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Patho > Topic 5.3 - Cardiovascular Disorders III > Flashcards

Topic 5.3 - Cardiovascular Disorders III Flashcards

1
Q

Which fetal structure permits blood flow between the aorta and pulmonary arteries?

A

Ductus arteriosis

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2
Q

Which fetal structure permits blood flow between the atria?

A

Foramen ovale

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3
Q

What are some causes of congenital heart malformations?

A

Both genetic and environmental influences are probable.

Studies show that teratogens may play a bigger role than genetics.

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4
Q

What is a right to left shunt? How else can this be described/classified.

A

A congenital heart malformation that allows unoxygenated blood to enter systemic circulation and bypass lungs.

aka cyanotic

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5
Q

What is a left to right shunt? How else is this classified/described?

A

A congenital heart malformation that allows oxygenated blood to flow back into pulmonary circulation. Creates extra work for right side of the heart.

aka acyanotic

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6
Q

How do congenital obstructions in the heart affect the infant? How are they classified?

A

They are classified as acyanotic and lead to increased workload for the side of the heart affected. Can lead to heart failure.

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7
Q

What is atrial septal defect? How is is classified?

A

Acyanotic (L-R shunt)
–>Abnormal opening between atria
(Failure of foramen ovale to close)

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8
Q

What kind of effects are seen on the rest of the heart due to an atrial septal defect?

A

Right side enlargement due to left to right shunting

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9
Q

What is ventricular septal defect? How is it classified?

A

Acyanotic (L - R shunt)
–> Abnormal communication between ventricles

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10
Q

How does a ventricular septal defect affect the rest of the circulatory system?

A

Increase in pulmonary flow leads to pulmonary HNT

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11
Q

Where does VSD usually occur?

A

Near the bundle of His

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12
Q

What is the most common congenital heart anomaly?

A

VSD

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13
Q

What is PDA? How is it classified?

A

Acyanotic (L - R defect)
–>Patent ductus arteriosus allows blood from aorta to enter pulmonary arteries

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14
Q

What are some effects of a patent ductus arteriosus?

A

Increased pulmonary bloodflow leads to increase venous return, which increases workload on the left side of the heart.

Increased pulmonary HNT can also lead to right-sided HF

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15
Q

What is coarctation of the aorta? How is it classified?

A

Acyanotic
–> Narrowing of aorta, usually just after the ductus arteriosus

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16
Q

What are some effects of coarctation of the aorta?

A

Low pressure in legs
Can lead to LV HNT + hypertrophy

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17
Q

What is tetralogy of Fallot? How is it classified?

A

Cyanotic (R - L Shunt)
1. Large VSD
2. Pulmonary stenosis
3. Overriding of aorta that straddles VSD
4. RV hypertrophy

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18
Q

What is transposition of the great arteries? How is it classified?

A

Cyanotic
–> When two separate, noncommunicating systems are established
–> Usually, the pulmonary arteries attach to the left ventricle, and the aorta attaches to the right
–> Incompatible with life, unless mixing occurs through other defects

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19
Q

What is Truncus arteriosus? How is it classified?

A

Cyanotic (R - L Shunt)
–> When the aorta and PA establish as one vessel that splits into three arms. All receive blood from both sides of heart and share a single valve due to a VSD

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20
Q

What are some effects of truncus arteriosus?

A

Increases pulmonary blood flow leads to pulmonary HNT and RV hypertrophy

Increases pulmonary resistance leads to increased cyanosis, because it forces more venous blood back into systemic circulation

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21
Q

What are the most important predisposing risk factors leading to CHF?

A

ischemic heart disease, HNT, and diabetes

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22
Q

What side of heart failure is most common?

A

Left-sided, but it will affect both sides over time

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23
Q

What is the commonly used criteria of diagnosis for heart failure? (7)

A

–> Dyspnea
–> Pulmonary rales
–> Cardiomegaly
–> Pulmonary edema
–> S3 gallop
–> Tachycardia
–> Neck vein distention

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24
Q

What is normal ejection fraction?

A

60-80%

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25
Q

What is reduced ejection fraction heart failure? What is its etiology?

A

Systolic heart failure with an EF < 40%
Characterized by reduced contractility, often onset by MI

26
Q

What is preserved ejection fraction heart failure? What is its etiology?

A

Inability of LV to fill during diastole with EF > 50%
Often caused by coronary artery disease, HNT, other anomalies that prevent cardiac filling.

27
Q

how does Left-failure affect pulmonary + systemic circulation?

A

Backward effects:
Increased pulmonary pressure leads to right ventricular hypertrophy (due to afterload) and pulmonary congestion

Forward effects:
Decreased cardiac output leads to decreased tissue perfusion and RAAS activation –> Fluid retention

28
Q

Whatare the backward and forward effects of right-side HF?

A

Backward effects:
Decreased ejection fraction and increased right ventricular preload leads to increased right atrial pressure and systemic congestion

Forward effects:
Decreased output by left ventricle leads to RAAS activation and decreased tissue perfusion.

29
Q

How does the body compensate for heart failure?

A

Baroreceptors trigger SNS –> Increased HR and contractility

RAAS activation –> Fluid retention and increased preload

Increased ventricular wall tension leads to myocyte growth and hypertrophy + Remodeling

30
Q

What might cause dysrhythmia? (both pathological and mechanisms)

A

Hypoxia, inflammation, electrolyte imbalance, drugs

Caused either by abnormal automaticity or triggered activity

31
Q

What causes disorders of impulse formation?

A

Dysfunction of the SA node, can lead to bradycardia or tachycardia

32
Q

What is sinus tachycardia?

A

A heart rate >100bpm

Often a compensatory response to increase demand or decreased stroke volume.

33
Q

What is sinus bradycardia? What causes it?

A

Heart rate <60 bpm
Causes by PSNS due to sleep, drugs, increased stroke volume or acute HTN.

34
Q

What is first degree heart block?

A

A prolonged PR interval

35
Q

What might cause disorders of impulse conduction?

A

Ischemia, infection, medication, inherited abnormalities.

36
Q

What is second degree heart block?

A

Some p-waves not conducted to ventricles

37
Q

What is third degree heart block?

A

No impulses conducted from atria to ventricle, ventricular escape rhythm present.

38
Q

How is third degree heart block treated?

A

With a pacemaker

39
Q

What is atrial flutter? Hows does it appear on an ECG?

A

Rapid atrial rate of 240-350 bpm
Sawtooth pattern of atrial depolarization present, with slow ventricular rate (VER)

40
Q

How is atrial fib/flutter treated?

A

With anticoagulants to prevent the formation of thrombi within atria due to stagnant blood

41
Q

What might cause v-fib?

A

MI/ischemia, myocardium damage, high catecholamine levels, abnormal electrolyte balance.

42
Q

What is shock?

A

An acute failure of the circulatory system to supply peripheral tissues and organs of the body with adequate blood supply resulting in hypoxia.

43
Q

What is cardiogenic shock?

A

Inadequate cardiac output despite sufficient vascular volume - hypotension and tissue hypoperfusion

44
Q

What causes cardiogenic shock?

A

Short term consequences of an MI or severe ischemia

45
Q

What are the clinical manifestations of cardiogenic shock?

A

Similar to end-stage heart failure
Decreased MAP + SV
Oliguria
Neurological changes

46
Q

What is obstructive shock? What causes it?

A

Mechanical obstruction prevents effective cardiac filling and stroke volume, manifests as right side heart failure
Commonly caused by pulmonary embolism, cardiac tamponade, or pneumothorax

47
Q

What is hypovolemic shock?

A

Shock caused by loss of blood, plasma, or interstitial fluid in large amounts - heart still functional

48
Q

What are the clinical manifestation of hypovolemic shock?

A

Thirst, tachycardia, cool & clammy skin, decreased arterial BP, oliguria, confusion

49
Q

What percent of intravascular volume can be lost before a person begins experiencing hypovolemic shock?

A

15%

50
Q

What is distributive shock?

A

Shock characterized by excessive vasodilation and peripheral pooling of blood

51
Q

What are the kinds of distributive shock?

A

Anaphylactic, neurogenic, and septic

52
Q

What causes anaphylactic shock?

A

Excessive mast cell degranulation mediated by IgE in response to hypersensitivity.

53
Q

What causes neurogenic shock?

A

Loss of SNS activation of arteriolar SM.
Might be caused by medullary depression due to injury or OD, or lesions in SNS fibers due to injury.

54
Q

What causes septic shock?

A

A severe systematic inflammatory response to a bacterial or fungal infection.

55
Q

What are the three stages of shock?

A
  1. Compensatory
  2. Progressive
  3. Refractory
56
Q

What occurs during the compensatory stage of shock?

A

Body can maintain adequate tissue perfusion despite CO reduction
SNS activation attempts to maintain BP even though cardiac output has fallen –> Increased CO + vascular resistance

57
Q

What occurs during the progressive stage of shock?

A

Hypotension and tissue hypoxia present
Lactate production increases with anaerobic metabolism, but eventual lack of ATP leads to cellular swelling, dysfunction, and death
Presence of free radicals, inflammatory cytokines, and activation of clotting cascade

58
Q

What occurs during refractory shock?

A

Constriction of splanchnic vessels, release of aldosterone + cortisol, cool & clammy skin with pallor/cyanosis due to reduces capillary refill. Eventual organ failure.
This kind of shock is lethal.

59
Q

How is shock treated?

A

Ventilation Support
—> O2 support prevents pulmonary HTN
Fluid Resuscitation
–> Improve microvascular flow

Vasopressors if hypotension persists despite fluid administration
Vasodilators reduce afterload and increase cardiac output without increasing myocardial demand for O2.
Inotropic agents increase CO.

60
Q

Which vasopressor is chosen to treat shock?

A

Adrenergic Agonists
–> First line vasopressors due to their rapid onset, high potency, and short-half life.

Patho (14 decks)

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