated right-sided failure results from any cause
of pulmonary hypertension

– Parenchymal lung diseases
– Primary pulmonary hypertension
– Pulmonary vasoconstriction

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19
Q

What occurs in PRIMARY right-sided heart failure?

A
  • pulmonary congestion is MINIMAL (unlike isolated failure!!!)
  • the venous system is markedly congested
  • Liver congestion (NUTMEG LIVER)
  • Splenic congestion leading to splenomegaly
  • Effusions involving peritoneal, pleural and pericardial spaces
  • Edema, especially in dependent areas (e.g., ankles)
  • Renal congestion
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20
Q

What is left-sided heart failure most commonly due to?

Symptoms are mainly a consequence of what?

A
  • ISCHEMIC heart disease, SYSTEMIC HYPERTENSION, MITRAL OR AORTIC VALVE disease, and
    primary diseases of the myocardium
  • Symptoms are mainly a
    consequence of PULMONARY CONGESTION AND EDEMA, although systemic hypoperfusion can cause secondary renal and cerebral dysfunction.
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21
Q

Right heart failure is most often due to what?

Symptoms are chiefly related to what?

A
  • Right heart failure is most often due to left heart failure, and less commonly to primary pulmonary disorders
  • Symptoms are chiefly
    related to PERIPHERAL EDEMA AND VISCERAL CONGESTION
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22
Q

Sporadic genetic abnormalities are the major known causes of what? Examples?

A
  • Sporadic genetic abnormalities are the major known causes of congenital heart disease
  • Examples: Turner syndrome, and trisomies 13, 18 & 21
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23
Q

What is the single most common genetic cause of congenital heart disease?

A

trisomy 21

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24
Q

About 40% patients with Down syndrome have at least one heart defect and it is usually derived from what?

A

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

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25
Q

Congenital Heart Dz:

Notch pathway are associated with a variety of congenital heart defects, including ?

A

bicuspid aortic valve (NOTCH1 ) and tetralogy of Fallot (JAG1 and NOTCH2)

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26
Q

Congenital Heart Dz:

Fibrillin mutations underlie what syndrome?

A

Fibrillin mutations underlie MARFAN syndrome—associated with valvular defects and aortic aneurysms

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27
Q

What are some examples of congenital heart disease?

A
  • Left-to-right shunts
  • Atrial Septal Defects (ASD)
  • Ventricular Septal Defects (VSD)
  • Patent Ductus Arteriosus (PDA)
  • Right-to-left Shunts
  • Obstructive lesions
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28
Q

What are the top 3 most frequent congenital cardiac malformations?

A
  1. Ventricular septal defect
  2. Atrial septal defect
  3. Pulmonary stenosis
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29
Q

What are the genes and gene product function for:

  1. ASD or conduction defects
  2. ASD or VSD
  3. Tetralogy of Fallot
A

1.
Gene: NKX2.5
Gene Product Function: Transcription factor

  1. Gene: GATA4
    Gene Product Function: Transcription factor
  2. Gene: ZFPM2 or NKX2.5
    Gene Product Function: Transcription factors
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30
Q

What is the most common congenital heart disease?

A

Left-to-Right Shunts

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31
Q

What are some examples of Left-to-Right shunts?

A

– ASD
– VSD
– PDA (patent ductus arteriosus)

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32
Q

Common Congenital Left-to-Right Shunts:

  • ? increases only RV and pulmonary outflow volumes
  • ? and ? cause increased pulmonary blood flow and pressure
A
  • ASD

- VSD and PDA

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33
Q

When do you start noticing symptoms for atrial septal defects?

A

Usually asymptomatic until adulthood (>30 year old)

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34
Q

90% of all ASDs; center of atrial septum; may be multiple or fenestrated

A

Secundum ASD

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35
Q

5% of all ASDs; adjacent to AV valves; often assoc with AV

valve abnormalities and/or VSD

A

Primum anomalie

36
Q

5% of all ASDs; near entrance of SVD; can be assoc with

anomalous pulmonary venous return to the R atrium

A

Sinus venosa defects

37
Q

The left-to-right shunting causes volume overload on the right side, which may lead to?

A

– Pulmonary hypertension
– Right heart failure
– Paradoxical embolization
– May be closed surgically, with normal survival

38
Q

Patent Foramen Ovale (PFO):

  • 80% of it closes permanently by what age?
  • The remaining 20% of the flap can open if there is what?
  • So even a temporary increase in pressure can produce brief periods of R-L ** shunting which can cause what conditions?

• Whats a big issue that is associated with PFO?

A
  • 2 years old
  • An increase in right sided pressure
  • Pulmonary HTN
  • Bowel movement
  • Coughing
  • Sneezing

• PARADOXICAL EMBOLUS

39
Q

What is the MOST COMMON form of congenital heart disease?

A

Ventricular Septal Defect (VSD)

40
Q

The effects of Ventricular Septal Defect (VSD) is dependent on its what?

A

SIZE and presence of other heart defects

41
Q

Ventricular Septal Defect (VSD):

  • 90% ? VSD in membranous interventricular septum
  • ? VSD: below Pulmonary valve, or within muscular septum
A
  • membranous

- Infundibular

42
Q

Large VSDs may cause significant shunting, leading to?

A

– Right ventricular hypertrophy
– Pulmonary hypertension
– Unclosed large VSD can ultimately result in shunt reversal, leading to cyanosis and death

43
Q

May fail to close when infants are HYPOXIC, and/or have defects associated with INCREASED PULMONARY VASCULAR PRESSURE (VSD)

A

Patent Ductus Arteriosus (PDA)

44
Q

What kind of noise does a Patent Ductus Arteriosus (PDA) make?

A

harsh, machinery-like murmur

Usually asymptomatic at birth

45
Q

The effect of Patent Ductus Arteriosus (PDA) is determined by what?

A

The shunt’s diameter

46
Q

Patent Ductus Arteriosus (PDA):

  • Large shunts can increase ? and eventually shunt
    reversal and cyanosis
  • Preservation of patency (via ?) can be lifesaving in infants with obstruction of pulmonary or systemic outflow
A
  • pulmonary pressure

- prostaglandin E

47
Q

Right-to-Left Shunts is strongly associated with what?

A

Cyanosis early in postnatal life

48
Q

What is considered the cyanotic congenital heart dz?

A

Right-to-Left Shunts

49
Q

What is the most common Right-to-Left Shunt?

A

Tetralogy of Fallot (TOF)

50
Q

What are some examples of Right-to-Left Shunts?

A 
– Tetralogy of Fallot (TOF) ***
– Transposition of the great arteries 
– Persistent truncus arteriosus 
– Tricuspid atresia 
– Total anomalous pulmonary venous connection
51
Q

What are the four cardinal features of Tetralogy of Fallot ?

A

1) VSD
2) Obstruction of RV outflow tract
3) Aorta overrides the VSD
4) RV hypertrophy

52
Q

Condition where the heart is enlarged and “BOOT SHAPED” because of the right ventricular
hypertrophy

A

Tetralogy of Fallot

53
Q

The clinical severity of Tetralogy of Fallot depends on the degree of what?

A

subpulmonary stenosis

54
Q

Tetralogy of Fallot:

  • MILD stenosis: ?
  • CLASSIC TOF is ?
  • Most infants CYANOTIC FROM BIRTH, or soon thereafter
A

– Mild stenosis: L to R shunt

– Classic TOF is R to L shunting with cyanosis

55
Q

Results in two separate systemic and pulmonary circulations,

incompatible with life after birth unless a shunt is present for mixing of blood from the two circulations

A

Transposition of the great vessels (TGA)

56
Q

Transposition of the great vessels (TGA):

– Approximately 1/3 have a ?
– 2/3 have a ? or ?
– ? ventricle becomes hypertrophic (supports systemic circulation) and the ? ventricle atrophies
– Without surgery, patients will die within a few months

A
  • VSD
  • a patent foramen ovale or PDA
  • Right … left
57
Q

Narrowing of the aorta, generally seen WITH a PDA (infantile form), or WITHOUT a PDA (adult form)

A

Coarctation of the Aorta

58
Q
  • What syndrome is associated with Coarctation of the Aorta?

- Are males or females more likely to have Coarctation of the Aorta?

A
  • Turner Syndrome (45,XO)

- Males 2X females

59
Q

Coarctation of the Aorta:

  • The clinical severity is dependent on what?
A
  • It depends on the degree of stenosis and patency of the ductus arteriosus
60
Q
  • Coarctation of the aorta WITH PDA manifests at birth: it may produce CYANOSIS in the ?
  • Coarctation WITHOUT PDA is usually ASYMPTOMATIC (in children and may go unrecognized well into adult life). Some things associated with this are?
A
  • lower half of the body
  • Without PDA:
  • HYPERTENSION in upper extremities, HYPOTENSION in lower extremities
  • CLAUDICATION AND COLD lower extremities
  • May eventually see concentric LV hypertrophy
61
Q

What are 3 examples of obstructive lesions?

A
  1. Coarctation of the aorta
  2. Pulmonary stenosis or atresia
  3. Aortic stenosis or atresia
62
Q

“Notching” on the undersurface of ribs is associated with what kind of Coarctation of the Aorta?

A

Aortic Coarctation WITHOUT PDA

63
Q

When does Eisenmenger syndrome occur?

A

Eisenmenger syndrome occurs when the PRESSURE IN THE PULMONARY ARTERIES BECOMES SO HIGH THAT IT CAUSES OXYGEN-POOR (BLUE) BLOOD TO FLOW FROM THE RIGHT TO LEFT VENTRICLE AND THEN TO THE BODY, CAUSING CYANOSIS. The high pressure also causes the wall of your heart’s right ventricle to thicken (HYPERTROPHY).

64
Q

Which disease results from insufficient perfusion to meet the metabolic demands of
the myocardium?

A

Ischemic heart Dz

65
Q

Ischemic heart Dz:

• Ischemia may result in?

A

– Myocardial infarction
– Angina pectoris
– Chronic ischemic heart disease, with heart failure
– Sudden cardiac death

66
Q

Which disease is the leading cause of death in the US, and >90% are secondary to
ATHEROSCLEROSIS?

A

Ischemic heart Dz

67
Q

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

A

Angina Pectoris

68
Q

What are the 3 clinical variants to Angina Pectoris?

A
  1. Stable angina
  2. Prinzmetal variant angina
  3. Unstable (or “crescendo”) angina
69
Q

What kind of Angina Pectoris involves:
• STENOTIC OCCLUSION OF CORONARY ARTERY

  • “squeezing” or burning sensation, RELIEVED BY REST or vasodilators
  • Induced by PHYSICAL ACTIVITY, stress
A

Stable Angina

70
Q

What kind of Angina Pectoris involves:
• Episodic coronary artery spasm, RELIEVED WITH VASODILATORS

• Unrelated to physical activity, HR or BP

A

Prinzmetal variant angina

71
Q

What kind of Angina Pectoris involves:

  • 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
A

Unstable (or “crescendo”) angina

72
Q

Myocardial infarction (MI):

• Age distribution and risk factors mirror those of atherosclerosis in general, because nearly 90% of infarcts are caused by an ?

A

atheromatous plaque

73
Q

What are some other causes of Myocardial Infarction?

A

– Embolus
– Vasospasm
– Ischemia secondary to vasculitis, shock, hematologic abnormalities

74
Q

What is the classic presentation of a Myocardial Infarction?

A 
• PROLONGED CHEST PAIN (>30 min)
- Crushing, stabbing, squeezing, tightness 
- Radiating down left arm, or left jaw
•  DIAPHORESIS 
•  Dyspnea 
•  Nausea-vomiting 
•  Up to 25% are asymptomatic
75
Q

What is the area of infarction associated with these coronary vessels:
• LAD (40-50%)
• RCA (30-40%)
• LCX (15-20%)

A

• LAD (40-50%)
- Apex, LV anterior wall, anterior two thirds of septum

• RCA (30-40%)
- RV free wall, LV posterior wall, posterior third of septum

• LCX (15-20%)
- LV lateral wall

76
Q

What morphological changes do we see in a light microscope with an MI at:
- 1/2 - 4 hours: ?

