Cardiovascular System Flashcards
1
Q
atrial and ventricular pressure when AV valve close
A
ventricular pressure > atrial pressure
2
Q
atrial and ventricular pressure when SL valve closed
A
ventricular pressure < aorta/pulm. artery
3
Q
Lub sound associated with
A
AV valves closing
4
Q
Dup sound associated with
A
semilunar valves closing
5
Q
Pericardial sac and names of its layers
A
- two-layer sac that covers the heart
- Visceral pericardium: fused to heart
- Parietal pericardium: outer layer from heart, reinforced with fibrous pericardium (dense CT)
6
Q
Cardiac tamponade
A
ompression of the heart caused by build up of fluid in pericardial sac; fibrous pericardium can’t expand well causing the heart to become strangulated
7
Q
Layers of pericardial sac
A
- Fibrous pericardium
- Parietal pericardium
- Pericardial cavity
- Visceral pericardium (also called epicardium)
8
Q
Phrenic Nerve: origin, what it innervates, where it passes
A
innervates diaphragm; descends between pericardial and pleural sacs; origin: C3-5
9
Q
Cardiopulmonary Resuscitation (CPR)
A
chest compressions to sandwich heart between sternum and spine to help squeeze blood from heart into circulation
10
Q
Heart Wall layers
A
- Epicardium (visceral pericardium)
- Myocardium
- Endocardium
11
Q
Histology of Heart Wall layers
A
- Epicardium – mesothelium, variable layer of adipose, coronary vessels
- Myocardium – cardiac muscle
- Endocardium – endothelium, thin layer loose CT, conducting system
12
Q
where is fossa ovalis located
A
right atrium
13
Q
pathway of conducting system
A
SA node → atria → AV node → AV bundle/bundle of His → right and left bundle branches → purkinje fibers → ventricles
14
Q
what is the conducting system of the heart
A
Specialized cardiac muscle cells that stimulate contraction; allows heart to contract w/o innervation
15
Q
coronary circulation: coronary arteries
A
16
Q
coronary circulation: coronary veins
A
17
Q
Myocardial Action Potential: Phase 0
A
rapid upstroke and depolarization; voltage-gated Na+ channels open
18
Q
Myocardial Action Potential: Phase 1
A
initial repolarization – inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open
19
Q
Myocardial Action Potential: Phase 2
A
platuea – Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux; Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction
20
Q
Myocardial Action Potential: Phase 3
A
rapid repolarization – massic K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels
21
Q
Myocardial Action Potential: Phase 4
A
resting potential – high K+ permeability through K+ channels
22
Q
Refractory period and actional potentials
A
period of time after a stimulation in which excitable cell cannot be stimulation again
23
Q
Absolute refractory period (ARP) vs Relative refractory period (RRP)
A
Absolute: action potential can’t be induced no matter the strength of the signal (phase 0 to 2)
Relative: action potential can be induced if stimulus is strong enough
(phase 3)
24
Q
Excitation-Contraction Coupling of cardiac muscle cells – physiology from actional potential to contraction of muscle
A
Myocyte depolarized by action potential; calcium ions enter cell in phase 2 of AP via L-type calcium channels in the sarcolemma
⇒ calcium triggers subsequent release of calcium from SR through ryanodine receptors (calcium-release channels)
⇒ calcium released SR ￪ intracellular calcium conc. ⇒ free calcium binds troponin-C on actin
⇒ contraction of muscle
25
calcium channel blockers affect on cardiac muscle cell excitation-contraction coupling
calcium channel blockers ￬ release of calcium from SR during action potential
26
action potential in cardiac pacemaker cells (nodal cells)
27
sympathetic and parasympathetic affect on nodal cell action potential
* Beta-AR/Gs: ↑ If, ↑Ica,L
* Sympathetic stimulation ⇒ steeper upstroke on action potential
* Muscarinic AchR/Gi: ↑ IK, Ach↓ If, ↓ Ica,L
* Parasympathetic inhibition ⇒ slower/less steep upstroke
28
how PQRST wave lines up with conduction pathway of heart
P – SA node, atrial muscle
QRS – purkinje fibers, ventricular muscles
T – repolarization
29
greatest and least automaticity in heart cells
SA node has greatest automaticity; vetricular and atrial myocytes have no automaticity under normal conditions
30
P wave of ECG
atrial depolarization
31
PR interval of ECG
time from start of atrial depolarization to start of ventricular depolarization (normally \<200 msec)
32
QRS complex of ECG
ventricular depolarization (normally \<120 msec)
33
QT interval of ECG
ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization
34
T wave of ECG
ventricular repolarization
\*T-wave inverion can indicate ischemia or recent MI
35
J point of ECG
junction between end of QRS complex and start of ST segment
36
ST segment of ECG
isoelectric, ventricles depolarized
37
U wave in ECG
prominent in hypokalemia, bradycardia
38
Quadrant Rule – alignment of QRS and estimating QRS axis
39
arrangemnent of limb leads in ECG
40
precordial leads in ECG
41
suggested method for reading ecg
rate, rhythm, axis, conduction, ischemia/injury/infarction, hypertrophy
42
sinus rhythm
originates from SA node, "normal" rhythm, P wave before QRS and in same direction
43
normal QT invernal in relation to R-R interval
QT interval should be less than half of the RR interval
44
QTc interval
(QT)/(RR^1/2) = corrected QT interval
called Bazett’s formula
45
causes of prolonged QTc interval
- Drugs (K channel blockers)
- Hypocalcemia, hypomagnesemia, hypokalemia
- Hypothermia
- Acute myocardial ischemia / infarction
- Congenital (inherited channelopathies)
- Increased intra-cranial pressure
46
Right Ventricular Hypertrophy Criteria
1. In V1, R wave is greater than the S wave
2. R wave in V1 greater than 7 mm
3. Right axis deviation
4. In V1, T wave inversion without etiology (posterior MI, ARVC, Brugada, etc.)
5. Prominent S waves in V5 and V6
47
Left Ventricular Hypertrophy ECG
- With LVH, the electrical balance is tipped further to the left
- looking at V6 lead: Tall R waves in the left chest leads
- Predominant S waves in the right chest leads
48
jugular venous pressure
reflects right atrial pressure
49
right atrial pressure wave
50
Pulmonary Capillary Wedge Pressure (PCWP)
Normal: 5-15 mmHG
Reflects left atrial pressure
51
PCWP \> LA pressure
pulmonary vein obstruction
52
PCWP \> LVEDP
mitral valve disease
53
LVEDP \> PCWP
aortic valve disease, hypertension
54
Stroke volume
amount of blood leaving heart during ejection; in healthy: 100% SV tranverses the SV valves (less than 100% indicates leak/hole)
LVEDV – LVESV
Depends on: chamber size, loading conditions, myocardial contractility
55
calculate cardiac output
CO = stroke volume (SV) x heart rate (HR)
56
Fick principle
CO = (rate of O2 consumption) / (arterial O2 content - venous O2 content)
57
Frank-Starling principle
Force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload)
58
preload
volume blood in ventricles at end of diastole; approximated by ventricular EDV; depends on venous tone and circulating blood volume
59
afterload
pressure against which heart must work to eject blood during systole (systolic pressure); estimated by MAP
60
ejection fraction
Good measure of myocardial contractility but can be skewed by loading conditions
EF = SV/EDV = (EDV-ESV)/EDV
Normal: 55-65%
61
systemic pressure difference
MAP = RAP
mean systemic arterial pressure - right atrial pressure
62
Pulmonary pressure difference
MPAP – LAP
Mean pulmonary artery pressure – left atrial pressure
63
how arterial pressure relates to resistance and cariac output
MAP = TPR x CO
TPR = total peripheral resistance
64
factors that increase stroke volume
increased: contractility, preload
decreased: afterload
SV CAP
65
M1 receptor (tissue, response)
**tissue:** autonomic ganglia
**response:** depolarizes postsynaptic neurons
66
M2 receptor (tissue, response)
**tissue**: heart (primarily atria), axon terminals
**response**: decreased heart rate, conduction velocity, and contractility
67
M3 receptor (tissue, response)
**tissue**: smooth muscle, eye bronchioles, GI tract, urogenital system)
**response:** contraction
**tissue:** vascular endothelium
**response:** dilates blood vessels
68
nicotinic receptor in adrenal medulla: response
depolarizes medullary cells --\> secretion of catecholamines (epinephrine, norepinephrine, dopamine)
69
alpha 1 (a1) receptor: tissue and response
**tissue:** smooth muscle (eye, vascular, urogenital, hair follicles)
**response:** contracts smooth muscle
70
alpha 2 receptor: tissue and response
**tissue:** vascular smooth muscle
**response**: contracts smooth muscle
**tissue:** platelets
**response:** aggregation
71
B1 receptor: tissue and response
tissue - heart
response - increase heart rate, conductive velocity, contractility
tissue - kidney
response - increase renin release
72
B2 receptor: tissue and response
tissue - heart
response - increase heart rate, contractility
73
D1 receptor: tissue and response
tissue - vascular smooth muscle, especially renal vasculature
response - dilates blood vessels
74
Epinephrine: receptor selectivity, clinical use
* B1 = B2\>a1\*= a2\*
* low doses produce cardiac stimulation and vasodilation, which turns to vasoconstriction at high doses
* used in anaphylactic shock; cardiogenic shock, cardiac arrest
75
bronchial smooth muscle M3 activation
M3 agonist and antagonist
M3 activation --\> muscle contraction --\> bronchoconstriction (narrowing of airway)
Agonist = methacholine
Antagonists: Ipratropium (SAMA – short-acting muscarinic antagonist) and Triotropium (LAMA – long-acting)
76
B2 activation in bronchial smooth muscles, agonist, and antagonist
B2 activation --\> muscle relaxation --\> bronchodilation
* Agonist: albuterol (SABA) and Salmeterol (LABA)
* Common treatments in asthma to open airways
* Antagonists: propanolol (binds to both B1 and B2)
77
M2 receptor activation in heart
* M2 receptors found in atria in SA nodal cells
* Release of Ach reduces slope of diastolic repolarization --\> bradycardia
* Decrease in AV node conductivity
* Decrease in atrial contractility
78
effects B1 and B2 activation in heart
* Tachycardia (increase HR) via increase slope of diastolic depolarization
* Increase in AV node automaticity and conductivity (faster action potential propagation)
* Increase His-Purkinje automaticity and conductivity
* Increase atrial and ventricular contractility
79
B1 agonist and antagonist
Agonist: dobutamine (B1-specific)
Antagonist: Metoprolol (B1-specific)
80
M3 activation on blood pressure/flow
M3 activation --\> relax --\> decrease in blood pressure
81
alpha1 and 2 on blood pressure/flow
Alpha1 and alpha2 activate (smooth muscle cells) --\> constrict --\> increase blood pressure
82
B2 activation on blood pressure and flow
Beta2 activation (liver and skeletal muscle) --\> relax --\> decrease in TPR --\> increase blood pressure
83
D1 activation on blood pressure and blood flow
D1 activation --\> dilation of renal arteries/arterioles --\> increase renal blood flow
84
B1 activation on blood pressure and flow
B1 activation --\> stimulates renin release from juxtaglomerular cells in the kidney
85
effect on increase calcium on heart contractility
⇑ calcium released from cell = ⇑ force generation
86
Beta Agonist effects on heart contractility
Activation of beta adrenergic agonist = ⇑ production of heart fxn
⇑ contraction, peak force, relaxation rate
Shifts velocity vs. Load graph to right: ⇑ vmax given the afterload
87
Bowditch (Treppe) Effect
Myocardial tension ⇑ when HR ⇑
88
pressure-volume loop in cardiac cycle
89
how pressure-volume loop changes in response to change in preload
90
how pressure-volume loop changes in response to change in afterload
91
Law of Laplace
wall tension (T) is proportionate to the pressure (P) times radius (r) for thin-walled spheres or cylinders
92
ejection fraction (EF)
EF = SV/EDV = (EDV - ESV)/EDV
93
systolic ejection murmur
diamond-shaped; harsh sound lower pitched
94
systolic regurgitant murmur
holocystolic, sounds consistent through systole; high pitched whispy sound
95
diastolic regugitant murmur
decrescendo, soft, higher pitch
96
diastolic filling murmur
sound dies off then picks up again; only two-component murmur
97
murmur for mitral stenosis
opening snap, two-component murmur
98
murmur for aortic stenosis
crescendo,decrescendo
99
murmur for mitral/tricuspid regurgitation
holocystric high-pitched blowing
100
murmur for mitral valve prolapse
midsystolic click
101
murmur for ventricular septal defect
holocystic, harsh
102
murmur for aortic regurgiation
descrendo, high-pitched
103
high pressure gradient makes what kind of murmur
high pitched murmur
104
low pressure gradient makes what kind of murmur
low pitched murmur
105
aortic stenosis can lead to:
SAD: syncope, angina, dyspnea
106
aortic stenosis most commonly due to:
* calcification of otherwise normalvalve leaflets with age; the prevalence increases rapidly in the 7th decade of life.
* Aortic stenosis commonly occurs at an early age in patients with congenital bicuspid aortic valves.
* can result from rheumatic fever
107
changes in the heart as a result of aortic stenosis
The left ventricle grows progressively hypertrophied as the myocardium contracts against the mounting afterload. The myocardium outgrows its blood supply, leading to ischemia that results in progressive chest pain, dyspnea, and pulmonary congestion
108
which heart sound is aortic stenosis associated with?
S4
109
Electrocardogram (ECG) of aortic stenosis
will often show left ventricular hypertrophy (LVH),left atrial enlargement, and left bundle branch block (LBBB)
110
definition of Aortic regurgitation, also known as aortic insufficiency
the retrograde flow of blood from the aorta into the left ventricle during diastole due to anomalies in the aortic valve or the aortic root.
111
most common causes of acute aortic regurgitation
* aortic root enlargement (usually trauma or aortic dissection)
* Congenital bicuspid aortic valve
* Calcific valve disease
In the developing world, the most common cause is rheumatic fever.
112
heart changes in chronic aortic valve insufficiency
the left ventricle dilates to accommodate the volume of the backflow without increasing filling pressure or left atrial pressure. These individuals may be asymptomatic until eventually the heart can no longer compensate and symptoms of congestive left heart failure develop.
Since aortic regurgitation leads to congestive left heart failure, it is exacerbated by volume overload conditions (such as a high-salt diet) and strenuous exercise.
113
murmur caused by aortic regurgitation
Aortic regurgitation causes a high-pitched diastolic murmur, often with a blowing quality, beginning immediately after A2. It may decrescendo or persist throughout diastole, and is enhanced by the patient leaning forward and holding his breath at end-expiration.
114
ECG of aortic regurgitation will show:
Electrocardiogram will show left ventricular hypertrophy, left atrial dilation, and abnormal repolarization with ST segment depression at rest or during exercise.
115
which heart sound is chronic aortic regurgitation associated with?
S3
116
what is rheumatic fever?
heumatic fever is an immunologically-mediated disease that can occur 2-4 weeks after an untreated group A β-hemolytic streptococcal pharyngitis.
117
which valve does rheumatic fever most often affect and what does it do to it?
mitral
The acute valvular complication of rheumatic heart disease is mitral valve regurgitation, while the chronic valvular complication is mitral stenosis. Note that rheumatic heart disease is virtually the only cause of mitral stenosis.
118
pressure effects of mitral stenosis
Mitral stenosis results in increased left atrial pressures which are eventually transmitted to the pulmonary venous circuit.
119
mitral stenosis murmur and heart sound
On auscultation a low-pitched diastolic rumble following an opening snap just after the second heart sound is heard best at the fourth intercostal space, midclavicular line, with the patient in left lateral decubitus position.
The murmur is often followed by a loud S1.
120
procedure for treatment of mitral stenosis
valvuloplasty, replacement
121
myxomatous degeneration of mitral valve
valve is thicker but weakerdue to an increase in spongiosa (composed of dermatan sulfate) and a decrease in fibrosa (which has more tensile strength).
Leaflets are oversized and the chords elongated causing abnormal motion of the valve -- turbulent flow
122
definition of mitral regurgitation, also known as mitral insufficiency
retrograde flow of blood through the mitral valve from the left ventricle to the left atrium during systole due to anomalies of the mitral valve or the papillary muscles
123
causes of mitral regurgitation
* Mitral valve prolapse is the most common cause of mitral regurgitation as the prolapsed and “floppy” valve is unable to hold against the pressure differences experienced during ventricular systole.
* Intrinsic valvular damage can be caused by infective endocarditis and rheumatic fever.
124
murmur of mitral regurgitation
Mitral regurgitation causes a high-pitched holosystolic murmur at the apex with radiation to the axilla. Remember that mitral regurgitation often occurs in patients with mitral valve prolapse, so the murmur of mitral regurgitation may co-occur with a mid-systolic click.
125
definition of pulmonic stenosis
Pulmonic Stenosis is a congenital disorder characterized by a narrowing of the right ventricular outflow tract or defect of the pulmonary valve that leads to decreased blood flow from the right ventricle into the pulmonary artery.
Almost always congenital (present from birth)
126
what is tricuspid stenosis?
n tricuspid stenosis narrowing of the tricuspid valve results in a persistent diastolic pressure gradient between the right atrium to the right ventricle.
127
The most common cause of acquired tricuspid stenosis
rheumatic fever
128
what is tricuspid regurgitation
Tricuspid regurgitation occurs when the tricuspid valve allows retrograde flow of blood from the right ventricle into the right atrium during systole.
129
pathophys development of tricuspid regurgitation
elevation of right ventricular end-systolic pressure (RVESP) causes progressive dilatation of the right atrium and ventricle thereby causing distortion of the annulus. This leads to valvular insufficiency, despite otherwise anatomically normal leaflets and chordae
130
what is endocarditis?
Endocarditis is an inflammation (most often caused by infection) of the endocardial surface of the heart, usually involving the surface of cardiac valves. Most cases are caused by a bacterial infection.
131
what is the visual hallmark of endocarditis?
Vegetations are the hallmark of endocarditis and are friable, bulky, and potentially destructive on heart valves. Vegetations generally consist of fibrin, inflammatory cells and bacteria or other infective organisms.
132
Endocarditis can arise in healthy valves, but the following can predispose individuals to endocarditis:
Rheumatic heart disease
Mitral valve prolapse
Degenerative calcific valvular stenosis
Bicuspid aortic valve
Prosthetic valves
Unrepaired and repaired congenital defects
133
The most commonly infected valve in bacterial endocarditis is
mitral valve
134
Acute endocarditis is most commonly caused by which bacteria? What is the result?
Staphylococcus aureus
It most commonly results in a large vegetation that rapidly destroys the affected valve
135
Subacute endocarditis is usually caused by
viridans group streptococci (e.g. S. mitis, S. mutans, S. sanguinis) in the presence of valvular pathology, and is characterized by an indolent presentation.
It most commonly results in a small vegetation that does not destroy the valve
136
Prosthetic valve endocarditis is most commonly caused by
S. epidermidis.
137
The most common symptoms of endocarditis can be remembered from the mnemonic \_\_\_\_
FROM JANE
Fever
Roth spots
Osler nodes
Murmur
Janeway Lesions
Anemia
Nail-bed hemorrhage
Emboli
138
Cutaneous manifestations of endocarditis include
* Osler nodes (tender subcutaneous lesions on finger or toe pads)
* Splinter hemorrhages
* Janeway lesions (painless erythematous lesions on palms or soles)
139
what is Libman-Sacks endocarditis caused by and what can it cause
Libman-Sacks endocarditis is due to non-bacterial vegetations on both surfaces of the mitral valve that may cause regurgitation and that form in association with SLE.
140
what is Nonbacterial thrombotic endocarditis (marantic endocarditis) (NBTE)
may be secondary to mucin producing adenocarcinoma, hypercoagulative state, or lupus and may result in vegetations along the lines of closure of the mitral valve and in mitral valve regurgitation.
141
what is myocarditis?
Myocarditis is caused by any inflammatory process involving the cardiac muscle. Usually this is an upper respiratory virus.
142
Viral infections are the most common cause of myocarditis. These include:
* Coxsackie B virus (most common)
* Parvovirus B-19 (also important to remember)
* Echovirus (sometimes 'enterovirus' more generically)
* Adenovirus
* EBV
* CMV
* HHV-6
143
A feared complication of myocarditis is
dilated cardiomyopathy, which may present with sudden onset of extreme fatigue, dyspnea, and decreased exercise capacity in a previously healthy patient
144
the pathoglogical phases of myocarditis:
Acute: days 0-3 : viral invasion/infection phase --\> macrophage activation --\> cytokine expression
* Subacute: days 4-14: inflammatory phase; natural killer cells , B and T cell action; most patients will clear virus
* Chronic: beyond 14 days: when infection not cleared off; fibrosis, cardiac dilation, heart failure
145
what is pericarditis?
inflammation of any of the layers of the pericardium. It often presents with the presence of fluid in the pericardial space. The fluid can be composed of blood, serous fluid, or transudate.
146
common causes of pericarditis
* Systemic lupus erythematosus
* Rheumatoid arthritis
* radiation exposure
* Dressler syndrome
* Uremia
* Myocardial infarction
* Acute rheumatic fever
* bacterial infection
147
treatment of long QT syndrome
on-cardioselective beta blockers. Propranolol and nadolol are the preferred choices.
In patients who are still symptomatic with the use of beta blockers, an implantable cardioverter-defibrillator should be considered.
148
classically associated arrhythmia with long QT syndrome
torsades de pointes
149
what is Dilated cardiomyopathy
dilation of all four heart chambers
decreased myocardial contractility -- systolic dysfunction
150
causes of dilated cardiomyopathy
Alcohol abuse
wet Beriberi
Chagas disease
Cocaine
Coxsackie B virus
peripartum Cardiomyopathy
Doxorubicin, Daunorubicin
hEmochromatosis
151
change in cardiac function in dilated cardiomyopathy
Systolic dysfunction in dilated cardiomyopathy manifests with decreased cardiac output and a reduced ejection fraction (typically around 25%).
152
treatment of dilated cardiomyopathy
* ACE inhibitors and other diuretics
* β-blockers
* Digoxin
* dietary sodium restriction
153
what is restrictive cardiomyopathy?
diastolic dysfunction that causes reduced diastolic filling and decreased ventricular compliance
154
most common causes of restrictive cardiomyopathy
* Amyloidosis
* Myocardial fibrosis after open heart surgery
* Radiatio
155
how do you differentiate between constrictive pericarditis and restrictive cardiomyopathy?
* Constrictive pericarditis - pericardial knock (an accentuated heart sound occurring slightly earlier than a third heart sound, which may be audible and rarely is palpable).
* Restrictive cardiomyopathy - S3 heart sound
Classic history seen with constrictive pericarditis:
* Pericarditis
* Trauma
* Cardiac surgery
* Systemic disease that affects the pericardium (e.g. tuberculosis, connective tissue disease, malignancy)
156
what is hypertrophic cardiomyopathy?
* Hypertrophic cardiomyopathy (HCM) is a condition characterized by hypertrophy of the myocardium leading to hypercontractile, non-compliant myocardium. It was formerly known as idiopathic hypertrophic subaortic stenosis (IHSS) and asymmetric septal hypertrophy (ASH).
* Hypertrophic cardiomyopathy is functionally characterized by diastolic dysfunction due to reduced ventricular compliance.
* Hypertrophic cardiomyopathy is the most common cause of sudden death in young individuals.
157
"An otherwise healthy young athlete suddenly passes out and dies" -- what cardiomyopathy is this history associated with?
hypertrophic cardiomyopathy
158
Histopathologically, tissue samples are characterized by “myocardial disarray” -- which cardiomyopathy does this describe?
hypertrophic cardiomyopathy
159
The two most commonly mutated proteins in hypertrophic cardiomyopathy are:
* β-myosin heavy-chain
* Myosin-binding protein C
160
what is arrhythmogenic right ventricular cardiomyopathy/dysplasia
Thinning of RV wall with fatty replacement and/or fibrosis; wall filled with adipose
Inherited disease causing RV failure and arrhythmias (often lethal)
161
which cardiomyopathy is septal hypertrophy seen in?
hypertrophic cardiomyopathy
162
what is atrial flutter?
a type of supraventricular tachycardia which arises due to a macro-reentry circuit within the atrium (most commonly involving irritable foci in the right atrium near the tricuspid annulus) and is characterized by an atrial rate 250-350 BPM (classically 300 BPM).
Since the atrioventricular (AV) node has a slower conduction rate than the atrial muscle, only some of the atrial depolarizations are conducted to the ventricles, resulting in a functional AV block. The ratio of atrial to ventricular depolarizations is used to describe the rhythm (i.e. atrial rate of 340 bpm and a ventricular rate of 170 bpm would be described as a 2:1 flutter).
163
appearance of atrial flutter on ECG
regular, sawtooth flutter waves of atrial contraction at a rate of 250-350 bpm
164
what is atrial fibrillation?
the quivering state of the atria that occurs when many ectopic atrial foci fire in a chaotic manner that prevents the normal coordinated atrial contraction.
165
ECG of atrial fibrillation
an irregularly irregular rhythm with a disorganized baseline electrical activity, the absence of p-waves, and narrow QRS complexes (since the signal originates above the AV node).
166
what is Atrioventricular Nodal Reentry Tachycardia (AVNRT)
originates within the AV node
The basis for AVNRT is the existence of two separate conduction pathways within the AV node: a slow pathway with a short refractory period and a fastpathway with a long refractory period which share a final common pathway
In the common form of AVNRT, a perfectly-timed premature atrial beat arrives while the fast pathway is refractory and the slow pathway is able to conduct, thus allowing a re-entry circuit to develop if the fast pathway has recovered by the time the impulse traverses the slow pathway
167
what is Wolff-Parkinson-White (WPW) syndrome?
a separate accessory pathwayknown as the Bundle of Kent is present between the atria and ventricles which allows aberrant conduction between the atria and ventricles to bypass the AV node.
The accessory Bundle of Kent conducts atrial impulses to the level of the ventricles faster than the AV node, which naturally delays AV conduction.
WPW syndrome is the basis for atrioventricular (AV) reentry/reciprocating tachycardia (AVRT), a type of supraventricular tachycardia (SVT).
shows a D wave on ECG
168
what is orthodromic AVRT
the most common type of AVRT, the reentry circuit involves forward conduction of atrial impulses to the ventricles via the AV node with retrograde conduction from the ventricles back up to the atria via the accessory pathway.
169
what is antidromic AVRT?
type of AVRT, the reentry circuit involves forward conduction down the accessory pathway with retrograde conduction up the His-Purkinje system through the AV node.
170
ECG of orthodromic AVRT
Orthodromic AVRT produces a regular, narrow-complex tachycardia with a ventricular rate of 150-250 BPM (may be greater) and inverted P waves on E\G
171
ECG of antidromic ECG
egular, wide-complex tachycardia with a ventricular rate of 150-250 BPM with inverted P waves on ECG
172
ventricular tachycardia on ECG
wide,regular QRS tachycardia with QRS complexes lasting longer than 140 msec
173
what is a junctional escape rhythm?
* A junctional rhythm with a rate of 40-60 bpm.
* QRS complexes are typically narrow (\< 120 ms).
* No relationship between the QRS complexes and any preceding atrial activity (e.g. P-waves, flutter waves, fibrillatory waves).
* may haev retrograde P wave in ST segment
supraventricular impulses are interrupted and AV node becomes the pacemaker for the heart transmitting impulses to the atria upwards (P waves) and ventricles downwards (QRS complex)
174
ECG PR \> 200 msec (200-220 ms depending on definition used)
First Degree AV block
175
ECG:
Progressing lengthening of the PR interval and then failure of AV conduction Blocks occurs in ratios (3:2, 4:3, 5:4, ect) As PR interval lengthens, the time between the QRS complexes (R-R interval) may shorten by an amount equal to the change in PR interval
Second Degree AV block: Type I (Mobitz I or Wenckebach)
176
P-wave fails to conduct to the ventricle without a preceding change in the PR interval
Typically due to block within the his-purkinjae system (below the AV node)
Second Degree AV Block Type II
177
ECG:
Multiple P-waves Blocked
“High Grade” AV Block
178
using intra cardiac recording to distinguish between reading of second degree type I and II AV blocks
no his signal - type I (block in AV)
his signal - type II (block in his)
179
ECG:
Complete dissociation of the atrium and ventricle
Atrial rhythm is often regular or sinus tachycardia
Ventricular rhythm is often junctional (narrow QRS, rate 40-60 bpm), and less frequently ventricular (wide QRS, rate 30-40 bpm)
Third Degree AV Block
180
ECG:
• Loss of septal Q in V6 • Late positive V6 • Late negative V1
Left Bundle Branch Block
181
ECG:
Preserves septal Q in V6 • Late positive V1 (rSR’) • Late negative V6 (also I, aVL)
Right Bundle Branch Block
182
ECG:
Left axis deviation (-45º- -90º)
QRS duration less than 120 ms
qR in I and aVL
rS in II, III and aVF
Left Anterior Fascicular Block
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ECG:
Right axis deviation (\>90º)
QRS duration less than 120 ms
rS in I and aVL
qR in II, III and aVF
Left Posterior Fascicular Block
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classes of antiarrythmic drugs
I - sodium channel blockers
II - Beta-blockers
III - potassium channel blockers
IV - calcium channel blockers
V - digoxin and other
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what is digoxin?
Binds to the Na+/K+ ATPase pump • Increases intracellular Na+ • Increases intracellular Ca+2 through Na+/Ca+2 exchange • Slows phase 4 in sinoatrial and AV nodal cells
increases contractility in heart failure
186
when is ANP released?
from atrial myocytes in response to increased blood volume and atrial pressure
187
what causes varicose veins?
Weakness of the tunica media in veins caused by increased pressure or defects in the structure or function of valves lead to varicose veins in the legs.
188
definition of edema vs effusion
Edema is the accumulation of excess fluid within the tissues whereas effusion indicates collection of fluid within a cavity of the body such as cranial cavity, in the middle ear, in joint spaces, pleural cavity, pericardial cavity or peritoneal cavity
189
what is pitting edema?
due to increased fluid movement from the blood vessels typically due to increased hydrostatic pressure (NFP positive). Accumulation of fluid in interstitial space due to failure of vital organs such as kidney, heart and liver or local conditions.
190
what is non-pitting edema (lymphoedema)?
Lymphoedema is accumulation of fluid in interstitial space, typically due to blockage of lymphatic vessels and swelling of lymph nodes. Filariasis, radiation, cogenital disease (Milroy’s disease) or surgery
191
what is peripheral artery disease?
injury to systemic arteries, usually atherosclerotic
Manifestations include claudication, renal artery stenosis, abdominal aortic aneurysm (AAA)
192
The tunica intima is lined by a single layer of endothelial cells, and these cells secrete several substances that control various aspects of blood vessel function. Which of the following substances, secreted by endothelial cells, influences shear stress and prevents adherence of leukocytes and platelets to the blood vessel wall?
nitric oxide
193
what is atherosclerosis?
disease of elastic arteries and large/medium sized muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol plaques
194
symptoms of atherosclerosis
195
presentation and pathophysiology of stable ischemic heart disease
**Presentation:**
Asymptomatic or chronic, predictable angina pectoris
**Pathophysiology:**
obstructive or non-obstructive coronary artery disease
intact fibrous cap
minimal platelet activation or thrombus
196
presentation and pathophysiology of Acute Coronary Syndrome
**Presentation:** Unstable Angina or Non-ST elevation MI or ST elevation MI
**Pathophysiology:**
obstructive coronary artery disease
plaque rupture or erosion platelet activation,
inflammation, and thrombus
197
Two diagnostic tests that are integral to the definition of acute coronary syndromes
* ECG
* serum biomarkers of myocardial cell necrosis, such as troponin I and troponin T
198
clinical definition of unstable angina
* Angina at rest
* New angina (within last 2 weeks is a particularly high risk category)
* Increasing/accelerating angina
199
The presence of a NSTEMI is defined by two criteria:
1. Evidence of myocardial necrosis (often elevated troponin).
2. No elevation of the ST-segment on the ECG.
200
If not treated quickly, ST-segment elevation will usually be followed by the development of abnormal Q-waves, which implies \_\_\_
completed transmural necrosis
201
Nitric oxide and prostacyclin in clotting and atherosclerotic plaques
both are potent inhibitors of platelet activation; reduced in the vicinity of the atherosclerotic plaque due to endothelial damage and dysfunction
202
serotonin: smooth muscles agonist or antagonist
agonist
203
thromboxane A2: smooth muscle agonist or antagonist
agonist
204
cause of NSTEMI vs. STEMI
NSTEMI typically results from rupture plaque and sub-occlusive thrombus, whereas STEMI typically results from ruptured plaque and occlusive thrombus
205
prinzmetal angina
intermittent chest pain secondary to coronary artery vasospasms. Variant angina pectoris is unrelated to physical activity and episodes usually occur at rest, especially at night and early in the morning.
206
symptoms of stable angina in "special" populations
Weakness of the arms • Shortness of breath • Dizziness
207
definition of heart failure
The clinical syndrome (characteristic signs & symptoms) that results when the heart cannot pump enough blood to adequately serve the body’s needs while at the same time maintaining normal pressures in the heart chambers and lung vessels
208
Left-sided heart failure
Signs (e.g. rales, narrow pulse pressure, pulsus alternans, cool extremities) and symptoms (e.g. PND, orthopnea, dyspnea, exercise limitations, fatigue, generalized weakness, confusion) of low cardiac output and pulmonary congestion due to high left sided filling pressures (increased left atrial pressure) leading to fluid backing up behind a dysfunctional left ventricle and/or left-sided valvular disease
209
changes in ejection fraction and end diastolic volume in systolic vs. diastic heart failure
210
Signs and symptoms that are most indicative of\_\_\_heart failure include:
## Footnote
Orthopnea
Paroxysmal nocturnal dyspnea
Pulmonary edema
LEFT
211
definition of orthopnea
shortness of breath that occurs in the recumbent position and improves upon elevation of the head (e.g. by sitting up or with pillows). It is caused by an acute increase in venous return upon lying down, which leads to pulmonary congestion.
212
what is paroxysmal nocturnal dyspnea
an acute shortness of breath that awakens a person after 1-2 hours of sleep. It is caused by increased venous return due to reabsorption of peripheral (especially lower extremity) edema during sleep.
213
Signs and symptoms that are most indicative of
\_\_\_ heart failure include:
Hepatomegaly (nutmeg liver)
Jugular venous distention
Peripheral edema
RIGHT
214
what is cor pulmonale
Isolated right heart failure is most commonly due to lung disease that leads to pulmonary hypertension
215
Agents commonly used in the treatment of congestive heart failure can be remembered with the mnemonic:
B-SAD
* β-blockers
* Spironolactone
* ACE inhibitors or ARBs
* Diuretics (furosemide, thiazide), Digoxin
216
Agents that improve mortality in heart failure include:
* β-blockers (avoid in acutely decompensated heart failure)
* Spironolactone
* ACE inhibitors / angiotensin II receptor blockers
217
location and action: a1 adrenergic receptor
CV system
location: arterioles, veins
action: vasoconstriction
218
location and action: B1 adrenergic receptor
CV system
location: SA node
action: increased heart rate
location: cardiac muscle cells
action: increased contractile strength
219
location and action: B2 adrenergic receptor
CV system
location: some arterioles
action: vasodilation
220
location and action: N-Ach (gang.) and N-Ach receptor
CV system
location: autonomic ganglia
action: postganglionic EPSP
location: SA Node
action: decreased heart rate
221
location and action: guanylyl cyclase receptors in CV system
location: arterioles
action: vasodilation
222
yay you're done
good job c:
