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CRRAB 1 > Nordgren Week 3 > Flashcards

Nordgren Week 3 Flashcards

1
Q

severe reduction in blood supply to the body tissues; metabolic needs of tissues not met

A

circulatory shock

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2
Q

What is the arterial pressure in circulatory shock?

A

arterial pressure is usually low

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3
Q

What leads to syncope in severe shock?

A

inadequate brain blood flow

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4
Q

how do you calculate MAP?

A

CO x TPR

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5
Q

Name three causes of accelerated cardiovascular crises (circulatory shock primary disturbances)?

A
  1. severely depressed myocardial functional ability 2. grossly inadequate filling dt low mean circulatory filling pressure 3. profound systemic vasodilation
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6
Q

Name two things that lead to profound systemic vasodilation?

A
  1. abnormal presence of powerful vasodilators 2. absence of neurogenic tone normally supplied by the sympathetic nervous system
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7
Q

What are 5 consequences of cardiovascular crises?

A

cardiogenic shock, hypovolemic shock, anaphylatic shock, septic shock and neurogenic shock

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8
Q

Name compromised cardiac pumping to decreased CO?

A

Cardiogenic shock

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9
Q

Causes of cardiogenic shock?

A

severe arrhythmias, abrupt valve malfunction, MI, coronary occlusions

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10
Q

Name depletion of body fluids to decreased blood volume to reduced cardiac filling to reduced SV?

A

hypovolemic shock

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11
Q

Causes of hypovolemic shock?

A

significant hemorrhage (>20% blood volume), fluid loss from severe burns, chronic diarrhea, prolonged vomitting

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12
Q

Name severe allergic rxn to antigen sensitivity to release of histamine, PG, leukotrienes, bradykinin to increased arteriolar vasodilation, increased microvascular permeability, loss of venous tone and decreased TPR and CO?

A

anaphylactic shock

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13
Q

Name severe vasodilation dt release of substances into blood stream by infective agents?

A

septic shock

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14
Q

Causes of septic shock?

A

endotoxin released from bacteria induces formation of a nitric oxide synthase in endothelial cells

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15
Q

Name loss of vascular tone dt inhibition of normal tonic activity of sympathetic vasoconstrictor nerves?

A

neurogenic shock

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16
Q

Causes of neurogenic shock?

A

deep general anesthesia, reflex response to deep pain associated with traumatic injury

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17
Q

What are the steps that lead to vasovagal syncope?

A

increased vagal activity to decreased heart rate

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18
Q

What type of shock can vasovagal syncope accompany?

A

neurogenic shock

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19
Q

What causes the common sx of shock?

A

increased sympathetic nerve activity

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20
Q

What are the common sx of shock?

A

pallor, cold clammy skin, rapid HR, muscle weakness, venous constriction

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21
Q

What happens if the compensatory response to shock is weak?

A

abnormally low arterial pressure, reduced cerebral perfusion–> dizziness, confusion, LOC

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22
Q

Compensatory Process: rapid, shallow breathing to?

A

promote venous return via action of the respiratory pump

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23
Q

Compensatory Process: increased renin release?

A

increased TPR via formation of angiotensin II

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24
Q

Compensatory Process: increased circulatory levels of ADH?

A

increases TPR

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25
Q

Compensatory Process: increased circulating levels of what neurotransmitter?

A

epinephrine

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26
Q

Compensatory Process: reduced capillary hydrostatic pressure resulting from intense arteriolar constriction?

A

reabsorption

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27
Q

Compensatory Process: increased glycogenolysis in the liver (via epi and norepi)?

A

release of glucose to rise in EC osmolarity (up to 20 mOsm); shifts fluid from intra to EC space

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28
Q

What is it called when: no intervention can halt the ultimate collapse of the CV system–>death?

A

irreversible shock

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29
Q

Type of shock where general CV situation progressively degenerates?

A

progressive shock

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30
Q

What is the most common form of heart disease in USA? MI, heart failur and arrhythmias?

A

coronary artery disease

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31
Q

Most common cause of coronary artery ds?

A

atherosclerosis of the large coronary arteries?

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32
Q

What can lead to increase vascular resistance and reduces coronary flow in coronary artery disease?

A

calcified plaques large enough to physically narrow lumen of arteries

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33
Q

What can compensate to reduce arteriolar resistance in order to improve coronary flow?

A

if not too severe: local metabolic vasodilator mechanisms

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34
Q

Physiological consequences of an MI are similar to those of what?

A

cardiogenic shock

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35
Q

ventricular function is depressed through myocardial damage, insufficient coronary flow, or anything that directly impairs mechanical performance

A

chronic heart failure

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36
Q

What defines failure-systolic dysfunction?

A

left ventricular EF of less than 40%

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37
Q

What happens to the cardiac function curve in heart failure-systolic?

A

lower than normal

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38
Q

What can lead to sustained cardiac challenges and induce a chronic state of systolic failure?

