Nordgren Week 3 Flashcards
(110 cards)
1
Q
severe reduction in blood supply to the body tissues; metabolic needs of tissues not met
A
circulatory shock
2
Q
What is the arterial pressure in circulatory shock?
A
arterial pressure is usually low
3
Q
What leads to syncope in severe shock?
A
inadequate brain blood flow
4
Q
how do you calculate MAP?
A
CO x TPR
5
Q
Name three causes of accelerated cardiovascular crises (circulatory shock primary disturbances)?
A
- severely depressed myocardial functional ability 2. grossly inadequate filling dt low mean circulatory filling pressure 3. profound systemic vasodilation
6
Q
Name two things that lead to profound systemic vasodilation?
A
- abnormal presence of powerful vasodilators 2. absence of neurogenic tone normally supplied by the sympathetic nervous system
7
Q
What are 5 consequences of cardiovascular crises?
A
cardiogenic shock, hypovolemic shock, anaphylatic shock, septic shock and neurogenic shock
8
Q
Name compromised cardiac pumping to decreased CO?
A
Cardiogenic shock
9
Q
Causes of cardiogenic shock?
A
severe arrhythmias, abrupt valve malfunction, MI, coronary occlusions
10
Q
Name depletion of body fluids to decreased blood volume to reduced cardiac filling to reduced SV?
A
hypovolemic shock
11
Q
Causes of hypovolemic shock?
A
significant hemorrhage (>20% blood volume), fluid loss from severe burns, chronic diarrhea, prolonged vomitting
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
13
Q
Name severe vasodilation dt release of substances into blood stream by infective agents?
A
septic shock
14
Q
Causes of septic shock?
A
endotoxin released from bacteria induces formation of a nitric oxide synthase in endothelial cells
15
Q
Name loss of vascular tone dt inhibition of normal tonic activity of sympathetic vasoconstrictor nerves?
A
neurogenic shock
16
Q
Causes of neurogenic shock?
A
deep general anesthesia, reflex response to deep pain associated with traumatic injury
17
Q
What are the steps that lead to vasovagal syncope?
A
increased vagal activity to decreased heart rate
18
Q
What type of shock can vasovagal syncope accompany?
A
neurogenic shock
19
Q
What causes the common sx of shock?
A
increased sympathetic nerve activity
20
Q
What are the common sx of shock?
A
pallor, cold clammy skin, rapid HR, muscle weakness, venous constriction
21
Q
What happens if the compensatory response to shock is weak?
A
abnormally low arterial pressure, reduced cerebral perfusion–> dizziness, confusion, LOC
22
Q
Compensatory Process: rapid, shallow breathing to?
A
promote venous return via action of the respiratory pump
23
Q
Compensatory Process: increased renin release?
A
increased TPR via formation of angiotensin II
24
Q
Compensatory Process: increased circulatory levels of ADH?
A
increases TPR
25
Compensatory Process: increased circulating levels of what neurotransmitter?
epinephrine
26
Compensatory Process: reduced capillary hydrostatic pressure resulting from intense arteriolar constriction?
reabsorption
27
Compensatory Process: increased glycogenolysis in the liver (via epi and norepi)?
release of glucose to rise in EC osmolarity (up to 20 mOsm); shifts fluid from intra to EC space
28
What is it called when: no intervention can halt the ultimate collapse of the CV system-->death?
irreversible shock
29
Type of shock where general CV situation progressively degenerates?
progressive shock
30
What is the most common form of heart disease in USA? MI, heart failur and arrhythmias?
coronary artery disease
31
Most common cause of coronary artery ds?
atherosclerosis of the large coronary arteries?
32
What can lead to increase vascular resistance and reduces coronary flow in coronary artery disease?
calcified plaques large enough to physically narrow lumen of arteries
33
What can compensate to reduce arteriolar resistance in order to improve coronary flow?
if not too severe: local metabolic vasodilator mechanisms
34
Physiological consequences of an MI are similar to those of what?
cardiogenic shock
35
ventricular function is depressed through myocardial damage, insufficient coronary flow, or anything that directly impairs mechanical performance
chronic heart failure
36
What defines failure-systolic dysfunction?
left ventricular EF of less than 40%
37
What happens to the cardiac function curve in heart failure-systolic?
lower than normal
38
What can lead to sustained cardiac challenges and induce a chronic state of systolic failure?
progressive coronary artery disease, sustained elevation in cardiac afterload, reduced functional muscle mass following MI (or primary cardiomyopathy-genetic)
39
What alterations do you see in failure-systolic dysfunction regarding Ca?
reduced Ca sequestration by SR, upregulation of NCX to lo intracellular Ca concentration, low affinity of troponin for Ca
40
In failure-systolic dysfunction what is the substrate metabolism change? is it more or less efficient?
fatty acid to glucose metabolism; less efficient
41
What is the primary disturbance of failure-systolic dysfunction?
decreased cardiac output to decreased arterial pressure
42
What type of compensatory mechanisms are important in chronic heart failure-long term or short term?
Long-term
43
What is one of the goals of long-term compensation of failure-systolic?
fluid retention: sympathetically incuded renin release, then return to normal sympathetic ouput
44
What effect does fluid retention have on both peripheral and central venous pressure?
much higher than normal (chronically high EDV)
45
Ho does increased volume leading to increased EDV lead to excessive cardiac impair cardiac function?
increased total wall tension/stress required to generate adequate pressure within the enlarged chamber
46
How does increased EDV affect myocardial oxygen demand?
increased
47
How does high venous pressure in systolic dysfunction lead to edema and congestion?
via transcapillary fluid filtration
48
What are the hallmarks that accompany left sided failure?
pulmonary edema, dyspnea, respiratory distress
49
What are the hallmarks that accompany right sided failure?
distended neck veins, ankle edema, fluid accumulation in the abdomen with liver congestion and dysfunction
50
Most common sx of systolic dysfunction?
inability to increase CO (low exercise tolerance, fatigue) and fluid accumulation (tissue congestion, SOB, peripheral swelling)
51
Define failure-diastolic dysfunction
implies a stiffened heart during diastole
52
Do increases in cardiac filling pressure in diastolic dysfunction increase EDV?
no, they do NOT produce normal increases in EDV
53
What is another name for failure-diastolic dysfunction?
heart failure with preserved systolic function?
54
Name the 5 possible causes of diastolic dysfunction?
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
Define pulmonary hypertension
pulmonary artery pressure > 20mmHg, systemic edema, chest pain, fatigue, linked to chronic hypoxia (COPD, cystic fibrosis)
56
Define systemic hypertension
elevation of mean systemic arterial pressure >140/90mmHg, >20% of adult western world population
57
What increases in risk with HTN?
CAD, MI, heart failure, stroke
58
Action of diruetic therapy in HTN?
inhibit renal tubular salt (and fluid) reabsorption
59
Action of beta blocker therapy in HTN?
inhibit sympathetic influences on heart and renal renin release
60
Action of ACE inhibitors and Angiotensin II receptor blockers therapy in HTN?
block the effects of the renin-angiotensin system
61
Name 4 causes of an arrhythmia
1. hyperkalemia 2. MI 3. Ischemia 4.other damage to myocardial tissue
62
Define Ischemia
loss of coronary blood flow to myocardium; decreased levels of O2 in tissue, cellular hypoxia, mitochondrial damage, diminished intracellular ATP levels
63
What happens in heart dt loss of ATP?
decreased activity of ATP transport systems
64
Action of Na+/K+/ATPase transport pump
cell repolarizes because this pumps out MORE Na+ than it brings in K+ ions leading to a net loss of + ions
65
What happens to membrane potential if Na+/K+/ATPase pump is not working?
Na+ cannot leave cell through this pump membrane and potential stays more +
66
What can result from Ca overload?
delayed after depolarizations to arrhythmia
67
What kind of ionotrope and chronotrope is Digoxin (blocks the Na+/K+ ATPase pump)?
positive ionotrope (increases contractility--> SV) and negative chronotrope (decreases SA nodal rate-> HR)
68
How is Digoxin a Negative Chronotrope?
