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Spring 2016 - CVPR > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Does the myocardium do anaerobic metabolism?

A

No. It is always aerobic because fatigued heart muscle is bad

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2
Q

In what part of the heart cycle is the LV perfused? Other parts of the heart?

A

Diastole. Systole compresses the intramural coronary vessels too much. Other parts are perfused all the time

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3
Q

What is the Law of Laplace?

A

Myocardial wall tension is proportional to cavity pressure, cavity dimension, and 1/ wall thickness

T oc P*L/WT

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4
Q

How do beta-blockers treat angina?

A

Slow heart rate -> longer diastole -> more coronary blood flow filling

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5
Q

What is the molecular cause of angina?

A

Production of ischemic metabolites like adenosine

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6
Q

Acute myocardial infarction is also called ___________

A

Unstable angina

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7
Q

What happens acutely in coronary occlusion?

A

Impairment of re-uptake of calcium into the SR

-> depletion of high-energy phosphates, intracellular acidosis

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8
Q

What is the main shortcoming of the ECG?

A

Insensitive at rest (also not super sensitive and specific during exercise)

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9
Q

2 anti-platelet drugs

A 
Aspirin
Plavix (clopidogrel)
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10
Q

What are the 2 most common vessels used for coronarybypass surgery?

A

Mammary artery

Saphenous vein

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11
Q

What is the primary component of large arteries, small arteries, and arterioles?

A

Elastin
Collagen
Smooth muscle

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12
Q

Nitric oxide is synthesized from ___________ by ___________

A

Arginine

Nitric oxide synthase

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13
Q

Can LDL enter the endothelium?

A

Not under normal conditions. It can only enter disrupted/abnormal endothelium

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14
Q

Foam cells secrete ___________ that degrade the fibrous cap of the atherosclerotic plaque

A

Matrix metalloproteases

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15
Q

2 markers of cardiac necrosis

A

Cardiac-specific troponins

Creatinine kinase MB isoenzyme

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16
Q

What is the composition of venous and arterial thrombi? Where do they occur? What drug classes are used to treat?

A

Venous: fibrin and RBC-rich. Occur in areas of stasis. Treat with anticoagulants.
Arterial: platelet-rich. Occur in areas of high flow. Treat with antiplatelets.

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17
Q

Which heparins can bind antithrombin+thrombin?

A

At least 18 saccharide units. Otherwise it just binds antithrombin?

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18
Q

What is the route of administration for heparin?

A

IV – immediate
SubQ – delayed
It is not absorbed from the gut!

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19
Q

What is the antidrug to heparin?

A

Protamine

It is a strongly + charged drug that complexes with the strongly – charged heparin

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20
Q

What are the advantages to low molecular weight heparin?

A

Longer half-life

Better bioavailability

More predictable dose response, so can be given outpatient

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21
Q

What does warfarin do?

A

Inhibits recycling of vitamin K, depleting it and some clotting factors (2,7,9,10,protein C)

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22
Q

Which drug acts in the plasma to directly inhibit the activity of factor Xa?

A

Rivaroxaban

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23
Q

Which drug do you use to prevent deep vein thrombosis after hip-knee replacement surgery?

A

Rivaroxaban

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24
Q

Which drug acts in the plasma to directly inhibit thrombin?

A

Dabigatran

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25
Q

What does streptokinase do?

A

Activates plasminogen

It’s from strep!

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26
Q

What is the Fick equation?

A

CO = VO2/(Ca-Cv)

CO=cardiac output
Ca = arterial O2 concentration
Cv = venous O2 concentration

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27
Q

Is increase in arterial O2 content a factor in the increase in muscle oxygen extraciton during exercize?

A

No

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28
Q

How does the heart meet increased oxygen demand during exercize?

A

Increased coronary blood flow.

O2 extraction is already high at rest, so it doesn’t increase by much during exercize

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29
Q

What is the Frank-Starling law?

A

Stroke volume increases in response to an increase in the volume of blood filling the heart (end diastolic volume) when all other factors are constant

Why? Increased stretching of ventricular wall causes cardiac muscle to contract more forecefuly

Why? Because when muscle fibers stretch , calcium sensitivity increases

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30
Q

What is the Frank-Starling curve?

A

Ventricular end-diastolic pressure vs. stroke colume

The more the LV is filled, the more it will contract

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31
Q

What measureable thing is elevated in myocyte necrosis?

A

Troponin enzymes (I and T)

Begin 3-12 hours after injury and peak 18-24 hours after necrosis begins

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32
Q

What does LDL bind to in the intima, resulting in entrapment?

A

ECM proteoglycans

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33
Q

What are dietary fats called when they are in the lymphatic system?

A

Chylomicrons

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34
Q

What is the main difference in composition between LDL and HDL cholesterol?

A

HDL has more protein and LDL has more lipid

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35
Q

What are apolipoproteins?

A

Proteins that bind lipids to carry them through the lymphatics and blood stream

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36
Q

Which apoplipoprotein is highly correlated with HDL cholesterol? non-HDL cholesterol?

A

Apolipoprotein A

Apolipoprotein B

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37
Q

What does apoplipoprotein C do?

A

It enhances the interactions of chylomicrons with lipoprotein lipases that hydrolize the triglycerides in them to free fatty acids

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38
Q

What are the 5 clnical indications of metabolic syndrome?