A

progressive coronary artery disease, sustained elevation in cardiac afterload, reduced functional muscle mass following MI (or primary cardiomyopathy-genetic)

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39
Q

What alterations do you see in failure-systolic dysfunction regarding Ca?

A

reduced Ca sequestration by SR, upregulation of NCX to lo intracellular Ca concentration, low affinity of troponin for Ca

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40
Q

In failure-systolic dysfunction what is the substrate metabolism change? is it more or less efficient?

A

fatty acid to glucose metabolism; less efficient

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41
Q

What is the primary disturbance of failure-systolic dysfunction?

A

decreased cardiac output to decreased arterial pressure

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42
Q

What type of compensatory mechanisms are important in chronic heart failure-long term or short term?

A

Long-term

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43
Q

What is one of the goals of long-term compensation of failure-systolic?

A

fluid retention: sympathetically incuded renin release, then return to normal sympathetic ouput

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44
Q

What effect does fluid retention have on both peripheral and central venous pressure?

A

much higher than normal (chronically high EDV)

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45
Q

Ho does increased volume leading to increased EDV lead to excessive cardiac impair cardiac function?

A

increased total wall tension/stress required to generate adequate pressure within the enlarged chamber

46
Q

How does increased EDV affect myocardial oxygen demand?

A

increased

47
Q

How does high venous pressure in systolic dysfunction lead to edema and congestion?

A

via transcapillary fluid filtration

48
Q

What are the hallmarks that accompany left sided failure?

A

pulmonary edema, dyspnea, respiratory distress

49
Q

What are the hallmarks that accompany right sided failure?

A

distended neck veins, ankle edema, fluid accumulation in the abdomen with liver congestion and dysfunction

50
Q

Most common sx of systolic dysfunction?

A

inability to increase CO (low exercise tolerance, fatigue) and fluid accumulation (tissue congestion, SOB, peripheral swelling)

51
Q

Define failure-diastolic dysfunction

A

implies a stiffened heart during diastole

52
Q

Do increases in cardiac filling pressure in diastolic dysfunction increase EDV?

A

no, they do NOT produce normal increases in EDV

53
Q

What is another name for failure-diastolic dysfunction?

A

heart failure with preserved systolic function?

54
Q

Name the 5 possible causes of diastolic dysfunction?

A
  1. decreased cardiac tissue passive compliance 2. increased myofibrillar passive stiffness 3. delayed myocyte relaxation in early diastole 4. inadequate ATP levels 5. residual, low grade cross-bridge cycling during diastole
55
Q

Define pulmonary hypertension

A

pulmonary artery pressure > 20mmHg, systemic edema, chest pain, fatigue, linked to chronic hypoxia (COPD, cystic fibrosis)

56
Q

Define systemic hypertension

A

elevation of mean systemic arterial pressure >140/90mmHg, >20% of adult western world population

57
Q

What increases in risk with HTN?

A

CAD, MI, heart failure, stroke

58
Q

Action of diruetic therapy in HTN?

A

inhibit renal tubular salt (and fluid) reabsorption

59
Q

Action of beta blocker therapy in HTN?

A

inhibit sympathetic influences on heart and renal renin release

60
Q

Action of ACE inhibitors and Angiotensin II receptor blockers therapy in HTN?

A

block the effects of the renin-angiotensin system

61
Q

Name 4 causes of an arrhythmia

A
  1. hyperkalemia 2. MI 3. Ischemia 4.other damage to myocardial tissue
62
Q

Define Ischemia

A

loss of coronary blood flow to myocardium; decreased levels of O2 in tissue, cellular hypoxia, mitochondrial damage, diminished intracellular ATP levels

63
Q

What happens in heart dt loss of ATP?

A

decreased activity of ATP transport systems

64
Q

Action of Na+/K+/ATPase transport pump

A

cell repolarizes because this pumps out MORE Na+ than it brings in K+ ions leading to a net loss of + ions

65
Q

What happens to membrane potential if Na+/K+/ATPase pump is not working?

A

Na+ cannot leave cell through this pump membrane and potential stays more +

66
Q

What can result from Ca overload?

A

delayed after depolarizations to arrhythmia

67
Q

What kind of ionotrope and chronotrope is Digoxin (blocks the Na+/K+ ATPase pump)?

A

positive ionotrope (increases contractility–> SV) and negative chronotrope (decreases SA nodal rate-> HR)

68
Q

How is Digoxin a Negative Chronotrope?

A
  1. direct: early, brief prolongation of AP followed by shortening of plateau phase (increase PR, decrease QT) 2. Autonomic: increases PNS activity
69
Q

What causes there to be fewer available Na channels?

A

fewer available when membrane potential is more positive

70
Q

What are the consequences of fewer available Na channels?

A

decreases the upstroke velocity of AP (amplitude of phase 0) and decreased conduction velocity of AP (slope of phase 0) to ALTER IMPULSE CONDUCTION AND IMPULSE FORMATION

71
Q

What can lead to a unidirectional block?

A

slowed conduction

72
Q

What can a unidirectional block lead to?

A

reentry

73
Q

What is ‘accomodation’ of the action potential?

A

many of the Na channels are inactivated and the length of recovery time has increased; AP can still be elicited via the slow inward current of Ca

74
Q

What is the cause of an altered IMPULSE FORMATION with digoxin?

A

accommodating cells resemble slow-response pacemaker cells and can display spontaneous depolarization and automaticity

75
Q

What is a problem caused by spontaneous deopolarization and automaticity?

A

ectopic beats and arrhythmia

76
Q

How to deal with reentry?

A

create a bidirectional block: slow conduction further, speed conduction, alter effective refractory period

77
Q

Action of a K channel blocker?

A

slows the efflux of K during phase 3, prolonging the refractory time of the cell

78
Q

Action of a Ca Channel Blocker

A

slows influx of Ca by blocking the T type channels, which are depolarized at relatively low membrane potentials; allows for Na channels to fully repolarize and excite the cell in a fast-response

79
Q

What is the basis for effectiveness of Na channel blockade?

A

effectiveness based on how quickly the drug associates/dissociates with channels

80
Q

What is the order of effectiveness of Na channel blockade?

A

IC>IA>IB

81
Q

What is the order of effective refractory period of Na channel blockade?

A

IA>IC>IB (decreases)

82
Q

Class 1A Na Channel Blocker

A

quinidine; moderate Na channel blockade, increase effective refractory

83
Q

Name the class of anti-arrhythmic: intermediate association, slows rate of rise (phase 0) of AP, prolongs AP (increases refractory period)

A

Class IA Na channel blocker

84
Q

Which class of Na channel blocker has intermediate rate of association?

A

Class IA

85
Q

Name the class of anti-arrhythmic: shortens refractory period (phase 3) and decreases duration of action potential

A

Class IB

86
Q

Which class of Na channel blocker has rapid rate of association?

A

Class IB

87
Q

Name the class of anti-arrhythmic: markedly slows phase 0 depolarization, no effect on refractory period

A

Class Ic

88
Q

Which class of Na channel blocker has slow rate of association?

A

Class Ic

89
Q

used to prevent and treat supraventricular arrhythmias and to reduce ventricular ectopic depolarization and sudden death in patients with MI

A

B-adrenoceptor blockers

90
Q

how do B blockers effect have antiarrhythmic effect

A

inhibit sympathetic activation

91
Q

Action of B blockers

A

slow the heart rate, decrease the AV node conduction velocity (increases PR interval), increase the AV refractory period, they have little to no effect on ventricular conduction and repolarization

92
Q

has some class I activity, but is a B blocker

A

propanolol

93
Q

AE of Propanolol

A

include bronchospasm, bradycardia, fatigue

94
Q

cardioselective B blocking drug, so better for use in patients with asthma

A

Acebutolol

95
Q

short acting B blocker used primarily for intraoperative and acute arrhythmias

A

esmolol

96
Q

non-selective B blocking drug that prolongs the AP (delays the slow outward current of K+)

A

Sotalol

97
Q

How do procainamide, disopyramide, quinidine effect the PR interval?

A

increase

98
Q

How do procainamide, disopyramide, quinidine effect the QRS interval?

A

increase

99
Q

How do procainamide, disopyramide, quinidine effect the QT interval?

A

increase

100
Q

How do lidocaine, mixiletine affect the EKG?

A

no effect

101
Q

How do flecainide effect the QT interval?

A

no change

102
Q

How do flecainide effect the PR interval?

A

slight increase

103
Q

How do flecainide effect the QRS interval?

A

increase

104
Q

What are the AE of procainamide (what class is it)?

A

torsades de pointes, syndrome resembling lupus erythematosus (Class IA Na channel blocker)

105
Q

What are the AE of Quinidine (what class is it)?

A

torsades de pointes (class 1A Na channel blocker)

106
Q

What med is does NOT recommend a loading dose?

A

Disopyramide (Class 1A Na channel blocker)

107
Q

What drug used prophylactically may actually increase total mortality and is NOT advised?

A

Lidocaine (Class 1B Na channel blocker)

108
Q

What med has significant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury (off-label use)?

A

Mexiletine (Class 1B Na channel blocker)

109
Q

What med is a potent blocker of Na and K channels with SLOW UNBLOCKING KINETICS (but does NOT prolong AP or QT interval)?

A

Flecainide (Class 1C Na channel blocker)

110
Q

What antiarrhythmic has slow upstroke of AP, WEAK B-BLOCKING ACTIVITY, but does not prolong AP?

A

Propafenone (Class 1C Na channel blocker)

CRRAB 1 (9 decks)

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