Cardiology 2 Flashcards
(100 cards)
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
2
Q
Location of SA and AV node
A
Atrium
3
Q
Left Heart
A
thicker wall
Mitral valve
Pumps into systemic circulation via aorta and great vessels
Innervated with LBB
4
Q
MAP
A
Average pressure over one full cardiac cycle
2/3 diastolic + 1/3 systolic
5
Q
Normal MAp
A
70-100
6
Q
Perfusion MAP
A
60-65 to perfuse coronary arteries, kidneys, brain
7
Q
Weights MAP not used
A
Pts <12 or <20kg
8
Q
Factors affecting MAP
A
Vascular tone
Fluid Status
Drugs
Cardiovascular and Neurogenic status
9
Q
Preload
A
RV wall stress at end diastole
10
Q
Increase Preload
A
NS/RL bolus
RBC bolus
Releasing intrathoracic pressure
Supine position
Vasopressors
11
Q
Decrease preload
A
Nitroglycerin
Morphine
Furosemide
PPV, AutoPEEP, increased intrathoracic pressure
Sitting
12
Q
Contractility
A
Squeeze or inotropy of cardiac muscle
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
14
Q
Afterload
A
Resistance against which ventricles contract
15
Q
Increased Afterload
A
Alpha agonists
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
17
Q
SNS Effect on Heart
A
Innervates all aspects of heart
Stimulation causes increased HR and contractility
Blockade decreases HR and contractility
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
19
Q
Sympathetic Stimulation
A
Increase Na and Ca influx
Able to reach threshold quicker
20
Q
Sodium
A
Influx increases charge towards threshold for AP
21
Q
Potassium
A
Increased K decreases membrane potential, decreases intensity of AP and decreases contractions
22
Q
Calcium
A
Increases contractions
23
Q
Aortic Arch Baroreceptors
A
Responds to increased Bp
Transmits via vagus nerve to medulla
24
Q
Carotid Body Baroreceptors
A
Transmit via glossopharyngeal nerve to medulla
Response to all Bp changes
25
Increased Carotid pressure
Increase stretch
Increase PSNS decrease SNS
Vasodilation and decreased HR
26
Decreased carotid pressure
Decreases arterial pressure, decreased stretch, increased sympathetic outflow and decreased PSNS
Vasoconstriction, increased HR, increased contractility, increased BP
27
Central Chemoreceptors
Respond to changes in pH and pCO2 in brain
28
Peripheral Chemoreceptors
Carotid and aortic bodies respond to decreased pO2 increased pCO2, and decreased pH
29
Chemoreceptors
Activation increases sympathetic outflow to compensate for vasodilation effects of hypoxia to redistribute blood flow
30
RAAS
Renin from juxtaglomerular cells (kidneys)
Renin turns angiotensinogen to angiotensin I
Angiotensin I to Angiotensin II by ACE from lungs
31
Angiotensin II
Vasoconstriction
Decreased excretion of salt + water
Increased BP
32
Hormones impacting Vasoconstriction
NE and Epi
ANgiotensin
Vasopressin
Endothelia
33
Ion Changes to Vasoconstriction
Increased calcion
Decrease in H
34
Decrease BP Hormones
Bradykinin
Histamine
35
Ion Changes to Decrease BP
Increase K
Increase Mg
Increase acetate and citrate
Changes in H
Increased CO2
36
Unstable Angina
No myocardial injury
T wave abnormality/ST depression
37
NSTEMI
Subendocardial injury with +ve troponin
TI > 99th percentile
38
STEMI
Transmural injury with ST elevation on ECG
39
3 Types of troponin
Troponin C (skeletal)
Troponin I (cardiac)
Troponin T ( cardiac)
40
Other causes of increased troponin
Myocarditis
Pericarditis
Heart failure
Valvular disease
Aortic dissection
Sepsis
Renal failure
PE
41
Primary Hemostasis
Utilizes platelets to form a plug at site of injured blood vessel
42
Secondary Hemostasis
Fibrin mesh formed by multiple coagulation factors to stabililze the plug
43
5 Phases of Primary Hemostasis
Endothelial injury
Exposure: underlying collagen release vWF
Adhesion: platelets bind to vWF
Activation: platelets become active
Aggregation: platelet cluster
44
Secondary Hemostasis Patho
Thrombin binds with receptor activating more platelets
Fibrinogen -> fibrin -> fibrin mesh
Stabilizing factor
45
Primary Hemostasis Treatments
ASA
Antiplatelets
46
ASA
Inhibits thromboxane A2 production (inhibits COX-1 and COX-2)
Decreases ability for clot to form
47
Antiplatelets
Prevent platelet aggregation and thrombus formation
Inhibit GP IIB/IIIA receptors
48
Secondary Hemostasis Treatments
Heparin
Coumadin
Direct Thrombin Inhibitors
Direct Factor Xa Inhibitors
49
Heparin
Binds to enzyme inhibitor anti-thrombin III
Inactivates thrombin, factor Xa and other proteases
50
Coumadin
Decreases active vitamin K
Decrease clotting ability
51
Direct Thrombin INhibitors
Bind to thrombin in circulation and those already forming clot
52
When is direct thrombin inhibitor useful
Heparin induced thrombocytopenia
53
Side effects of direct thrombin inhibitors
GI symptoms, dyspepsia, gastritis
54
Direct Factor Xa inhibitors
Act on factor X of coagulation cascade
55
International Normalized Ratio
Lab value of how long it takes for blood to clot
56
Therapeutic iNR
2-3s
57
Nitroglycerin Action
Converted to NO in cell
Causes vascular smooth muscle relaxation and vasodialtion
Reduces oxygen demand
Decreases preload, afterload, and dilates coronary arteries
58
Phosphodiesterase Inhibitors
Inhibit phosphodiesterase III -> cAMP breakdown
Unable to activate platelets
59
MOA Morphine
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
Morphine effects of inhibition of nerve firing
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
Cardiogenic Shock
Acute physiological condition caused by inability of heart to pump blood for needs of body
62
S/Sx of Cardiogenic Shock
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
Causes of Cardiogenic Shock
Decreased function or performance of myocardium
Abnormalities leading to decrease in LV EDV
Structural defects or obstructions leading to shock
64
Dopamine Classifications
Sympathomimetic
Alpha Adrenergic Agonist
Beta Adrenergic Agonist
Dopaminergic Agent
65
Dopamine 2-5mcg/kg/min
Dopaminergic stimulation
Dilation vessels in mesentery and kidney
Increased blood flow to kidney and gut
66
5-10mcg/kg/min dopamine
Beta I stimulant
Positive inotropic
Positive chronotropic
67
10-20mcg/kg/min dopamine
Alpha I stimulant
Peripheral vasoconstriction
Beta I stimulation
Reversal of dopaminergic effects
68
ACS definitive treatment
Antiplatelets, antithrombins, abtianginal
Primary PCI for balloon angioplasty
Thrombolysis (TNK)
69
Atropine Classification
Parasympatholytic
Anticholinergic
Antimuscarinic
Antidote for cholinergic OD, cholinesterase inhibitors and amanita muscaria
Diagnostic agent
Belladonna alkaloid
Antiparksonian
70
MOA Atropine
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
Atropine Precautions
Can cause paradoxical bradycardia if administered slowly
May not work in heart blocks
Increases workload of heart
72
Transcutaneous Pacemaker
External
Non-invasive
Pacing through skin
73
Transvenous Pacemaker
Electrodes via large central vessels to right chambers of the heart
74
Epicardial Pacemaker
Internal implanted
Electrodes on surface of heart
75
Permanent Pacemaker
Venous or epicardial
Implanted
Electrodes on surface of heart
76
Fixed Rate Pacemaker
Fires constantly at preset rate without regard for inherent beats
77
Demand Pacemakers
Sensing device that will only discharge when natural rate of heart falls below present value established for pacer
78
Single Chamber Pacemaker
Either ventricle or atria
79
Dual chamber Pacemaker
Stimulate atria then ventricles
80
Pacemaker Failure to Sense
Inability to identify ECG waveforms
Paced beats early, late, or not at all
81
Failure to Fire
Pacing spike fails to appear when it should
82
failure to Capture (electrical)
Waveform fails to appear after pacing spike and depolarization of heart does not occur
83
Failure to Capture (mechanical)
Spike appears, no mechanical output
Pulse doesn't match
84
Adenosine Class
Anti-arrhythmic
Diagnostic agent
85
MOA Adenosine
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
Adenosine Half life
<10s
87
Lidocaine Class
Anti-arrhythmic Class Ib
Sodium channel blocker
Local anesthetic
88
Indications lidocaine
Cardiac irritability
Refractory VF or VT
Topical administration pre ETT
89
MOA Lidocaine
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
Precautions Lidocaine
Pt with perfusion disorder, hepatic disease, elderly
91
Lidocaine toxicity
3.0mg/kg
92
S/Sx of lidocaine toxicity
Drowsiness
Slurred speech
Dysrhythmias
CNS depression
Seizure
Coma
Death
93
Amiodarone Class
Class III antiarrhythmic
Adrenergic blocker
Na, K, Ca blocker
Acts on all cardiac tissue
94
Indications Amiodarone
Refractory VF VT
Refractory PSVT or A-fib
Symptomatic atrial flutter
95
MOA Amiodarone
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
Electrical Phase Cardiac Arrest
0-4min
Electrical conduction chaotic with lots of irritable foci
Defibrillation needed
97
Circulatory Phase Cardiac Arrest
4-10min
Drop in BP without perfusion to heart or brain
CPR needed
98
Metabolic Phase Cardiac Arrest
>10 min
Metabolic acidosis kicks in due to anaerobic metabolism
Decreased transport of O2 needed for perfusion
Possible sodium bicarb
99
Ventricular Fibrillation
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
Cardioversion
Place all cardiac cells in depolarized state, allowing dominant pacemaker to proceed
