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Block 7 > Cardio > Flashcards

Cardio Flashcards

1
Q

What does angina mean?

A

Chest pain due to reduced blood flow (ischemia) to the heart
The coronary arteries supplying blood to the heart itself have more than 70% stenosis (note: <70% stenosis would be asymptomatic and 100% stenosis/ blockage would be an MI)

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2
Q

What are the 3 causes of holosytolic murmurs (same level of loudness throughout systole)?

A
  1. Tricuspid Regurgitation
  2. Mitral Regurgitation
  3. VSD (Ventricular Septal Defect)
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3
Q

What defect produces a continuous, “machine-like” murmur?

A

PDA (Patent Ductus Arteriosus)

*The reason it is continuous is an open PDA means there is a shunt causing blood to flow from aorta—> pulm. Arteries. This is outside the heart, so not dependent on systole or diastole.

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4
Q

You’re listening to the heart at the 4 different valves. What are the landmarks of where to listen?

A

AORTIC- 2nd intercostal space on the patient’s right/ right upper sternal border

PULMONIC- 2nd intercostal space on the patient’s left/ left upper sternal border

TRICUSPID- left lower sternal border on the patient’s left

MITRAL- 5th intercostal space on the patient’s left, mid-clavicular line

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5
Q

Are systolic murmurs always pathological? Diastolic murmurs?

A

Systolic murmurs can be normal/ innocent in kids, young thin patients, and pregnant women.
Diastolic murmurs are always pathologic!

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6
Q

The main side effect of statins is myopathy. What does that mean?

A

Problems with muscles. Muscle fibers not functioning properly, muscle aches

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7
Q

What does myalgia mean?

A

Muscle pain (a major side effect of statins)

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8
Q

Some symptoms of pericarditis= fever, leukocytosis, high ESR (inflammation). What does leukocytosis mean?

A

High WBC count

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9
Q

What EKG changes are seen in acute pericarditis? How is this distinguished from ischemia like in an MI?

A

ST elevations all over the EKG (whereas, just in one heart region in ischemia) and/or PR depression

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10
Q

What is the most common cause of pericarditis?

A

A viral infection- often Coxachie

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11
Q

What does myopericarditis mean?

A

Myocarditis + pericarditis (patient has inflammation of the myocardium/ heart muscle AND the pericardium/ heart covering)

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12
Q

If a patient has an elevated JVP (jugular venous pressure), what does that tell you?

A

Fluid from the RA is getting backed up (because the jugular vein turns into the SVC and dumps into the RA). There’s increased pressure in the RA and some heart pathology going on (ex: pericarditis)

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13
Q

What EKG findings do you see in cardiac tamponade?

A

Low-voltage QRS (lower peaks) and electrical alternans

The electrical recording isn’t as strong because the heart is swinging around in fluid in the pericardial sac

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14
Q

What are the 3 layers of the pericardium (heart covering)? Other heart layers?

A

Fibrous pericardium—> parietal layer of the serous pericardium—> visceral layer of the serous pericardium a.k.a. Epicardium—> myocardium (heart muscle)—> endocardium (inner lining)

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15
Q

Which valves have chordae tendonae (heart strings attached to papillary muscles)?

A

The AV valves (tricuspid + mitral/bicuspid)

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16
Q

Conceptually, what does cardiac output (CO) mean? What is its equation?

A

CO is the amount of blood your heart pumps out per minute (L/min)
CO= SV * HR

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17
Q

Conceptually, what is stroke volume (SV)? What is its equation?

A

The volume of blood that gets pumped out (closely related to the contractility of the heart) SV= EDV- ESV (blood your heart is filled with at the end of diastole minus blood that’s still in your heart after it contracts in systole= blood that got pumped out)

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18
Q

Conceptually, what is contractility?

A

How hard the heart muscle squeezes (closely related to stroke volume, or SV)

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19
Q

Conceptually, what is myocardial oxygen demand?

A

How much oxygen/ energy the heart needs to do its work

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20
Q

Conceptually, what is preload? Afterload?

A

Preload- VOLUME of blood available to load into the LV before it gets pumped out
Afterload- PRESSURE the LV has to develop/ overcome to pump

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21
Q

Conceptually, what is ejection fraction (EF)? What is normal EF?

A

% of blood pushed out the LV with each heartbeat

Normal= about 55-60%

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22
Q

What is the ejection fraction (EF) formula?

A

SV/ EDV= (EDV-ESV)/ EDV

What’s getting pumped out over the total amount of blood the heart initially was filled with before it pumped

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23
Q

Conceptually, what is mean arterial pressure (MAP)? What are the 2 equations?

A

The average pressure in arteries during 1 cardiac cycle.
MAP= CO* Resistance (TPR or SVR)
…and…
MAP= 2/3 diastolic BP + 1/3 systolic BP
(*you can’t take the average BP like a normal mean bc 2/3rds of time is spent in diastole, 1/3rd in systole and you have to account for that)

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24
Q

What happens to BP and blood flow in (1) vasoconstriction and (2) vasodilation?

A

(1) vasoconstriction: increases BP; decreases blood flow

(2) vasodilation: decreases BP; increases blood flow

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25
Q

What’s the difference between VASOconstriction and VENOconstriction?

A

Vasoconstriction is talking about the arteries (away from the heart)
VENOconstriction is talking about the veins (to the heart)

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26
Q

How does VENOconstriction effect preload?

A

It increases it because you are increasing “milking” of blood up to the heart, so the heart will fill with more blood

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27
Q

What 4 heart-related things happen when the sympathetic nervous system is activated?

A

(1) increase in HR (NE released from sympathetic nerves—> increases cAMP—> stimulates more Na+ to come in through channels—> faster depolarization/ contraction of heart)
(2) increase in contractility
(3) VENOconstriction (increase in “milking” up of blood to the heart= increase of preload)
(4) vasoconstriction (increases BP, decreases blood flow to less critical organs like GI organs because skeletal muscles, for example, are more important in a fight or flight situation)

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28
Q

What 4 things does cardiac output (CO) depend on?

A

(1) preload (2) afterload (3) contractility (4) HR

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29
Q

Describe blood flow all the way through the heart

A

Enters SVC/ IVC—> RA—> tricuspid valve—> RV—> pulmonic valve—> pulmonary artery—> lungs to get oxygenated—> pulmonic veins—> LA—> mitral (bicuspid valve)—> LV—> aortic valve—> aorta—> out to body

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30
Q

What are all the heart valves and how many leaflets do they each have normally?

A

AV valves= tricuspid valve and mitral (bicuspid) valve
Semilunar valves= pulmonic and aortic valve

They all have 3 leaflets except mitral (bicuspid) valve only has 2.

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31
Q

The ductus arteriosus (shunt from pulmonary arteries to aorta to bypass lungs) normally closes at birth. What is the remnant of this called?

A

Ligamentum arteriosum

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32
Q

What are the 3 shunts in fetal circulation and what do they bypass?

A

(1) DUCTUS VENOSUS- shunts blood coming in from umbilical vein to IVC (bypasses hepatic circulation)
(2) FORAMEN OVALE- shunts most of the blood from the RA to the RV (bypasses the RV to the lungs)
(3) DUCTUS ARTERIOSUS- shunts blood that went through the RV—> pulmonary arteries to the aorta (bypasses the lungs)
* The liver doesn’t need all the blood flow and the lungs are filled with amniotic fluid and not yet working so that’s why blood skips these structures

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33
Q

In terms of veins and arteries/ oxygenated and deoxygenated blood, what is different about fetal circulation (in the womb) vs. adult circulation?

A

Veins are to the heart, arteries away from the heart (same)

Veins carry OXYGENATED blood, arteries carry deoxygenated blood as it gets distributed to tissues (opposite)

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34
Q

What does “placental abruption” mean?

A

The placenta detaches from the uterus (usually the baby dies)

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35
Q

What is cyanosis

A

Blue-ish discoloration of skin due to low oxygen saturation

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36
Q

What do prostaglandins (PG’s) like E1= Alprostadil and E2 do to the ductus arteriosus (DA)? How about Indomethacin?

A

PG’s keep the DA open/ patent. Indomethacin is an NSAID, so inhibits PG’s and therefore may help close the DA.
*The placenta provides a lot of PG’s to keep the DA shunt (pulm arteries—> aorta, bypassing lungs) open in fetal circulation. Once born, the DA normally closes. If it remains open/ patents, we may give Indomethacin to close it. If the baby has cyanosis (lack of oxygen), we may give PG’s to keep it open (aortic pressure rises after birth so will now shunt aorta—> pulm arteries) to get more blood into lungs for oxygenation until we fix the underlying problem.

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37
Q

(Congenital heart disease) Why is a right to left shunt worse than a left to right shunt?

A

In a left to right shunt, oxygenated blood from the left side of the heart is shunted to the right, causing volume overload. This causes a heart murmur, but only becomes a real problem (cyanosis, “blue kids”) if it is left untreated for a long time and the pulmonary circuit builds up so much pressure (pulm hypertension) that the shunt switches directions. NOT AS BAD
In a right to left shunt, deoxygenated blood from the right side of the heart is shunted to the left to get pumped out to the body—> cyanosis (“blue babies”). BAD!!

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38
Q

About 25% of people have a patent (open) foramen ovale (fetal shunt between atria). Is this a problem? If it can be, why?

A

Usually not a problem because just a little oxygenated blood from the higher pressure LA will leak into the lower pressure RA—> higher pressure in the RA. BUT, can lead to paradoxical emboli (if you get a blood clot, it can come in through the RA and take advantage of the shunt/ opening and move directly to the LA even though that’s against the pressure gradient and get pumped out systemically possibly leading to a stroke) **also seen in atrial septal defect (ASD)

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39
Q

If the septal defect is smaller, will the heart murmur be softer or louder?

A

Louder (blood traveling through a smaller space will produce a louder sound)
Smaller septal defect= less symptoms but louder heart murmur

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40
Q

What does tachypnea mean?

A

Rapid, shallow breathing

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41
Q

What’s central cyanosis vs peripheral cyanosis?

A

Central cyanosis- heart is pumping enough blood (normal CO, warm extremities) but it doesn’t have enough oxygen in it
Peripheral cyanosis= heart is not pumping enough blood (HF), which is why you’re body isn’t getting enough oxygen

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42
Q

Describe Tetrology of Fallot.

A

Congenital defect/ displacement of the infundibular septum (smooth funnel connecting the RV and the pulmonary arteries). Leads to 4 problems: (1) narrowing/ stenosis of the pulmonic valve (2) displacement/ overarching of the aorta (3) hypertrophy/ thickening of the RV walls (4) ventricular septal defect (VSD)

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43
Q

What is angina? Why would giving nitrates help?

A

Angina= chest pain from ischemia/ decreased blood flow to the heart
Nitrates primarily cause venodilation, but they also cause vasodilation. The vasodilation of the coronary arteries in the heart will open up the arteries where the infarct is so the infarct isn’t blocking as much/ isn’t as much of a problem

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44
Q

What is the main mechanism of nitrates?

A

Venodilation (decreasing preload to the heart)

But they also cause vasodilation (decreasing afterload on the heart)

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45
Q

During exercise, where do you get vasoconstriction? Where do you get vasodilation? Explain.

A

You get vasoconstriction as a part of the sympathetic response increasing BP and decreasing blood flow to less critical organs at the time, like the gut. You get vasodilation to increase blood flow to muscles.

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46
Q

Why do you get cyanosis in Tetrology of Fallot?

A

2 reasons:

1) the aorta is misplaced/ overarching so you get shunting of deoxygenated blood from the RV through the aorta and out to the body
2) there is stenosis of the pulmonary artery so less blood gets through to the lungs for oxygenation

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47
Q

Which valve defects cause systolic heart murmurs?

A

Tricuspid insufficiency, mitral insufficiency, pulmonic stenosis, and aortic stenosis

**Remember: AV valves are open, semilunar valves are closed in systole. Stenosis= problem with opening the valve. Insufficiency= regurgitation= problem with closing the valve.

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48
Q

Which valve defects cause diastolic heart murmurs?

A

Tricuspid stenosis, mitral stenosis, pulmonic insufficiency, and aortic insufficiency

**Remember: AV valves are open, semilunar valves are closed in systole. Stenosis= problem with opening the valve. Insufficiency= regurgitation= problem with closing the valve.

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49
Q

Which layer of the heart is the most vulnerable to ischemia (such as angina)?

A

The subendocardium (because it is the layer that is furthest away from the coronary arteries, so receives less blood flow)

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50
Q

What does inotrophy mean?

A

Contractility (agents that alter contractility)

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51
Q

What blood vessels feed the heart/ supply the heart itself with blood?

A

Coronary arteries

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52
Q

What are examples of ischemic heart disease?

A

Stable angina, unstable angina, MI
*can result in sudden cardiac death or chronic ischemic heart disease (if chronic damage from ischemia progresses to CHF)

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53
Q

Describe stable angina

A

STABLE ANGINA- you have >70% stenosis in coronary arteries supplying the heart and this is a problem during exercise when your body needs to pump out more blood to meet increased metabolic demands (the blockage makes it harder to push blood through)

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54
Q

Does inspiration make heart murmurs louder or quieter? Expiration?

A

Inspiration makes right heart murmurs louder (negative pressure increases preload/ blood coming up through the SVC/ IVC and dumping into the right side of the heart)

Expiration makes left heart murmurs louder (positive pressure squeezes blood out of the lungs and into the left side of the heart)

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55
Q

What does standing up do to the intensity of heart murmurs (most murmurs, hypertrophic cardiomyopathy, and mitral valve prolapse)? Explain.

A

Standing up—> DECREASES PRELOAD (blood pools by gravity).
MAKES MOST MURMURS QUIETER (Less preload= less blood to flow through defected valve= less turbulent flow= quieter murmurs).
MAKES HYPERTROPHIC CARDIOMYOPATHY MURMUR LOUDER (Less preload= less blood to fill the LV and push the defect out of the way= more aortic outflow obstruction causing a murmur).
YOU HEAR THE MITRAL VALVE PROLAPSE CLICK EARLIER (Less preload causes the valve to be more floppy= more turbulent flow= murmur from ballooning out of valve heard sooner)

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56
Q

What does the Valsava maneuver (bearing down) do to the intensity of heart murmurs (most murmurs, hypertrophic cardiomyopathy, and mitral valve prolapse)? Explain.

A

Valsava=Bearing down—> DECREASES PRELOAD (squeezing abdominal muscles—> clamping off of IVC).
MAKES MOST MURMURS QUIETER (Less preload= less blood to flow through defected valve= less turbulent flow= quieter murmurs).
MAKES HYPERTROPHIC CARDIOMYOPATHY MURMUR LOUDER (Less preload= less blood to fill the LV and push the defect out of the way= more aortic outflow obstruction causing a murmur).
YOU HEAR THE MITRAL VALVE PROLAPSE CLICK EARLIER (Less preload causes the valve to be more floppy= more turbulent flow= murmur from ballooning out of valve heard sooner)

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57
Q

What is the valsava maneuver (phase II)?

A

Bearing down (like on the toilet or trying to blow out to make your ears pop with your mouth closed)

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58
Q

What does handgrip do to the intensity of the following heart murmurs: mitral regurgitation, aortic regurgitation, and VSD? Explain.

A

Handgrip—> INCREASES AFTERLOAD (due to increased SVR aka BP from you gripping those hand muscles)
MAKES THESE MURMURS LOUDER (increased afterload= increased pressure the LV has to pump against to get the blood out= so the blood will take the path of least resistance, for example, will go from LV->LA rather than LV->aorta in a mitral regurgitation= and more blood through bad valve= more turbulent flow= louder murmur)

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59
Q

What does handgrip do to the intensity of the following heart murmurs: hypertrophic cardiomyopathy, aortic stenosis, and mitral valve prolapse? Explain.

