Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patient Care > Cardiology 2 > Flashcards

Cardiology 2 Flashcards

1
Q

Right Heart

A

Thinner wall
Tricuspid valve
Pumps into pulmonary circulation via pulmonary arteries
Receives blood from IVC and SVC
Innervated with RBB no fascicels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Location of SA and AV node

A

Atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Left Heart

A

thicker wall
Mitral valve
Pumps into systemic circulation via aorta and great vessels
Innervated with LBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MAP

A

Average pressure over one full cardiac cycle
2/3 diastolic + 1/3 systolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Normal MAp

A

70-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Perfusion MAP

A

60-65 to perfuse coronary arteries, kidneys, brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Weights MAP not used

A

Pts <12 or <20kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Factors affecting MAP

A

Vascular tone
Fluid Status
Drugs
Cardiovascular and Neurogenic status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Preload

A

RV wall stress at end diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Increase Preload

A

NS/RL bolus
RBC bolus
Releasing intrathoracic pressure
Supine position
Vasopressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Decrease preload

A

Nitroglycerin
Morphine
Furosemide
PPV, AutoPEEP, increased intrathoracic pressure
Sitting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Contractility

A

Squeeze or inotropy of cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Increases of contractility

A

Increased preload
Reducing tension in cardiac muscle caused by ischemia
Correcting electrolyte abnormalities
Reversing acidosis
Giving drugs that stimulate Beta I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Afterload

A

Resistance against which ventricles contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Increased Afterload

A

Alpha agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PSNS Effect on Heart

A

Innervates SA and AV node
Stimulation decreases HR by decreasing conduction velocity
Reduces contractile force of atrial and ventricular cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SNS Effect on Heart

A

Innervates all aspects of heart
Stimulation causes increased HR and contractility
Blockade decreases HR and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

PSNS Stimulation of SA node

A

Releases acetylcholine at both nerve terminals
Dominate activity at SA node
Decreased Ca channels increasing efflux of K, decreases HR and conduction through AV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sympathetic Stimulation

A

Increase Na and Ca influx
Able to reach threshold quicker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sodium

A

Influx increases charge towards threshold for AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Potassium

A

Increased K decreases membrane potential, decreases intensity of AP and decreases contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Calcium

A

Increases contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Aortic Arch Baroreceptors

A

Responds to increased Bp
Transmits via vagus nerve to medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Carotid Body Baroreceptors

A

Transmit via glossopharyngeal nerve to medulla
Response to all Bp changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Increased Carotid pressure

A

Increase stretch
Increase PSNS decrease SNS
Vasodilation and decreased HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Decreased carotid pressure

A

Decreases arterial pressure, decreased stretch, increased sympathetic outflow and decreased PSNS
Vasoconstriction, increased HR, increased contractility, increased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Central Chemoreceptors

A

Respond to changes in pH and pCO2 in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Peripheral Chemoreceptors

A

Carotid and aortic bodies respond to decreased pO2 increased pCO2, and decreased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chemoreceptors

A

Activation increases sympathetic outflow to compensate for vasodilation effects of hypoxia to redistribute blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

RAAS

A

Renin from juxtaglomerular cells (kidneys)
Renin turns angiotensinogen to angiotensin I
Angiotensin I to Angiotensin II by ACE from lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Angiotensin II

A

Vasoconstriction
Decreased excretion of salt + water
Increased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hormones impacting Vasoconstriction

A

NE and Epi
ANgiotensin
Vasopressin
Endothelia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Ion Changes to Vasoconstriction

A

Increased calcion
Decrease in H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Decrease BP Hormones

A

Bradykinin
Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Ion Changes to Decrease BP

A

Increase K
Increase Mg
Increase acetate and citrate
Changes in H
Increased CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Unstable Angina

A

No myocardial injury
T wave abnormality/ST depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

NSTEMI

A

Subendocardial injury with +ve troponin
TI > 99th percentile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

STEMI

A

Transmural injury with ST elevation on ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

3 Types of troponin

A

Troponin C (skeletal)
Troponin I (cardiac)
Troponin T ( cardiac)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Other causes of increased troponin

A

Myocarditis
Pericarditis
Heart failure
Valvular disease
Aortic dissection
Sepsis
Renal failure
PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Primary Hemostasis