1. direct: early, brief prolongation of AP followed by shortening of plateau phase (increase PR, decrease QT) 2. Autonomic: increases PNS activity
69
What causes there to be fewer available Na channels?
fewer available when membrane potential is more positive
70
What are the consequences of fewer available Na channels?
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
What can lead to a unidirectional block?
slowed conduction
72
What can a unidirectional block lead to?
reentry
73
What is 'accomodation' of the action potential?
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
What is the cause of an altered IMPULSE FORMATION with digoxin?
accommodating cells resemble slow-response pacemaker cells and can display spontaneous depolarization and automaticity
75
What is a problem caused by spontaneous deopolarization and automaticity?
ectopic beats and arrhythmia
76
How to deal with reentry?
create a bidirectional block: slow conduction further, speed conduction, alter effective refractory period
77
Action of a K channel blocker?
slows the efflux of K during phase 3, prolonging the refractory time of the cell
78
Action of a Ca Channel Blocker
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
What is the basis for effectiveness of Na channel blockade?
effectiveness based on how quickly the drug associates/dissociates with channels
80
What is the order of effectiveness of Na channel blockade?
IC>IA>IB
81
What is the order of effective refractory period of Na channel blockade?
IA>IC>IB (decreases)
82
Class 1A Na Channel Blocker
quinidine; moderate Na channel blockade, increase effective refractory
83
Name the class of anti-arrhythmic: intermediate association, slows rate of rise (phase 0) of AP, prolongs AP (increases refractory period)
Class IA Na channel blocker
84
Which class of Na channel blocker has intermediate rate of association?
Class IA
85
Name the class of anti-arrhythmic: shortens refractory period (phase 3) and decreases duration of action potential
Class IB
86
Which class of Na channel blocker has rapid rate of association?
Class IB
87
Name the class of anti-arrhythmic: markedly slows phase 0 depolarization, no effect on refractory period
Class Ic
88
Which class of Na channel blocker has slow rate of association?
Class Ic
89
used to prevent and treat supraventricular arrhythmias and to reduce ventricular ectopic depolarization and sudden death in patients with MI
B-adrenoceptor blockers
90
how do B blockers effect have antiarrhythmic effect
inhibit sympathetic activation
91
Action of B blockers
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
has some class I activity, but is a B blocker
propanolol
93
AE of Propanolol
include bronchospasm, bradycardia, fatigue
94
cardioselective B blocking drug, so better for use in patients with asthma
Acebutolol
95
short acting B blocker used primarily for intraoperative and acute arrhythmias
esmolol
96
non-selective B blocking drug that prolongs the AP (delays the slow outward current of K+)
Sotalol
97
How do procainamide, disopyramide, quinidine effect the PR interval?
increase
98
How do procainamide, disopyramide, quinidine effect the QRS interval?
increase
99
How do procainamide, disopyramide, quinidine effect the QT interval?
increase
100
How do lidocaine, mixiletine affect the EKG?
no effect
101
How do flecainide effect the QT interval?
no change
102
How do flecainide effect the PR interval?
slight increase
103
How do flecainide effect the QRS interval?
increase
104
What are the AE of procainamide (what class is it)?
torsades de pointes, syndrome resembling lupus erythematosus (Class IA Na channel blocker)
105
What are the AE of Quinidine (what class is it)?
torsades de pointes (class 1A Na channel blocker)
106
What med is does NOT recommend a loading dose?
Disopyramide (Class 1A Na channel blocker)
107
What drug used prophylactically may actually increase total mortality and is NOT advised?
Lidocaine (Class 1B Na channel blocker)
108
What med has significant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury (off-label use)?
Mexiletine (Class 1B Na channel blocker)
109
What med is a potent blocker of Na and K channels with SLOW UNBLOCKING KINETICS (but does NOT prolong AP or QT interval)?
Flecainide (Class 1C Na channel blocker)
110
What antiarrhythmic has slow upstroke of AP, WEAK B-BLOCKING ACTIVITY, but does not prolong AP?
Propafenone (Class 1C Na channel blocker)