A

Handgrip—> INCREASES AFTERLOAD (due to increased SVR aka BP from you gripping those hand muscles)
MAKES HYPERTROPHIC CARDIOMYOPATHY MURMUR QUIETER (More afterload will make it even harder for blood to get out through the aorta= so less blood will make it through to aorta past the defect and high pressure= less turbulent flow= quieter murmur)
MAKES AORTIC STENOSIS MURMUR QUIETER (More afterload will make it even harder for blood to get out through the aorta= so less blood will make it through aorta= less turbulent flow= quieter murmur)
YOU HEAR THE MITRAL VALVE PROLAPSE CLICK LATER (More afterload/ pressure pushes the valve back in place= less turbulent flow= murmur from ballooning out of valve heard later)

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60
Q

What does rapid squatting do to the intensity of the following heart murmurs: aortic stenosis, mitral regurgitation, and VSD? Explain.

A

Rapid squatting—> INCREASES PRELOAD (kink veins in legs= increased “milking” up of blood to heart) and also afterload (increased SVR aka BP from you contracting muscles)
MAKES THESE MURMURS LOUDER (increased preload= increased blood that will go through the defected valves= increased turbulent flow= louder murmurs)

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61
Q

What does rapid squatting do to the intensity of the following heart murmurs: hypertrophic cardiomyopathy and mitral valve prolapse? Explain.

A

Rapid squatting—> INCREASES PRELOAD (kink veins in legs= increased “milking” up of blood to heart) and also afterload (increased SVR aka BP from you contracting muscles)
MAKES HYPERTROPHIC CARDIOMYOPATHY MURMUR QUIETER (More preload expands the LV and pushes the defect out of the way so it’s not such a problem= decreases turbulent flow= quieter murmur)
YOU HEAR THE MITRAL VALVE PROLAPSE CLICK LATER (More preload/ blood pushes the valve back in place/ makes it more crisp= less turbulent flow= murmur from ballooning out of valve heard later)

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62
Q

In general, if you have greater preload what will that do to the loudness of a murmur?

A

More blood flow through bad valve= louder murmur

Less blood flow through bad valve= quieter murmur

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63
Q

What is mitral valve prolapse?

A

Ballooning up of valve leaflets (note: more preload/ afterload will help push the valve back into place/ make it more crisp so it’s less of a problem and there’s less of a murmur. Less preload will make the valve even more floppy so it’s more of a problem and there’s more of a murmur.)

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64
Q

What does a crescendo-decrescendo murmur mean?

A

It gets louder, then it gets quieter again

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65
Q

What is total peripheral resistance (TPR) aka systemic vascular resistance (SVR)?

A

Pretty much the same thing as BP

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66
Q

Explain what endocarditis is.

A

Inflammation of the endocardium= inner layer of heart= infection of the valves.
(Example: patient may have vegetations= grape-like collections of bacteria on their valve from a strep epidermidis infection following a valve replacement surgery. These vegetations can go to anywhere in the body and cause lots of symptoms, like in fingernail beds causing splinter hemorrhages.)

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67
Q

How long does it take for the heart to beat in embryo?

A

4 weeks (heart is beating by week 4)

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68
Q

Is RA pressure higher or lower before birth? After birth?

A

RA pressure is higher before birth; lower after birth.
REMEMBER: right heart pressures are higher before birth (lungs not working). Left heart pressures are higher after birth (the right heart only has the job of pumping to the lungs, while the left heart has the greater job of pumping to the body)

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69
Q

Why would you give PG’s to a baby with Tetralogy of Fallot temporarily before that congenital heart defect can be surgically fixed?

A

PG’s will keep the ductus arteriosus open, allowing blood to shunt from the higher pressure aorta—> lower pressure pulmonary arteries= more blood flow to the lungs. Why does this help? In Tetralogy of Fallot, you have early cyanosis because (1) deoxygenated blood from the RV is shunting into the overarching aorta and (2) blood is having a hard time getting through the stenosed pulmonary artery to the lungs to get oxygenated. So you have the aorta pumping out deoxygenated blood and little oxygenated blood. By shunting some of that deoxygenated blood in the aorta back to the pulmonary arteries so they can get to the lungs (bypassing the stenosis early on in pulmonary artery), you are giving the blood a chance to get oxygenated by the lungs and making the cyanosis not as bad so the baby can live until surgery.

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70
Q

Why would you give PG’s to a baby with Total Anomalous Pulmonary Venous Return (TAPVR) temporarily before that congenital heart defect can be surgically fixed?

A

PG’s will keep the ductus arteriosus open, allowing blood to shunt from the higher pressure aorta—> lower pressure pulmonary arteries= more blood flow to the lungs. Why does this help? In TAPVR, you have the pulmonary veins dumping into the right heart (so oxygenated blood gets put back into compartment with deoxygenated blood). So, only the right side of your heart is working—> right side has more pressure than left side, unlike normal. So a PDA will cause shunting from the right side (pulmonary arteries)—> left side (aorta). This will help pump blood out to sustain life until surgery (you need a R—> L shunt to live in this condition).

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71
Q

What’s the difference between coarctation of the aorta that is pre-ductal and post-ductal? What does that means in terms of collateral artery development?

A 
PRE-DUCTAL= the narrowing of the aorta is before the ductus arteriosus, so a PDA (patent/ open ductus arteriosus) would help by shunting blood across to the aorta after the problem. 
POST-DUCTAL= the narrowing of the aorta is after the ductus arteriosus, so the PDA doesn’t help because it would shunt blood across the aorta, THEN the blood would run into the problem of a narrowed aorta. In this case, the body would compensate by making new vessels= collateral vessels to feed the lower half of the body with blood.
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72
Q

Turner syndrome is associated with what heart problems?

A

Bicuspid aortic valve and coarctation of the aorta (“Turner syndrome turns the aorta into a problem”)

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73
Q

What heart problems are associated with Down syndrome?

A

Down syn is associated with endocardial cushions (giving rise to atrioventricular (AV) septum + valves) not developing right—> AV septal defect, ASD (atrial septal defect), and VSD (ventricular septal defect).

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74
Q

Babies born to diabetic moms are most likely to have what congenital heart problem?

A

Transposition of the great vessels

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75
Q

What is systolic BP associated with? Diastolic BP? (Options: CO, PVR, preload, afterload)

A 
Systolic BP (pumping out) is associated with afterload (pressure the LV has to pump against) and CO (how much blood gets pumped out over a given time).
Diastolic BP (filling) is associated with preload (blood that is available to fill the LV) and PVR (the blood that’s in the periphery and available to go back up to the heart)
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76
Q

What’s the difference between eccentric and concentric hypertrophy?

A

Eccentric= myocytes are added sideways/ in series (LV gets stretched out).
Concentric- myocytes are added on top of each other/ in parallel (LV thickens to where it looks like a bullseye).

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77
Q

In what case would you see both elevated JVP and enlarged liver?

A

Right heart failure

Because blood backs up to SVC—> jugular vein & IVC—> liver venous system

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78
Q

What is the feared complication of prolonged QT intervals on EKG?

A

TORSADES DE POINTES (“twisting of the points”).
This is a ventricular tachycardia arrhythmia with QRS (ventricular depolarization) getting smaller and larger and smaller and larger…

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79
Q

What is congenital long QT syndrome? What 2 specific disorders does this include?

A

You are born with defective Na/K channels in your heart—> takes longer for ventricles to depolarize and repolarize—> prolongs the QT interval on EKG (QT= whole systole; depolarization + repolarization). Prolonged QT=> Torsades de Pointes (can result in sudden cardiac death).
Includes: ROMANO-WARD SYNDROME (autosomal dominant) and JERVELL AND LANGE-NIELSEN SYNDROME (autosomal recessive, includes deafness).

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80
Q

You can get Torsades de Pointes (V tach arrhythmia with shifting waveforms of QRS getting smaller and larger and smaller and larger…) from prolonged QT intervals (systole= depol. + repol.). What are causes of this (hint: there are 5)?

A

Causes of prolonged QT—> Torsades de Pointes:

  1. Drugs (ABCD: antiArrhythmics 1a and 3, antiBiotics like macrolides, antiCychotics, antiDepressants, and antiEmetics (stop vomiting).
  2. Hypokalemia (low K+)
  3. Hypomagnesemia (low Mg2+)
  4. Hypocalcemia (low Ca2+) RARELY
  5. Congenital abnormalities (ex: congenital long QT syndrome)
    * *Anti-arrhythmic drugs cause this if they prolong QT too much. Low K+/ low Mg can cause this bc these electrolyte abnormalities mess up ventricular depolarization.
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81
Q

V tach arrhythmia with shifting waveforms of QRS getting smaller and larger and smaller and larger…knows as “twisting of the points.” What is this called?

A

Torsades de pointes

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82
Q

When do you see peaked T waves?

A

Hyperkalemia (high K+) and early ischemia

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83
Q

When do you see U waves? (2 cases)

A

Hypokalemia (low K+) and bradycardia (low HR)

*they follow T waves

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84
Q

Inverted T waves on EKG may indicate what?

A

Ischemia or recent MI

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85
Q

What enables depolarization to travel from one myocyte to the next? (Note: this is different from skeletal muscle where cells are individually depolarized.)

A

Gap junctions

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86
Q

Think about the cardiac pacemaker (SA node, AV node) action potential. What does it mean to increase/ decrease the slope of phase 4?

A

Phase 4= ventricular diastole (resting/ refilling) but Na+ is slowly coming in through “funny channels” till it reaches threshold that triggers full-on depolarization.
Increase slope of phase 4= increase Na+ influx= increase rate at which you depolarize= increase HR (sympathetic NS and sympathomimetic drugs do this).
Decrease slope of phase 4= decrease HR (PNS, beta-blockers, and Adenosine do this).

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87
Q

Heart sounds: What is S1? S2?

A 
S1= closure of mitral/ tricuspid valves (AV valves)
S2= closure of aortic/ pulmonic valves (semilunar valves)
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88
Q

Explain the physiologic splitting of S2.

A

Inspiration—> increases venous return (blood dumped into right heart)—> since there’s more blood/ pressure in the right side of the heart, the pulmonic valve will take a little longer to close than the aortic valve—> subtle spit of the S2 heart sound

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89
Q

When do you hear S3 and S4 heart sounds- systole or diastole? Be specific.

A

Both are pathologic/ abnormal, heard in diastole. S3= early filling sound (heard right after S2). S4= late filling sound (heard right before S1).

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90
Q

What kind of patients have S3 gallop heart sounds?

A

Acute heart failure patients. The S3 sound is blood slamming into an already overfilled ventricle. (High LA pressure—> rapid early filled of LV—> S3. “Pushers” meaning they push blood into the LV.) *S3 can sometimes be normal in young patients or pregnant women.

91
Q

Explain the 4 types of shock.

A
  1. CARDIOGENIC- heart problem (MI, HF, valvular dysfunction, arrhythmia)—> low CO—> low BP—> lack of perfusion
  2. HYPOVOLEMIC- loss of blood volume (hemorrhage, dehydration, burns)—> low CO—> low BP—> lack of perfusion
  3. DISTRIBUTIVE- massive cytokine release (sepsis, anaphylaxis/ severe allergic reaction, CNS injury)—> systemic vasodilation—> low BP—> lack of perfusion
  4. OBSTRUCTIVE- something is obstructing the outflow of blood from the heart (cardiac tamponade, PE, tension pneumothorax)—> low CO—> low BP—> lack of perfusion
92
Q

What are ways the body controls BP?

A
  1. Nervous system: sympathetic and parasympathetic
  2. Hormones: catecholamine (NE, epi), natriuretic peptides (ANP, BNP), ADH, and RAA system
    (*note: heart transplants are made possible bc of the hormonal control over BP, since nerve connections are lost)
93
Q

Where are catecholamine (epi, NE) released from in the body?

A

The adrenal gland (on top of the kidneys- specifically in the medulla)

94
Q

In general, when are ANP and BNP released from the heart? What do they do?

A

When you have an increase in blood volume (preload)—> increase myocyte stretch—> ANP and BNP get pumped out from heart—> carried through bloodstream to kidneys to tell them to excrete more Na+ and water to lower blood volume back to normal (they inhibit the RAA system, cause vasodilation, decrease Na+ and water appetite and ADH)

95
Q

Why is there a such thing as chronic hypertension? In other words, why don’t the baroreceptors correct for the high BP?

A

In chronic hypertension, your BP stays high because the baroreceptors sensing BP have become desensitized and think the high BP is the new norm so they don’t trigger hormone release to correct for it.

96
Q

In hypoxia, what local metabolites act on the heart to do autoregulation (local regulation of BP)?

A

Low oxygen—> adenosine, NO, CO2 cause vasodilation of coronary arteries—> increases blood flow to compensate

97
Q

What are the “Jones criteria” for diagnosis of Rheumatic fever?

A 
Joints (migratory polyarthritis)
<3 (carditis) 
Nodules in skin (subcutaneous) 
Erythema marginatum 
Sydenham chorea (jerking movement disorder)
98
Q

Older patient with hx of hypertension has sudden-onset chest pain radiating to the back and markedly unequal BP in both arms. What do you think?

A

Aortic dissection

99
Q

Flat facial profile, protruding tongue, small ears, VSD (holosystolic heart murmur). What are you thinking and what is the underlying genetic defect?

A

Down syndrome. Trisomy 21 from nondisjunction (chromosomes fail to separate, allowing an extra copy to get passed on).

100
Q

What are complications associated with coarctation of the aorta?

A

HF, increased risk of cerebral hemorrhage from “berry aneurysms” (due to pressure differences), aortic rupture, and possible endocarditis (inflammation of inner layer of heart/ valves)

101
Q

What embryo structure is the SVC derived from?

A

The common cardinal veins.

102
Q

Long standing pulmonary hypertension leads to what gross anatomy finding of the heart?

A

Hypertrophy (thickening) of the RV

103
Q

What does orthopnea mean?

A

Discomfort breathing while laying down flat

103
Q

What is “cor pulmonale?”

A

Isolated right HF due to a pulmonary cause (for example, pulmonary HTN leading to right-sided HF)

104
Q

What heart problem can Lyme disease cause?

A

AV block (oftentimes 3rd degree, or complete AV block)

105
Q

What is AV block in general? Describe 1st degree AV block.

A

AV block is when the AV node is having a problem sending the electrical signal from the atria down to the ventricles for depolarization.
1st degree—> prolonged PR interval only (the atria is communicating/ sending signal down to ventricles fine, but this AV conduction is SLOW) *not a concern, seen in athletes, patients on Ca2+ channel blockers, beta-blockers (bc they slow HR).

106
Q

What is AV block in general? Describe 2nd degree AV block (include both subtypes in description).

A

AV block is when the AV node is having a problem sending the electrical signal from the atria down to the ventricles for depolarization.
2nd degree includes Mobitz I (Wenckebach) and Mobitz II.
Mobitz 1–> PR interval gets longer and longer…then dropped beat/ P wave without QRS following it (AV conduction is slow, then communication between atria and ventricles gets lost at a point). *caused by disease of the AV node itself.
Mobitz II—> PR interval is not affected…see dropped beat/ P wave without QRS following it (Communication is lost between atria and ventricles at a point). *worse bc its caused by disease of His-Purkinje system.

107
Q

What is AV block in general? Describe 3rd degree AV block.

A

AV block is when the AV node is having a problem sending the electrical signal from the atria down to the ventricles for depolarization.
3rd degree—> complete AV block. No communication between atria and ventricles at all. You see regular R-R intervals (this is how you distinguish it from Mobitz I) but no QRS’s following P waves.

108
Q

What is “complete heart block?”

A

Same thing as 3rd degree AV block. Means the atria are not communicating with the ventricles at all/ depolarization signal is not being sent down for the ventricles to contract when they are supposed to.

109
Q

In heart block/ 3rd degree/ complete AV block, do the ventricles get depolarizer?

A

Yes. In this problem, the atria aren’t communicating with the ventricles. It’s an AV nodal problem. But, one of the “back up pacemakers” will take over to pace the heart, so depolarization of ventricles does occur but at a much slower rate.

110
Q

If both bundle branches of the heart are blocked, what do we call this?

A

AV block. (Now there is a blockage preventing the AV node from relaying the electrical impulse from the atria to the ventricles)

111
Q

If only one bundle branch is blocked (left OR right bundle branch block), is that considered an AV block?

A

No. The AV is not blocked. It still has a route to take to transmit electrical impulse from atria to ventricles (but there will be problems with this. You’d see a normal PR interval (because AV node is getting the electrical message from the atria to the ventricles in a normal time) but prolonged QRS (because the ventricles do take longer to contract given that one bundle branch is blocked).

112
Q

In heart failure, which drugs decrease mortality (based on clinical studies) and which ones are just used for symptomatic relief?

A

ACE inhibitors/ ATII receptor blockers, beta-blockers (except in late stage), and spironolactone decrease mortality. Thiazide or loop diuretics are just for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patients.

113
Q

What does atrial kick mean?

A

Atrial contraction. The “final push” of blood the atria contracts out.

114
Q

What is the S4 heart sound?

A

The sound blood is making when it bounces off the thick/ hypertrophied walls. You hear it in pathology at the end of diastole (before the S1 sound in systole).

115
Q

Why is dry cough a side effect of ACE inhibitors?

A

ACE (angiotensin converting enzyme) breaks down Bradykinin. So a side effect of an ACE inhibitor is dry cough because Bradykinin will build up (ACE is prevented from breaking it down).

116
Q

What 3 drugs are known to cause drug-induced lupus as a side effect? (Note: we see anti-histo next antibodies in drug-induced lupus)

A

1) Hydralazine (HTN drug)
2) Procainamide (anti-arrhythmic)
3) Isoniazid (TB drug)

117
Q

What 2 things do Ca2+ channel blockers do? Explain the basic mechanism.

A

1) vasodilation (dec BP, inc blood flow)
2) dec contractility

How? Ca2+ normally helps muscles contract. It causes vasoconstriction of the smooth muscle in arteries and contraction of the muscle in the heart. So, Ca2+ channel blockers will inhibit these effects—> vasodilation and dec contractility.

118
Q

Which class of Ca2+ channel blockers acts more on vascular smooth muscle (to cause vasodilation and dec BP)? How about on the heart (to dec contractility)?

A

Dihydropyridines act on vascular smooth muscle to vasodilate (these drugs end in “-divine”).
Non-dihydropyridines act on the heart to dec contractility.

119
Q

Most common cause of subarachnoid hemorrhage is what?

A

Rupture of inter-cranial aneurysm

120
Q

Polycystic kidney disease can present with what type of aneurysm in the brain?

A

Berry aneurysms (“bubbles in the kidneys, bubbles in the brain”)

121
Q

What are 2 signs of HF?

A

Edema and SOB

122
Q

Would you put a Mobitz I AV block patient on a pacemaker? How about a Mobitz II patient?

A

Mobitz I- don’t need pacemaker (this is a AV node disease)
Mobitz II- give pacemaker bc high risk for developing into type III AV block aka full heart block (this is a His-Purkinje disease)

123
Q

What is “cardiac glycoside?”

A

Digoxin (just another name for it)

124
Q

What’s the most likely valve affected in IV drug users who develop endocarditis? What organism is most likely to cause it?

A

Tricuspid valve. Staph Aureus.

125
Q

Systolic HF is associated with what abnormal heart sound? Diastolic HF is associated with what abnormal heart sound?

A 
Systolic HF (pumping problem) is associated with S3 (blood slamming into overfilled ventricle).
Diastolic HF (filling problem) is associated with S4 (blood slamming into stiff ventricular wall).
126
Q

What does diaphoresis mean?

A

Sweating

127
Q

Explain the development of an atherosclerotic plaque (possibly leading to MI).

A

1) things like hyperlipidemia, hypertension (too much pressure on vessels overtime causes damage), hyperglycemia, and smoking trigger endothelial injury—> inc vascular permeability, WBC adhesion
2) lipoproteins (LDL) enter into the arterial wall intima layer and accumulate. Monocytes—> macrophages—> foam cells (engulf lipid particles). Platelets adhere to endothelium and become activated.
3) PDGF (platelet derived growth factor) are released from platelets, macrophages, and endothelial cells

128
Q

When you decrease contractility you decrease work on the heart. Explain.

A

Contractility is how hard the hard is pumping. If it is having to pump really hard, it will require more blood flow/ oxygen to do its work. If it doesn’t have to pump as hard/ do as much work, it won’t demand as much blood flow/ oxygen.

129
Q

What 2 things do we give Digoxin to patients for?

A

1) systolic HF (pumping problem)- digoxin acts on myocytes to increase contractility
2) a fib- digoxin also stimulates the vagus (parasympathetic) nerve to dec HR at the SA and AV node pacemaker cells, so it has anti-arrhythmic properties

130
Q

What does Inotrophy mean? What does chronotrophy mean?

A

Inotrophy means contractility (a positive Inotropic agent inc contractility). Chronotrophy means rate at the SA node (a positive chronotrophic agent inc HR).

131
Q

Why does aortic regurg lead to a widened pulse pressure?

A

Aortic regurgitation= blood flowing back from aorta into LV during DIASTOLE. At this time in diastole, there’s less blood so less pressure in the aorta, so decreased diastolic pressure. Pulse pressure= systolic BP- diastolic BP. Lower diastolic BP= wider PP.

132
Q

Why are nitrates contraindicated in patients with HOCM (hypertrophic obstructive cardiomyopathy)?

A

Nitrates decrease preload (by venodilation). A decrease in preload will make HOCM worse! (Lack of blood in the LV—> less LV expansion—> thickened septum gets in the way more, making it harder for the blood to get through aortic outflow tract. Whereas, an increase in preload expands the LV more—> pushes defect out of the way—> makes the problem not bad.)

133
Q

What does thrombocytopenia mean?

A

Low platelets

134
Q

What’s the difference between SVT (supraventricular tachycardia) and VT (ventricular tachycardia)?

A

SVT is arrhythmia that originates in the atria. VT originates in the ventricles.

135
Q

What are the layers of artery walls?

A

Intima (innermost layer)—> media—> adventitious (outer layer).
**Intima is a single layer of endothelial cells with BM. Media is smooth muscle cells and elastin. Adventitious is connective tissue, vasa vasorum (blood supply to artery wall) and nerve fibers.

136
Q

How can you treat angina?

A

Can place a stent or give a drug that will decrease O2 demand (by dec HR, contractility, afterload, or preload) since demand exceeds the supply of O2 getting through the partially occluded coronary vessel. Nitrates are the go-to angina drug bc they venodilate—> dec preload—> dec blood the heart has to push through—> dec work on heart, so heart requires less oxygen supplied by blood in coronary arteries, so occlusion becomes less of a problem.

137
Q

What is claudication?

A

Pain with activity due to ischemia (ex: temporal artery disease involves ischemia to jaw so you get pain with chewing, angina involves ischemia to heart so you get chest pain typically with exercise, peripheral artery disease involves poor blood flow/ ischemia to extremities like legs so you get leg pain when walking)

138
Q

Loud S2 heard at left 2nd intercostal space. What are you thinking?

A

Pulmonary HTN (at the location where you hear pulmonic valve and the fact that it’s loud indicates you have excess fluid)

139
Q

Wide S2 split that doesn’t change on inspiration. Murmurs going on. What are you thinking?

A

ASD. Blood is shunting from higher pressure left heart—> lower pressure right heart. So the right heart builds up pressure and the pulmonic valve will take longer to close= wide S2 split regardless of inspiration.
Murmurs can occur due to excess blood shunted over to right heart.

140
Q

What is a “tet spell”? What can help it?

A

Tet spell= cyanotic episode from Tetrology of Fallot. Rapid squatting makes it feel better because it increases afterload (from inc SVR *also inc preload) which reverses the R—> L shunt to L—> R. (Blood was being shunted from RV to aorta, but if you inc the pressure in the aorta, it will shunt from LV back to RV so more blood will get to the lungs for oxygenation)

141
Q

3 days after an MI you get a friction rub and chest pain that worsens with deep breathing/ movement. What are you thinking?

A

Fibrinous pericarditis

142
Q

Rapid heartbeats. No chest pain. EKG shows delta waves. What are you thinking?

A

WVW (Wolff-Parkinson-White Syndrome). Some excitation signals go through accessory “secret pathway” that bypasses the rate-slowing AV node—> ventricles get depolarized before they should and you see delta waves.

143
Q

An immigrant kid who is not vaccinated is most likely to have what congenital heart defect?

A

PDA from congenital rubella (ToRCHeS infection)

144
Q

If the question stem describes a baby with cyanosis and an out-of-place aorta, what are the 2 heart defects you should think of?

A

Tetrology of Fallot or Transposition of the Great Vessels.

145
Q

Persistent truncus arteriosis is due to what problem in embryo development?

A

Failure of the acorticopulmonary septum to form (from NCCs). Another way to say this is septation.

146
Q

Transposition of the great vessels is caused by what problem in embryo development?

A

Failure of the aorticopulmonary septum to spiral (the spiraling is what positions the pulmonary arteries on the right and the aorta on the left where they’re supposed to be).

147
Q

Elevated homocysteine means you can’t make what?

A

Methionine (amino acid).

If you have an enzyme deficiency that prevents the conversion of homocysteine—> Met, then homocysteine builds up.

148
Q

Think about coronary artery anatomy. What does right-dominant mean (in 85% of people)? What about left-dominant?

A 
Right-dominant= PDA comes off of the RCA.
Left-dominant= PDA comes off of the LCX (left circumflex).
149
Q

Tachycardia, irregularly irregular rhythm, no P waves, narrow QRS. What is it?

A

A fib.
No P waves means the atria are not contracting (they are just freaking out). The EKG is irregular and you have narrow QRS from the tachy (ventricles contracting rapidly, increasing HR).

150
Q

You see a low GFR. What 2 elevated lab values would you expect to see?

A

Elevated BUN and Cr.
Why? Because low GFR= kidneys not doing their job of filtering well= kidney failure.
You’d see high BUN because urea not getting filtered and becoming part of urine as much as it should, so more stays behind in blood.
You’d see high Cr bc that gets freely filtered, but you aren’t filtering as well since kidneys are damaged.

151
Q

If an atherosclerotic plaque ruptures, why does that put you at risk for MI and thrombus—> stroke?

A

Rupture of a plaque could completely occlude the vessel—> MI.
Rupture of a plaque also makes the platelets go ahhh! There’s damage to vessel wall. So they go in and form a clot to repair the damage (normal body process, though happening within the vessel wall) and if a piece of this clot breaks off and embolizes and blocks blood flow to the brain that’s a stroke.

152
Q

Elderly man. Just underwent cystoscopy a month ago. No history of heart problems but now presents with a diastolic murmur. What gram (+) organism that can grow in 6.5% bile is probably responsible?

A 
Enterococcus faecalis (or enterococcus faecium). Why? This organism is usually found in the urinary tract (often causes UTIs) so manipulation of the urinary tract (cystoscopy= scope up the bladder) can cause this bacteria to migrate to where it’s not supposed to be and cause problems, including endocarditis). 
From sketchy: “do U love trees?” —> UTIs, endocarditis, and biliary tree infection.
153
Q

How can you treat a patient with a DVT?

A

Give anticoagulants. (But if the patient has a high risk of bleeding out like history of hemorrhages in which case anticoagulant therapy is contraindicated, you can instead place an IVC filter to prevent the clot from embolizing to the lungs: DVT—> PE)

154
Q

At what spinal level do the renal veins join the IVC? At what level do the common iliac veins merge to become the IVC?

A

Renal veins join the IVC at L1-L2.

The common iliac veins merge to the IVC at L5.

155
Q

How are CO (cardiac output) and EF (ejection fraction) affected in diastolic HF? systolic HF?

A

Diastolic HF= problem filling. Lowered CO bc not filling with as much blood= not as much blood to pump out. Preserved ejection fraction bc no problems with pumping (the PERCENTAGE of the blood that is pumped out remains the same).
Systolic HF= problem pumping. Lowered CO and EF.

156
Q

What are side effects of Digoxin?

A

GI symptoms (nausea, omitting, diarrhea) & neurological symptoms (fatigue, confusion, weakness). A specific but rare side effect is changes to color vision (Xanthopsia= blurry yellow vision). Life threatening complications from digoxin toxicity include fatal arrhythmias (because it acts on pacemaker cells to dec HR in addition to acting on myocytes to inc contractility).

157
Q

Teenage athlete dies from sudden cardiac death. What is the most likely cause and what 2 findings would you see on autopsy?

A

Hypertrophic (obstructive) cardiomyopathy (HCM, of the subtype HOCM)

1) massive myocyte hypertrophy (usually at the septum, making it hard for blood to get through from LV to aorta)
2) myocyte fiber disarray (irregular arrangement of myocytes with lots of connective tissue)

158
Q

Patient with recent dental procedure and pre-existing heart condition comes in for evaluation and presents with a new murmur. The gram (+) organism that synthesizes dextrans most likely responsible for causing the new murmur will adhere where in the heart?

A

Strep viridans. Causes endocarditis. Will adhere to FIBRIN-PLATELET AGGREGATES deposited at sites of endothelial trauma.

159
Q

Most common nephrotic syndrome in kids age 2-6 is what?

A

Minimal change dz

160
Q

Little kid with recent URI presents with edema and proteinuria >3.5 g/day. What is the most likely diagnosis?

A

Minimal change dz.

161
Q

Strep Bovis (aka Step Galloclyticus) is known for causing what 2 problems?

A

1) subacute bacterial endocarditis

2) colon CA

162
Q

What is the clearance equation?

A

Clearance of X= ([X]in urine * V) / ([X]in plasma)

Where V= urine flow rate (mL/min).

163
Q

What can be used to estimate the GFR (glomerular filtration rate)? What can be used to estimate the RPF (renal plasma flow)? What is the equation for FF (filtration fraction)? What’s a normal FF?

A 
The Cl (clearance) of inulin or creatinine can be used to estimate the GFR (inulin is the gold standard bc it is freely filtered through, but creatinine is used clinically since it’s naturally occurring in the body—it slightly overestimates since a tiny bit is secreted/ added into kidney tubules). 
The Cl of PAH can be used to estimate the RPF. 
FF= GFR/ RPF (what’s getting filtered divided by total flow of blood) 
Normal FF= 20%.
164
Q

Laboratory studies of post-strep GN would show what?

A

Elevated titers of strep antibodies and decreased levels of complement C3 (due to consumption).

165
Q

What drug can be given to treat HTN and at the same time, help with migraine headaches?

A

Beta blocker

166
Q

How do beta-blockers help treat HTN?

A

They inhibit the beta-1 receptor (stimulates renin release by the kidney)—> dec renin—» dec BP

167
Q

Why isn’t it a good idea to give a beta-blocker to treat HTN in a patient with a low HR?

A

A beta-blocker will dec HTN, but will also dec HR. So if you give it to someone who is already bradycardic, you can dec HR too much= bad!

168
Q

What heart problem can cause head-bobbing?

A

Aortic regurgitation (due to wide pulse pressure from high systolic BP and low diastolic BP)

169
Q

Enlargement of what chamber of the heart can compress the esophagus leading to dysphagia (difficulty swallowing)?

A

The left atria (the LA resides on the posterior surface of the heart and is adjacent to the esophagus).