  • 4-12 hours: ?
  • 12-24 hours: ?
  • 1-3 days: ?
  • 3-7 days: ?
  • 7-10 days: ?
  • 10-14 days: ?
  • 2-8 weeks: ?
  • > 2 months: ?
A
  • 1/2 - 4 hours: Waviness of fibers at border
  • 4-12 hours: Edema; hemorrhage
  • 12-24 hours: PYKNOSIS of nuclei; myocyte HYPEREOSINOPHILIA; marginal CONTRACTION BAND necrosis; early NEUTROPHILIC infiltrate
  • 1-3 days: COAGULATION NECROSIS, with LOSS OF NUCLEI; early NEUTROPHILIC infiltrate.
    • Gross feature: Yellow-tan infarct center
  • 3-7 days: BEGINNING DISINTEGRATION OF DEAD MYOFIBERS, with dying neutrophils; early phagocytosis of dead cells by MACROPHAGES at infarct border
    • Gross feature: Hyperemic border
  • 7-10 days: Well-developed PHAGOCYTOSIS of dead cells; GRANULATION TISSUE at margins
    • Gross feature: Maximally yellow-tan and soft, with DEPRESSED red-tan margins
  • 10-14 days: Well-established GRANULATION TISSUE with NEW BLOOD VESSELS and collagen deposition
  • 2-8 weeks: INCREASED COLLAGEN
    - Gross feature: Gray-white scar
  • > 2 months: DENSE collagenous scar
77
Q

Restoring blood flow to an area of ischemia and impending infarction

  • Examples?
A

Reperfusion

  • Examples: Thrombolysis, angioplasty and stent placement, CABG
78
Q

Lab Evaluation of an MI:

What are the most useful molecules for measuring the blood levels of proteins that leak out of irreversibly damaged myocytes?

A

cardiac-specific troponins T and I (cTnT and cTnI), and the MB fraction of creatine kinase (CK-MB

79
Q

Lab Evaluation of an MI:

What are the most sensitive and specific biomarkers of myocardial damage?

A

cardiac-specific proteins, particularly cTnT and cTnI(proteins that regulate calcium-mediated contraction of cardiac and skeletal muscle)

80
Q

Lab Evaluation of an MI:

• ? are NOT normally detectable in the circulation.
– Following an MI, levels of both begin to rise at ? hours;

– cTnT levels peak somewhere between ? hours while cTnI levels are maximal at 24 hours

A

• Troponins I and T

  • 3-12 hours
  • 12-48 hours
81
Q

Lab Evaluation of an MI:

• What enzyme is expressed in brain, myocardium, and skeletal muscle; And is a dimer composed of two isoforms designated “M” and “B”

– While ? homodimers are found predominantly in cardiac and skeletal muscle, and ?
homodimers in brain, lung, and many other tissues, ?heterodimers are principally localized to cardiac muscle (with considerably lesser amounts found in skeletal muscle)

  • Thus, the MB form of creatine kinase (CK-MB) is sensitive but NOT ?, since it can also be elevated after skeletal muscle injury
A

• Creatine kinase

  • MM … BB… MB
  • specific
82
Q

Lab Evaluation of an MI:

? begins to rise within 3 to 12 hours of the onset of MI, peaks at about 24 hours,
and returns to normal within approximately 48 to 72 hours

A

CK-MB

83
Q

“Cardiac Enzymes”

– Time to elevation of CKMB, cTnT and cTnI is ? hours

– CK-MB and cTnI peak at ? hours

– CK-MB returns to normal in ? hrs, cTnI in ? days, and
cTnT in ? days

A
  • 3 to 12 hrs
  • 24 hours
  • 48-72 hrs, .. 5-10 days…, 5 to 14 days
84
Q

Complications of MI:

Half of all MI deaths occur within 1 hour of onset, and are usually secondary to an ?

A

Arrhythmia

85
Q

Complications of MI:

  • Contractile dysfunction is dependent on what?
A

Dependent on size of the infarct and associated loss of function

86
Q

Complications of MI:

What condition is associated with a MI?

A

Fibrinous pericarditis **

87
Q

Complications of MI:

• Myocardial rupture

  • Typically requires a transmural infarct
  • Occurs ? days post MI, when inflammation and necrosis have weakened the wall
  • Risk factors: Increased age, large transmural anterior MI, first MI, absence of LV hypertrophy

• Infarct expansion
– Muscle necrosis which leads to weakening, stretching and thinning of the wall
– Mural thrombus often seen

• Ventricular aneurysm**
– ? 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

A

• Myocardial rupture
- 2-4 days

• Ventricular aneurysm
- Late

Cardiopulm Exam 1 (13 decks)

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