A 
Large abdominal circumference
Triglycerides >150 mg/dL
Reduced HDL
BP > 130/85
Glycemia >100
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39
Q

What 3 things does insulin do?

A

It mostly promotes caloric storage

Protein metabolism: increased AA transport, decreased proteolysis, increased protein synthesis

Carbohydrate metabolism: decreased glycogenolysis, gluconeogenesis, increased glucose transport, glycogen synthesis, glucose oxidation

Fat metabolism: decreased lipolysis, VLDL secretion, muscle lipoprotein lipase . Increased lipogenesis, apoB degradation, adipose tissue LPL

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40
Q

What is the best treatment for metabolic syndrome?

A

Lifestyle change

Genetics play a very small role and environment is the biggest factor

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41
Q

What are the 3 risk factors for peripheral artery disease?

A

Diabetes
Smoking
Lipids

In order - diabetes is largest

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42
Q

What are the 2 symptoms of peripheral artery disease?

A

Claudication caused by reversible muscle ischemia

Ischemic rest pain/ischemic ulcers

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43
Q

How do you diagnose peripheral artery disease?

A

Ankle-brachial index

Abnormal if ankle systolic BP/arm systolic BP >0.9

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44
Q

Aortic aneurysm involves which layers of the blood vessel?

A

All 3

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45
Q

What are the 2 ‘shapes’ of aneurysm?

A

Fusiform - entire circumference

Saccular - evagination of a segment of the circumference

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46
Q

What does risk of aneurysm rupture correlate with?

A

Size

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47
Q

At what fetal day does the heart begin to beat?

A

22 or 23

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48
Q

In the end of the 5th week, 2 masses appear in the truncus of the developing heart:

A

Dextrosuperior -> aortic cusp

Sinistroinferior truncal swellings -> anterior pulmonary cusp

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49
Q

What are the 3 major layers of the heart?

A

Epicardium - connective tissue and fat
Myocardium - cardiac myocytes
Endocardium - ECs

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50
Q

What encloses the heart? What are its material properties?

A

Pericardium

Is noncompliant

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51
Q

What are the 4 valves?

A

Tricuspid - right AV
Pulmonic
Mitral - left AV
Aortic

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52
Q

The SA node’s intrinsic activity is ___________bpm

A

100

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53
Q

What does the His-Purkinje system do?

A

Conduct rapid depolarization to trigger coordinated ventricular contraction

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54
Q

What are the 3 layers of an artery?

A

Adventitia
Media
Intima

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55
Q

What is the definition of microcirculation?

A

The vasculature from the first-order arterioles to the venules

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56
Q

Which valves have chordae tendinae?

A

AV valves

The semilunar valves don’t have them!

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57
Q

How does the time to repolarization of cardiac muscle differ from skeletal muscle? Why?

A

It is much longer in order to prevent tetanus

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58
Q

What is the molecular structure of myosin?

A

2 heavy chains, 4 light chains

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59
Q

Why is blood flow fastest in the aorta?

A

Because its cross-sectional area is smallest

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60
Q

Flow equation

A

Q = dP/R where R is resistance

Analogous to V=IR

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61
Q

What is the ratio between flow and resistance?

A

F=r^r

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62
Q

Equation for mean arterial pressure

A

Diastolic P + 1/3(systolic P - diastolic P)

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63
Q

Equation for vessel compliance

A

C = dV/dP

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64
Q

How many liters of blood do we have?

A

5

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65
Q

For the left ventricle, preload is equal to ________

Afterload is equal to________

A

End diastolic volume

Aortic pressure

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66
Q

What is the bainbridge reflex?

A

A way (in addition to starling’s law) in which increased venous return causes increased cardiac output

Increased venous return stretches sinus node -> HR increase

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67
Q

What is the pulse pressure?

A

Systolic-diastolic pressure

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68
Q

Inotropy is also called ______________

Lusitropy is ________

A

Contractility

Rate of myocardial relaxation

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69
Q

How does cardiac ATPase compare to that of skeletal and smooth muscle?

A

It is slower than skeletal muscle but faster than smooth muscle

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70
Q

Cardiac muscle cells are connected by _________________

A

Intercalated discs

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71
Q

What are the 5 steps of the cardiac muscle contraction-relaxation cycle

A
  1. Action potential leads to calcium release
  2. Calcium binds to troponin C
  3. Troponin complex undergoes structural change, moving tropomyosin out of the way
  4. Myosin binds actin and the crossbridge moves
  5. Calcium is released and tropomyosin reblocks the binding site, causing relaxation
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72
Q

Thick filaments are ______________ and thin filaments are ______________

A

Myosin

Actin + troponin + tropomyosin

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73
Q

______________ blocks binding sites on actin

A

Tropomyosin

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74
Q

What does troponin do?

A

When bound by calcium, displaces tropoyosin, freeing up binding sites on actin

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75
Q

Calcium in cardiac cells is stored in the ______________

A

Sarcoplasmic reticulum

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76
Q

What does titin do? (2)

A

It helps tether myosin to the Z line of the sarcomere

Also forms an elastic spring, and is responsible for much of the passive elastic properties of the cell/heart

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77
Q

How is a GPCR (G protein-coupled receptor) deactivated?

A

Autodephosphorylation of GTP to GDP allows subunits to rebind

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78
Q

What are the 5 steps of vascular smooth muscle cell activation?

A
  1. Calcium enters cytoplasm (from SR and through channels)
  2. Calcium binds calmodulin
  3. Ca-CaM binds to myosin light chain kinase and activates
  4. Activated MLCK phosphoylates the light chain of myosin, so cross bridge cycling can occur
  5. Contraction is halted by dephosphoylation of myosin light chain by myosin light chain phosphatase
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79
Q

What does cAMP do to vascular smooth muscle?

A

Relaxes

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80
Q

Where are the arterial baroreceptors (2)?

A

Aortic arch

Carotid sinus

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81
Q

What is the set point for the baroreceptor reflex?

A

~100mmHg

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82
Q

What does endothelin do? What enzyme makes it?

A

Vasoconstrict

Endothelin converting enzyme

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83
Q

What 3 things stimulate renin release?

A

Sympathetic stimulation of juxtaglomerular cells

Decreased blood pressure in renal artery
Decreased Na+ reabsorption in the kidney

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84
Q

What does renin do?

A

Cleaves angiotensinogen to angiotensin I

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85
Q

What cleaves angiotensin I to angiotensin II?

A

ACE

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86
Q

What are the 5 effects of angiotensin II?

A

Systemic vasoconstriction via binding to GPCRs on vascular SMCs

Stimulates sympathetic activity

Stimulates aldosterone release from adrenal cortex

Stimulates release of endothelin from vascular endothelium

Stimulates ADH release from pituitary

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87
Q

What does aldosterone do?

A

Promotes reabsotpion of Na+ and water in kidney collectin ducts

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88
Q

What does ADH do? (2)

A

Increases water reabsorption in kidneys

Vasoconstriction

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89
Q

Timothy syndrome is a defect in which channel? What ECG finding does this result in?

A

L-type calcium

Long QT

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90
Q

What ECG finding does Brugada syndrome result in?

A

Short QT

Sodium-channel mutation

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91
Q

What is the behavior of the funny current channel?

A

Permeable to Na+ below -30 mV and K+ above this

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92
Q

What are the phases and ion activity of a fast cardiac action potential? Draw!

A 
0 - rise
1 - partial repolarization
2 - plateau
3 - repolarization 
4 - resting
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93
Q

What are the phases and ion activity of a slow cardiac action potential? Draw!

A

0 - ast fdepolarizaton
3 - repolarization
4 - resting (but really slowly depolarization)

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94
Q

What cause phase 0 of the fast action potential?

A

Influx of Na+ through voltage-activated channels

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95
Q

What causes phase 1 of the fast action potential?

A

Inactivation of sodium current and activation of transient potassium current

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96
Q

What causes phase 2 of the action fast potential?

A

Voltage-activated L-type calcium channels
Delayed rectifier potassium channels

Calcium influx is balanced by potassium eflux

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97
Q

What causes phase 3 of the fast action potential?

A

Calcium channel inactivation

Delayed rectifier potassium channels

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98
Q

What are the only drugs that have been demonstrated to reduce the incidence of sudden cardiac death?

A

Beta blockers!

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99
Q

How do defective potassium channels cause long QT?

A

There are fewer of them (b/c misfolded proteins aren’t let out and about), reducing current amplitude, delaying repolarization

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100
Q

How do defective sodium channels cause long QT?

A

They don’t completely inactivate so there is still sodium flowing during phase 2, prolonging it

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101
Q

What causes early vs. late afterdepolarizations?

A

Early - reactivation of Ca2+ channels in response to elevated Ca2+ in the prolonged QT

Delayed - Elevated Ca2+ from the Na/Ca exchanger (NCX)

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102
Q

What are the 3 degrees of conduction block?

A

1 - long PR interval
2 - some P waves are not followed by QRS
3 - complete block. No relationship between timing of P and QRS

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103
Q

What are the 2 requirements for re-entrant arrhythmias?

A

Unidirectional conduction block in a functional circuit

Conduction time > refractory period

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104
Q

What is the principle of use-dependence in anti arrhythmics?

A

Blocking agents can more easily inactivate active channels (because they physically slip in there) so they tend to preferentially work on overactive regions of the heart or ones with abnormal resting potentials

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105
Q

What are the 2 ways class I antiarrhythmic drugs can suppress re-entrant arrhythmias?

A

Slowing conduction velocity (by slowing current)

Prolonging refractory period

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106
Q

Which neurotransmitter is released by the preganglionic sympathetic neurons? Postganglionic sympathetic neurons?

A

Acetylcholine

Norepinephrine

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107
Q

What transmitter is released by post and preganglionic parasympathetic neurons?

A

Acetylcholine

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108
Q

What are the 2 types of cholinergic receptors? Where are they located? What type of receptor are they?

A

Nicotinic. Cell body of postganglionic neurons. Na/K ion channel.

Muscarinic. Effector cells. G protein-coupled.

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109
Q

What is the problem in diastolic vs. systolic heart failure?

What does diastolic heart failure results in? Systolic heart failure? (in terms of heart size)

A

Filling. Hypertrophy

Squeeze. Dilation

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110
Q

What is the suffix for ACE inhibitors?

What is the suffix for angiotensin receptor blockers?

What is the suffix for aldosterone receptor blockers?

What is the suffix for beta-blockers?

A
  • pril
  • sartan
  • one
  • olol
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111
Q

Which way does electrical signal flow through the atrial septum?

A

L to R

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112
Q

Draw cardiac output diagram

A

:)

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113
Q

Draw pressure volume loops for normal, increased preload, increased inotropy, increased afterload

A

:)

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114
Q

Draw His bundle conduction system through the ventricles

A

:)

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115
Q

What are the 3 troponin isoforms?

A

C - calcium-binding
I - inhibits myosin ATPase
T - tropomyosin-binding

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116
Q

What are the 2 titin isoforms? How do their material properties differ?

A

N2B

N2BA, which is less stiff

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117
Q

Where do slow action potentials occur?

A

SA and AV node

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118
Q

How do action potentials of endocardial and epicardial cells compare?

A

Endocardial cells depolarize slightly before and their repolarization is longer

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119
Q

Draw an EKG and explain the parts

A

:)

120
Q

In which leads is the QRS upright?

A

Left-sided leads

It is downwards in right-sided leads

121
Q

What are the effects of R, L, and L fascle bundle blocks?

A

R - wide QRS with delayed RV conduction

L - wide QRS with delayed LV conduction

Fasicle - QRS is not widened, but direction of depolarizaiton altered (frontal plane mean axis is altered)

122
Q

What happens in Finnish familial arrhythmia?

A

Mutant K+ channel is not properly upregulating during increased sympathetic activity. There is not enough repolarizing K+ current to match the increased depolarizing Ca2+ current

This prolongs phase 2 triggering afterdepolarizations

123
Q

Which channel is responsible for early afterdepolarizaitons? Delayed afterdepolarizaitons?

A

Late-calcium

NCX

124
Q

What are the 4 classes of antiarrhythmics?

A

I - block voltage-gated Na+ channels
II - beta-blockers
III - prolong fast response phase 2 by delaying repolarization
IV - block voltage-gated Ca2+ channels

125
Q

What are the 3 subclasses of class I antiarrhythmics? Draw their voltage charts. What are examples of each.

A

:)

1a: quinidine, procainamide, disopyramide
1b: lidocaine, tocainide, mexeletine, phenytoin (lettuce, tomato, mayo, pickles)
1c: propafenone, flecainide, ecainide

126
Q

What is measurement of conduction velocity used as a surrogate for?

A

Current density

127
Q

Which 3 currents do class II/beta blockers reduces?

A

Funny
Long-type Ca2+
K+

128
Q

What 2 effects do beta blockers have on the slow response?

A

Decreased phase 4 slope -> decreased firing rate

Prolonged repolarizaiton -> increased refractory period

129
Q

What channel is responsible for Ca2+ influx out of the SR? What opens it?

A

RyR (ryanodine receptor)

Ca2+

130
Q

Does skeletal muscle contraction require entry of external calcium?

A

No, only cardiac muscle does

Calcium does the same thing in both cell types though. It binds to troponin on thin filaments and activates contraction.

131
Q

What 3 channels remove calcium from the cytosol?

A

SERCA - puts into SR
NCx - puts outside
PMCA - puts outside

In order of importance

132
Q

What is the ratio for NCX?

A

3 Na for 1 Ca

It can actually run in either direction (calcium into cell during depolarization and out of the cell upon repolarization.)

133
Q

What happens in catecholaminergic polymorphic ventricular tachycardia?

What ion channel is it a defect in?

A

ECG abnormalities upon exercize

Mutations in RyR2, which allows Ca2+ to leak out of the SR during resting phase

134
Q

What role does GTP play in G-proteins?

A

The activated subunits bind GTP and the inactivated subunits bind GDP

135
Q

The main target of G-proteins is _______

A

cAMP

136
Q

The main target of cAMP is _______

A

PKA

Activated by cAMP binding

137
Q

What does the sympathetic nervous system do to the L-type calcium channel?

A

L-type Ca2+ - slowed inactivation -> increased inotropy (contractility)

138
Q

What does the sympathetic nervous system do to troponin?

A

Troponin I - causes increased ca dissociation -> increased lusitropy (relaxation)

139
Q

What does the sympathetic nervous system to do phospholamban?

A

Inhibits, so it doesn’t inhibit SERCA

  • > faster resetting of Ca2+ levels in SR
  • > increases inotropy (increased SR load), lusitropy (faster removal of Ca2+)
140
Q

How is the HCN (funny current) channel activated?

A

cAMP directly

Most other ones are phosphorylated by PKA

141
Q

What 4 channels do the sympathetic and parasympathetic nervous systems act on to increase/decrease HR?

A

HCN
L-type Ca2+
RyR
NCX

Sympathetic - more cAMP by Gs
Parasympathetic - less cAMP by Gi

142
Q

What is the primary mechanism for parasympathetic control of heart rate?

A

The gamma G-protein subunit activates GIRK (G protein inward rectifier K channel), hyperpolarizing the cell

143
Q

Do smooth muscle cells have sarcomeres, troponin, or tropomyosin?

A

No

144
Q

How does sympathetic stimulation cause vasoconstriction?

A

NE activates AARs (alpha adrenergic receptors) on vascular SMCs

AARs are coupled to Gq (G-quirky.)

Increased IP3

Increases Ca2+ release from SR

145
Q

Where in the brain is the cardiovascular control center?

A

Medulla

146
Q

What is the primary mechanism by which blood flow in capillaries is matched to metabolic demand?

A

Vasoactive metabolites produced by metabolically active tissue act on receptors on VSMCs

147
Q

What is the myogenic response?

A

A feedback mechanism of VSMCs to maintain constant flow even with changes in pressure

Stretching causes vasoconstriction

148
Q

What are the 2 Mobitz types of 2nd degree AV blocks?

A

1 - PR lengthens until a P does not conduct

2 - PR interval is constant

149
Q

What is the ECG difference between atrial flutter and fibrillation?

A

flutter has P waves but fibrillaiton does not

150
Q

What causes a junctional rhythm? What does the ECG look like?

A

Where the AV node causes most of the heart’s beating

P waves are in the wrong place

151
Q

What does a premature ventricular contraction or ventricular tachycardia look like?

A

Wide, abnormal QRS

No P wave

152
Q

What are the ECG effects of hyper and hypocalcermia?

A

Shortens QT interval

Lengthens QT interval

153
Q

What are 3 ECG effects of hypokalemia?

A

Lengthened QT interval
Prominent U waves
T waves may be inverted

154
Q

What does the ECG reveal in acute pericarditis?

A

DIffuse ST elevation

155
Q

What is the drug of choice for acute pericarditis? What are 2 alternatives??

A

Ibuprofen

Aspirin, colchicine (for preventing recurrent pericarditis)

156
Q

What are 5 causes of pericardial iffusion?

A 
Pericarditis
Metastatic malignancy
Uremia
Autoimmune disease
Hypothyroidism
157
Q

What is the distinguishing symptomatic feature of pericardial pain vs. acute coronary pain?

A

It is aggravated by deep breathing and relieved by sitting up/postural changes

158
Q

What are 3 important effects of quinidine not related to Na+ channel block?

A

Blocks K+ channels real well -> prolongs AP duration

Vagal inhibitor

Alpha-adrenergic receptor antagonist

159
Q

What is cor pulmonale?

A

When primary lung disease causes right heart failure

160
Q

Is the autonomic nervous system part of the central or peripheral nervous system?

A

The peripheral

161
Q

How does the speed and specificity of the autonomic and somatic motor systems compare?

A

The autonomic system is slower and has diffuse projections

162
Q

What are 2 important inputs to the autonomic nervous system?

A

Nucleus of the solitary tract

Hypothalamus

163
Q

Comparing the sympathetic and parasympathetic systems,

Where do neurons originate?
Where are the ganglia located?
Which has the larger ratio of pre to post ganglionic neurons?

A

Sympathetic: Thoracic and lumbar spinal cord, near spinal cord (sympathetic chain), less (1:10 ratio)

Parasympathetic: brainstem and sacral spinal cord, near target organs, more (1:3 ratio)

164
Q

What does the subfornical organ do in terms of the CV system?

A

Detects low blood pressure

Causes release of vasopressin in posterior pituitary

165
Q

What does vasopressin do? (2)

A

Vasoconstriction

Increase water retention in kidneys

166
Q

What is the positive feedback input to the subfornical organ?

A

Angiotensin II activates neurons in the subfornical organ

167
Q

Calcium is sequestered in the SR by binding to _______

A

Calsequestrin

168
Q

What does phospholambin do?

A

Inhibits the SERCA calcium pump

169
Q

How are cardiac output and peripheral vascular resistance altered durig weight training?

A

Peripheral resistance is increased

CO stays the same

170
Q

How do the ATPase levels and myosin isotype ratio change with pathological hypertrophy? With physiological hypertrophy?

A

Decrease in ATPase and increase in BB MHC

Increase in ATPase and aa MHC

171
Q

What is orthopnea?

A

Immediate shortness of breath when lying flat due to blood pooling in the legs in heart failure

172
Q

What is pulse pressure like in heart failure with low flow?

A

It is low due to low output

173
Q

What are the 3 waves of jugular venous pressure? Draw

A

A - atrial contraction
C - closing of tricuspid valve in early systole
V - movement of right ventricle annulus and tricuspid valve backwards at the end of systole

174
Q

What causes S3?
When does it occur?
What sound does it make?

A

Rapid expansion of ventricular walls in early diastole

Dilated heart

‘kentucky’

175
Q

What causes S4?

What sound does it make?

A

Atria contracting against a stiff LV

‘tennessee’

176
Q

What 4 things cause B-type natriuretic peptide release?

A

Ventricular stretch (primary)

Secondary:
Hyperadrenergic state
RAAS activation
Ischemia

177
Q

What 2 tests are there for B-type natriuretic peptide level?

A

BNP

NT-proBNP, N-terminalbreakdown product of BNP (much higher)

178
Q

What is the diagnostic use of BNP (B-type natriuretic peptide)

A

Negatively predictive - a low BNP makes HF unlikely as the cause of symptoms

179
Q

What are the 2 groups of diuretics?

A 
Loop directics (usually sulpha drugs)
Thiazide diuretics (use to augment loop diuretics)
180
Q

What are 3 loop diuretics we care about?

A

Furosemide (most commonly used)
Bumetanide
Torsemide

181
Q

What are 3 ACE inhibitors we care about? What is ther dosing schedule?

A

Lisonipril - qd (most commonly used)
Enaliapril - bid
Captopril- tid

182
Q

What are 3 angiotensin receptor blockers? What is their dosing regimen?
When do you use them?

A

Valsartan BID
Candesartan QD
Losartan QD

‘The valiant knight Candy loses’

Use when patients develop cough to ACE inhibitors - they have been shown to be equivalent in studies

183
Q

What are the 2 mineralocorticoid receptor antagonists?

What are 2 side effects?

A

Spironolacetone
Eplerenone

Hyperkalemia
Gynecomastia (spironolactone only)

184
Q

What are the 2 side effects of beta-blockers?

A

Negative inotropy: fluid retention, hypotension, decreased CO

Bronchoconstriction

185
Q

The combination of which 3 drug classes decrases remodeling in heart failure?

A

Ace inhibitors/angiotensin receptor blockers (add first)

Beta blockers (add second)

Aldosterone receptor blockade

186
Q

What other drug class do you give for African Americans with heart failure in addition to the 3?

A

Arterial vasodilation antihypertensives: hydralazine/isosorbide dinitrate

187
Q

What is the clinical indication for cardiac resynchronization therapy (biventricular pacemakers)

A

Bundle branch block -> QRS >150 ms

188
Q

What are 3 positive inotropic agents, how are they administered, and how do they work?

A

Digoxin (PO) - K/Na exchange
Dobutamine (IV) - beta agonist
Milrinone (IV) - phosphodiesterase inhibitor, similar effect as above

189
Q

ACE inhibitors also act on______, causing ______

A

Kinin II -> increase in bradykinin (which is protective!)

Cough (a pulmonary irritant)

190
Q

6 side effects of ACE inhibitors

A 
Cough
Hyperkalemia (becaus angiotensin II gets rid of potassium)
Angioedema
Renal dysfunction
Neutropenia
Hypotension
191
Q

What are the side effects of angiotensin inhibitors?

A

Less angioedema, cough than ACE inhibitors

Also hyperkalemia
Uricosuric effects (can make gout worse)
192
Q

What are the only 3 beta blockers that have been shown to reduce mortality?

A

Bisoprolol BID
Carvedilol BID
Metroprolol succinate QD

193
Q

HFpEF is also known as _______ heart failure

A

Diastolic

194
Q

What are the unipolar limb leads of the EKG?

A

aVR - to right arm
aVF - to left foot
aVL - left arm

AV = augmented vector

195
Q

What are the bipolar limb leads of the EKG?

A

In an equilateral triangle of each arm and left leg

I points straight across from right arm to left arm
II is from right arm to left leg
III is from left arm to left leg

196
Q

What defines Q, R, and S waves?

A

Q is downward deflection
R is upward deflection
S is downward deflection following an upwards one

197
Q

What are the grid lines on the EKG?

A

.1 mV / .5 mV

0.04s/0.2s

198
Q

What are the steps for analyzing an EKG?

A 
Voltage
Rhythm
Rate
Intervals
Mean QRS axis
P wave abnormalities
QRS abnormalities
ST abnormalities
199
Q

What are 5 class III antiarrhythmic drugs?

A 
Ibutlide
Dofetilide
Amiodarone
Sotalol (also a beta-blocker)
Bretylium
200
Q

What are 2 class IV antiarrhythmic drugs?

A

Verapamil

Diltiazem

201
Q

Does OTC cough medication work on kinin cough?

A

No, because it is a different mechanism

202
Q

What are 5 drugs that interact with ACE inibitors?

A

Lithium and other salt substitutes
NSAIDS
Loop diuretics
K+ sparing diuretics (because can cause hyperkalemia)

203
Q

What happens to receptor selectivity as beta blocker dose increases?

A

Selectivity decreases (for either beta1/beta2/alpha1). For heart, I think we want beta receptors

204
Q

Which organ metabolizes beta blockers?

A

The liver, so don’t use in liver failure

205
Q

What blood pressure defines hypertension?

A

> 140/90

206
Q

Which type of heart failure can lead to liver congestion?

A

Right heart

207
Q

What is myxomatous degeneration?

A

Pathological weakening of connective tissue (usually used in context of mitral valve prolapse)

208
Q

Rheumatic fever is when antibodies form against ______ of which bacteria?
What does this cross-react with?

A

M protein
Group A strep (GAS)
Glycoproteins

209
Q

What is the Jones Criteria for rheumatic fever?

A 
Joints
O - myocarditis
Nodules, subcutaneous
Erythema merginatum
Syndenham chorea
Minor:
CRP increased
Arthralgia
Fever
Elevated ESR

Prolonged PR
Anamnesis of rheumatism
Leukocytosis

210
Q

What are Aschoff bodies?

A

Collectionsof mononuclear cells in the myocardium during carditis

211
Q

Which valves are usually affected in endocarditis? (2)

A

Mitral (65-75%)

Aortic (25%)

212
Q

What is a sterile/marantic/non=bacterial vegetation from?

A

Thrombus on valve

213
Q

Which is the most common primary tumor of the heart in teens and adults? Where is it located?

A

Cardiac myxoma

LA&raquo_space; RA > other sites

214
Q

Mutations to which 3 proteins are present in 70-80% of hypertrophic cardiomyopathies?

A

Myocin-binding protein C
Beta-myosin heavy chain
Cardiac troponin T

215
Q

Mutations to which 4 proteins are oten found in dilated cardiomyopathy?

A

Desmin
Dystrophin
Sarcoglycans
Lamin

216
Q

How much of hypertrophic cardiomyopathy is due to genetics?

A

All of it

217
Q

What structural change occurs in hypertrohic cardiomyopathy?

A

Thickened interventricular septum bulges into the LV outflow tract during early systole -> outflow obstruction

218
Q

What is Sq? What is S2?

A

Closeure of the AV valves

Closure of the semilunar valves

219
Q

What causes the vast majority of mitral stenosis?

A

Rheumatic (80-99%)`

Second most is calcific (3%)

220
Q

How is a tricuspid regurgitation murmur affected by breathing?

A

It becomes louder during inspiruation

221
Q

What happens to the jugular during tricuspid regurgitation (2)?

A

Jugular venous distension

Systolic V wave

222
Q

What is the most common cause of tricuspid regurgitation?

A

From RV pressure/volume overload

223
Q

What is the most common congenital cardiac defect?

A

Bicuspid aortic valve

Like 1% of people

224
Q

When do you treatbicuspid aortic valve?

A

When symptoms begin. Otherwise, you die pretty quickly

225
Q

Should you use ACE inhibitors and angiotensin II receptor blockers at the same time?

A

No. THere is no added benefit

226
Q

What are 2 aldosterone antagonists we care about?

A 
Spironolactone
Eplerenone (use if edocrine side effects occur with spinonolactone)
227
Q

Digoxin works via the _______

A

Neurohormonal modulator

228
Q

How is digoxin excreted?
How long does it take to reach steady state?
What is its volume of distribution?

A

Renally
7-10 days
5-7 L (so, blood volume)

229
Q

What disease is digoxin used to manage?

A

HFrEF (heart failure with reduced ejection fraction)

It reduces hospitalizations

Does not benefit HFpEF

230
Q

What 5 drug classes are indicate careful digoxin dosing? (a 50% dicrease in dosing)

A 
Antiarrhytymics
Antifungals
Calcium channel blockers (particularly verapamil)
Quinine
Macrolides
231
Q

Digoxin toxicity can cause changes to which 3 ions?

A

Hypokalemia
Hypercalcemia
Hypomagnesemia

232
Q

What are the 2 drugs to increase inotropy?

A

Dobutamine - Beta1 agonist, slight peripheral vasodilation
Milrinone - phosphodiesterase inhibitor (something about heart disease), increases myocyte Ca2+ utulization, moderate peripheral vasodilation

233
Q

What does dopamine administration do to the heart

A

Stimulates adrenergic receptors

Releases norepinephrine form nerve terminals (not sure what this does)

234
Q

What is the difference between pericardial effuson and tamponade?

A

Tamponade is a worse effusion, where there is a decrease in blood output to the body

235
Q

What is the clinical presentation of pericardial effusion with tamponade (3)?

A

Decreased RV diastolic filling during inspiration
Distended neck veins
Inspiratory decrease in arterial pressure (paradoxical pulse) - because RV filling squishes LV filling

236
Q

What happens to the IVC during tamponade?

A

It doesn’t have the normal 50% reduction during inspiration. It remains dilated.

237
Q

What are 2 EKG findings in cardiac tamponade?

A

Sinus tachycardia
Low voltage
Electrical alternans (alternating QRS height that reflects swinging of heart in pericardium(

238
Q

What happens to RV and LV diastolic pressures during constrictive pericarditis?

A

They become equal

Both become elevated and equal because heart filling is restricted

239
Q

How do you calculate heart rate from an EKG?

A

300/# heavy lines between QRS

1500/# small lines between QRS

240
Q

Which 2 leads monitor the RV?

Which 2 leads monitor the LV?

A

V1,V2

V5,V6

241
Q

What causes ST depression?

A

Ischemia due to sudden high oxygen demand that can’t be met (coronary blood flow can’t be increased)

242
Q

What cause T wave inversion?

A

Ischemia due to acute coronary artery obstruction during low oxygen demand (coronary blood flow suddenly is lessened)

243
Q

What EKG findings do transmural infarcts produce?

What about subendocardial infarcts?

A

Q waves - a negative deflection in leads over the infarcted myocardium

ST depression

244
Q

What is heart failure?

A

When the heart can’t pump enough blood forward to meet the demands of the body (forward), or can only do so if cardiac filling pressures are super high (backward failure)

245
Q

What is chronotropic incompetence?

A

An inability of the heart to regulate its rate appropriately in response to physiologic stress

246
Q

What are 2 indications for teatment of bradyarrhythmias?

A

When the patient is symptomatic

When the rhythm is below the AV node

247
Q

Which of the AV blocks are infranodal?

A

2 and 3 (idk why…)

248
Q

How you distinguish single and multifocal atrial tachycardia?

A

3+ p-wave morphologies

249
Q

When do you cardiovert people?

A

If a rhythm is hemodynamically unstable (syncope, confusion, end organs aren’t perfused)

250
Q

What does adenosine do for arrhythmias?

A

It temporarily blocks the AV node

251
Q

What is the pathophysiology of Atrioventricular nodal reentrant tachycardia

A

fast and slow pathway through AV node
A properly timed extra beat can go down the slow and up the fast pathway

Atria and ventricles depolarize simultaneously

252
Q

What does the EKG look like in atrioventricular reentrant tachycardia?

A

Shortened P-R interval
Slurred QRS with delta wave

Because, there is no pause between atrial and ventricular contraction

253
Q

What is a nonpharmacologic maneuver for atrial tachycardias?

A

Vagal maneuvers - slow AV conduction

254
Q

What are the 5 C’s of atrial fibrillation management??

A 
reverse Cause
Control rate
antiCoagulate
Control rhythm (consider)
Catheter ablation (consider)
255
Q

What 2 drug types are used for rhythm control in supraventricular tachycardia?

A

CLass 1C agents

CLass III agents

256
Q

What 4 medication classes are for ventricular tachyarrhythmmias?

A

Beta blockers, calcium channel blockers, class iC, class III

257
Q

Nearly all diruretic agents exert their effects ath the_____ surface of renal tubule cells

A

Luminal (urine)

258
Q

Na+ is the major extracellular cation and its movement between compartments is controlled by regulated active transport via _________ activity at the ______ surface

A

Na/K ATPase

Interstitial (blood)

259
Q

What does acetazolamide do?

A

ReInhibits carbonic anhydrase, resulting in retention of HCO3- in urine and mild alkaline diuresis (so… we don’t really use it as a diuretic)

260
Q

Draw the sites of diuretic action

A

:)

261
Q

What is the range (in degrees) of the normal QRS axis?

A

-30-+90

262
Q

What does the P-wave look like in RA and LA enlargement? Draw!

A

mrr

263
Q

What 2 drugs are for ventricular arhythmias?

A

Beta-blockers - proven benefit

Amiodarone - maybe benefit

264
Q

What is a disadvantage of Angiotensin II receptor antagonists compared to ACEIs?

A

They don’t have bradykinin actions

265
Q

How does serum K+ affect condctance?

A

Low - decreased conductance despite increased electrochemical gradient

High - increased conductance despite decreased electrochemical gradient

266
Q

How does QT length affect risk of torsades?

A

QT prolongation increases risk of torsades and this further increases with low K+

267
Q

What loop diuretic substitute can be used if there is a sulfa sallergy?

A

Ethacrynic acid

268
Q

How does the AHA organize cardiomyopathies?

A

Genetic
Acquired
Mixed

269
Q

Sarcomeres are added in _____________ in eccentric hypertrophy

A

Series

270
Q

What is outflow tract obstruction? What condition is it often seen in?

A

Mitral valve in mid-systole covers outflow tract to the aortic valve

Hypertrophic cardiomyopathy

271
Q

What are the murmur characteristics in hypertrophic cardiomyopathy?

A

Systolic

Louder with standing/valsalva (increases LV volume) and softer with squatting

272
Q

What is restrictive cardiomyopathy?

A

Decreased ventricular volumes with normal ventricular wall thickness

273
Q

How does digoxin slow the AV node?

A

Increasing vagal tone, probably via the neurohormonal modulator

274
Q

What drug is good to combine angiotensin 1 receptor blockers with?

A

Neprilysin inhibitor

275
Q

Are there any diuretics that inhibit Na/K ATPase?

A

No! They just decrease Na+ reabsorption at vairous sites in the nephron

276
Q

What EKG change is evident in hyperkalemia?

A

Peaked T waves

277
Q

What happens to the pacemaker rate in n hyperkalemia? Action potential duration? Conduction rate?

A

HR slows
AP is shorter
Conduction rate is slower

278
Q

How do loop diuretics work?

A

They inhibit NaCl transport via the Na/K/2Cl transporter

279
Q

What happens to blood pH with loop diuretics

A

Hypokalemic metabolic alkalosis because more Na+ is absorbed at the collecting tubule, resulting in more K+ and H+ excretion

280
Q

Draw effect of diuretic agents on plasma electrolytes

A

Mrr

281
Q

How do thiazide diuretics work?

A

They inhibit the Na/Cl cotransporter

282
Q

What do thiazides do to serum calcium levels?

A

The increase reabsorption (ice cream fall out of slide)

283
Q

What are 5 side effects of thiazides?

A 
Hypokalemia
Hyperglycemia
Hyperuricemia (gout!)
Hyperlipidemia
Allergy - sulfa
284
Q

Which 2 diuretic classes increase K+?

A

ACE inhibitors

Aldosterone receptor inibitors

285
Q

What are the 2 ways K+-sparing diuretics work?

A

Competitive antagonist at aldosterone receptor (spironolactone/eplerenone)

Direct block of Na+ channels (triamterene/amiloride) - not used in HF

286
Q

How does spironolactone help in heart failure besides being a diuretic?

A

Blocks aldosterone receptors in heart, reducing remodeling

287
Q

Which 3 drugs can you use on stable ventricultachyarrhythmias (like after shock)

A

Amiodarone
Lidocaine
Procainamaide

288
Q

What is a dyhydropyridine we care about?

A

Nifedipine

289
Q

How does adenosine work?

A

Agonist at A1 receptor ast AV node
It hyperpolarizes by increasing K current and reduces phase 0 Ca current, thereby inhibiting AV node and increasing its refractory period

290
Q

How do you treat bradyarrhythmias?

A

Pacemaker if symptomatic

Very limited role for medications

291
Q

What 3 drugs can increase vagal tone, reducing AV block?

A

Dopamine
Epinephrine
Atropine

Only for short term
Long-term pharmacotherapy is not possible and requires pacemaker

292
Q

Which potassim state can cause early afterdepolarizastions?

A

Hypokalemia

293
Q

Which drug is a parasympathomimetic?

A

Digoxin

294
Q

Does the aortic of pulmonic valve close first?

A

Aortic

295
Q

When is S2 1 sound? When is it 2 sounds?

A

Expiration

Inspiration (A2 P2)

296
Q

WHEN are S3 and S4 heard in the heart cycle?

A

S3 - diastole systole

S4 - late diastole

297
Q

PHosphorylation of troponin I weiincreases ______

A

LUsitropy/relaxation

Spring 2016 - CVPR (4 decks)

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