170
Q

Class 3 antiarrythmic drugs (and class 1a) lengthen the QT interval and therefore come along with the adverse effect of Torsade de Pointes. Of the class 3 drugs, which is known for being the safest/ least likely to cause Torsade de Pointes?

A

Amiodarone

171
Q

What 2 things are risk factors for developing aortic stenosis?

A

Old age (calcifications) and bicuspid aortic valve (normally the aortic valve is tricuspid)

172
Q

How do elderly people with aortic stenosis get the calcifications on their aortic valve?

A

Calcifications grow on damaged/ necrotic tissue from old age in the setting of normal calcium levels in the blood (has nothing to do with having hypercalcemia).

*Metastatic calcifications tend to form in the setting of hypercalcemia, but these tend to deposit in other organs—not the heart.

173
Q

What is the difference between hypertensive urgency and emergency?

A

Both defined by BP > 140/90 but in hypertensive urgency, there is no evidence of end-organ damage. In hypertensive emergency, there is.

174
Q

What are the 2 equations to calculate cardiac output (CO)? The easy one and Fick’s principle.

A

CO= SV* HR

Fick’s principle: CO= (rate of oxygen consumption) / (arterial oxygen content - venous oxygen content)

175
Q

How would age-related stiffness of the aorta affect BP?

A

It would increase systolic BP, but not affect diastolic BP. So you’d see isolated systolic hypertension.

176
Q

What 3 symptoms (Beck’s triad) may be found in a patient with cardiac tamponade?

A

Hypotension (low BP), distended neck veins (elevated JVP), and distant heart sounds.

*in cardiac tamponade, the heart is compressed by fluid and is “swinging around”. Usually due to trauma—> pericardium doesn’t have time to stretch so even just a little fluid in the sac can restrict filling of the heart—> low CO—> low BP. You get low-voltage QRS on EKG and pulses paradoxus (low amplitude of systolic BP >10 during inspiration).

177
Q

Lady had an MI and 5 days later died suddenly. How?

A

Most likely due to rupture of the ventricular free wall (4-7 days post-MI)—> hypotension and sudden death.

178
Q

A patient has a dilated coronary sinus. What’s the most likely cause of this?

A

Pulmonary hypertension. Why? The coronary sinus is the big vein on the posterior side of the heart that drains blood from the heart. It empties into the right atrium (RA), so anything that increases the pressure within the RA will dilate the coronary vein. Pulmonary hypertension= backing up of fluid into the lungs—> backs up further to right heart—> more pressure in RA—> dilated coronary sinus draining into the RA.

**note: coronary artery disease would NOT affect the size of the coronary sinus vein.

179
Q

Young guy comes in with fatigue, crackles upon lung auscultation, elevated JVD, and lower extremity edema. He recently got over a viral infection. What is the most likely diagnosis?

A

VIRAL MYOCARDITIS—> leading to DILATED CARDIOMYOPATHY (systolic dysfunction/ pumping problem)

Crackles indicate backing up of fluid from left heart to lungs. High JVD and edema indicate further backing up of fluid from lungs to right heart to venous system (left-sided HF—> pulmonary edema—> right-sided HF). Fatigue is from heart not adequately pumping blood for oxygen to be delivered to tissues to supply energy. This is the picture of end-stage CHF, but this dude is young and recently had a virus. Viruses like Coxsachie, adenovirus, and influenza are capable of damaging the heart muscle leading to this (rare).

180
Q

What class of drugs are helpful to give to patients with vasospasm (Prinzmental angina, Raynaud phenomenon)?

A

Ca2+ channel blockers

181
Q

What drugs are a good pick to treat both BPH (benign prostatic hyperplasia) and HTN?

A

Alpha-1 blockers

Alpha-1 receptors such as Doxazosin, Prazosin, and Terasonin (sympathetic) will lead to urinary retention (you don’t want to pee in a fight or flight situation) and vaso/venoconstriction—> inc BP (again, think fight or flight). SO…blocking alpha-1 means peeing and dilating vessels—> dec BP. This is exactly what you want to treat BPH and HTN.

182
Q

ArteriOLOsclerois (thickening/ narrowing of the small arterioles) is divided into hyaline (hyaline membranes from protein leakage into the vessel walls) and hyperplastic (thickened vessel walls by hyperplasia of smooth muscle). BENIGN HTN or diabetes would cause which? MALIGNANT HTN would cause which?

A 
Benign HTN or diabetes—> hyaline arteriOLOsclerosis
Malignant HTN (severe HTN with end-organ damage)—> hyperplastic arteriOLOsclerosis
183
Q

Orthopnea is a sign of what?

A

Left-sided heart failure

(Orthopnea= backing up of fluid from failing left heart into lungs—> pulmonary edema and you have to sleep with multiple pillows to breathe well. This is a noticeable problem upon laying down, not standing up, because when you stand up gravity pulls some fluid down. When you lay, your vessels are now on an even plane and backing up of fluid is able to happen more with left-sided HF.)

184
Q

Why syndrome can lead to dextrocardia, meaning the heart is placed on the right side of the chest instead of the left? Why?

A

Kartagener syndrome, which is a defect of the dynein arm of cilia. Cilia are required to move the heart over ride—> left side during development, so if they are defected you get a heart that remains on the right side (also you can get infertility in men due to sperm immobility and sinus infections due to defected mucociliary escalator to push gunk out)

185
Q

What is the most common congenital cardiac anomaly, usually occurring in the membranous septum?

A

Ventricular septal defect (VSD)

186
Q

Transposition of the Great Vessels, Tetrology of Fallot, and Persistent Truncus Arteriosus can arise from failure of what type of cells to migrate during development?

A

NCCs (neural crest cells).

NCCs and endocardial cells migrate—> truncal and bulbar ridges spiral and fuse to form the septum separating the pulmonary artery and aorta. If this process is disrupted, you get truncal abnormalities (problems involving the pulmonary arteries/ aorta).

187
Q

What are the names of the 3 shunts in cardiac embryo?

A
  1. Ductus venousus
  2. Foramen ovale
  3. Ductus arteriosus (PDA)
188
Q

What happens to SVR (systemic vascular resistance), PVR (pulmonic vascular resistant), RA pressure, and LA pressure before and after birth (higher or lower)?

A

In utero: low SVR, high PVR (lungs filled with amniotic fluid), high RA pressure, low LA pressure (everything is flipped—right heart has more pressure than left)
After birth: high SVR, low PVR (lungs filled with air), low RA pressure, high LA pressure (left heart is higher pressure bc it has to pump to whole body, not just lungs)

189
Q

What are the postnatal derivatives of the following: ductus arteriosus and ductus venosus (after birth once these structures “go away” what are their remnants called)?

A

Ductus arteriosus—> ligamentum arteriosum

Ductus venosus—> ligamentum venosum

190
Q

If someone is stabbed in the heart from the front side, which chamber is most likely to be penetrated? What about from the back side?

A

The right ventricle in the front. Left ventricle in the back.

Remember the orientation of the heart in the chest. On the anterior side, the RV takes up most space, but there’s also the RA and the LV. On the posterior side, the LV takes up most space, but there’s also the RA (the RA is the one heart chamber that cannot be seen from the front side).

191
Q

What are the 2 equations for mean arterial pressure (MAP)?

A
  1. MAP= CO * resistance (TPR or SVR)

2. MAP= 2/3(diastolic BP) + 1/3(systolic BP)

192
Q

What is the equation for wall stres and wall thickness of the ventricle (LaPlace’s law)?

A

Wall stress (proportional to tension)= (pressure * radius)/ (2 * wall thickness)

193
Q

Which blood vessels account for most of the TPR (total peripheral resistance)? Which vessels provide the most blood storage capacity?

A

Arteriole account for most of the TPR (largest BP drop across these vessels).
Veins provide most of the blood storage capacity.

194
Q

What is orthopnea?

A

Discomfort, hard to breathe when laying down flat (from HF—> pulmonary HTN)

195
Q

Dobutamine is given to a HF patient. Why? What mechanism of action does it use?

A

Dobutamine is primarily a beta-1 agonist (beta-1 > beta-2, alpha) so it inc HR, contractility, and BP. It can help with HF (systolic dysfunction/ pumping problem) by increasing contractility. It uses Gs GPCR pathway—> activates adenyl cyclase—> inc cAMP—> PKA—> inc Ca2+ (contractility) in heart, inhibits myosin light chain kinase in smooth muscles to dilate.

196
Q

Pulmonary capillary wedge pressure measures approx. pressure in which chamber of the heart?

A

The Left Atrium
(catheter is advanced through the IVC—> RA—> RV—> pulm arteries where it can approximate the pressure of the LA to see how well the heart is working).

197
Q

What are the side effects of Digoxin?

A
  1. GI symptoms (like vomiting)
  2. neurological symptoms
  3. Color vision issues

*also causes hyperkalemia and low HR (see FA page 307 for channels it acts on)

198
Q

What heart problem can lupus cause?

A

Endocarditis

199
Q

Wide, fixed splitting of S2 (doesn’t change with inspiration). What are you thinking?

A

ASD (atrial septal defect).
In ASD, you have a left-to-right shunt (blood from higher pressure LA goes into RA). Since you always have more blood flow to the right heart, you always have delayed pulmonic valve closure (aortic valve closes, then pulmonic valve) regardless of breath.

200
Q

Explain the psychological splitting of S2.

A

You breathe in (inspiration) and diaphragm moves down (neg pressure)—> inc venous return—> more blood to right heart (RA—> RV)—> delayed closure of the pulmonic valve—> aortic valve closes in S2, then pulmonic valve slightly after

201
Q

In what 2 conditions do you hear wide splitting of S2 (exaggeration of the normal “physiological splitting of S2”)?

A 
Pulmonic stenosis (problem opening pulmonic valve, so it will also close later) and right bundle branch block (RV takes longer to contract bc it has to wait for the LV to send the signal over, and since the RV contraction is delayed the pulmonic valve opening is delayed).
*In these cases, the split is even bigger during inspiration.
202
Q

What is paradoxical splitting and in which 2 conditions is it heard?

A

Paradoxical splitting is closure of the aortic valve before the pulmonic valve in S2 (since inspiration causes the pulmonic valve to close before the aortic valve, inspiration will make it to where there’s less of a physiological split). This occurs in aortic stenosis (problem opening the aortic valve, so it will also close later) and left bundle branch block (LV takes longer to contract bc it has to wait for the RV to send the signal over, and since LV contraction is delayed the aortic valve opening and closing is delayed too).

203
Q

What is the inheritance pattern of HOCM (hypertrophic obstructive cardiomyopathy)?

A

Autosomal dominant

204
Q

What is “sputum with light pink color” suggestive of?

A

CHF

205
Q

What does “hibernating myocardium” mean?

A

LV systolic dysfunction (pumping problem) due to reduced coronary blood flow at rest that is partially or completely reversible by revascularization.

206
Q

After total ischemia (like in an MI), how long does it take for the heart (cardiac myocytes) to stop contracting (due to lack of blood= lack of oxygen= lack of ATP/ energy to contract)?

A

Within 60 seconds! (This is why heart attacks are sudden and happen fast).
*note: ischemic injury can be reversible within 30 min (you give back blood and fix the problem and contractility will come back with time, just maybe not as good as it was before). But after 30 min, it becomes irreversible.

207
Q

What is Endothelin 1?

A

A vasoconstrictor within endothelial cells.

208
Q

Guy breaks a long bone or pelvic bone in an automobile accident. Now presents with hypoxemia, confusion, and petechial rash. What happened?

A

Fat emboli—> PE

209
Q

Explain Reynaud phenomenon (associated with smoking).

A

“Red white and blue syndrome”

White—> cut blood supply to fingers/ toes (most distal points blood has to flow too)
*this is usually triggered by the cold bc cold—> sympathetic response and vasoconstriction (dec blood flow) of vessels supplying skin so blood can be more available to more critical organs)

Blue—> cyanosis (blood supply/ Oxygen has been cut for too long)

Red—> re-perfusion (usually when patient warms hands coloration will return due to vasodilation, inc blood flow)

210
Q

What is the major determinant of symptom severity in a patient with Tetrology of Fallot?

A

The degree of RV outflow tract obstruction (how stenotic the pulmonic valve is) is the major determinant of R—> L shunting and cyanosis (how severe).

211
Q

Blowing diastolic murmur accompanied by a wide pulse pressure (patient can feel palpitations) and head bobbing. What is it?

A

Aortic regurgitation!

212
Q

Mitochondrial vacuolarization is a sign of irreversible cell injury. What does this even mean?

A

The involved mitochondria are permanently unable to make ATP.

213
Q

What parameter is DECREASED during exercise?

A

Systemic vascular resistance (SVR)

Due to vasoDILATION to muscles

214
Q

Talking about acute pericarditis, what are common symptoms/ signs that point to the diagnosis? What’s the difference between fibrinous pericarditis, hemorrhagic pericarditis, and purulent pericarditis?

A

Pericarditis= inflammation of the pericardium (sac surrounding the heart). Patients get sharp chest pain that can radiate to shoulder or back, gets worse on inspiration, and gets better when they lean forward. You hear a friction rub on auscultation. EKG has ST elevations all over (inflammation is all over, there’s not just ST elevations corresponding to one affected area of the heart as in an MI).
FIBRINOUS- most common, pericardium is filled with fibrin-containing exudate (due to viral infection like Coxaschie, MI, uremia, lupus, RA)
HEMORRHAGIC- pericardium is filled with blood mixed with fibrinous exudate (due to cancer, TB, coagulation problem, post-surgery)
PURULENT- from an active bacterial infection going on in the pericardial space (staph, strep)

215
Q

Women had joint pain and a rash a week ago, no significant medical or family history. Presents now with chest pain radiating to left shoulder, friction rub, and ST elevations all over in her EKG. Diagnosis?

A

Fibrinous pericarditis (most likely due to lupus).

216
Q

Patient has nodules in the apex of their lungs, which is confirmed to be a type of pneumoconioses. What occupational exposure would this be due to?

A

Silicosis (remember this is the one where you get APICAL lung nodules!, inc risk for TB)

217
Q

Which pneumoconioses increases risk for TB?

A

Silicosis (remember this is the one where you get APICAL lung nodules!, inc risk for TB)

218
Q

A guy is a sandblaster for his work. He presents with “eggshell calcification” in upper lungs. What is this?

A

Silicosis (pneumoconioses from occupational exposure of silica)

219
Q

How can COPD lead to isolated right sided heart failure, or cor pulmonale?

A

COPD—> widespread vasoconstriction in the lungs to shunt blood away from poorly ventilated areas and to better ventilated areas (though the lungs are all kinda bad in COPD)—> increases hydrostatic pressure in the vessels of the lungs—> fluid leaks out and backs up to right side of the heart

220
Q

In COPD or another pathology that leads to backing up of fluid and right-sided HF, it is possible that the patient does NOT have peripheral edema. Why is this?

A

Increased tissue lymphatic drainage

221
Q

How can sleep apnea cause pulmonary HTN and right-sided HF?

A

Sleep apnea involves episodes where the individual stops breathing at night (usually due to obstruction from having excess fat in the neck or big tonsils, etc.)—> poor oxygenation to lungs (low O2, high CO2)—> vasoconstriction in lungs to shunt blood away from poorly ventilated areas (in effort to get good V/Q, or ventilation/ perfusion, matching)—> pulmonary HTN (bc vasoconstriction increases BP)—> high hydrostatic pressure leads to fluid leakage from vessels—> backing up of fluid to right heart

222
Q

Vasodilation is accomplished by Nitric Oxide (NO) release. NO is made from what amino acid?

A

Arginine.
*note: for this reason, Arginine can be given as a supplement to help with conditions that improve by vasodilation, like angina (take work off the heart)

Block 7 (5 decks)

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