Download Practice Questions - Answers Which of the following is not an effect

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Cardiovascular disease wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Electrocardiography wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Heart failure wikipedia , lookup

Coronary artery disease wikipedia , lookup

Artificial heart valve wikipedia , lookup

Cardiac surgery wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Myocardial infarction wikipedia , lookup

Jatene procedure wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Aortic stenosis wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Transcript
Practice Questions - Answers
1. Which of the following is not an effect of Catecholamines on cardiac myocytes
a. increased intracellular cAMP
b. Phospholamban Phosphorylation
c. Increased Sarcolemmal Calcium flux
d. Enhanced Troponin-C Calcium binding
e. Increased activity of Sarcosplasmic Reticulum Ca+2 pump
2. Describe what is meant by preload and afterload
Preload refers to myocardial stretch (related to end diastolic volume,
but not exactly equivalent), which alters the amount of tension a
myocyte can develop during contraction. Afterload refers more directly
to the pressure working against the ejection of blood from the ventricle
(in the case of the left ventricle, this would be aortic pressures).
3. What is the chemical/mechanical basis for the Frank-Starling relationship?
The contractile unit of the myocyte is the sarcomere, made up of actin
and myosin thin/thick filaments. These filaments overlap, and when
activated, undergo a cross-bridge cycling which produces sarcomere
shortening. The amount of cross-bridges which can be formed is
intrinsically related to the amount of overlap between thick and thin
filaments. Varying sarcomere length (i.e. increased myocardial stretch)
thus effects the degree of cross-bridge formation, and hence force
production.
Match the following terms with the phrase best associated with it
a.
b.
c.
d.
e.
f.
Membrane invagination which helps spread action potentials
Connects individual cells to form a functional syncytium
Separates cytosplasmic and extra-cellular spaces
Calcium induced Calcium release
Sarcosome
Dense structures located at the ends of myocardial fibers
4. Ryanodine Receptor D
5. T-Tubule A
6. Sarcolemma C
7. Mitochondria E
8. Gap Junctions B
9. Intercalated Discs F
10. Digitalis is a drug sometimes used in heart failure to improve cardiac
contractility, whose pharmacologic target is the Na/K ATP-ase in the sarcolemma.
How might affecting intracellular Na levels serve to increase inotropy? (hint: what
other non-ATP dependent transporters are in the sarcolemma?)
Contractility depends upon intracellular calcium levels, with increased
calcium leading to increased contractility. Although not directly targeted by
digitalis, poisoning of the Na/K+ pump increases intracellular Na, and hence
impairs the function of the Na/Ca exchanger leading to increased intracellular
calcium.
11. S3 and S4 (sometimes referred to as gallops due to their characteristic rhythm)
are additional heart sounds occurring at the beginning of diastole and towards the
end of diastole respectively, typically in the setting of heart disease (but not always).
Postulate the underlying mechanical cause of both these extra sounds.
The point of this question was more to get you thinking about the origins of
heart sounds, and realizing that not always do they occur due to valve closure.
S3 is an abnormal sound caused by fluid turbulence during the rapid filling
phase of diastole. Blood rushes into the ventricle and slams into a stiff
ventricular wall, producing the characteristic gallop. S3s can be heard in some
healthy individuals, including children and athletes, but also in patients
suffering from disorders related to stiffening of the myocardium.
S4 is also caused by turbulent flows, but is slightly different in origin. S4
occurs late in diastole, right after atrial contraction. In sick patients with
abnormally dilated hearts, this column of blood sploshes into the ventricle
and impacts a standing volume which failed to eject during the last beat (or so
is thought).
12. Deep inhalation increased blood return to the right heart, and decreased blood
return to the left heart. What differences in heart sounds might you encounter if you
were listening with a stethoscope during this maneuver?
Most commonly a split S2 would be heard, but may be difficult to detect. The
key to this question is to realize that S1 and S2, while appearing to be singular
sounds, are each constructed of two sounds coming from the right and left
sides of the heart. However, the right and left heart do not always contract in
synchrony, and this asynchrony can be made more apparent through
maneuvers which increase right ventricular filling while decreasing left
ventricular filling. Pulmonic sounds are often quieter than aortic sounds, and
therefore to maximize chances of hearing a split S2 it would be best to listen
over the 2nd intercostal space at the left sternal border.
13. Draw left ventricular and aortic pressure tracings (wiggers diagram) for a
patient suffering from aortic valve stenosis, labeling the different parts of the
cardiac cycle.
Note that the Ventricular pressure tracing (shown in red) is substantially
elevated during the ejection phase compared to the aortic pressure tracing.
Aortic stenosis is a disease in which the aortic valve leaflets undergo
calcification and hardening, thus increasing flow resistance across the valve.
Hence, pressure upstream of the valve must increase to maintain downstream
pressure.