Cardiovascular Flashcards
(80 cards)
1
Q
truncus arteriosus
A
ascending aorta and pulmonary trunk
2
Q
bulbus cordis
A
smooth part (outflow tract) of left and right ventricles
3
Q
primitive atria
A
trabeculated part of left and right atria
4
Q
primitive ventricle
A
trabeculated part of left and right ventricles
5
Q
primitive pulmonary vein
A
smooth part of left atrium
6
Q
left horn of sinus venosus
A
coronary sinus
7
Q
right horn of sinus venosus
A
smooth part of right atrium
8
Q
right common cardinal vein and right anterior cardinal vein
A
SVC
9
Q
heart morphogenesis
A
first functional organ (beats spontaneously at 4 weeks)
10
Q
cardiac looping
A
heart tube elongates on the right side (first visual sign of left-right asymmetry)
begins 4 weeks gestation
11
Q
dextrocardia
A
dextrocardia of embryonic arrest - heart is further right in thorax than is normal
dextrocardia situs inveersus - heart is mirror image on right side
12
Q
steps of separation of chambers - atria
A
- septum primum grows toward endocardial cushions, narrowing foramen primum
- foramen secundum forms in septum primum (foramen primum disappears)
- septum secundum develops as foramen secundum maintains right-to-left shunt
- septum secundum expands and covers most of the foramen secundum (the residual foramen is the foramen ovale)
- remaining portion of septum primum forms valve of foramen oval
- septum secundum and septum primum fuse to form the atrial septum
- foramen ovale closes soon after birth due to increased LA pressure
13
Q
patent foramen ovale
A
casued by failure of the septum primum and septum secundum to fuse after birth (generally left untreated)
can lead to paradoxical emboli - venous thromboemboli that enter systemic arterial circulation
14
Q
paradoxical embolism
A
potentially caused by patent foramen oval
NORMALLY - emboli from veins enter right side of heart and move to lungs = pulmonary embolism
WITH PATENT FORAMEN OVALE - emboli can pass directly from venous circulation to arterial circulation and may enter brain = stroke
15
Q
steps of separation of chambers - ventricles
A
- muscular ventricular septum forms - opening is called interventricular foramen
- aorticopulmonary septum rotates and fuses with muscular ventricular system to form membranous interventricular septum, closing interventricular foramen
- growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum
16
Q
ventricular septal defect
A
most commonly occurs in membranous septum
acyanotic at birth due to left-right shunt
17
Q
acyanotic congenital heart defects
A
“3 D’s”
- VSD
- ASD
- PDA
18
Q
cyanotic congenital heart defects
A
“5 T’s”
- truncus arteriosus
- transposition of the great vessels
- tricuspid atresia
- tetralogy of fallot
- total anomalous pulmonary venous return
19
Q
outflow tract formation
A
- truncus arteriosus rotates - neural crest an endocardial cell migrations
- truncal and bulbar ridges that spiral and fuse to form aortic pulmonary septum - ascending aorta and pulmonary trunk
20
Q
conotruncal abnormalities
A
- transposition of the great vessels
- tetralogy of fallot
- persistent truncus arteriosus
21
Q
fetal erythropoiesis (when is blood being produced)
A
“Young Liver Synthesizes Blood”
- Yolk sac (3-8 weeks)
- Liver (6 weeks - birth)
- Spleen (10-28 weeks)
- Bone marrow (18 weeks - adult)
22
Q
fetal hemoglobin
A
HbF (alpha2gamma2)
higher affinity for oxygen than adult hemoglobin due to less avid binding of 2,3-BPG (allows fetal hemoglobin to extract oxygen from maternal hemoglobin (HbA - alpha2beta2) across the placenta
“alpha always, gamma goes, becomes beta”
23
Q
fetal circulation
A
blood in umbilical arteries (mixed/unoxygenated blood from aorta) has low O2 saturation
blood in umbilical veins has PO2 of 30mmHg and is 80% saturated (oxygenated at placenta)
24
Q
fetal circulation - shunts
A
- ductus venosus - blood entering fetus from the placenta (in umbilical veins) bypasses hepatic circulation via ductus venous (moves directly in IVC)
- foramen ovale - highly oxygenated blood reaching the right atrium from the placenta (via IVC) passes from right atrium to left atrium through the foramen oval (pumped out the aorta to the head and body)
- ductus arteriosus - blood exiting the right ventricle passes directly from the pulmonary artery to the aorta through the ductus arteriosus (high fetal pulmonary artery resistance)
25
circulation changes at birth
1. fetus takes first breath = decreased resistance in pulmonary vasculature = increased left atrial pressure as compared to right atrial pressure (more blood entering left side from lungs now) = foramen ovale closes (FOSSA OVALIS)
2. increased oxygen (from respiration) and decreased prostaglandins from (placental separation) cause closure of the ductus arteriosus (LIGAMENTUM ARTERIOSUM)
* **INDOMETHACIN helps close patent ductus arteriosus
* **PROSTAGLANDINS E1 and E2 maintain PDA
26
umbilical vein
ligamentum teres heaptis (contained in falciform ligament)
27
umbiLical arteries
mediaL umbilical ligaments
28
ductus arteriosus
ligamentum arteriosum
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ductus venosus
ligamentum venosum
30
foramen ovale
fossa ovalis
31
allaNtois
mediaN umbilical ligament
32
notochord
nucleus pulposus of intervertebral disc
33
blood supply to SA and AV nodes
right coronary artery
infarct = nodal dysfunction (bradycardia or heart block)
34
right-dominant circulation
85% of cases
posterior descending/interventricular artery arises from right coronary artery
35
left-dominant circulation
8% of cases
posterior descending/interventricular artery arises from left circumflex coronary artery
36
blood supply to lateral and posterior walls of left ventricle
left circumflex coronary artery
37
blood supply to interventricular septum/anterior papillary muscle/anterior surface of left ventricle
left anterior descending artery
38
blood supply to interventricular septum/posterior walls of ventricles
posterior descending/interventricular artery
39
blood supply to right ventricle
acute marginal artery
40
codominant circulation
7% of cases
posterior descending/interventricular artery arises from left circumflex coronary artery AND right coronary artery
41
coronary artery occlusion
most commonly occurs in left anterior descending artery (LAD)
42
enlargement of left atrium
left atrium is most posterior portion of the heart
enlargement can cause dysphagia = compression of the esophagus OR horsiness = compression of recurrent laryngeal nerve (branch of the vagus nerve)
43
cardiac output (CO)
stroke volume (SV) X heart rate (HR)
early exercise - cardiac output maintain by increased SV and HR
late exercise - CO maintained by increased HR only (SV can only increase to a certain point and plateaus)
***diastole is preferentially shortened with increased HR = less filling time = decreased CO (ventricular tachycardia)
44
Fick Principle
CO= (rate of O2 consumption)/(arterial O2 content - venous O2 content)
45
mean arterial pressure (MAP)
CO X TPR
2/3 diastolic pressure + 1/3 systolic pressure
46
pulse pressure
systolic pressure - diastolic pressure
proportional to SV (increased SV = increased PP); inversely proportional to arterial compliance (increased arterial compliance = decreased PP)
47
causes of increased pulse pressure
1. hyperthyroidism (increases systolic BP)
2. aortic regurgitation (causes a decreased diastolic BP)
3. arteriosclerosis (increase in SBP due to decreased arterial compliance)
4. obstructive sleep apnea (increase in sympathetic tone)
5. exercise (transient)
48
causes of decreased pulse pressure
1. aortic valve stenosis (decreased systolic BP - less blood flow through the system)
2. cardiogenic shock (inadequate circulation of blood due to failure of the ventricles to pump effectively)
3. cardiac tamponade
4. advanced heart failure
49
stroke volume (SV)
end diastolic volume - end systolic volume
SV CAP - Stroke Volume affected by Contractility, Afterload, adn Preload (increased SV for increased contractility/preload and decreased afterload)
50
ischemic heart disease
group of syndromes related to myocardial ischemia (not enough blood flow to the tissues)
leading cause of death in USA
usually due to atherosclerosis of coronary arteries (decreases flow to myocardium) - incidence increases with age
51
angina
