9 Heart

q123456's version from 2016-05-30 14:09


Question Answer
aortic coarctionKA33-35
In fully compensated aortic coarctation
1) blood flow is normal in upper and lower
2) blood pressure is high in upper
3) vascular resistance in upper is high
4) vascular resistance in lower is low due to arteries and arterioles dilation
fibromuscular dysplasiarenovascular stenosis in women of middle age KA31-12
Ergonovineprinzmetal's angina
Decreasing venous return increase the murmur of ?Hypertrophic cardiomyopathy
the premature contraction of the ventricleno normal ventricular filling, preload is reduced>>>decreased left ventricular end -diastolic volume
arterioles and capillariesarterioles: the greatest wall thickness(relative)
capillaries: the minimal wall thickness but the largest cross-sectional area, the velocity of blood flow is lowest in the capillaries (v=flow/area)
Hypertrophic cardiomyopathyMitral valve cusp and interventricular septum
suddenly dies, young adult, myosin heavy chain

septal thickening
decreased ventricular size
normal contractile function
decreased diastolic function
Congenital bicuspid aortic valvesPremature calcific aortic stenosis in the sixth and seventh decades
Turner Syndrome: Bicuspid aortic valve (12.5%, most common), aortic coarctation (6.9%), cystic hygroma (cavernous lymphangioma of the neck)
Dilated cardiomyopathy1 CoxsackieB
2 alcohol abuse/thiamine deficiency
3 doxorubicin
4 Acute rheumatic fever: rheumatic pancarditis>>>cardiac dilation>>>functional mitral regurgitation(MR)
5 Duchenne and Becker Muscular Dystrophy can cause dilated cardiomyopathy

pulmonary edema
jugular venous distention
peripheral edema

decreased ventricular wall thickness
increased ventricular size
decreased contractile function
normal diastolic function
e.g. Ischemic heart disease
Dystrophic calcificationcell injury and death, necrotic tissue
Hypertensive heart diseaseinceased ventricular wall thickness
decreased ventricular size
normal contractile function
decreased diastolic function
hemorrhagic streaks in the nail bedInfectious endocarditis
congenital long QT syndromesdeafness
mutations in a K+ channel protein
sudden cardiac arrhythmia
Torsades de pointes and sudden death
Myxomasvalve obstruction
Scattered cells within a mucopolysaccharide stroma
small heartaging
appetite suppressants (fenfluramine)pulmonary hypertension>>>Right ventricular hypertrophy
inhibit platelet aggregation and adhesion, vasodilates, vascular permeability and leukocyte chemotaxisprostacyclin
PDA: continuous murmur in newborn: indomethacin
enhances platelet aggregation, vasoconstrictionthromboxane A2
SLE induced pericarditispericarditis:most common cardiovascular syndrome associated with SLE
normal coronary arteries, acute MI, mitral valve thickening with vegetations (infectious endocarditis)
chronic aortic stenosis and left ventricular hypertrophyatrial fibrillation>>>loss of atrial contraction>>>reduce left ventricular preload and cardiac output >>>systemic hypotension
after MImyocardial ischemia: increase in size of myocardial cells
without ATP>>> Increased intracellular Na+ and Ca2+
loss of cardiomyocyte contractility occurs within´╝Ü60 seconds after the onset of total ischemia

<4 hours:Minimal change
1-5days after MI: neutrophilic infiltrate
5-10days after MI: Macrophage phagocytosis of dead cells
2 weeks after MI: fibrovascular granulation and Scar formation

early onset pericarditis:
2-4 days following a transmural MI
sharp chest pain
exacerbated by swallowing or relieved by leaning forward
friction rub

A ruptured ventricular free wall:
occurs 3-7 days after the onset of myocardial infaction: A ruptured ventricular free wall

dressler's syndrome
late onset post MI pericarditis: autoimmune reaction to necrtic tissue

atherosclerotic plaque obstructing >75% of the coronary artery lumen, no thrombus: chest pain, relieved within 5 min by rest
ruptured atherosclerotic plaque with fully obstructive thrombus/acute transmural MI:chest pain and dyspnea, not respond to aspirin or sulingual nitroglycerin
Pressure5 mmHg right atrium
5-25 mmHg right ventricle
10-25 mmHg pulmonary artery

12 mmHg left atrium
10-130 mmHg left ventricle
70-130 mmHg aorta
pufferfish>>>tetrodotoxinbinds to sodium channel>>>preventing sodium influx and depolarization>>>dizziness, weakness, loss of reflexes, hypotension and paralysis
the most atherosclerotic involvement vesselAbdominal aorta
new onset cardiac murmur in a young adultbacterial endocarditis
kawasaki diseasefever, vomiting, conjunctivitis, red tongue,
coronary artery aneurysms in <5 years kids
bruit of the carotid arterylisten to the arteries in your neck with a stethoscope. If an abnormal sound, called a bruit, reflect turbulent blood flow. That could indicate carotid artery disease.
Trousseau syndromemigratory
spontaneous venous thrombosis
the upper and lower extremities
VISCERAL carcinoma.
kussmaul's signincrease in the jugalar venous pressure with inspiration

The internal jugular vein

present in most anything that prevents Right heart filling

During inspiration, the intrathoracic pressure is negative (suction of air into the lungs), and abdominal pressure is positive (compression of abdominal organs by diaphragm). This makes a pressure gradient between the infra- and supradiaphragmatic parts of v. cava inferior, "pulling" the blood towards the right atrium and increasing venous return.

kussmaul's sign:pericarditis
pulsus paradoxusa decrease in SBP more than 10mmHg during inspiration
tamponade, constrictive pericarditis, obstructive pulmonary disease and restrictive
cardiomyopathy>>>pulsus paradoxus

1) In normal breathing, more blood fill in the ventricle during the inspiration
2) Systolic contraction prevents the filling of the heart,
3) A decreased SBP during inspiration.
4) Any condition which prevents lung expansion (asthma and COPD) or heart expansion (pericarditis and tamponade)-->greater decrease

The blood pressure cuff inflated to 130 mmHg and the pressure is very slowly decreased. At 100mmHg, intermittent korotkoff sounds are heard only during experation. At 78 mmHg, korotkoff sounds are heard throughout the respiratory cycle
Hypovolemic shocksympathetic nervous system is activated
1) constriction of the arteriolar>>>increased total peripheral resistance
2) constriction of the venous circulation >>>increases blood return to he heart, maintaining preload
3) stimulation of the heart>>>increased contractility and heart rate

blood losses of up to 10% of the circulating blood volume: A normal blood pressure
rapid infusion of blood or normal saline>>>increase the preload>>>extends the end diastolic sarcomere length>>> increasing stroke volume and cardiac output
Exercisestimulation of the sympathetic nervous system
1) increased cardiac output
2) increased preload (contraction of the venous system)
3) contraction of the arterioles in all tissue except the actively working muscles>>> shunt blood toward the exercising muscle
4) exercising muscle releases local vasodilatory factors>>>decrease in the systemic vascular resistance
e.g. runs on a treadmill for 30 mins. which of the follow sets of physiologic changes in most likely to be seen in this man in response to the exercise? vascular resistance: decreased!!! >>> decreased BP and increased HR
severe anemiahypoxia>>>small arteries and arterioles to dilate>>> increased arteriolar diameter-->decreased peripheral vascular resistance
anemia-->decreased blood viscosity
kids, cyanosis of the lower extremities but not the upper bodyPDA L to R>>>R to L
PDA: left sternal border, infant, continuous murmur
tetralogy of fallot (squatting posture)squatting posture=diagnostic significance.
Squatting increases peripheral vascular resistance -->decreases the right-to-left shunt across the ventricular septal defect (VSD).
atrial natriuretic peptide1) Myocytes of the cardiac ventricles express mRNA for natriuretic peptides tipically synthesized by the atria, this findng is associated with which of the following conditions? Hypertrophy
2) deposition of atrial natriuretic peptide-derived proteins:Isolated atrial amyloidosis, aging
Defect in interatrial septumdown syndrome
which of the anatoic sites would normally have a blood oxygen content that differs the most from the valve obtained from this healthy volunteer's aorta?coronary sinus
the cardiac function curveincrease in the height of the cardiac function curve: increase cardiac output
increase slope of both the cardiac function curve and the venous return curve: decreased total peripheral resistance TPR
An increased mean systemic pressure: rightward shift of the venous return curve along the x-axis
arteriovenous fistula: decrease in total peripheral resistance TPR
Increased CO
increased venous return
decreased stroke volume and increased end systolic volume:decreased cardiac contractility
external pressure on the carotid sinusesCN IX
stimulate baroreceptors in the carotid sinus walls>>>vasodilatation>>>
decreased in heart rate
low blood pressure
the ventricular pressure volume loop shows elevated pressures during the isovolumetric ventricular contraction phase before the aortic valve opensventricular afterload is increased
S3early in diastole
dilated ventricle

myocardial ischemia>>>systolic dysfunction>>>decreased the ejection fraction >>>increased left ventricular end-systolic volume. blood rushing into a partially filled ventricle

lie in the left lateral decubitus position, exhale completely (listening at end expiration)
by decreasing the volume of the lungs and bringing the heart closer to the chest wall.
presystolic sound, turn left side and hold the breath
Increased stiffness of the left ventricular wall (L ventricular hypertrophy/hypertesive heart disease)
Skeletal musclecalcium channel blockers do not affect skeletal muscle>>>Skeletal muscle does not require calcium to enter from the extracelluar space to cause calcium release from within the cell
No dependence on extracellular calcium
complete (3rd degree) atrioventricular AV blockSA node impulses cause atrial contraction/AV node cause ventricular contraction complete (3rd degree) atrioventricular AV block
The atria and ventricles depolarize indenpendently of each other>>>AV dissociation
45-55 beats per minute>>>AV node
60-100 beats per minute>>> SA node

fastest-->slowest: Park at Ventura Avenue (purkinje-atrial-venricular-AV)


Question Answer
V of jugular venous pressurevenous return
mitral regurgitation: a high V of jugular venous pressure during systole
Y of jugular venous pressuretricuspid valve open>>>blood flows into the R ventricle
a of jugular venous pressureR atrial contraction
atrial fibrillation: "a" wave in the JVP is absent
tricuspid stenosis: large "a" waves
C of jugular venous pressurebulging of the tricuspid valve into the right atrium druing ventriclualr systole (isovolumic phase)
x of jugular venous pressureR atrial relaxation/ventricular systole
tricuspid regurgitation:x wave become a positive wave
jugular venous pulseA-C-X-V-Y
3 waves: a, c, v. a=Atrial contraction, c=early Systole, v=Venous return
Absent in patients with atrial fibrillationa wave of jugular venous pressure
a of jugular venous pressureS4


Question Answer
Pulmonary embolismIn the lower lobes (Perfusion is greater than ventilation in the lower lobes)
Heparin or low-molecular-weight heparin; warfarin for extended therapy
Lower extremity deep venous thrombosis (DVT) e.g Hip surgery, after operation, decompensation>>>chest pain and dyspnea
V/Q scan reveals a large perfusion defect, chest pain, dyspnea>>>deep vein thrombosis
Low dose of aspirinrecurrent coronary artery thrombosis and ischemic strokes
Chest pain, hypercholesterolemiaDefects in the LDL receptor
Lipoprotein lipase deficiencyHypercylomicroemia/hypertriglyceridemia
Kids, Pancreatitis, lipemia retinalis, skin xanthomas, hepatosplenomegaly
neoplasm under the nailglomus tumor (glomangioma)
lymphangiosarcoma (arm swelling)radical mastecotomy for breast cancer
hypertensive arteriolar sclerosisa 58 year old man: sudden right hand weakness, decreased strength in his right hand only. Initial CT scan without contrast showed no abnormalities. Four weeks later, repeat brain imaging show a 9 mm cavitary lesion in his left internal capsule. this patient's condition is most likely casused by?

a 56 year old man with a history of hypertension, tingling sensation on the left side of his body, diminished sense of touch and position in the left arm and leg. an MRI of brain is shown (KA25-30), which structurs is most likely damaged? internal capsule
Abrupt onset severe chest pain, hypertension, normal serum troponin levels, ECG negativea tear in the aortic intima>>>aortic dissection
aortic dissection: hypertension
***aortic aneurysm:
high cholesterol, atherosclerosis
abdominal aortic aneurysm(AAA): abdominal pain that radiates to the back
abdominal bruit is auscultated
intermittent claudicationatherosclerosis
Liver angiosarcoma (arsenic, polyvinyl chloride)
hyaline arteriolosclerosisnon-malignant hypertension or diabetes
Homogeneous deposition of eosinophilic hyaline material n the intima and media of small arteries and arterioles
malignant hypertensionhyperplastic arteriolosclerosis
Homogeneous onion like concentric thickening of the walls of arterioles
recurrent severe nosebleeds+telangiectasiasosler weber rendu syndrome
L. heart failureChronic left heart failure:hemosiderin containing macrophages in the alveoli
Acute left heart failure: transudate (filtration of plasma water and electrolytes into the lung interstitium and alveoli) not exudate