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Physiology 2 > KIN 407 Midterm 2 > Flashcards

KIN 407 Midterm 2 Flashcards

1
Q

Acute coronary artery syndromes?

A

Stable angina pectoris, unstable agina, acute MI, sudden cardiac death

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2
Q

What determines myocardial oxygen supply?

A

O2 content from coronary blood flow…coronary perfusion pressure, coronary vascular resistance (external compression and intrinsic regulartion via neural innervation, endothleial factors, and local metabolites)

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3
Q

What determines myocardial oxygen demand?

A

Wall stress and heart rate and contractility

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4
Q

Situational triggers of coronary events?

A

Physical exertion, emotional excitement or anger, large meal, cold weather (vasoconstriction)…all constrict arteries or rupture plaque

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5
Q

Stenosis at 70% versus 90%?

A

70%, BF is adequate at rest but becomes a challenge with stress…stenosis at >90% is insufficient BF at rest

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6
Q

5 types of angina pectoris?

A

Stable angine, silent angina, variant angina, unstable angina, postprandial angina

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7
Q

What is stable angina?

A

chronic pattern of angina, narrow lumen, vasoconstriction, relieved by rest, NO PERMANENT DAMAGE

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8
Q

Variant angina?

A

pain at rest, coronary artery spasm, but if severe enough can cause sudden cardian death. “Prinzmental angina”

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9
Q

Silent angina?

A

No symptoms/pain, detected by EMG, diabetics, women and old people are most common, damage to microvasculature of heart

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10
Q

unstable angina?

A

Increased frequency and duration of angia, platelets –> thrombus, pain during less exertion or rest, high freqency of progression to an MI

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11
Q

Postprandial angia?q

A

After a meal, a marker of extensive CAD and can precipitate to an MI

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12
Q

Consequences of ischemia?

A

1) Swithch from aerobic to anaerobic metabolism because of inadequate O2 2) Impaired contraction (both systolic contraction and diastolic relaxation…both require O2) 3) Increased LV diastolic pressure –> pulmonary congestion (dyspnea) 4) Waste products (esp. H+) activate peripheral pain receptor in the C7-T4 causing angina and triggers arrhythmia 5) Increased SNS, leading to sweating, high HR and BP

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13
Q

Symptoms of angina?

A

Chest pain (pressure, discomfort, tightness, burning, heaviness. location is diffuse not localized). tachycadria, sweating, nasusea, fatigue and weakness. ECG changes

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14
Q

Diagnosis of ischemia/angina/

A

history, physical exam, ECG, stress testing, nuclear imaging studies, echocardiogram, coronary angiography

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15
Q

Treatment for ischemia?

A

restore O2 supply balance, pharmacology, revascularization, coronary bypass sutgery

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16
Q

What is an MI?

A

A myocardial infarction…death of tissues (myocardial necrosis)…prolonges cessation of blood supply…acute thrombus,,,depends on amount of occlusion and extent of collateral circulation…damage is IRREVERSBLE

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17
Q

SIgns of unstable angina?

A

ST depression, no tissue damage, partial occlusion, no necrosis of tissues, no TN-T or TN-I in blood

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18
Q

Signs of a non-St-elevation MI (NSTEMI)?

A

ST depression, damage, partial occlusion, necrosis of tissue, TN-I an TN-T in blood

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19
Q

ST-Elevation MI (STEMI)?

A

ST elevation, damage (most), complete occlusion, necrosis of tissues, TN-I and TN-T in blood

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20
Q

What is a transmural infarct?

A

Entire thickness of myocardium, and results from total prolonged occlusion

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21
Q

What is a subendothelial infarct?

A

Inner most layer of the myocardium…some contraction may still occur

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22
Q

Amount of tissue affected from a MI depends on?

A

Mass of affected myocardium, magnitude and duration of impaired flow, O2 demand at that region, collateral circulation (more collaterals = less damage), the degree of tissue response that modifies the ischemic response

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23
Q

Metabolic changes occur hoe long after blood flow decreases?

A

Decrease function in 2 minutes

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24
Q

When does irreversible cell injury occur?

A

20 minutes

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25
Q

WHen does edema occur in an infarcted heart?

A

4-12 hours

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26
Q

When do wavy myofibrils appear after an infarct?

A

1-3 hours

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27
Q

When does total necrosis of cardiac tissue occur following an infarct?

A

2-4 days

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28
Q

When does clearing of the necrotic myocardium happen in an infarcted area?

A

5-7 days

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29
Q

WHen does the deposition of collagen to form scar tissue begin in the infarcted heart?

A

7 weeks

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30
Q

What are the functional alterations of ischemia?

A

Systolic dysfunction, wall motion abnormalities, diastolic dysfunction, ventricular remodelling

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31
Q

Ventricular remodeling due to ischemia causes what?

A

Thinning and infarcted tissues (increases wall stress, impairs systolic contraction, increases likelihood of aneurysm), dilation of noninfarcted wall (increases Q at first, but leads to heart failure/arrhythmias later on)

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32
Q

Systolic dysfunction due to ischemia is caused by?

A

Lack of ATP and death of cells…leads to impaired ventricular contraction

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33
Q

What are the wall motion abnormalities caused by ischemia?

A

Hypokinetic (low functional movement), Akinetic (no movement), Dyskinetic (outward bulge instead of contracting)

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34
Q

Diastolic dysfunction due to ischemia is caused by?

A

lack of ATP…impaired diastolic relaxation, which causes the intraventricualr pressure to being to rise leading to dyspnea

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35
Q

What are the 4 ways a MI is diagnosed?

A

Patient’s symptoms, Acute ECG abnormlaities (ST segment elevation, T wave inversion, Q wave developments), Detection of specific serum markers of necrosis (cTNI, cTNT), Imaging

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36
Q

Clinical features of a MI?

A

chest pain, shortness of breath, anxiety, weakness, tiredness, sweating, dizziness, palpitations, nausea, vomiting

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37
Q

Sympathetic effects of a MI?

A

triggered by pain, diaphoresis, cool/clammy skin, anxiety, dizziness, palpitations

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38
Q

Parasympthetic effects of a MI?

A

nausea, vomiting, weakness

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39
Q

WHen do serum markers appear in the blood following an MI, when do they peak?

A

3-4 hours after pain, peak 18-36 hours

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40
Q

Main serum markers of a MI?

A

cTNT and cTNI

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41
Q

Imaging techniques for discovering a MI?

A

echocardiography, stress test, angiography

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42
Q

Immediate care for a MI?

A

ECG, pain control, pharmacology (anti-ischemic, anti-thrombotic, anticoagulant), adjuvant (statin and ACE inhibitors)

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43
Q

What is the fibrinolytic therapy for acute treatment of STEMI?

A

Recombinant tissue-type plasminogen activator such as Alteplase, reteplase, or tenectplace, which all stimulate the natural fibrinolytic system to break down blood clots. Complications = bleeding

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44
Q

Triggers of sudden cardiac death?

A

transient ischemia, hemodynamic fluctuations, neurovascular fibrillation, environmental factors

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45
Q

Predominant cause of sudden cardiac death in adults?

A

CAD…plaque disruption with thrombus occlusion

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46
Q

Triggers of CAD that lead to sudden cardiac death?

A

wall stress, flexing of artery, augmenting catecholamine-induced platelet aggregation, coronary artery spasm/variant angina

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47
Q

hypertrophic cardiomyopathy and sudden cardiac death?

A

inherited condition…enlargement of the cells in the heart wall, especially the left ventricle, thickens the heart muscle, decreases stroke volume, inefficient contraction of sarcomeres, can cause electrical conduction disturbances and lethal heart rhythms

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48
Q

3 rules of cardiac vectors?

A
  1. Toward + electrode = upright deflection 2. away from + electrode = downward reflection 3. Perpendicular to + electrode = biphasic deflection or no signal
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49
Q

dEPOLARIZATION towards a negative electrode = ?

A

negative deflection

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50
Q

depolarization towards a positive electrode = ?

A

upward deflection

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51
Q

DIrection and magnitude of an ECG depends on?

A

how the electrical forces are aligned to a specigic reference axis (ECG leads)

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52
Q

Positive and negative electrode of lead 1?

A

Positive on left arm, negative on right arm

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53
Q

Positive and negative electrode on Lead 2?

A

Positive and left leg, negative on right arm

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54
Q

Positive and negative electrode on Lead 3?

A

Positive on left leg, negative on left arm

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55
Q

Location of aVR?

A

Right arm

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56
Q

Location of aVL?

A

Left arm

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57
Q

Location of aVF?

A

Left leg?

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58
Q

Criteria for a normal P wave?

A

<0.25 mV high

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59
Q

Criteria for a normal PR interval?

A

0.12-0.2 s

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60
Q

A PR internval that isn’t between 0.12-0.2 s means?

A

Problem between the SA node and AV node

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61
Q

Criteria for a normal QRS complex?

A

0.12s

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62
Q

Criteria for a normal corrected QT inteval?

A

0.35-0.44s

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63
Q

Criteria for a normal ST segment?

A

should be isoelectric

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64
Q

Criteria for a normal T wave?

A

same orientation as QRS

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65
Q

What is an R wave?

A

A positive reflection

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66
Q

What is any positive reflection called?

A

A R wave

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67
Q

What is a Q wave?

A

A negative deflection before an R wave

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68
Q

What is a S wave?

A

A negative deflection after an R wave

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69
Q

Standard calibration of an ECG reading?

A

10 mm - 1 mV, 1 mm = 1 mV, 1 mm = 0.4 s at 25 mm/s

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70
Q

Summary of steps for 12 lead analyses?

A

1) Check rates 2) Rhythm 3) Axis–calculate mean QRS 4) hypertrophy 5) ischemia and infarction 6) conclusions

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71
Q

Quickest way to determine heart rate?

A

1500/#mm per beat

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72
Q

PR interval greater than 0.2s?

A

AV block

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73
Q

PR internval less than 0.12?

A

pre-excitation syndrome

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74
Q

QRS greater than 0.12s?

A

Bundle branch block

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75
Q

QTc greater than 0.44?

A

Long QT syndrome

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76
Q

How to correct for QT (how to calculate QTc)?

A

QT/ square root of R-R interval

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77
Q

If +ve in Lead 1 and aVF?

A

normal axis

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78
Q

If +ve in Lead 1 and -ve in aVF?

A

left axis deviation

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79
Q

If -ve in Lead 1 and +ve in AVF?

A

right axis deviation

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80
Q

Normal axis range?

A

-30 degrees to 90 degrees

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81
Q

Left axis deviation range?

A

-30 to -90 degrees

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82
Q

Right axis deviation?

A

90 to 150

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83
Q

Possible cause of left axis deviation?

A

Left ventricular hypertrophy

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84
Q

Possible cause of right axis deviation?

A

Right ventricular hypertrophy, left ventricular infarction

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85
Q

Right Atrial Hypertrophy showings in an ECG?

A

Tall peaked waves >2,5 mm in LEAD 2. Diphasic P waves with initial phase larger than terminal phase in V1

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86
Q

Left atrial hypertrophy showings in an ECG?

A

Wide notched P wave (>0.12 s wide, >1 mm) in Lead 2. Diphasic waves with initial phase smaller than terminal phase in V1.

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87
Q

Right ventricular hypertrophy showings in an ECG?

A

R/S ratio >1.0 in V1. Right axis deviation.

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88
Q

Left ventricular hypertrophy showings in an ECG?

A

R wave in V5+ S wave in V1 = >35mm. Left axis deviation.

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89
Q

Ischemia showings in an ECG?

A

ST segment depression >0.5 mm (most common) OR T-wave inversion

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90
Q

Injury or infarction showings in an ECG?

A

ST-segment elevation above isoelectric line >1mm. Significant Q wave that is 1/4 the height of R wave or Q >0.04 s duration

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91
Q

What is the criteria for a significant Q wave?

A

1/4 height on R wave or Q >0.04s duration

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92
Q

Acute MI signs in an ECG?

A

ST segment is still elevated

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93
Q

Old MI signs in an ECG?

A

ST segment normalized, significant Q wave persists.

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94
Q

Significant Q waves must be found in what leads for a lateral MI?

A

Lead 1, aVL, V5, V6

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95
Q

Significant Q waves must be found in what leads for an inferior MI?

A

Lead 2 and 3, and aVF

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96
Q

Significant Q waves must be found in what leads for an anterior MI?

A

V1, V2, V3, V4

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97
Q

What is sinus bradycardia?

A

HR <60 bpm…normal if well-trained or caould be pathological (bad pacemaker) or drug-induced

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98
Q

What is sinus tachycardia?

A

HR > 100 bpm. Could be normal id from exercise or pathological if there is a fever, hypoxia, or anemia. QT waves blend together.

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99
Q

What does sinus arrythymia look like on an ECG?

A

Normal PQRST (each complex looks the same), but the rate varies

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100
Q

What does a wandering pacemaker ECG look like?

A

P-shape changes (something else in the atria besides SA node is firing). QRST is consistent.

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101
Q

What does atrial fibrillation look like on an ECG?

A

No P-wave, multiple atrial firings (just quivering, so no real P-wave), very varying QRS.

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102
Q

What is the biggest concern with atrial fibrilllation?

A

Low CO, so feel lightheaded. When the blood isn’t being pumped from the hear, it sits there and begins to coagulate. If the heart goes to a normal rhythm, clot is ejected = stroke

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103
Q

What are premature beats?

A

beats that occur early, followed by a pause

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104
Q

What are escaped beats?

A

Beats the occur late, normal pacemaker fails to elicit a stimulus

105
Q

What does premature atrial contraction look like on an ECG?

A

Abnormal P-wave, foci in atrium (AV-node, Purkinje fibers, etc.), appears earlier and is followed by a pause. Common in healthy individuals without any symptoms

106
Q

What does premature nodal contraction look like on an ECG?

A

NO P-wave (so must be a problem with the SA node). Complex early followed by a pause. Normal QRS

107
Q

What does premature ventricular contraction look like on an ECG?

A

early beat followed by a pause, then normal rhythm resumes. Wide/tall distorted QRS. No related P-wave.

108
Q

Uni-focal PVC?

A

QRS complexes look like the same in an ECG, multiple of them

109
Q

Multi-focal PVC?

A

Very dangerous arrhythymia because there are multiple cells firing, not just one

110
Q

Bigamy PVC?

A

Every 2nd beat, not too dangerous.

111
Q

Trigamy PVC?

A

Every 3rd beat

112
Q

Couple PVC?

A

2 in a row with different foci…very dangerous because 2 different irritable cells are firing, which reduced CO, leading to ischemia

113
Q

What are the criteria for dangerous PVCs?

A

1) PVC strikes on the T wave of the preceding beat (RON-t) 2) PVCs are multilocal 3) Pairs or couplets or runs

114
Q

What is RON-T, and why is it so dangerous?

A

PVC strokes on the T wave of the preceding beat…heart never repolarizes, meaning it isn’t relaxing, no O2 through the coronary arteries = ischemia = MI.

115
Q

What would an atrial escape ECG look like?

A

abnormal looking P wave that appears late, foci in atrium

116
Q

What is an escaped beat?

A

when a normal pacemaker fails to elicit a stimulus for one or more beats

117
Q

What would a nodal escape look like on an ECG?

A

no p wave, normal QRS, late

118
Q

What would a ventricular escaped beat look like on an ECG?

A

abnormal QRS, no p-wave, late.

119
Q

What is the way to not get ventricular escape/ventricular arrhythmias confused with ST segment depression?

A

It is an isolated beat.

120
Q

What would paroxysmal atrial tachycardia (PAT) look like on an ECG?

A

sudden onset or termination of tachycardia, atrial rate of 140-250 bpm, all waves present, but P and T run together

121
Q

What would paroxysmal ventricular tachycardia look like on an ECG?

A

Rate > 100 bpm. Wide QRS.

122
Q

What would atrial flutter look like on an ECG?

A

atrial rate of 180-300 bpm, “saw toothed” pattern, multiple atrial contractions,, occasional ventricular contraction, some ouput but there is still potential for clotting.

123
Q

How are atrial flutter and atrial fibrillation different?

A

Atrial flutter is saw-toothed and a rate can distinctly be counted. Atrial fibrillation is a bunch of p-waves that don’t look the same and cannot count the rate.

124
Q

What would ventricular flutter look like on an ECG?

A

“smooth sine” wave appearance, 200-300 bpm, and not sudden like PAT

125
Q

What would ventricular fibrillation look like on an ECG?

A

Many ventricular foci, chaotic rhythm and ineffective pumping of the heart, no recognizable wave forms, people are unconscious

126
Q

What would Wolf-Parkinson look like on an ECG?

A

Short PR interval ( to spread electrical activity to ventricles. Delta-wave present (slurred upstroke of QRS).

127
Q

What would a heart block look like on an ECG?

A

Prolonged P-R interval (>0.2s)

128
Q

What would a RBBB look like on an ECG?

A

Wide QRS (>0.12 s). Wide S in V6. RSR’ in V1.

129
Q

What would a LBBB look like on an ECG?

A

sinus rhythm with wide QRS, absent R and prominent S in V`, widened QRS, broad, notched R in V6

130
Q

What are some technical problems that would cause you to stop an ECG?

A

loose electrode or broken wire, muscle tremor (ECG picking up EMG of heart), wandering baseline, bad grounding (picking up lights in the room)

131
Q

What are the 3 reasons for using a stress test?

A

diagnostic (determine disease and severity, determine additional assessments), prognostic (risk of future cardiac events, assist in management decisions), therapeutic/functional capacity (pre discharge for ADL and medication effectivness, post discharge for obtaining a “true” measure of CRF, to obtain data fro Ex RX, to monitor progress, change medications, return to work)

132
Q

When is a medical exam needed before a GTX?

A

moderate risk for vigorours activity. High risk for moverate and vigorous activity.

133
Q

When is an exercise test required?

A

high risk for moderate and vigorous activity

134
Q

When is a physician required for supervision?

A

high risk for moderate and vigorous activity

135
Q

Angina scale for a GTX?

A

1 = light, barely noticeable 2 = moderate, bothersome 3 = severe, very uncomfortable 4 = most severe pain ever experienced

136
Q

Why should you stop a GTX when there is a drop in systolic BP greater than 10 mmHg with an increase in work rate?

A

A sign of CVD, myoccardial ischemia, or LV dysfunction —> shows there is poor contraction and inability to increase Q –> ischemia

137
Q

Why should you stop a GTX if there is 3/4 on the angina scale?

A

Indicates severe ischemia, low O2 to the heart —> MI or arrhythymias

138
Q

Why should you stop a GTX if there are increasing nervous system symptoms or signs of poor profusion?

A

important to prevent an event from happening that may cause them to fall off the treadmill

139
Q

Why should you stop a GTX if you experience technical difficulties or the subject desires to stop?

A

Unable to monitor properly can lead to negligence on your part if something happens, and as per informed consent, the participant has the right to stop whenever.

140
Q

Why should you stop a GTX if there is sustained ventricular tachycardia (200-300bpm)?

A

Inappropriate blood flow to heart leading to ventricular fibrillation

141
Q

Why should you stop a GTX is there is an ST elevetaion greater than 1 without diagnostic Q waves (other than V1 or aVR)?

A

indicative of an injury to the myocardium or an MI

142
Q

Why should you stop a GTX is there is a ST depression greater than 2 mm or a marked axis shift?

A

ischemia –> low O2 –> arrhythymias and MI

143
Q

Why should you stop a GTX is there are arrhythymias?

A

irritable heart or lack of proper conduction –> ineffective pumping –> ischemia

144
Q

Why should you stop a GTX is there is fatigue, shortness of breath, wheezing, leg cramps, or claudication?

A

Indicative of respiratory stress or ischemia in legs

145
Q

Why should you stop a GTX if SBP is greater than 250 mmHg?

A

risk of arterial rupture

146
Q

Why should you stop a GTX if DBP is greater than 115 mmHg?

A

Increases afterload/work of the heart, decreases BF, leading to ischemia

147
Q

Why should you stop a GTX if there is a ST segment depression greater than 1mm?

A

indicative of CAD

148
Q

Three steps in interpreting the results of a GTX?

A

diagnostic:state whether the test is positive for CAD, prognostic using funtional VO2, exercise prescription.return to work.

149
Q

What is a positive GTX for CAD?

A

1) drop in SBP >10 mmHg despite increase in work rate 2) failure of HR to increase despite increasing work rate 3) SBP > 250 mmHg, DBP >115mmHg 4) Moderate to severe angina (2 on a scale 0-4) 5) ST segment depression > 1mm or ST elevation > 1 mm 6) Arrhythmias (milt-focal PVC, sustained ventricular tachycardia, atrial tachycardia, heart blocks, bardyarrhythmias

150
Q

Less than 4.9 METS for a VO2 is…

A

poor

151
Q

5-8 METS for VO2 is…

A

fair

152
Q

9-11 METS for VO2 is…

A

good

153
Q

Greater than 12 METS for VO2 is…

A

excellent

154
Q

<5 METS increases mortality by…

A

4:1

155
Q

When would you use a pharmacological stress test?

A

to evoke myocardial ischemia in those who can’t exercise

156
Q

How can you measure heart function in someone who can’t exercise?

A

ECG, echocardiography, or coronary perfusion tests

157
Q

2 ways to induce ischemia?

A

use a drug to dilate an artery or use a drug to increae myocardial demand

158
Q

Best method for testing heart function of people who can’t exercise?

A

use both a drug that dilates arteries and one that increases myocardial demand

159
Q

How is using a drug to dilate an artery help assess heart function?

A

Intravenous administration of Persantine or adenosine –> vasodilators –> relax coronary artery smooth muscle –> decreased vascular resistance –> increased coronary blood flow. There is only vasodilation in non-diseased arterty –> “Steals” blood from artery with diminished flow (i.e. atherosclerotic artery)

160
Q

How does using a drug to increase myocardial demand useful for assessing heart function?

A

dobutamine or arbutamine…beta effect to increase HR and SV, in the presence of atherosclerosis, ischemia occurs (O2 demand > O2 supply)

161
Q

What is Holter Monitoring?

A

continuous ambulatory ECG…computer program idientifies abnormalities, and then this is compared to patient’s daily activities to determine cardiac response to lifestyle events. Helps to evaluate therapeutic interventions.

162
Q

What is echocardiography?

A

Uses ultrasound to examine the heart…transducer sends out sound waves that reflect off tissue and return waves to be processed

163
Q

Reasons for using an echocardiography?

A

Assess 4 chambers of heart, wall thickness, wall motion and volumes, valves structure and fucntion, blood vessels entering and leaving heart, look at the pericardial sac ad how much fluid surrounds the heart. Abnormalities (thrombus, growth, and congenital defects)

164
Q

Things an echocardigram can tell you related to CAD?

A

Ventricular assessment of EDV, ESV, SV, and EF. Coronary artery disease (abnormal wall motion or thinning, thrombus for atrial fib or flutter, aneursyms)

165
Q

What can nuclear perfusion imaging show in the heart?

A

1) myocardial perfusion imaging 2) assessment of blood flow throughout the heart 3) to localize and quantify ischemia and infarction 4) assessment of myocardial metabolism

166
Q

What are the radioactive tracers used in nuclear perfusion imaging?

A

Thalium-201 and Technetium-99m

167
Q

What is SPECT imaging?

A

a series of planar images are obtained over a 180 degree arc around the patient’s chest to form several 3-D images

168
Q

How does a myocardial perfusion imaging test work?

A

1) Inject radioactive tracer into vein 2) tracer emits gamma rays 3) Gamma camera and computer constructs images 4) at max exercise the heart is assesed 5) wait 406 hours and view again to see if cold spot went away

169
Q

In a nuclear perfusion imaging test, if the cold spot goes away after 6 hours what is the diagnosis?

A

ischemia (reversible)

170
Q

In a nuclear imaging test, if the cold spot does NOT go away after 6 hours, what is the diagnosis?

A

MI

171
Q

What is MUGA, and what does it asses?

A

Multiple Gated Acquisition. Tells how well the heart pumps blood (ventricular function) by injecting RBC attached with 99Tmc.

172
Q

What is MUGA used for?

A

ventricular function, ventricular volumes, EF, CAD, valve disease, congenital heart disease, cardiomyopathy

173
Q

What is the gold standard and most reliable test for assessing the heart?

A

Coronary angiography…but it is invasive

174
Q

What is coronary angiography used for?

A

identify and quantify coronary stenosis (if in advanced stages), pressure in the chambers, wall motion and size, and determines need for angioplasty, stent, or bypass.

175
Q

How does an angiogrpahy work?

A

The guide wire is loaded with a coronary catheter and is fed through the femoral arterty. Guided under x-ray and then a radiactive agent is injected. X-rays produce “angiographs”. Various instruments such as a pressure transducer, ultrasound, lasers and blades, balloons, and stents can be placed on the catheter tip.

176
Q

What are the six drugs used to treat hypertension?

A

1) ACE inhibitors 2) angiotensin II receptor blockers 3) diuretics 4) beta-adrenergic antagonists 5) alha adrenergic blockers 6) calcium channel blockers

177
Q

“Pril”?

A

ACE inhibitor

178
Q

What is the effect of ACE inhibitor drugs?

A

Peripheral vasodilation (dec. TPR - dec. BP), decreases aldosterone (increases Na2+ and water loss so a dec. in blood volume and therefore BP), decrease in bradykinin breakdown (vasodilation via NO and prostaglandin), decreases SNS (dec. renin = decreases ANG I = dec. ANG II)

179
Q

What is the exercise effect of ACE inhibitors?

A

decreases rest and exercise BP, exercise prescription is not altered, may cause post exercise hypotension

180
Q

“Sartan”

A

ANG II receptor blocker

181
Q

How does a ANG II receptor blocker work, and what are its effects?

A

Competes with receptor for ANG II, same effects as ACE inhibitors

182
Q

3 types of diuretics?

A

loop diuretics, distal convoluted tubule diuretics, and K+ sparing diuretics

183
Q

What do diuretics do, and what is their effect?

A

Decrease reabsorption of Na_ into kidney and increase fluid retention, thus decreasing vascular volume and blood pressure. Decrease prload = decrase Q = decrease BP.

184
Q

Exercise effect of diuretics?

A

Decreases resting and exercise BP, no effect on HR

185
Q

Side effects of diuretics?

A

Intravascular volume decreases, which may cause postural hypotension and post exercise hypotension. Leads to hypokalemia and alkalosis, which can cause an electrolyte imblance leading to muscle cramps, fatigue, and PVCs. ENSURE PROPER HYDRATION!

186
Q

How do beta blockers work?

A

Decrease sympathetic effects because it blocks NE and P on beta receptors

187
Q

1st generation beta blockers?

A

non-selective (block beta 1 and 2)…propranolol

188
Q

“Ol”?

A

beta blocker

189
Q

“Ide”

A

diurectic

190
Q

“Mide”

A

loop diuretics

191
Q

“One”

A

potassium sparing diuretics

192
Q

2nd generation beta blockers?

A

cardioselective (block beta 1 only)…atenolol

193
Q

Beta 1 receptor blockers on heart?

A

Block E and NE for decreased sympathetic response…decreases in HR, contractility, and conduction velocity = decrease in Q = decrease in BP

194
Q

Beta-2 receptors in blood vessels?

A

Block E and NE…decreased vasodilation (not a huge effect because there are so many alpha-1 receptors)

195
Q

Beta-1 blockers on the kidney?

A

Decrease renin, which decreases ANG I, which decreases ANG II, which decreases vasoconstriction and promotes vasodilation.

196
Q

Effects of Beta blockers on exercise and some considerations?

A

1) decrease resting and exercise HR, BP – blunted response 2) dose and time effect (may wear off) 3) decreased ischemia with exercise 4) increase exercise capacity in patients with angina and decreased exercise capacity in clients with no angina 5) GXT done on medications 6) DO NOT use age-adjusted HR, use actual values obtained rom GXTand RPE scales

197
Q

GTX done on medication for?

A

exercise prescription

198
Q

GTX done without medication for?

A

diagnostics

199
Q

Beta blockers are not recommended for?

A

Asthmatic paitents, COPD patients, diabetic patients, people with AV conduction problems, sinus bradycardia, and heart failure.

200
Q

Why are BBs not recommended for people with asthma or COPD?

A

Blocking Beta2 receptors causes bronchoconstriction

201
Q

Why are BBs not recommended for diabetics?

A

Beta-2 receptors in liver and pancreas are respnsible for glucose release, so by blocking B1 receptors causes a masking of sympathetic signals, leading to a blunted hypoglycemic response

202
Q

How do alpha blockers work, and what are their effects?

A

Block alpha-1 receptor, which causes vasodilation and decreased TPR, so decreased BP

203
Q

Effects on exercise and considerations of alpha-blockers?

A

no change in RHR or RBP, decrease resting and exercise BP, may cause postural hypotension

204
Q

Calcium channel blockers can causes effects in what 3 places?

A

vascular smooth muscle, SA and AV node, cardiac myocardium

205
Q

Effect of calcium channel blockers on VSM?

A

decreases TPR

206
Q

Effect of calcium channel blockers on SA and AV node?

A

decrease HR and conduction of AP

207
Q

Effect of calcium channel blockers on cardiac myocardium?

A

decreases contractility via negative inotropy

208
Q

3 groups of calcium channel blockers and what they do?

A

1) non0dihydropyradine cardiac calcium channels (verapamil) 2) non-dihydropyridines for vascular or cardiac (ditiazem) 3) dihydropyridines for vascular smooth muscle (amlodipine)

209
Q

What two groups of calcium channel blockers should you NOT use predicted heart rate with?

A

Non-dihydropyridines for cardiac and intermediate (cardiac and vascular smooth muscle)

210
Q

Effects of calcium channel blockers on exercise and some considerations?

A

decrease resting and exercise BP, increase exercise capacity in angina paitents, GXT on medication, posterual and post exercise hypotension

211
Q

3 drug types used to treat angina?

A

beta blocker, calcium blockers, nitrates and nitroglycerine

212
Q

How do beta blockers work fro decreasing angina?

A

Block beta-1 receptors so decreases HR and SV, so decrease RPP and O2 demand

213
Q

How do calcium channel blockers help with angina?

A

Block Ca2_ channels in heart leads to decreased SV and therefore decreased work of heart and O2 demand. Block Ca2+ in VSM = vasodilation = dec afterload = dec wall stress = dec work of heart = dec O2 demand

214
Q

What is main effect of nitrates and nitroglycerine for angina treatment?

A

Dilation of peripheral veins = blood pooling in peripheral veins = dec SV due to dec preload = dec wall stress = dec myocardial VO2

215
Q

How do nitrates and nitrogylcerin work?

A

Get converted to NO = vasodilation

216
Q

How do nitrates and nitrogylcerin affect peripheral arteries?

A

increases dilation, which decreases afterload

217
Q

How do nitrates and nitroglycerin affect coronary arteries?

A

dilate them causing increased O2 supply

218
Q

Effects on exercise and considerations of angina medication?

A

1) increase RHR may increase ex HR 2) decreases RBP, may decrease ex BP 3) postural hypotension 4) increase exercise capacty

219
Q

What is the main anti-platelet drug given?

A

Aspirin

220
Q

How does aspirin act as an anti-platelet drug?

A

Inhibits COX-1, which is the enzymes that converts arachadonic acid into thromboxane A2, leading to clotting. So, by blocking this reaction from occurring, there is decreased clotting, and therefore a decreased risk in stroke and heart attack

221
Q

What is thrombaxane A2?

A

An enzyme responsible for platelet aggregation and vasoconstriction

222
Q

Minor side effects of aspirin?

A

upset stomach and heart butn

223
Q

Major side effects of aspirin?

A

GI tract bleeding and hemorrhage stroke

224
Q

Recommendations of who SHOULD take a daily aspirin, and who should NOT take a daily aspirin?

A

People > 50 with no CVD symptoms but one major risk factor or diabetics with one major risk factor SHOULD take it. Men under age 45 and women under 55 who have never had a heart attack or stroke should not take aspirin.

225
Q

3 types of Class I arrhythmia drugs

A

IA: moderate, IB: weak, IC: strong Na2+ channel blockers

226
Q

What do CLass I arrhythymia drugs do the AP in heart cells?

A

Block the Na channels, so there is a decrease in Phase 0 upstroke velocity, leading to a decrease in conduction velocity, and thus decreased reentry.

227
Q

How are Ia Na2+ channel blockers different than Ib and Ic?

A

Block K+ channels, too, so there is prolonged repolarization and an increase in the effective refractory period, so decreased reeentry

228
Q

What do Type I arrhythymia drugs do to the SA and AV node?

A

Increase threshold potential and decrease Phase 4 slope, which decreases rate of firing, and decreases automaticity.

229
Q

Effect of a Type IA arrhythmia drugs?

A

moderate

230
Q

Effect of a Type IB arrhythymia drugs?

A

weak

231
Q

Effect of a Type IC arrhythymia drugs?

A

strong

232
Q

What are Class II arrythymia drugs?

A

Beta blockers

233
Q

What do class II arrhythymia drugs do?

A

Beta blockers that decrease sympathetic activity in the oacemaker cells, so they decrease rate and conduction velocity

234
Q

What are Class III arrhythmia drugs?

A

K+ channel blockers

235
Q

What do Class III arrhythmia drugs do?

A

Block K+ channels, so tehy delay repolarization, thus increasing action potential duration and a longer refractory period (promotes the plateau stage in phase 3 of the AP)

236
Q

What are Class IV arrhythmia drugs?

A

Ca2+ channel blockers

237
Q

How do Class IV arrhythmia drugs work?

A

Block Ca2+ channels on the SA and AV node, thereby decreasing rate and conduction (verapamil and diltazem)

238
Q

What is the most prescribed drug for dyslipidemia?

A

Statins (HMG-CoA reductase inhibitors)

239
Q

How do statins work?

A

Inhibits HMG-CoA reductase in the liver, which decreases the amount of cholesterol made and put into the blood. In turn, hepatocytes increases LDL receptors, which leads to a decrease in LDL levels, VLDL levels, and TG levels.

240
Q

What are the side effects of statins?

A

liver and kidney damage, muscle structural breakdown

241
Q

Exercise effects of statins?

A

may cause muscle aches and joint stiffness

242
Q

Additional benefits of statins?

A

improve endothetlial function (enhances synthesis of NO), inhibit monocyte entry into arterial wall (decreases atherosclerosis), reduce oxidation of LDL (also decreases atherosclerosis), suppressess inflammatory response (good for everything, including CAD)

243
Q

Besides statins, what are some other drugs used for dyslipidemia?

A

Resisins/bile acid sequestrants, fibrates, niacin/nicotinic acid

244
Q

5 types of surgical interventions for CAD?

A

1) Percutaneous transluminal coronary intervention (PTCI) 2) Coronary artery bypass graft surgery 3) Pacemaker 4) Ventricular assists 5) transplants

245
Q

Treatment for what type of surgical intervention that is used is based on?

A

patient age, co-moribidities, extent of disease (number of location of affected coronary arteries), disease severity

246
Q

Types of percutaneous transluminal coronary intervention (PTCI)?

A

Angioplasty, stent, atherectomy

247
Q

What is an angioplasty?

A

A balloon cathether is passed through the guiding catheter up the femoral artery or an artery in the arm to the area near the narrowing. Inflate balloon, compress plaque, and restore the size of the artery.

248
Q

What is a stent?

A

A stent is on the balloon catheter. Inflate the balloon, expand stent to fit into artery wall, deflate balloon. Stents can be drug-eluting stents that release sirolimus that prevents scar tissue formation over the stent.

249
Q

What is an atherectomy?

A

Rotating shaver on tip of catheter, used to cut away plaque. Laser on the tip uses a pulse of light from the laser to vaporize plaque deposits.

250
Q

Risks of PCTI?

A

bleeding, damage blood vessel, allergic reaction, arrhythymia, emergency bypass, heart attack, stroke

251
Q

What is a coronary artery bypass surgery?

A

healthy blood vessel is removed from leg, arm, or chest. Blood vessel is used to create new blood flow path in your heart. The “bypass graft” enables blood to reach your heart by flowing around (bypassing) the blocked portion of the diseased artery. The increased BF reduces angina and the risk of heart attack.

252
Q

Risks of bypass surgery?

A

Risks associated with anesthesia, death, angina, heart attack, stroke, excessive bleeding, infection, subtle problems in long-term memory, comprehension, calculation skills, and concentration.

253
Q

What is an off-pump bypass>

A

Not on a heart or lung machine, mechanically stabilizing the hear

254
Q

Why is an off pump bypass recommended?

A

less trauma, shorter hospital stay, multiple vessels, less infection, same outcome

255
Q

What is a pacemaker?

A

Artificial implanted source that stimulates the heart to produce a normal rate and sufficient Q OR an implantable cardioverter defibrillator

256
Q

How does a pacemaker function?

A

Senses physiological, mechanical, or electrical signals and paces the heart OR a fixed rate pacemaker

257
Q

What is an orthotopic heart transplant?

A

remove recipients heart and attach donor’s heart to the great vessels and the atria

258
Q

What is a heteroptropic heart transplant?

A

Both hearts remains in recipient and are connected in parallel

259
Q

Types of rejection in a heart transplant?

A

1) hyperacture (early after surgery when acute inflammatory infiltration with vessel necrosis) 2) Acute cellular rejection (first 6 motnhs, T-lymphocytes and macrophage infiltration of the myocardium) 3) Acute humoral (vascular rejection) 4) Chronic rejection

Physiology 2 (16 decks)

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