chest pain
stable angina
unstable angina
prinzmetal angina
52
stable angina
chest pain arising with exertion or emotion - generally secondary to atherosclerosis of coronary arteries (greater than 70% stenosis)
pain lasts less than 20mins, radiates to left arm/jaw, diaphoresis(sweating), shortness of breath - resolves with rest
***decreased blood flow due to stenosis is not able to meet the metabolic demands of the heart during exertion = chest pain
reversible injury with NO NECROSIS
subendocardial ischemia = ST depression
TREAT: nitroglycerin (dilate arteries and restore blood flow), rest
53
unstable angina
chest pain at rest - caused by rupture of atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of coronary artery (still small amount of blood flow)
reversible injury with NO NECROSIS
subendocardial ischemia = ST depression
TREAT: nitroglycerin (vasodilation = decrease preload= decrease work required by heart)
***high risk of progression to myocardial infarction
54
Prinzmetal angina
episodic chest pain unrelated to exertion - caused by transient coronary artery vasospasm
reversible injury = NO NECROSIS
transmural ischemia = ST elevation
TREAT: nitroglycerin or calcium channel blockers, smoking cessation if applicable
triggers include tobacco, cocaine, and triptans
55
coronary steal syndrome
vessels after area of coronary stenosis are maximally dilated at baseline - when vasodilatory drugs are given, blood is shunted to well-perfused areas and post-stenotic regions become ischemic
drugs: dipyridamole, regadenoson
principle behind pharmacological stress tests
56
myocardial infarction
crushing chest pain lasting more than 20 mins - caused by thrombosis of atherosclerotic plaque and COMPLETE occlusion of coronary artery (OR coronary vasospasm - prinzmetal angina or cocaine, emboli, or vasculitis)
GENERALLY INVOLVED LEFT VENTRICLE (RV and atria generally spared)
57
clinical features of myocardial infarction
severe, crushing chest pain lasting more than 20 mins
pain radiates to left arm and jaw
diaphoresis
dyspnea
***symptoms not relieved by nitroglycerin
58
occlusion of left anterior descending artery (LAD)
infarction of anterior wall and anterior septum of LV
most commonly involved artery in MI (45% of cases)
59
occlusion of right coronary artery (RCA)
infarction of posterior wall, posterior septum, and papillary muscles of LV
second most commonly involved artery
60
occlusion of left circumflex artery
infarction of lateral wall of LV
61
phases of infarction
initial: subendocardial ischemia with subendocardial necrosis involving less than 50% of the myocardium = ST depression
later: transmural ischemia with transmural necrosis = ST elevation
62
lab tests for elevated cardiac enzymes
elevated cardiac enzymes indicate irreversible damage to myocardium
1. troponin 1: gold standard (most sensitive and specific) - levels rise 2-4 hours after infarction and remain elevated for 7-10 days
2. CK-MB: useful for detecting reinfarction (troponin remains elevated) - levels rise 4-6 hours after infarction and return to normal by 72 hours
63
myocardial infarction treatment
1. aspirin or heparin = limits thrombus
2. supplemental O2 = minimizes ischemia
3. nitrates= vasodilate veins and coronary arteries (decrease preload and thus decrease work required by heart)
4. B-blocker = slow HR (decrease need for O2 an decrease risk for arrhythmia
5. ACE inhibitor = decrease LV dilation (block production of Ang II to decrease after load
6. fibrinolysis or angioplasty = open blocked vessel
64
risk with restoring blood flow in myocardial infarction
1. reperfusion of irreversible damaged cells causes calcium influx = hyper-contraction of myofibrils (contraction band necrosis)
2. reperfusion injury - return of O2 and inflammatory cells may lead to free radical generation causing further injury to myocytes ***will see cardiac enzymes continue to rise after reperfusion***
65
morphologic changes in myocardial infarction - <4 hours
no changes to tissue
concerned about cardiogenic shock with massive infarctions, congestive heart failure (due to decreased ejection fraction), and arrhythmia
66
morphologic changes in myocardial infarction - 4-24 hours
gross: dark discoloration
microscopic: coagulative necrosis (nucleus removed from cells) (no neutrophils)
concerned about arrhythmia sue to damaged conduction system
67
morphologic changes in myocardial infarction - 1-3 days
gross: yellow pallor (WBCs in myocardium)
microscopic: neutrophil invasion (acute inflammation)
concerned about fibrinous pericarditis (presents as chest pain with friction rub) ***only with transmural infarction
68
morphologic changes in myocardial infarction - 4-7 days
gross: yellow pallor (WBCs in myocardium)
microscopic: macrophages (destroy necrotic debris = wall is weakest)
concerned about rupture of ventricular free wall - blood moves into pericardium and causes cardiac tamponade
concerned about interventricular septum rupture (causes shunt)
concerned about rupture of papillary muscles (causes mitral valve insufficiency
***concern depends on which coronary artery is infarcted
69
morphologic changes in myocardial infarction - 1-3 weeks
gross: red border emerges as granulation tissue enters from edge of infarct
microscopic: granulation tissue with plump fibroblasts, collagen, and blood vessels
***heart tissue is permanent and won't regenerate - scar tissue replaced dead heart tissue
70
morphologic changes in myocardial infarction - months
gross: white scar
microscopic: fibrosis
concerned about aneurysm (scar is not as strong as myocardium), mural thrombus (stasis), and Dressler syndrome (in transmural infarction, pericardial Ags exposed to immune system = pericarditis
71
sudden cardiac death
unexpected death due to cardiac disease that occurs within 1 hour of symptoms or without any symptoms at all - generally due to fatal arrhythmia (ventricular arrhythmia)
associated with coronary artery disease (70%), cardiomyopathy (hypertrophy and dilation), cocaine abuse, and hereditary ion channelopathies
72
chronic ischemic heart disease
poor myocardial function due to chronic ischemic damage (with or without infarction)
progresses to congestive heart failure
73
characteristics of transmural infarct
necrosis
affects entire thickness of heart wall
ST elevation on EKG, pathologic Q waves
74
characteristics of subendocardial infarct
ischemic necrosis of less than 50% of the wall thickness
subendocardium vulnerale to ischemic damage
ST depression on EKG
75
dilated cardiomyopathy
dilation of all four chambers of the heart (most common form of cardiomyopathy - 90%) - massive stretching of the heart causes decreased pumping ability leading to systolic problems
leads to biventricular CHF; mitral and tricuspid valve dysfunction (valves are stretched and can't close properly); arrhythmia (conduction system stretched and dysfunctions)
TREAT: heart transplant
76
common causes of dilated cardiomyopathy
1. most common: genetic mutation (autosomal dominant)
2. myocarditis (coxsackie A or B) - lymphocytic infiltrate in the myocardium resulting in chest pain, arrhythmia with sudden death, heart failure ***dilated cardiomyopathy is a late complication
3. alcohol abuse
4. beriberi
5. drugs (cocaine, doxorubicin)
6. Chagas disease
7. childbirth (late pregnancy or soon after birth)
8. hemochromotosis
77
hypertrophic cardiomyopathy
massive hypertrophy of left ventricle
commonly caused by genetic mutations in sarcomere proteins (generally autosomal dominant)
MYOFIBER HYPERTROPHY WITH DISARRAY
S4 and systolic murmur
78
clinical features of hypertrophic cardiomyopathy
1. decreased cardiac output - LV hypertrophy restricts filling ability = diastolic dysfunction
2. sudden death due to ventricular arrhythmias (common cause of sudden death in young athletes)
3. syncope with exercise - sub-aortic hypertrophy of ventricular septum results in functional aortic stenosis (can't increase blood output to match need)
79
restrictive cardiomyopathy
decreased compliance of ventricular endocardium that restricts filling during diastole
presents as CHF, classic finding is low-voltage EKG with diminished QRS amplitude
80
causes of restrictive cardiomyopathy
amyloidosis, sarcoidosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia
