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Pharma 2 > Lecture 4 - Cardiac Pathology & Pharmacology > Flashcards

Lecture 4 - Cardiac Pathology & Pharmacology Flashcards

1
Q

What creates the P wave?

A

Atrial contraction

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2
Q

What causes the QRS wave?

A

Ventricular contraction

NOTE: the atrium is still contracting at this point, however, its covered because ventricular contraction is so much more

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3
Q

KNOW: Myocardial perfusion = the fluid (blood) that your heart gets

A
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4
Q

When does myocardial perfusion happen?

A

Diastole - Happens during periods of relaxiation (when the ventricles arent actively contracting)

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5
Q

KNOW: The heart has many collateral vessels - just like the circle of willis - to keep blood from being blocked

A
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6
Q

What inhibits myocardial perfusion?

A

Resistance - such as atherosclerosis

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7
Q

Where does plaque buildup originate?

A

Tunica intima

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8
Q

What is coronary perfusion pressure?
* What happens if this is inadequate?

A

The pressure gradient that moves blood through the hearts coronary arteries to supply the myocardium w/ O2

If its not enough it could lead to ischemia which could lead to a MI

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9
Q

Cornary Perfusion Pressure equation

A

Cornary Perfusion Pressure = Aortic diastolic pressure - left ventricular end diastolic pressure

Cornary perfusion pressure. represents the net pressure driving blood into the coronary arteries to supply the heart muscle

Aortic Diastolic Pressure - BP in the aorta during diastolie - its the pressure available to push blood into the coronary arteries, which supply blood to the artery

LVEDV - pressure inside LV at the end of diastole - represent the back pressure or resistance that opposes the flow of blood into the coronary arteries

The higher the aortic diastolic pressure, the more force there is to push blood into the coronary arteries

However, the LVEDV acts as a resistance opposing force. If LVEDP is high, it reduces the effective pressure available for cornary blood flow

If CPP is too low, the heart may not get enough blood, leading to conditions like ischemia which lead to MI

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10
Q

What is the occulsive force in endocardium?

A

Left ventricular end diastolic volume - because it can push on the endocardium (exert pressure) blocking the blood flow to it

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11
Q

Coronary perfusion pressure = aortic driving pressure

A
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12
Q

2 biomarkers for acute coronary syndrome and heart failure?

A

1) Troponins
2) Natriuretic Peptides

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13
Q

TEST Troponins have a high specificity for myocardial cell injury or infarct (they exist when these things are going on).

What is the norm for cardiac Troponin T?

What is the norm for cardiac Troponin I?

What is the norm for High-Sensitivity Cardiac Troponin (Men and Women)?

A

Troponin T = <0.1 ng/L (over this # is abnormal)

Troponin I: <0.03 ng/mL (over this number is abnormal)

High-Sensitivity Cardiac Troponin: Women < 14 ng/L; Men <22 ng/L (greater than these #’s is abnormal)

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14
Q

Troponin #’s have to be trending down for PT to see them. Describe the trend

A

3 consecutive labs trending down

They can still be elevated, they just need to b going down

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15
Q

Why might we not want to do exercise w/ someone w/ heart pathology?

A

Because at rest all the blood is routed to vital organs; however, w/ EX, some of that blood is routed to external musculature, not leaving as much blood for internal viscera, meaning they won’t have as much blood to work with, and if they’re already ischemic this could be problematic.

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16
Q

KNOW: Natriuretic Peptides are made by the heart, and commonly used to assess for heart failure.

A
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17
Q

Brain Natriuretic Peptide (BNP) is releated in response to what two things?

A

Artiral or Ventricular Stretch

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18
Q

A Brain Natriuretic Peptide (BNP) count of what indicates heart failure? Which number is a normal #?
* What causes an increase in this?

A

> 400 indictes that heart failure is likely

<100 is normal

NOTE: This # increases over the lifetime because it responds to increase stretch in the heart, and we have cardiac enlargement as we age

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19
Q

Which sex has more Brain natriuretic peptide?

A

Female

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20
Q

Does Obesity cause more or less brain natriuretic peptide and why is that an issue?

A

Causes Lower BNP

It’s an issue because we might not know they’re at risk for heart failure
* I think the reasoning is due to increased blood volume in obese people

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21
Q

N-terminal fragment of pro-brain natruiretic peptide (NT-pro-BNP) is another fariation of natriuretic Peptides. What number is normal?

A

<300 pg/mL

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22
Q

TEST A value off 200 is normal for Brain natruitetic Peptide (BNP) or N-terminal frament of pro-brain natriuretic peptide (NT-pro-NBP)?

A

NT-pro-NBP

Anything under 100pg/mL is normal for BNP

Anything under 300 pg/mL is normal for NT-pro-NBP

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23
Q

Symptoms that signify an acute MI, as a result of insufficient supply to cardiac muscle =

A

Acute Coronary Syndrome

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24
Q

What causes a type 1 myocardial infarction?

What causes a type 2 myocardial infarction?
* What sex does this happen more in?

A

A blockage = type 1

Mismatch of supply and deman ratio = type 2
* can also be due to spasm
* Women > men

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25
Q

KNOW: Diagnosis of mycardiac infacrtion made by a rise/fall/both in a blood test sensitive to myocardial damage with at least one value above the 99th percentile of the upper reference limit with cinical evidence
* labs and clinical symptoms
* mainly looking at the 3 troponin levels

A
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26
Q

A patient has a full thickness myocardial infarction. What does this mean and what structure gets affected thats really important?

A

Full thickness means that cell death happens all the way down to the endocardium

Its super bad because the cardiac valves originate from the endocardium, meaning there can now be backflow/valve pathologies.

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27
Q

STEMI/NSTEMI are cnosidered type 1 or type 2 maycardial infarctions?

A

They’re both considered type 1

caused by some kind of blockage

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28
Q

3 things that make up NSTEMI

A

1) No ST elevation
2) Less Necrosis
3) Elevation of cardiac biomarkers (think tropinin)

Remember, this is classified as a type 1 myocardial infarction.

NOTE: Stands for No ST elevation Myocardial infarction

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29
Q

What 3 things make up a STEMI myocardial infarction?

A

1) ST elevations in lateral leads (V5-6)
2) Most severe
3) Abnormal cardiac markers

NOTE: Stands for ST elevation myocardial infarction

Classified as a type 1 myocardial infarction (some kind of blockage caused it)

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30
Q

Whats more severe STEMI or NSTEMI?

A

STEMI

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31
Q

Which one of these is a STEMI ECG?

A

2

Notice the ST segment elevation

NOTE: The isoelectric line is in yellow

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32
Q

Which of these is classified as a NSTEMI ECG

A

3

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33
Q

When is ST segment is above the isoelectric line is it considered STEMI or NSTEMI?

A

STEMI

34
Q

The ST segment is at the isoelectric line. Is it STEMI or NSTEMI?

A

NSTEMI

Its only STEMI if that ST segment is elevated

35
Q

KNOW: Risk factors for STEMI:
* Dyslipidemia
* Diabetes mellitus
* Hypertension
* Smoking
* Family hx of coronary artery disease

A
36
Q

Refferal patterns

A
37
Q

A 69 year old female presents to the ER with chest pains. Which of the following lab values will most likely indicate an MI?

1) Cardiac Troponin T = 0.9
2) High-Sensitivity Cardiac Tropnin = 20
3) NT-pro BNP = 300
4) BNP = 400

A

They’re all tehcnically positive

38
Q

Heart failure = heart slowly giving up
*deconditioned

Myocardial infarction = acute failure

A
39
Q

Signs of heart attack
* Notice lots of these symptoms are prolonged, not just for a second

A
40
Q

What are prodromal Symptoms?

A

Any of those heart attack symptoms that can occur 1 month prior to MI

They’re like warning signs

41
Q

percutaneous coronary intervention (PCI) is what and what is it used for

A

group of interventions –> when they go in and make sure there is no blockage
* used to widen the arteries

Its the perfurred medical management for a stemi

However, you need to get to a hospital that performs these within 30 minutes of the initial incident

42
Q

What do thrombolytics do and what are they used for?

A

Break up blood clots
* Must be used within 6-12 hours within onset of symptoms

Used for STEMI when PCIs are unavailable

43
Q

What two treatments are used for STEMI and which one if perfurred?
* Time of administration?

A

Precutanous coronary intervention = perfurred (within 30 minutes)

Thrombolytics (within 6-12 hours)

44
Q

Perfurred treatment for a NSTEMI?

A

Coronary angiography for majoirty
* Little camera put through vessel and up to heart to make sure blodo vessel isnt spasmsing or kinked / other pathologies, and make sure vessel is opened up.

45
Q

KNOW: Medical clearance is needed to exercise following MI

A
46
Q

Submax EX is recommended within how many days after an MI?

A

within 3 days

47
Q

Progressive phyiscal activity (not exercise) and pacing must beging within ___ hours after hospitization of an MI?

A

within 24 hours PA should start

48
Q

Light intensity EX = how many METS?

A

< 3 = light

49
Q

Moderate PA METs

A

3 to 6

50
Q

Vigrous intensity activities

A

> 6

51
Q

In acute cardiac rehab how do we EX a cardiac patient? (this is phase 1 of cardiac rehab)

A

Start at 1-2 METs and progress to 3-6 METs (moderate EX) and then discharge

52
Q

How long should you wait to exercise following a tPA infusion?

A

24 hours

typically given after stroke =, but a myocardial infarction is much like a stroke

53
Q

know roughly which category each activity falls in

A
54
Q

Contraindication to exercise w/ MI (11)

A

1) Unstable angina (unpredictable)
2) Less than 1 or 2 days post MI (more for Exercise in moderate/vig category - METS 3+)
3) New ECG changes - since the MI
4) Si/Symptoms of MI
5) Oxygen saturation < 85%
6) Suspected dissecting aneurysm (burning/lightheadedness)
7) RR > 45
8) Polmonary emblism
9) Uncontrolled hypertension or Diabetes
10) Acute injection
11) Digoxin Toxicity - medication used for heart failure

55
Q

KNOW: In a Coronary aryery Angioplasty they use the radial or femoral artery to stick a tube up to the heart and remove plaque, put in stents, or blow up a baloon

Patient is normally awake

A
56
Q

Disturbances in heart rate or cardiac rhythm (conduction pattern [SA node –> AV node, bundle of HIS –> Perk)

A

Arythmia

57
Q

What are the 3 ways arythmias are classified

A

1) Origin
2) Pattern
3) Speed

Can be ventircular or supraventricular, fibrillation or flutter, tachy or brady.

58
Q

When looking for arythmias you’re looking to see that the R waves are regular

(can also see the same thing by taking a pulse)

A
59
Q

Where is the SA node located?

A

R atrium

pacemaker

NOTE: AV node also located in R atrium - delays to give atrium time to eject all blood into ventricles

60
Q

Risk factors for arythmias: (10)

A

1) Diabetes
2) Obstructive sleep apnea
3) Smoking
4) Alcohol
5) Increased pulse pressure
6) Family hx
7) Left ventricle enlargement
8) Increased left ventricular wall thickness
9) High BMI
10) Heart failure

this things will all alter the conductivity of the heart

61
Q

TEST What is normal pulse pressure

A

40-60

62
Q

S/S of arythmia (4)

A

1) Rate: Significant devation from the normal range
2) Rhythm: Variation from normal heart rhythm
3) Palpitations, fatigue, shortness of breath, syncope (fainting)
4) Some people can be asymptomatic

63
Q

KNOW: Different kinds of arrhythmias
* Sinus arrhythmia (SA node - R atrium)
* PACs
* Atrial Tachy
* PAT oR PSVTAtrial Flutter
* Atrial Fibrillation
* Junctional (nodal) Rhythm
* PVCs
* Ventricular Tachy (torsades de pointes)
*** Ventricular fibrilation **

A
64
Q

what are these

A

Torsades de pointes (happen w/ ventircular tachy)
* heart can’t refukk

65
Q

Know: If PVCs arrhthmia occurs in 3 or more they become ventricular tachycardia –> that becomes serious when you get torsades de pointes (looks like a coil), heart is not able to relax and fill blood and pump if its just a coil.

A
66
Q

What is cardioversion?

A

Low levels of electrical stimulation w/ the goal of regulating the heart. It is timed w/ the hearts electrical system

67
Q

defibrilator

A

electrical current given to the heart - not timed w/ hearts electrical system

68
Q
A
69
Q

What is timed w/ the hearts electrical system, a defibrilator or cardioversion?

A

cardioversion is a shock thats timed w/ the hearts electrical system.

70
Q

KNOW: Everytime you have a flutter you can throw a clot

A
71
Q

Defibrillators are paired with what drug and why?

A

Anticoagulant therapy

because w/ every flutter they can throw a clot

72
Q

KNOW: Surgical options for arrythmias

Ablation: can essentially burn around where the signal travels to get it to go in the right direciton

pacemakers

Maze procedure

A
73
Q

TEST What are the 4 drugs used to treat arrhythmias and there classes?

A

Class I - Sodium Channel Blockers
Class II - Beta Blockers
Class III - Potassium Channel Blockers
Class IV - Calcium Channel Blockers

74
Q

What drug do you use for a tachycardia arrhythmia?

A

beta blockers (class 2)
* Slows down HR

75
Q

what do potassium channel blockers do for arrhythmias?

A

Prolong reportization (rest period)
* makes sense - they block some of the potassium coming back in making reporization take longer

76
Q

What do calcium channel blockers do as medication for arrhythmias?

A

Work best for bradycardia (speed up HR)

77
Q

MOA for sodium channel blockers? (arrythmias)

A

Bind to membrane sodium channels in various excitable tissues, including myocardial cells

act during phase 0 of the cardiac action potential

78
Q

Most common side effect of anti arrhythmia class 1 drugs (sodium blockers)

A

arrhymias

drugs that are used to treat arrythmias may increase arrythmias

drugs are also associated with a variety of side effects such as dizziness, visual distrubances, nausea, vomiting, and dirrhea

79
Q

Class II antiarrhytmia drugs are beta blockers. explain their MOA?
* What condition are they best used to treat?
* What suffix do they end in

Adverse effects?

A

There are beta-1 receptors on the myocardium

they act antagonisticlly to block epi/nor from binding to beta 1 receptors on the myocardium

**They decrease cardiac HR/contractility and prolong effects of refractory period, so work really well for tachycardia. **

End in -lol

Adverse effects = Can produce excessive slowing of cardiac conduction and thus cause arrhythmias (causes bradycardia)

Beta 1 = 1 heart
Beta 2 = 2 lungs

80
Q

What do potassium channel blockers do for arrythmias? MOA?
* what kind of arrhythmia is it for (2)
* specific calcium channel blockers name

A

Prolong reporization = longer refractory period = slower HR

mediated by inhibition of potassium efflux during repolorization (blocks potassium from going in and slowering it down)

Selective ability to block calcium entry into myocardial and vascular smooth muscle cells
* This blocks the binding of actin and myosin filaments and decreases the contractility (slows everything down)

ventircular arrythmia and supra ventircular arrhythmias

81
Q

Adverse effects of calcium channel blockers

A

increase in cardiac arrhythmias (proarrhythmic effect)

because they slow and steady the heart they can create PVCs –> ventricular tachy –> Torsades de pointes

Bradycardia

in smooth muscle: vasodilation leading to dizziness and HA’s

82
Q

(

A

Pharma 2 (23 decks)

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