Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Patho > Topic 5.3 - Cardiovascular Disorders III > Flashcards

Topic 5.3 - Cardiovascular Disorders III Flashcards

(60 cards)

Start Studying
1
Q

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

A

Ductus arteriosis

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

Which fetal structure permits blood flow between the atria?

A

Foramen ovale

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

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

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

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

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

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

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

What is ventricular septal defect? How is it classified?

A

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

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

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

A

Increase in pulmonary flow leads to pulmonary HNT

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

Where does VSD usually occur?

A

Near the bundle of His

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

What is the most common congenital heart anomaly?

A

VSD

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

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

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

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

A

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

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

What are some effects of coarctation of the aorta?

A

Low pressure in legs
Can lead to LV HNT + hypertrophy

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

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

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

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

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

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

A

ischemic heart disease, HNT, and diabetes

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

What side of heart failure is most common?

A

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

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

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

What is normal ejection fraction?

A

60-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is reduced ejection fraction heart failure? What is its etiology?
Systolic heart failure with an EF < 40% Characterized by reduced contractility, often onset by MI
26
What is preserved ejection fraction heart failure? What is its etiology?
Inability of LV to fill during diastole with EF > 50% Often caused by coronary artery disease, HNT, other anomalies that prevent cardiac filling.
27
how does Left-failure affect pulmonary + systemic circulation?
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
Whatare the backward and forward effects of right-side HF?
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
How does the body compensate for heart failure?
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
What might cause dysrhythmia? (both pathological and mechanisms)
Hypoxia, inflammation, electrolyte imbalance, drugs Caused either by abnormal automaticity or triggered activity
31
What causes disorders of impulse formation?
Dysfunction of the SA node, can lead to bradycardia or tachycardia
32
What is sinus tachycardia?
A heart rate >100bpm Often a compensatory response to increase demand or decreased stroke volume.
33
What is sinus bradycardia? What causes it?
Heart rate <60 bpm Causes by PSNS due to sleep, drugs, increased stroke volume or acute HTN.
34
What is first degree heart block?
A prolonged PR interval
35
What might cause disorders of impulse conduction?
Ischemia, infection, medication, inherited abnormalities.
36
What is second degree heart block?
Some p-waves not conducted to ventricles
37
What is third degree heart block?
No impulses conducted from atria to ventricle, ventricular escape rhythm present.
38
How is third degree heart block treated?
With a pacemaker
39
What is atrial flutter? Hows does it appear on an ECG?
Rapid atrial rate of 240-350 bpm Sawtooth pattern of atrial depolarization present, with slow ventricular rate (VER)
40
How is atrial fib/flutter treated?
With anticoagulants to prevent the formation of thrombi within atria due to stagnant blood
41
What might cause v-fib?
MI/ischemia, myocardium damage, high catecholamine levels, abnormal electrolyte balance.
42
What is shock?
An acute failure of the circulatory system to supply peripheral tissues and organs of the body with adequate blood supply resulting in hypoxia.
43
What is cardiogenic shock?
Inadequate cardiac output despite sufficient vascular volume - hypotension and tissue hypoperfusion
44
What causes cardiogenic shock?
Short term consequences of an MI or severe ischemia
45
What are the clinical manifestations of cardiogenic shock?
Similar to end-stage heart failure Decreased MAP + SV Oliguria Neurological changes
46
What is obstructive shock? What causes it?
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
What is hypovolemic shock?
Shock caused by loss of blood, plasma, or interstitial fluid in large amounts - heart still functional
48
What are the clinical manifestation of hypovolemic shock?
Thirst, tachycardia, cool & clammy skin, decreased arterial BP, oliguria, confusion
49
What percent of intravascular volume can be lost before a person begins experiencing hypovolemic shock?
15%
50
What is distributive shock?
Shock characterized by excessive vasodilation and peripheral pooling of blood
51
What are the kinds of distributive shock?
Anaphylactic, neurogenic, and septic
52
What causes anaphylactic shock?
Excessive mast cell degranulation mediated by IgE in response to hypersensitivity.
53
What causes neurogenic shock?
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
What causes septic shock?
A severe systematic inflammatory response to a bacterial or fungal infection.
55
What are the three stages of shock?
1. Compensatory 2. Progressive 3. Refractory
56
What occurs during the compensatory stage of shock?
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
What occurs during the progressive stage of shock?
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
What occurs during refractory shock?
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
How is shock treated?
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
Which vasopressor is chosen to treat shock?
Adrenergic Agonists --> First line vasopressors due to their rapid onset, high potency, and short-half life.

Patho (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions