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CVS > Review Q's Week 3 > Flashcards

Review Q's Week 3 Flashcards

1. physio of cardiac cycle (1-29) 2. pathology of myocardium + myocarditis & cardiamyopathies (30-62) 3. phy regulation of cardiac volume (63-88) 4. hypertension management pharma (89-107) 5. anatomy lab 1 structure of heart (108-120) 6. physio regulation of contraction of cardiac muscle (121-153) 7. physio Cardiac Out (154-178) 8. drugs to treat HF (179-199) 9. pathology practical 1 CF (200-211) 10. clinical med HF (212-243) 11. seminar 4 physio cardiac function (244-264)

1
Q

In which stage are the semilunar valves open?

a. diastole
b. systole

A

b. systole

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2
Q

In which stage does the blood flow out of the ventricles?

a. diastole
b. systole

A

b. systole

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3
Q

T/F: blood flow from the ventricles is continuous

A

false, its pulsatile

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4
Q

T/F: blood flow to the body is continuous

A

true, this is due to aortic storage

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5
Q

When do the atria contract?

A

at the end of ventricular filling, phase 1 in the cardiac cycle

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6
Q

How long does the cardiac cycle last? (in 75bpm) and how is it divided into systole and diastole?

A
  1. 8sec per cycle
  2. 5 diastole and 0.3 systole
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7
Q

How do you calculate stroke volume?

A

EDV - ESV=SV

EDV= end diastolic volume (the max amount of blood in the heart)

ESV= end systolic volume (the one third of blood left in the ventricle after ejection)

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8
Q

When does ventricular ejection begin?

A

When the left ventricle pressure is higher than the aortic pressure

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9
Q

When do the semilunar valves close?

A

When the atrial pressure is higher than ventricular pressure

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10
Q

When do the AV valves open?

A

when ventricular pressure is bellow atrial pressure

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11
Q

What sound is made when the AV valves close?

a. lub
b. dub

A

a. lub

(S1)

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12
Q

During isovolumic/isovolumetric contraction, what occurs to pressure and volume?

A

increase in pressure

no change in volume

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13
Q

During rapid ejection of the ventricles, what is happening in the atria?

A

the pressure begins to rise as blood fills it

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14
Q

What heart sounds can be heart in children?

A

S1, S2, S3 (S3 because their ventricles are smaller and more compliant, not due to pathology)

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15
Q

Why does the S3 heart sound (aka ventricular gallop) occur?

A

The S3 sound is produced by a large amount of blood striking a very compliant left ventricle.

S3= often a sign of systolic heart failure

Heard in: congestive heart failure+dilated cardiomyopathy

(it’s also heard normally in children and well-trained athletes because of the compliance of the ventricles)

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16
Q

Why does the S4 heart sound (aka atrial gallop) occur?

A

If the left ventricle is noncompliant, and atrial contraction forces blood through the AV valves, S4 sound is produced by the blood striking the left ventricle.

S4 = sign of diastolic heart failure

Heard in: left ventricular hypertrophy or any condition that makes the ventricles stiffer

(very rarely occurs in normal conditions, unlike S3)

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17
Q

Which phase of the cardiac cycle does the AV valves close?

A

phase 2

(Isovolumic contraction)

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18
Q

Which phase of the cardiac cycle do the semilunar valves open?

A

phase 3

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19
Q

Which condition causes murmurs to start at the beginning of systole and continues throughout diastole?

A

Patent ductus arteriosus

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20
Q

What causes the blood flow to continue from the ventricle to the aorta?

A

Kinetic energy (this occurs during reduced ejection- which is phase 4- not rapid ejection)

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21
Q

Which phase of the cardiac cycle do the AV valves open?

A

phase 6

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22
Q

What conditions cause holosystolic (pansystolic) murmurs?

A

mitral/tricuspid regurgitation + ventricular septal defect

holosystolic= high amplitude throughout systole

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23
Q

Which condition causes mid-systolic murmurs?

A

aortic or pulmonic stenosis

mid-systolic murmurs= starts softly and become loudest near mid-systole then decrease

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24
Q

What percent of the ventricular filling is due to the atrial kick when patient is at rest VS during exercise?

A

At rest, the atrial kick is responsible to 20% but during exercise it does up to 40%

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25
Q

Which 2 areas reach maximum systolic pressure?

A

aorta and pulmonary artery

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26
Q

When does isovolumetric relaxation occur?

A

at the beginning of diastole, phase 5

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27
Q

Systolic murmurs versus Diastolic murmurs

A

Systolic murmurs= occur between S1 and S2

Diastolic murmurs= occur after S2

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28
Q

Which of the following causes a mid/ late diastolic murmur?

a. aortic stenosis
b. pulmonic stenosis
c. mitral stenosis

A

c. mitral stenosis

(A&B cause mid-systolic murmur)

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29
Q

Which of the following causes a diastolic murmur?

a. mitral regurgitation
b. aortic regurgitation
c. tricuspid regurgitation

A

b. aortic regurgitation

(A&B= Holosystolic murmur)

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30
Q

What kind of heart failure is expected after long-standing pulmonary hypertension?

A

Right ventricle failure

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31
Q

What are two causes of increased pressure in the ventricles?

A

systemic increase in pressure (systemic hypertension) OR a valvular stenosis

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32
Q

What’s the most common cause of weakening of the heart muscles, leading to a weaker pump?

A

myocardial infarction/ ischemia

(AKA commonest cause of left ventricular failure)

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33
Q

What’s the best way to check for cardiomegaly?

A

chest X ray

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34
Q

Previous MI patient comes in pregnant, what should you be wary of?

A

cardiac failure; pregnancy (as well as infection) is a contributory factor to cardiac failure due to the increased cardiac output. Monitor patient carefully.

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35
Q

What are some signs and symptoms of cardiac failure (left ventricular failure)?

A

less oxygen to tissue → hypoxia

less blood to brain→ loss of consciousness

less blood to heart→ arrhythmia or ischemia

less blood to kidney→ renal failure/no urine

less blood to liver→ high hepatic enzymes

+ cyanosis in extremities

+ pulmonary edema because the right heart isn’t taking the blood back from the lungs

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36
Q

What’s the cardinal sign of right ventricle failure?

A

raised jugular venous pressure (blood in veins doesn’t get drained)

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37
Q

What’s the most common cause of right ventricular failure?

A

left ventricular failure

after the L ventricle fails, blood pools in the lungs and the right heart has to push against the high force until it also fails (biventricular failure)

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38
Q

Patient with known heart condition comes in complaining of shortness of breath, which side of the heart is most likely compromised?

A

Left side; left ventricular failure. The left side brings the blood from the lungs to the heart, so when this is compromised the blood stays in the lungs and causes pulmonary edema

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39
Q

Which causes hepatomegaly and splenomegaly?

a. left heart failure
b. right heart failure

A

b. right heart failure

(as well as edema and ascites)

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40
Q

A patient has left ventricular failure and pulmonary edema. Suddenly, the pulmonary edema improved. What caused this to happen?

A

the right ventricle also failed and is now NOT pushing blood to the lung, thus causing the edema to improve.

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41
Q

A patient has an MI and comes in days later with SOB. Diagnose.

A

histology shows fluid build up in alveoli. Left ventricular failure due to weakened muscle (because of MI)

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42
Q

Which causes cyanosis and renal failure?

a. left heart failure
b. right heart failure

A

a. left heart failure

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43
Q

diagnose

A

chronic pulmonary congestion (irreversible and high mortality rate)

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44
Q

What is this?

A

nutmeg…

(nutmeg liver is a sign of chronic venous congestion)

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45
Q

Diagnose. Where is this histology sample from? What are the dark shapes in it?

A

Left ventricular failure (chronic systemic venous congestion)

sample from spleen, congestive splenomegaly

Gamna-Gandy bodies

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46
Q

What are the three criteria needed to diagnose myocarditis?

A

no ischemia

inflammatory infiltrate

necrosis

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47
Q

23 y/o patient comes in with cardiac failure symptoms (ex/ pulmonary edema) What do you suspect?

A

obviously you need more data but due to age you can assume it’s myocarditis, not ischemia (which is common among the elderly)

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48
Q

T/F: myocarditis can be diagnosed clinically

A

false, it can be suspected clinically, but it needs tests to prove it (ex/ MRI, Xray, histology, FISH, PCR, blood tests, culture)

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49
Q

What’s the treatment for myocarditis?

A

usually observation, unless the cause is bacterial then antibiotics

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50
Q

Describe the size of the heart

A

cardiomegaly; heart should be half (or less) of maximal horizontal thoracic diameter

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51
Q

19 y/o patient comes in with coughing, shortness of breath, and palpitations. He states that he had a fever days ago. Blood tests reveal leukocytosis. Whats the most likely diagnosis.

A

myocarditis

it’s hard to diagnose, but viral cause is most common cause and the fact that he has inflammation (leukocytosis) can help point you to the right direction.

(coughing and shortness of breath= pulmonary edema)

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52
Q

Diagnose this cardiac histology slide

A

toxoplasmosis myocarditis

(Toxoplasma gondii parasite= get it by eating undercooked contaminated meat or from exposure from infected cat feces)

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53
Q

Diagnose this cardia histology slide of a 25 y/o Brazilian man

A

chaga’s disease

Trypanosoma Cruzi; spread mostly by insects known as Triatominae

(common cause of myocarditis in south America)

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54
Q

Patient comes in with rapidly progressing symptoms of swelling of the ankles, chest pain, heart palpitations, and fatigue. Doctor thought he has TB or sarcoidosis, but tests revealed both those negative. Diagnose.

A

giant cell myocarditis

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55
Q

Tests show all the chambers of the heart are dilated. diagnose

A

Dilated Cardiomyopathy Definition

(heart muscle is weakened and cannot pump effectively)

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56
Q

35 y/o man died suddenly due to a heart condition. diagnose.

A

Hypertrophic Cardiomyopathy

thick left ventricle/septum leads to obstruction of the blood flow into the aorta

histology shows microfiber disarray (this is due to genetic disorder)

(he said to think of this when sudden death of relatively young man)

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57
Q

diagnose

A

dialated cardiomyopathy

all chambers are hypertrophied

fibrosis + Loss of myofibrils

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58
Q

Patient with diastolic failure and amyloid and hemosiderin deposits in heart. diagnose.

A

restrictive cardiomyopathy

(rigid ventricular wall causes impaired filling= diastolic failure because it can’t relax. This causes the atria to work harder and dilate over time.)

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59
Q

21 y/o previously healthy Italian male comes in with arrhythmia and palpitation. Strong family history of heart conditions. Diagnose.

A

Arrhythmogenic Right Ventricular Cardiomyopathy

Italian/ Mediterranean= disease more common in that region

the disease is autosomal dominant

Right ventricle failure due to lipid deposition

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60
Q

Which (1 or more) cardiomyopathy causes arterial dilation?

a. Restrictive cardiomyopathy
b. Arrhythmogenic right ventricular cardiomyopathy
c. Hypertrophic cardiomyopathy
d. Dilated cardiomyopathy

A

a. Restrictive cardiomyopathy (atria dilated only)

+

d. Dilated cardiomyopathy (all chambers dilated)

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61
Q

Which (1 or more) cardiomyopathy is due to myofiber disarray?

a. Restrictive cardiomyopathy
b. Arrhythmogenic right ventricular cardiomyopathy
c. Hypertrophic cardiomyopathy
d. Dilated cardiomyopathy

A

c. Hypertrophic cardiomyopathy

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62
Q

Which (1 or more) cardiomyopathy has a diastolic error/dysfunction?

a. Restrictive cardiomyopathy
b. Dilated cardiomyopathy
c. Hypertrophic cardiomyopathy

A

a. Restrictive cardiomyopathy

ventricles stiff so they don’t expand fully

B= systole problem because the heart is weak due to all the chambers being dilated

C= systole problem because the ventricle has hypertrophied causing a low volume of blood. This causes an obstruction during contraction.

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63
Q

Describe the relationship between preload and stroke volume

A

directly proportional

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64
Q

Describe the relationship between afterload and stroke volume

A

inversely proportional

wide aorta→ high afterload → low aortic pressure → low stroke volume

narrow aorta→low afterload→high aortic pressure→high SV

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65
Q

How is the force of contraction determined?

A

preload and inotropy

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66
Q

When does preload = end-diastolic volume?

A

right before contraction, the start of systole

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67
Q

What increases VS decreases preload?

A

increase= fluids (they increase ventricular stretch)

decrease= diuretics (less water, less volume, less stretch)

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68
Q

relationship between venous return and preload

A

directly proportional (duh)

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69
Q

Describe what occurs to stroke volume when the aorta is more compliant.

A

the stoke volume increases

SV= EDV - ESV (original)

↑SV= EDV - ↓ESV

(the SV increased by decreasing the end-systolic volume, which is the volume of blood in a ventricle at the end of contraction/systole. The ventricle was able to push more blood out since the aorta is compliant, so it had less blood left at the end)

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70
Q

Describe the effect of increased venous return on the stroke volume.

A

increased venous return → increase stretch of cardiomyocytes → increases the preload → increase SV

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71
Q

explain why the stroke volume is unable to make a remarkable increase after a certain point?

A

the pericardium that acts to protect the heart stops in from stretching further. (stops the linear relationship between SV and preload)

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72
Q

T/F: more overlap between myosin and actin always means stronger contraction

A

false, when there’s complete overlap or no overlap the contraction power will be decreased

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73
Q

How can stroke volume increase without EDP or preload increase?

A

the contractility of the ventricles (inotropy) may change and directly increase the SV, while the preload and EDP remain unchanged.

***length independent SV increase***

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74
Q

Using what mechanism does contractility change?

A

via Ca channels

Ca comes in from extracellular space (in phase 2)

Ca increases when it comes from the sarcoplasmic reticulum

troponin C sensitivity to Ca is increased

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75
Q

Describe the relationship between afterload and stroke volume

A

inversely proportional

(more afterload more resistance against ejection, less stroke volume)

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76
Q

How does increasing afterload decrease stroke volume?

A

by increasing the end-systolic volume (it increases because of higher resistance, lower shortening speed, more energy needed to open aortic vales, etc.)

SV= EDV - ESV (original)

↓SV= EDV - ↑ESV

(the ESV increases along with afterload, decreasing SV)

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77
Q

T/F: increasing the afterload decreases the cardiac output of every heart equally

A

False; cardiac output (CO) of a healthy heart isn’t as affected as the CO of a heart with dysfunction

(more dysfunction in heart = more CO decrease when afterload increases)

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78
Q

Which of the following points is when the aortic valve closes?

A

1

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79
Q

Which of the following points is when the mitral valve opens?

A

3

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80
Q

In of the following intervala is when ventricular filling occurs?

A

D

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81
Q

In of the following intervals is when isovolumic contraction occurs?

A

C

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82
Q

Which of the following points is preload?

A

4

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83
Q

Which of the following points is afterload?

A

2

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84
Q

What occurs when the pressure-volume loop is shifted to the left?

A

reduced end systolic volume

increased SV

increased inotropy

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85
Q

What occurs when the pressure-volume loop is shifted to the right?

A

increase end-systolic volume

increase end-diastolic volume

increase afterload

(this heart is a failing/dilated heart)

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86
Q

What occurs to cardiac efficiency with less oxygen uptake?

A

increased efficiency

CE = CW/O2uptake

(CE= cardiac efficiency)

(CW= cardiac work)

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87
Q

Which ventricle has higher cardiac work?

A

left ventricle

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88
Q

How does aortic stenosis affect cardiac efficiency?

A

aortic stenosis increases the pressure, and that increases the stroke work. Stroke work is directly proportional to O2 consumption. Higher O2 consumption decreases cardiac efficiency.

↑SW = SV x ↑MAP

↑ SW= ↑ O2 demand

↓CE = CW/ ↑O2uptake

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89
Q

Which system is for short term blood pressure control?

a. sympathetic nervous system
b. renin-angiotensin-aldosterone system

A

a. sympathetic nervous system

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90
Q

How do diuretics work in the short term versus the long term?

A

short term= decrease plasma volume + cardiac output

long term= vasodilation & decreased vascular resistance

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91
Q

What are the side effects of diuretics

A

Hypokalemia + Hyperglycemia (cause a reduction in insulin secretion)

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92
Q

Which is a renin inhibitor?

a. chlorothiazide
b. hydrochlorothiazide
c. furosemide
d. aliskiren

A

d. aliskiren

(the rest are diuretics)

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93
Q

What are some ACE inhibitors? Why do they not work in some individuals?

A

captopril, enalapril, lisinopril

Don’t work in some people because the ACE enzyme isn’t the only one capable of making angiotensin 1 to 2

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94
Q

What is the main side effect of ACE inhibitors? explain the mechanism.

A

dry cough

ACE destroys bradykinin, and since we’re blocking ACE, bradykinin builds up and causes the coughing.

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95
Q

What are two angiotensin II receptor blockers? What do they specifically block?

A

losartan, telmisartan

they block the AT1 receptors to stop angiotensin 2 stimulation

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96
Q

Orthostatic hypotension is a side effect of angiotensin 2 receptor blockers. explain the mechanism.

A

the blockers prevent contraction of veins

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97
Q

Which of the following Ca channel blockers is a nondihydropyridine?

a. Nifedipine
b. Verapamil
c. Amlodipine
d. Diltiazem

A

b. Verapamil

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98
Q

Which Ca channel blockers is a smooth muscle selective?

a. Nifedipine
b. Verapamil
c. Amlodipine
d. Diltiazem

A

a. Nifedipine

+

c. Amlodipine

(the Dihydropyridines)

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99
Q

Which Ca channel blockers can occasionally cause the heart rate to slow too much?

a. Nifedipine
b. Verapamil
c. Amlodipine
d. Diltiazem

A

b. Verapamil

(the nondihydropyridine, because its cardioselective)

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100
Q

Which Beta Adrenoceptor Blocking Agent is nonselective?
a. Propranolol

b. Atenolol

A

a. Propranolol

Atenolol= beta-1 adrenoceptor selective

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101
Q

Antagonism of which receptor causes a side effect of bronchospasm?

a. Alpha 1 Adrenoceptor
b. Alpha 2 Adrenoceptor
c. Beta 1 Adrenoceptor
d. Beta 2 Adrenoceptor

A

d. Beta 2 Adrenoceptor

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102
Q

Which drugs relax the muscles around the bladder and prostate?

A

Alpha-1 Adrenoceptor Blocking Agents=

Doxazosin, Prazosin, Terazosin

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103
Q

What type of drug is Carvedilol? When is it contraindicated?

A

it’s an alpha and beta-blocker (along with Labetalol), anti-oxidant, anti-inflammatory

contraindicated in conditions including bronchial asthma and severe bradycardia

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104
Q

Which drug is used to treat pregnancy-induced hypertension?

A

Methyldopa

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105
Q

What type of drugs are Alpha-Methyldopa + Clonidine? How do they work?

A

Centrally acting Alpha-2 Adrenergic Agonists

They stimulate alpha-2 receptors within the medulla, preventing the release of noradrenaline

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106
Q

What’s the side effect of direct vasodilators (EX/Hydralazine + Nitrates)

A

headache, swelling in the lower legs

107
Q

Minoxidil side effect

A

excessive hair growth

108
Q

Which site do vasodilators mostly act on?

A

mostly in arteries and arterioles (bind to vascular smooth muscle cell and relax them)

109
Q

identify 1-3

A

1 Superior vena cava

2 Right atrium

3 Inferior vena cava

110
Q

identify 4-7

A

4 Aortic arch

5 Main pulmonary artery

6 Left atrial appendage

7 Left ventricle

111
Q

compare A to B

A

A is the endocardium, its more pale, less dense, and has less intercalated discs

B is the myocardium, its more dense, has branched fibers, and more intercalated discs

112
Q

What are the nuclei identified in the figure?

A

they’re the nuclei of parasympathetic ganglionic cells

113
Q

Is this ventricular septal defect a membranous or muscular defect?

A

muscular septal defect

114
Q

Where is the coronary sulcus? What two things does it divide?

A

The atria of the heart are separated from the ventricles by the coronary sulcus

(AKA coronary groove, auriculoventricular groove, atrioventricular groove, AV groove).

115
Q

What is the interventricular groove and what two structures does it separate?

A

It’s a furrow on the anterior and posterior surfaces of the heart that marks the boundary between the right and left ventricles

116
Q

Which is a direct branch of the aorta?

a. Right common carotid artery
b. Left common carotid artery

A

b. Left common carotid artery

(and the Left subclavian artery)

the right’s come from the brachiocephalic trunk

117
Q

What are the two prominent anastomoses in the heart?

A

between the anterior and posterior interventricular arteries

between the circumflex artery and the terminal branch of the right coronary artery

118
Q

Identify A, B, C

A

A= brachiocephalic trunk

B= L common carotid artery

C= L subclavian artery

119
Q

between which layers of the heart do the arteries lie?

A

between the epicardium and muscle

120
Q

Which veins of the heart drain directly into the right atrium? (instead of the to the coronary sinus)

A

anterior cardiac veins

121
Q

moderator band?

A

A thick muscular ridge only found on the right ventricle. Travels from the ventricular septum to the base of the anterior papillary muscles.

* the right branch of the AV bundle does through the moderator band

122
Q

Why do the papillary muscles get conduction signals before the rest of the ventricle?

A

they need to be used to keep the tricuspid valve closed before the contraction of the ventricles occurs.

123
Q

Dihydropyridine channels are also known as

A

L-type calcium channels

124
Q

T/F: pacemaker cells don’t have sarcomeres

A

true

125
Q

What induces Ca release from ryanodine receptor channels?

A

Ca entering from outside the cell via voltage gates Ca channels

126
Q

Where are gap junctions of myocytes located?

A

at the intercalated disc

127
Q

How can the autonomic nervous system release hormones to increase heart rate?

A

they release epinephrine and norepinephrine, which activate beta 1 adrenergic receptors and act to increase the rate and strength of contractility (HOW? by increasing Ca current, release and reuptake)

128
Q

What two things determine contractile force?

A

intracellular Ca concentration

sarcomere length

129
Q

What are the three factors that control the number of cross-bridge activation?

(number of cross-bridge activation determines…?)

A

Ca concentration

troponin C to Ca affinity

Number of sarcomeres present

(number of cross-bridge activation determines the force of contraction)

130
Q

What controls the troponin C to Ca affinity?

A

the autonomic nervous system

the stretch (of cardiac muscle)

131
Q

Why is the force of contraction reduced in the cardiac muscle of older patients?

A

the force of contraction depends on the number of active cross bridges, and the number of cross-bridges depend on the number of sarcomeres present. Older patients have fewer sarcomeres due to apoptosis.

132
Q

We stated that the stretch of cardiac muscle gives the optimal overlap between actin and myosin, this causes the length-dependent change in troponin sensitivity. What law/mechanism does this showcase?

A

frank-starling law

133
Q

How does the frank starling law explain the lower resting heart rate observed in athletes?

A

they have longer sarcomeres, so each contraction produced is stronger and results in higher stroke volume. (so the heart doesn’t have to work as hard)

134
Q

Explain the link between end-diastolic volume and contractility

A

When EDV is high, the heart is maximally filled, which stretches the heart and increases contractility

135
Q

Explain the relationship between increased heart rate and…

1- filling time

2- stroke volume

3- cardiac output

A

When heart rate increases, the filling time decreases (not enough time for blood to go in maximally)

Because there’s not enough blood inside the heart when it contracts, the stroke volume decreases. HOWEVER, the stroke volumes per minute increase (less stroke volume, but more of them… quantity over quality).

This explains how cardiac output increases, due to the increase in number not the increase in volume. **this is true when when heart rate is 80-150bpm**

136
Q

Explain how age and stroke volume are related.

A

the greater the age the lower the stroke volume. This is due to the arteries losing their compliance and not being able to hold as much blood. This causes the venous return to decrease, which decreases stretch and stroke volume.

137
Q

How does high end systolic volume (ESV) change stroke volume in normal hearts versus in failing hearts?

A

when ESV is high (more blood left over in heart after contraction) the normal heart stretches, which increases contactility and thus stroke volume.

when ESV is high in a failing/dilated heart, the contractility and stroke volume are unchanged because the overlap in actin and myosin is decreased.

(remember= dilated/failing/systolic failure heart decreases contractility)

138
Q

What does inotropy depend on?

A

The entry of external calcium by L-type Ca-channels

Calcium release from sarcoplasmic reticulum (CICRC)

TnC affinity to calcium

139
Q

T/F: sympathetic activity speeds up the hearts contraction and slows down its relaxation

A

false, it speeds up both contraction and relaxation, that’s how it increases heart rate

(Ca release from L type channels and ryanodine receptors and Ca reuptake from SERCA is sped up)

140
Q

How does systolic failure and increased afterload affect inotropy?

A

systolic failure = heart cannot contract well so it lowers inotropy

increased afterload = increased pressure makes the heart push harder to counteract it, so increased inotropy

141
Q

Which most accurately describes positive inotropy changes the ventricle curve shift?

A

B

Higher stroke volume without a change in diastolic pressure

142
Q

Explain the Staircase phenomenon aka Treppe effect

A

As the time interval between each beat gets shorter, the Ca has no time to decrease (go to SR) so it builds up. That means the higher the heart rate increases, the calcium builds up (higher tension) until it hits a plateau.

(with each beat, the calcium levels get higher and higher- stair case/treppe- until maximum heart rate is reached)

143
Q

What is it called when the heart skips a beat? Explain why the force of the beat after the pause is greater than the rest.

A

heart skips beat= potentiation

the force is increased because of both frank starling mechanism and inotropy. frank s because during the missed beat, the blood filled the heart more, which caused increase in length. inotropy because the calcium levels accumulated causing a higher contractility.

144
Q

What mechanism/law causes the change from point A to point B?

A

higher inotropy

(or lower afterload?)

145
Q

What mechanism/law causes the change from point A to point B?

A

frank starling

146
Q

After an increase in venous pressure, where would the operational point be?

A

Point B, EDP would increase. Frank starling law.

147
Q

Which has a lower efficiency? explain.

a. inotropy
b. frank starling

A

b. frank starling

because it causes a larger ventricular volume, and that would cause an increase in oxygen consumption = lower efficiency

148
Q

Which increases stroke volume by decreasing the end systolic volume?

a. inotropy
b. frank starling

A

a. inotropy

149
Q

Which has beat to beat adjustments?

a. inotropy
b. frank starling

A

b. frank starling

150
Q

Explain how inotropy makes adjustments/adaptations.

A

it adapts based on large hemodynamic changes. So, after a strong contraction, the ESV decreases and thus increases SV. Over time, the stroke volume goes through the body and comes back to the heart and (slightly) increases the ESV. In exercise, this becomes more apparent (because the changes would be bigger).

151
Q

A 140-150 bpm, describe the relationship between heart rate and cardiac output. Why?

A

directly proportional

from 80-150bpm: when the heart rate increases, the stroke volumes decreases (cuz less filling time) BUT the stroke volume per minute increase and compensate for that fact… so CO increases

(more SV’s > less volume in the SV’s)

152
Q

A 150-170 bpm, describe the relationship between heart rate and cardiac output.

A

inversely proportional

from 150bpm and above: when the heart rate increases, the stroke volumes decreases (cuz less filling time) AND the stroke volume per minute increase but cannot compensate for that fact… so CO decreases

(more SV’s

153
Q

At which heart rate does the atrial pressure start to increase?

A

at 150bpm, there isn’t enough time for the ventricles to fill up with blood between each contraction (decreased filling time), that means that the extra blood gets stuck in the atria and increase their pressure

154
Q

Which has a greater effect on heart rate, parasympathetic or sympathetic system?

A

parasympathetic. When we block the parasympathetic effect with atropine, there’s much more of a drastic change than when we block the sympathetic system with propanolol.

155
Q

How does the heart rate get affected by Ca concentrations, K concentrations, and pH?

A

↑Ca= ↑HR (hypercalemia)

↑K= ↓HR (hyperkalemia)

↑pH=↑HR (alkalosis)

156
Q

T/F: a hypertrophic heart is hypoeffective

A

false; this is not always the case. A physiologically hypertrophic heart is hyperreflective while a pathologically hypertrophic heart is hypoeffective

157
Q

T/F: cardiac output of elders is decreased mainly due to the increase stiffness of vessels

A

false, its mainly due to the higher surface area

158
Q

How do you correct the cardiac output to body size?

A

divide it by body surface area

CO/BSA = cardiac index (the corrected CO)

159
Q

Which two reflexes are located on the aortic arch and carotid sinus?

a. Baroreceptor reflex
b. Cardiopulmonary reflex
c. Chemoreceptor reflex

A

a. Baroreceptor reflex

+

c. Chemoreceptor reflex

160
Q

Which reflexes detect stretch?

a. Baroreceptor reflex
b. Cardiopulmonary reflex
c. Chemoreceptor reflex

A

a. Baroreceptor reflex

+

b. Cardiopulmonary reflex

161
Q

Which reflex detects CO and O2 levels?

a. Baroreceptor reflex
b. Cardiopulmonary reflex
c. Chemoreceptor reflex

A

c. Chemoreceptor reflex

162
Q

How does the expiration affect venous return?

A

Exhaling increases intrathoracic pressure (abdominal pressure low in comparison) so the venous return is lowered

163
Q

What’s the relationship between total peripheral resistance and stroke volume

A

inversely proportional

(EX/ patient has hypertension, that increases resistance and decreases SV)

164
Q

Explain how increased resistance decreases stroke volume

A

more resistance means less venous return. less venous return means less CO, and that means less stoke volume.

(keep in mind that the area where CO and venous return cross is SV)

165
Q

When contractility increases, what occurs to SV, EDV, and ESV?

A

SV increases

EDV increases

ESV decreases

166
Q

How does the heart adjust to increased peripheral resistance?

A

↑ resistance

↓ SV

↑ EDV

↑stretching

↑force

167
Q

What occurs to stoke volume and venous return when central venous pressure increases?

A

the central venous pressure increases, pushing the blood to both sides: the heart and the periphery.

↑ stroke volume

↓ venous return

168
Q

How do you calculate venous return?

A

(peripheral venous pressure - central venous pressure)/venous resistance

169
Q

Describe the relationship between central venous pressure and venous return

A

inversely proportional

170
Q

What is the normal level of central venous pressure, cardiac output, and venous return?

A

CVP= 2

CO/venous return=5

(CO/venous have to be equal for no change to occur)

171
Q

Explain the events that must occur for central venous pressure to go from a high pressure back to a normal pressure.

A

high CVP means that venous return is low and cardiac function is high. The CO would work hard to push the blood out harder until the pressure is evened out, leading the venous pressure is to get back to normal (=to CO)

changes in central venous pressure go to an automatical adjustment

172
Q

What is cardiac tamponade? Which phase of the cardiac cycle does it affect? What can it lead to?

A

cardiac tamponade is when blood fills the pericardial sac. This compresses the heart and reduces the filling/stretching of the left ventricle (diastole affected). The right heart is also compressed so atrial pressure increases, which causes the blood to back up into the veins (blood in veins increase, distended jugular vein). Because the L ventricle isn’t taking enough blood, so the blood stagnates in the lung and causes pulmonary edema.

173
Q

What occurs when you breathe against a closed glottis?

A

Valsalva maneuver. The intrapleural pressure increases and reduces ventricular return. Less venous return leads to less SV and CO.

174
Q

What two things increase venous pressure?

A

higher blood volume

vasoconstriction

175
Q

Assuming the red point is the normal intersection point, which point represents what occurs in heart failure? explain.

A

point A

When heart failure occurs, ↓SV and ↓CO, which would drag the cardiac function curve downwards. This change increases the central venous pressure.

176
Q

Which point would the red dot shift to when the sympathetic stimulation increases? explain.

A

point H

The sympathetic stimulation increases contractility and CO, so the cardiac function curve increases.

(now it gets confusing) Venous constriction is also activated by the sympathetic stimulation, and that decreases compliance and increases CVP (it looks like it decreases in the graph? and in class he said CVP doesn’t change)

177
Q

Where does the red point shift during hemorrhage?

A

point B

↓CO because ↓venous return, so ↓CVP

178
Q

Explain how expiration affects SV

A

when we expire, the diaphragm rises and the pressure in the thorax increases. This compresses the right atrium and ventricle, decreasing CO+SV.

The venous return decreases because the pressure gradient between the peripheral venous pressure and central venous pressure has decreased

179
Q

During cardiac failure, how does the body compensate?

A

by increasing blood volume via vasoconstriction. This decreases compliance and increases venous resistance

(point C moves to point D, decreasing the right arterial pressure and central pressure.)

180
Q

Explain how the therapeutic interventions given improve cardiac function (in heart failure) work.

EX/ beta adrenergic receptors blockers, ANG II receptor blockers, ACE inhibitors and aldosterone receptor antagonists.

A

they function by increasing the venous resistance and decreasing central venous pressure to maintain the venous gradient.

** moves shifts the venous curve to the right **

181
Q

Which is made up of plants?

a. digoxin
b. digitoxin
c. both
d. neither

A

c. both

182
Q

Which of the following does liver failure enhance toxicity? How about renal failure

a. digoxin
b. digitoxin
c. both
d. neither

A

renal failure= increase toxicity in a. digoxin

liver failure= increase toxicity in b. digitoxin

** both have a low therapeutic index

183
Q

Explain the mechanism of action of digoxin

A

stop Na+/K+ ATPase (↑Na in cell), less effective Na+ /Ca2+ exchange (due to ↑Na), so now ↑Ca in cell= ↑ contraction force

184
Q

T/F: Digoxin is used to treat heart failure because of its ability to increase HR

A

false, it increases contractility and decreases HR

185
Q

In which condition does giving Digitalis Glycosides lead to toxicity?

a. hypokalaemia
b. hypocalcemia

A

a. hypokalaemia

(hypocalcemia= Digitalis Glycosides are less effective)

186
Q

How do Inotropic Drugs increase cAMP levels?

A

by inhibiting phosphodiesterases (stop using cAMP)

OR

activating adenylyl cyclase (to produce cAMP)

187
Q

Which of the following Inotropic Drugs can be given orally?

a. Amrinone
b. Milrinone
c. both
d. neither

A

c. both

(both orally or parenterally)

188
Q

T/F: Amrinone and Milrinone have vasoconstrictive effects

A

false, they have a vasodilating effect (which may contribute to their therapeutic effect.)

189
Q

Mechanism of action of Dobutamine

A
190
Q

How do dilator drugs aid in treating heart failure?

A

decreasing preload (venodilation)

decreasing afterload (arteriolar dilation)

191
Q

Mechanism of action of Thiazides

A
192
Q

Which blocks β1-and β2-adrenoceptors?

a. Atenolol
b. Carvedilol
c. both
d. neither

A

b. Carvedilol

(Atenolol= only block β1-adrenoceptors)

193
Q

Which exhibits anti-oxidant activity?

a. Atenolol
b. Carvedilol
c. both
d. neither

A

b. Carvedilol

194
Q

ACE inhibitors mechanism of action

A
195
Q

Patient comes in with diabetic nephropathy and some swelling in the ankles. Which do you prescribe?

A

Angiotensin-converting enzyme inhibitors to prevent loss of kidney function associated with diabetic nephropathy

196
Q

What’s the most common side effect of ACE inhibitors?

A

dry cough

197
Q

Which undergoes extensive first-pass hepatic metabolism?

a. telmisartan
b. losartan
c. both
d. neither

A

b. losartan

198
Q

T/F: both Angiotensin II receptor blockers and ACE inhibitors are contraindicated in pregnant women

A

true

(ACEIs are contraindicated during pregnancy because they cause fetal injury and death.)

199
Q

Which do Angiotensin II receptor blockers (ex/losartan, telmisartan) block?

a. AT1 receptors
b. AT2 receptors
c. both
d. netiher

A

a. AT1 receptors

200
Q

Which of the following can cause hyperkalemia?

a. Eplerenone
b. Spironolactone
c. both
d. neither

A

c. both

201
Q

Which of the following is a selective aldosterone receptor antagonist?

a. Eplerenone
b. Spironolactone
c. both
d. neither

A

a. Eplerenone

202
Q

Which of the following reduces K reabsorption?

a. Eplerenone
b. Spironolactone
c. both
d. neither

A

d. neither

(both reduce Na+ reabsorption)

203
Q

Which of the following has less hormonal side effects?

a. Eplerenone
b. Spironolactone
c. both
d. neither

A

a. Eplerenone

204
Q

What is LCZ696? How does it work?

A

Sacubitril/valsartan, its a combination drug for use in heart failure

Sacubitril= neprilysin inhibitor→ neprilysin degrades natriuretic peptides and bradykinin. These increase and cause vasodilation + sodium excretion

valsartan= angiotensin receptor blocker→ prevent stimulation by angiotensin II

205
Q

Which of the following is associated with jugular vein distention?

a. right side failure
b. left side failure

A

a. right side failure

206
Q

diagnose. Which side of the heart has most likely failed?

A

pulmonary edema, alveoli filled with fluid (hemosiderin is sometimes found too)

left-sided heart failure is most likely (blood pumped to body defectively, so it backs up into lungs)

207
Q

Which of the following is defective due to chronic lung disease?

a. right heart
b. left heart

A

a. right heart

208
Q

What are three things that cause dilated cardiomyopathy?

A

genetic causes

alcoholic dilated cardiomyopathy (long term alcohol abuse)

viral myocarditis (can cause fibrosis, decreased contractility, then the heart dilated to compensate)

peripartum cardiomyopathy (pregnancy)

209
Q

diagnose

A

Hypertrophic cardiomyopathy

(myofiber disarray!)

210
Q

How does Systemic amyloidosis affect the heart? is it a diastole or a systole problem?

A

causes Restrictive cardiomyopathy and heart failure

(a problem in relaxation, so diastole dysfunction)

211
Q

Patient with acute onset of heart failure. Histology is provided, diagnose.

A

myocarditis due to Chagas disease (Trypanosoma Cruzi)

212
Q

What does cor pulmonale mean?

A

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels

(ex/ pulmonary hypertension leading to right ventricular dilation)

213
Q

Which belongs to a patient with Pulmonary hypertension? A or B?

A

B

214
Q

A disease of the myocardium that may be associated with mutations of the gene encoding the sarcomeric protein Titin is:

a. Hypertrophic cardiomyopathy
b. Arrhythmogenic right ventricular cardiomyopathy
c. Restrictive cardiomyopathy
d. Dilated cardiomyopathy
e. Duchenne muscular dystrophy

A

d. Dilated cardiomyopathy

215
Q

How do you tell the difference between Hypertrophic cardiomyopathy and Hypertensive heart disease?

A

Hypertrophic cardiomyopathy= more septal hypertrophy

Hypertensive heart disease= symmetric hypertrophy of left ventricle (due to hypertension)

***not all cases of hypertrophic cardiomyopathy are asymmetrical (so this method doesn’t work all the time)

216
Q

This is the heart of a chronic alcoholic who developed congestive heart failure before he died. What is the diagnosis?

a. Myocardial infarction
b. Restrictive cardiomyopathy
c. Dilated cardiomyopathy
d. Hypertrophic cardiomyopathy
e. Amyloid deposition

A

c. Dilated cardiomyopathy

(associated with alcohol)

217
Q

What is a pathognomonic symptom of heart failure?

A

Paroxysmal nocturnal dyspnea or paroxysmal nocturnal dyspnoea (PND) is an attack of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep, and may be quite frightening.

218
Q

How do you treat patients that are cold and dry?

A

cold and dry means they have hypoperfusion but are not congested. Give them epinephrine to increase the cardiac output.

219
Q

How do you treat patients that are warm and wet?

A

they’re congested. give diuretics.

(if cold and wet, give both diuretics and epinephrine)

220
Q

a broadened/laterally displaced apical beat indicates…

A

a dilated heart

221
Q

Diagnose.

A

Pulmonary edema due to left ventricle systolic dysfunction

Kerley b lines are seen, indicates interstitial pulmonary edema.

222
Q

T/F: left ventricular systolic dysfunction is always present along with cardiomegaly

A

false, not always. If the systolic dysfunction is acute, the heart may not have has enough time to enlarge

223
Q

What do high Natriuretic Peptides indicate? explain.

A

Natriuretic Peptides are high in heart failure. They’re released with the atrial pressure is high and its dilated, they act to reduce the BP. (by natriuresis- the excretion of sodium by the kidneys)

224
Q

What conditions can increase the heart rate and mimic cardiac diseases?

A

anemia, high HR due to low RBC’s delivering oxygen

hyperthyroidism, can increase the metabolic rate so drastically that the body can’t keep up and thus increases HR

225
Q

What test can prove and classify heart failure?

A

Echocardiography

classify it into heart failure with reduced ejection fraction OR with sustained ejection fraction

226
Q

What is the normal left ventricular ejection fraction? How is it calculated?

A

50-75%

Ejection Fraction= SV/EDV

227
Q

How do you treat patients with heart failure and sustained ejection fraction?

A

They have a filling issue and not a contraction error, so can minimally help them bu giving diuretics, controlling blood pressure, and heart rate.

228
Q

give an example of heart failure with reduced ejection fraction and with sustained ejection fraction.

A

reduced ejection fraction= dilated cardiomyopathy
sustained ejection fraction= Left ventricular hypertrophy

229
Q

How do neurohormones react to a decrease in CO?

A

SNS is activated and epinephrine is released to so it increases SV and HR via beta receptors. This aids the heart initially, but epinephrine is toxic to myocardial tissue

230
Q

How does the renin angiotensin aldosterone system react to low CO? How can this be bad?

A

due to the low CO and reduced renal perfusion, renin is released to increase the BP and volume. This acts to improve the CO initially, but then the volume increases the afterload, which decreases CO furthur.

231
Q

What are three ways to stop the actions of the renin angiotensin aldosterone system?

A

1- ACE inhibitor→ stop angII synthesis, increase bradykinin

2- angiotensin receptor blocker (ARB’s)→ stop the effects of angII by blocking its receptors (AT1)

3- Mineralocorticoid Receptor Antagonist (MRA)→ stop aldosterone from retaining Na and water

232
Q

T/F: digoxin and diuretics aid to improve survival in HF patients

A

false, they act to improve the symptoms (the neurohormonal antagonists are the ones improving survival)

233
Q

Which heart failure drug must you give the least effective dose?

A

drugs that only improve symptoms (digoxin and diuretics), you give as little as possible

234
Q

Which heart failure drugs must you give the highest tolerated dose?

A

Neurohormonal Antagonists

(they decrease death)

235
Q

hydralazine–isosorbide dinitrate (H-ISDN) is given to treat heart failure. What is the target population for the drug?

A

Black Americans (increases their survival rate more)

236
Q

When should you use ACE inhibitors and when should you use angiotensin receptor blockers (to treat HF)?

A

use angiotensin receptor blockers if ACE inhibitors are intolerated

237
Q

What does it mean when a heart failure patient is given optimal medical therapy (OMT)?

A

ACE inhibitors

beta-blockers

MRA (mineralocorticoid antagonists)

(the first 2 are given, then if symptoms persist, MRA’s also given)

238
Q

T/F: all beta blockers can be used in heart failure

A

false, there are four that can be used:

bisoprolol, carvedilol, nebivolol, metoprolol succinate XL

239
Q

Which of the following do Mineralocorticoid Receptor Antagonists (MRA) end with?

a. sartan
b. lol
c. one
d. pril

A

c. one

240
Q

Which of the following do Angiotension receptor blockers (ARB) end with?

a. sartan
b. lol
c. one
d. pril

A

a. sartan

241
Q

How do you treat a heart failure patient who’s still symptomatic after optimal medical therapy (OMT)?

A

give ARNI, a new class of drugs called angiotensin receptor neprilysin inhibitor

242
Q

What is angiotensin receptor neprilysin inhibitor (ARNI) made up of?

A

made up of Valsartan/Sacubitril

Valsartan= angiotensin receptor blocker

Sacubitril= neprilysin inhibitor

243
Q

Which of the following do beta blockers end with?

a. sartan
b. lol
c. one
d. pril

A

b. lol

244
Q

Which two systems does ARNI (Valsartan/Sacubitril) interfere with? How?

A

The natriuretic peptide system and RAAS system

Valsartan= angiotensin receptor blocker (↓vasoconstriction)

Sacubitril= neprilysin inhibitor

neprilysin is an enzyme that deactivates brain natriuretic peptide (BNP; which decreases BP). So if we stop the degradation of BNP we enhance its action.

245
Q

Which of the following do ACE inhibitors end with?

a. sartan
b. lol
c. one
d. pril

A

d. pril

246
Q

What is a hibernating myocardium?

A

metabolically inactive myocardium (not dead, so if you improve the circulation to it, it gets activated)

247
Q

When is Implantable cardioverter-defibrillator (ICD) used?

A

used to prevent ventricular arrhythmia (the most common cause of sudden death). So we give them to patients with a reduced ejection fraction (below 35%) because we want to reduce the chance of sudden cardiac death.

(the device senses ventricular arrhythmia and sends a shock to the heart)

248
Q

When is cardiac resynchronization therapy (CRT) used?

A

For patient with electrical dissociation (ex/ right or left bundle branch block). So when the ventricles aren’t contracting at the same time, the CO and ejection fraction decreased.

This therapy makes the heart a new conduction system via wires. This is only used when conventional therapy fails and the ejection fraction is less than 25% or QRS complex is wide.

249
Q

Pulmonary capillary wedge pressure reflects the pressure of which chamber of the heart? explain.

A

When you block the pulmonary artery pressure (by inflating the balloon), the pressure would reflect the next chamber0 which is the left arterial pressure

250
Q

Which has a higher diastolic pressure?

a. right ventricular pressure
b. pulmonary artery pressure

A

b. pulmonary artery pressure

251
Q

What are two reasons the Pulmonary capillary wedge pressure would be high?

A

left ventricular failure

arterial stenosis

Pulmonary capillary wedge pressure = left arterial pressure

252
Q

Which chamber of the heart does this pressure cycle represent?

A

Its the right ventricle, the pressure only does as high as 25mmHg. The left ventricle goes above that because it has to pump for the whole body, so it has to be the right ventricle.

253
Q

What does this pressure cycle represent?

A

The right atrial pressure (aka the central venous pressure)

254
Q

What do the three peaks represent?

A

peak a= atrial contratction

peak c= bulging of tricuspid valve into atrium at start of ventricular contraction

last peak = passive filling of right atrium and vena cava when tricuspid valve
closes

255
Q

What are the three things you need to calculate the CO via Fick’s principle?

A

spirometer, venous, and arterial blood sample

256
Q

How would End-diastolic (EDPVR) and end-systolic (ESPVR) pressure-volume relationship change during low contractility?

A

ESPVR would go to point B

(in ESPVR, stiffness and pressure are inversly proportional)

EDPVR would do to point D

(in EDPVR, stiffness and pressure are directly proportional)

257
Q

What does this shift indicate? How is the ejection fraction and EDV affected?

a. increase in preload
b. decrease in preload
c. increase in afterload
d. decrease in afterload

A

a. increase in preload

ejection fraction increased

EDV increased

258
Q

What does this shift indicate? What occurs to ESV and ejection fraction?

a. increase in preload
b. decrease in preload
c. increase in introphy
d. decrase in introphy

A

c. increase in introphy

(ESPVR shifts up when contractility increases!)

ESV decreases

ejection fraction increases

259
Q

Which of the following readings most likely belongs to a failing heart? A, B, C

A

C

increased difficulty in building pressure (less steep)

260
Q

What does this shift indicate? How is the ESV and ejection fraction affected?

a. increase in lusitropy
b. decrease in lusitropy
c. increase in afterload
d. decrease in afterload

A

c. increase in afterload

ESV increase

ejection fraction decreased

261
Q

What does this shift indicate? How is the ESV and ejection fraction affected?

a. increase in lusitropy
b. decrease in lusitropy
c. increase in afterload
d. decrease in afterload

A

b. decrease in lusitropy (=decreased rate of myocardial relaxation)

EDPVR shifts up similarly to what would happen if stiffness increased

262
Q

Which occurs in reduced myocardial contractility?

a. high preejection time
b. low preejection time

A

a. high preejection time

263
Q

Which does it mean when the PET/LVET ration is increased?

a. more myocardial contractility
b. less myocardial contractility

PET= preejcetion time

LVET= left ventricular ejection time

A

b. less myocardial contractility

PET increases and LVET decreases

264
Q

What is the most commonly used index of the global ventricular function?

A

Ejection Fraction

EF = (SV/EDV)*100

CVS (13 decks)

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