A

Utilizes platelets to form a plug at site of injured blood vessel

42
Q

Secondary Hemostasis

A

Fibrin mesh formed by multiple coagulation factors to stabililze the plug

43
Q

5 Phases of Primary Hemostasis

A

Endothelial injury
Exposure: underlying collagen release vWF
Adhesion: platelets bind to vWF
Activation: platelets become active
Aggregation: platelet cluster

44
Q

Secondary Hemostasis Patho

A

Thrombin binds with receptor activating more platelets
Fibrinogen -> fibrin -> fibrin mesh
Stabilizing factor

45
Q

Primary Hemostasis Treatments

A

ASA
Antiplatelets

46
Q

ASA

A

Inhibits thromboxane A2 production (inhibits COX-1 and COX-2)
Decreases ability for clot to form

47
Q

Antiplatelets

A

Prevent platelet aggregation and thrombus formation
Inhibit GP IIB/IIIA receptors

48
Q

Secondary Hemostasis Treatments

A

Heparin
Coumadin
Direct Thrombin Inhibitors
Direct Factor Xa Inhibitors

49
Q

Heparin

A

Binds to enzyme inhibitor anti-thrombin III
Inactivates thrombin, factor Xa and other proteases

50
Q

Coumadin

A

Decreases active vitamin K
Decrease clotting ability

51
Q

Direct Thrombin INhibitors

A

Bind to thrombin in circulation and those already forming clot

52
Q

When is direct thrombin inhibitor useful

A

Heparin induced thrombocytopenia

53
Q

Side effects of direct thrombin inhibitors

A

GI symptoms, dyspepsia, gastritis

54
Q

Direct Factor Xa inhibitors

A

Act on factor X of coagulation cascade

55
Q

International Normalized Ratio

A

Lab value of how long it takes for blood to clot

56
Q

Therapeutic iNR

A

2-3s

57
Q

Nitroglycerin Action

A

Converted to NO in cell
Causes vascular smooth muscle relaxation and vasodialtion
Reduces oxygen demand
Decreases preload, afterload, and dilates coronary arteries

58
Q

Phosphodiesterase Inhibitors

A

Inhibit phosphodiesterase III -> cAMP breakdown
Unable to activate platelets

59
Q

MOA Morphine

A

Binds with opiate receptors throughout CNS
Hyperpolarization of nerve cells, inhiibitions of nerve firing
Pain relief decreases sympathetic outflow, catecholamine release, MVO2, MI progression

60
Q

Morphine effects of inhibition of nerve firing

A

Alter’s brain perception of pain
Decreases pain perception at spinal cord
Binds to perihheral terminals to decrease pain stimuli
Reduces sensitivity of respiratory centre to CO2
Histamine release causing hypotension
Enhances PNS stimulus
Stimulates chemoreceptor trigger for vomiting

61
Q

Cardiogenic Shock

A

Acute physiological condition caused by inability of heart to pump blood for needs of body

62
Q

S/Sx of Cardiogenic Shock

A

Rapid breathing
Severe shortness of breath
Sudden tachycardia
LoC
Weak pulse
Low BP
Sweating
Pale skin
Cold hands or feet
Urinating less than normal

63
Q

Causes of Cardiogenic Shock

A

Decreased function or performance of myocardium
Abnormalities leading to decrease in LV EDV
Structural defects or obstructions leading to shock

64
Q

Dopamine Classifications

A

Sympathomimetic
Alpha Adrenergic Agonist
Beta Adrenergic Agonist
Dopaminergic Agent

65
Q

Dopamine 2-5mcg/kg/min

A

Dopaminergic stimulation
Dilation vessels in mesentery and kidney
Increased blood flow to kidney and gut

66
Q

5-10mcg/kg/min dopamine

A

Beta I stimulant
Positive inotropic
Positive chronotropic

67
Q

10-20mcg/kg/min dopamine

A

Alpha I stimulant
Peripheral vasoconstriction
Beta I stimulation
Reversal of dopaminergic effects

68
Q

ACS definitive treatment

A

Antiplatelets, antithrombins, abtianginal
Primary PCI for balloon angioplasty
Thrombolysis (TNK)

69
Q

Atropine Classification

A

Parasympatholytic
Anticholinergic
Antimuscarinic
Antidote for cholinergic OD, cholinesterase inhibitors and amanita muscaria
Diagnostic agent
Belladonna alkaloid
Antiparksonian

70
Q

MOA Atropine

A

Competitively blocks effects of AcH at muscarinic receptors of PNS
Inhibits vagal influence of HR
Depresses salivation and bronchiole secretion, relaxes GI
Relaxes pupils

71
Q

Atropine Precautions

A

Can cause paradoxical bradycardia if administered slowly
May not work in heart blocks
Increases workload of heart

72
Q

Transcutaneous Pacemaker

A

External
Non-invasive
Pacing through skin

73
Q

Transvenous Pacemaker

A

Electrodes via large central vessels to right chambers of the heart

74
Q

Epicardial Pacemaker

A

Internal implanted
Electrodes on surface of heart

75
Q

Permanent Pacemaker

A

Venous or epicardial
Implanted
Electrodes on surface of heart

76
Q

Fixed Rate Pacemaker

A

Fires constantly at preset rate without regard for inherent beats

77
Q

Demand Pacemakers

A

Sensing device that will only discharge when natural rate of heart falls below present value established for pacer

78
Q

Single Chamber Pacemaker

A

Either ventricle or atria

79
Q

Dual chamber Pacemaker

A

Stimulate atria then ventricles

80
Q

Pacemaker Failure to Sense

A

Inability to identify ECG waveforms
Paced beats early, late, or not at all

81
Q

Failure to Fire

A

Pacing spike fails to appear when it should

82
Q

failure to Capture (electrical)

A

Waveform fails to appear after pacing spike and depolarization of heart does not occur

83
Q

Failure to Capture (mechanical)

A

Spike appears, no mechanical output
Pulse doesn’t match

84
Q

Adenosine Class

A

Anti-arrhythmic
Diagnostic agent

85
Q

MOA Adenosine

A

Endogenous nucleoside acting at adenosine A receptors in heart
Decrease adenylyl cyclase, resulting in decreased SA discharge and AV conduction
Efflux of potassium from cell, hyper polarization of cell
Decreases automaticity of AV node, causing complete AV bock

86
Q

Adenosine Half life

A

<10s

87
Q

Lidocaine Class

A

Anti-arrhythmic Class Ib
Sodium channel blocker
Local anesthetic

88
Q

Indications lidocaine

A

Cardiac irritability
Refractory VF or VT
Topical administration pre ETT

89
Q

MOA Lidocaine

A

Shortens phase 3 decreasing myocardial excitability
Decreases slope of phase 0
Increases fibrillation threshold
Decreases conduction in ischemic cardiac tissue without adversely affecting normal conduction

90
Q

Precautions Lidocaine

A

Pt with perfusion disorder, hepatic disease, elderly

91
Q

Lidocaine toxicity

A

3.0mg/kg

92
Q

S/Sx of lidocaine toxicity

A

Drowsiness
Slurred speech
Dysrhythmias
CNS depression
Seizure
Coma
Death

93
Q

Amiodarone Class

A

Class III antiarrhythmic
Adrenergic blocker
Na, K, Ca blocker
Acts on all cardiac tissue

94
Q

Indications Amiodarone

A

Refractory VF VT
Refractory PSVT or A-fib
Symptomatic atrial flutter

95
Q

MOA Amiodarone

A

Increases vF threshold by blocking K channels and prolonging repolarization and refractory period
Relaxes vascular smooth muscle to decrease PVR and increase coronary perfusion
Negative chronotrope
Negative inotrope
Negative dromotrope

96
Q

Electrical Phase Cardiac Arrest

A

0-4min
Electrical conduction chaotic with lots of irritable foci
Defibrillation needed

97
Q

Circulatory Phase Cardiac Arrest

A

4-10min
Drop in BP without perfusion to heart or brain
CPR needed

98
Q

Metabolic Phase Cardiac Arrest

A

> 10 min
Metabolic acidosis kicks in due to anaerobic metabolism
Decreased transport of O2 needed for perfusion
Possible sodium bicarb

99
Q

Ventricular Fibrillation

A

Multiple ectopic foci in ventricles at rates up to 500bpm
Rapid and irregular activity rendering ventricles unable to contract in synchronized manner
Loss of heart as a pump

100
Q

Cardioversion

A

Place all cardiac cells in depolarized state, allowing dominant pacemaker to proceed

Patient Care (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions