cardio Flashcards

(204 cards)

1
Q

right side of heart

A

receives O2-poor blood from tissues
pumps blood back to lungs to get rid of CO2, pick up O2 via pulm. circuit

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2
Q

left side of heart

A

receives oxygenated blood from lungs
pumps blood to body tissues via systemic circuit to deliver O2, and pick up CO2

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3
Q

atria

A

receiving chambers of heart
right and left

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4
Q

right atrium

A

receives deoxygenated blood returning from systemic circuit (from tissues)
SVC, IVC, coronary sinus empty into RA

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5
Q

left atrium

A

receives oxygenated blood returning from pulm. circuit (from lungs)
4 pulm. veins empty into LA

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6
Q

ventricles

A

pumping chambers of heart

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7
Q

right ventricle

A

pumps blood through pulm. circuit (pulm. trunk/artery to lungs)
most of anterior surface

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8
Q

left ventricle

A

pumps blood through systemic circuit (aorta to tissues)
posterioinferior surface

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9
Q

pleural cavities

A

2- each surrounds one lung

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10
Q

mediastinum

A

2- superior and inferior

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11
Q

superior mediastinum

A

surrounds other thoracic organs and structures, such as esophagus, trachea, thymus, aortic arch (and its 3 branches), SVC, and thoracic duct (lymphatic vessel)

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12
Q

inferior mediastinum

A

contains pericardial cavity
encloses the heart

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13
Q

location of heart

A

in mediastinum
b/w 2nd and 5th rib ICS
superior surface of diaphragm
2/3 of heart to left of midsternal line
anterior to vertebral column
posterior to sternum

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14
Q

base of heart

A

top
leans towards right shoulder

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15
Q

apex of heart

A

bottom
points towards left hip

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16
Q

apical pulse

A

palpated b/w 5th and 6th ribs in MCL

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17
Q

pericardium

A

double-walled sac that surrounds heart
2 layers- fibrous pericardium and serous pericardium

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18
Q

fibrous pericardium

A

1 layer
protect, anchor heart to the surrounding structures
prevent overfilling

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19
Q

serous pericardium

A

2 layers- parietal and visceral layer (separated by pericardial cavity)
deep to FP
allows the “heart works in a friction-less environment

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20
Q

parietal layer of SP

A

lines internal surface of fibrous pericardium and thoracic wall

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21
Q

visceral layer of SP

A

on external surface of heart

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22
Q

pericardial cavity

A

decreases friction
lets the heart work “easier”

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23
Q

anterior intraventricular sulcus

A

Anterior position of interventricular septum

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24
Q

posterior intraventircular sulcus

A

Landmark on posteroinferior surface

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25
coronary sulcus
Encircles junction of atria and ventricles AV groove
26
interatrial septum
separates atria contains fossa ovalis
27
fossa ovalis
remnant of foramen ovale of fetal heart
28
interventricular septum
separates ventricles
29
SVC
returns blood from the body regions above the diaphragm
30
IVC
returns blood from body regions below diaphragm
31
coronary sinus
returns blood from coronary veins
32
4 pulm. veins
return blood from lungs
33
papillary muscle
project into ventricular cavity Anchor chordae tendineae that are attached to AV valves of the heart
34
ventricles
thicker walls than atria left ventricle 3x thicker than right
35
heart valves
ensure unidirectional BF through heart open and close in response to pressure changes-> causes normal heart sounds (lub dub) 2 major types- AV and SL
36
AV valves
located between atria and ventricles prevent backflow into atria when ventricles contract 2- tricuspid and mitral (bicuspid)
37
SL valves
located between ventricles and major arteries exiting the heart prevent backflow from major arteries back into ventricles – Open and close in response to pressure changes – Each valve consists of three cusps that roughly resemble a half moon 2- pulm. and aortic
38
tricuspid valve
right AV valve made up of three cusps and lies between right atria and ventricle
39
mitral valve
left AV valve made up of two cusps and lies between left atria and ventricle
40
pulm. SL valve
located between right ventricle and pulmonary trunk/artery
41
aortic SL valve
located between left ventricle and aorta
42
pathway of blood through right side of heart
Superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus → – Right atrium → – Tricuspid valve → – Right ventricle → – Pulmonary semilunar valve → – Pulmonary trunk → – Pulmonary arteries → – Lungs (to pick up O2 and drop off CO2)
43
pathway of blood through left side of heart
Four pulmonary veins → – Left atrium → – Mitral (bicuspid) valve → – Left ventricle → – Aortic semilunar valve → – Aorta → – Systemic circulation/all tissues (to drop off O2 and pick up CO2)
44
pulm. circuit
short low pressure
45
systemic circuit
long high-friction
46
coronary circulation
Functional blood supply and O2 supply to heart muscle itself – Shortest circulation in body – Delivered when heart is relaxed – Left ventricle receives most of coronary blood supply
47
coronary arteries
Both left and right coronary arteries arise from base of the ascending aorta and supply arterial blood to heart – Both encircle heart located in coronary sulcus – Branching of coronary arteries varies among individuals
48
arteries
contain many anastomoses (junctions) * Provide additional routes for blood delivery * Cannot compensate for coronary artery occlusion
49
heart
receives 1/20th of body’s blood supply
50
LCA
supplies interventricular septum, anterior ventricular walls, left atrium, and posterior wall of left ventricle; has two branches: * Anterior interventricular artery * Circumflex artery
51
RCA
supplies right atrium and most of right ventricle; has two branches: * Right marginal artery * Posterior interventricular artery
52
cardiac muscle cells
striated, short, branched, interconnected – One central nucleus (at most, 2 nuclei) – Contain numerous large mitochondria (25–35% of cell volume) that afford resistance to fatigue – Rest of volume composed of sarcomeres – T tubules are wider, but less numerous – SR simpler than in skeletal muscle no triads
53
intercalated discs
are connecting junctions between cardiac cells that contain: – Desmosomes
54
desmosomes
hold cells together; prevent cells from separating during contraction
55
gap junctions
allow ions to pass from cell to cell electrically couple adjacent cells * Allows heart to be a functional syncytium, a single coordinated unit/one organ * Gaps: Intercalated discs
56
blood vessels
delivery system of dynamic structures that begins and ends at heart Work with lymphatic system to circulate fluids tunica intima, media, externa
57
arteries
carry blood away from heart oxygenated except for pulmonary circulation and umbilical vessels of fetus
58
capillaries
direct contact with tissue cells directly serve cellular needs exchange zones for nutrition and waste made up of endothelium (epithelium) with sparse basal lamina
59
veins
carry blood toward heart deoxygenated except for pulmonary circulation and umbilical vessels of fetus
60
lumen
central blood-containing space surrounded by a wall
61
tunica intima
Innermost layer that is in “intimate” contact with blood
62
tunica media
Middle layer composed mostly of smooth muscle and sheets of elastin * Sympathetic vasomotor nerve fibers innervate this layer, controlling: * Vasoconstriction: decreased lumen diameter * Vasodilation: increased lumen diameter * Bulkiest layer responsible for maintaining blood flow and blood pressure
63
tunica externa
Outermost layer of wall – called tunica adventitia * Composed mostly of loose collagen fibers that protect and reinforce wall and anchor it to surrounding structures * Infiltrated with nerve fibers, lymphatic vessels * Large veins also contain elastic fibers in this layer
64
vasa vasorum
in tunica externa system of tiny blood vessels found in larger vessels * Function to nourish outermost external layer
65
muscular arteries
Elastic arteries give rise to muscular arteries * Also called distributing arteries because they deliver blood to body organs * Have thickest tunica media with more smooth muscle, but less elastic tissue * Active in vasoconstriction
66
arterioles
smallest of all arteries: – Larger arterioles contain all three tunics – Smaller arterioles are mostly single layer of smooth muscle surrounding endothelial cells * Control flow into capillary beds via vasodilation and vasoconstriction of smooth muscle * Also called resistance arteries because changing diameters change resistance to blood flow * Lead to capillary beds
67
capillaries
Microscopic vessels; diameters so small only single RBC can pass through at a time * Walls just thin tunica intima Supply almost every cell, except for cartilage, epithelia, cornea, and lens of eye * Functions: exchange of gases, nutrients, wastes, hormones, etc., between blood and interstitial fluid drain into postcapillary venule
68
pericytes
spider-shaped stem cells help stabilize capillary walls, control permeability, and play a role in vessel repair
69
intercellular clefts
allow passage of fluids and small solutes in capillaries
70
continuous capillaries
Abundant in skin, muscles, lungs, and CNS * Continuous capillaries of brain are unique * Form blood brain barrier, totally enclosed with tight junctions and no intercellular clefts
71
fenestrated capillary
Found in areas involved in active filtration (kidneys), absorption (intestines), or endocrine hormone secretion * Endothelial cells contain Swiss cheese–like pores called fenestrations: * Allow for increased permeability * Fenestrations usually covered with thin glycoprotein diaphragm
72
sinusoidal capillary
Fewer tight junctions; usually fenestrated with larger intercellular clefts incomplete basement membranes: – Usually have larger lumens ▪ Found only in the liver, bone marrow, spleen, and adrenal medulla ▪ Blood flow is sluggish—allows time for modification of large molecules and blood cells that pass between blood and tissue ▪ Contain macrophages in lining to capture and destroy foreign invaders
73
capillary bed
interwoven network of capillaries between arterioles and venules
74
microcirculation
flow of blood through capillary bed from arteriole to venule
75
terminal arteriole
branch off arteriole that further branches into 10 to 20 capillaries (exchange vessels) that form capillary bed: – Exchange of gases, nutrients and wastes from surrounding tissue takes place in capillaries
76
vascular shunt
channel that directly connects arteriole with venule (bypasses true capillaries): - consists of metarteriole and thoroughfare channel
77
precapillary sphincter
cuff of smooth muscle surrounding each true capillary that branches off metarteriole acts as valve regulating blood flow into capillary bed: - controlled by local chemical conditions (not innervated)
78
veins
carry blood toward the heart * Formation begins when capillary beds unite in postcapillary venules and merge into larger and larger veins
79
venules
Capillaries unite to form postcapillary venules: – Consist of endothelium and a few pericytes – Very porous; allow fluids and WBCs into tissues * Have all tunics, but thinner walls with large lumens compared with corresponding arteries * Tunica media is thin, but tunica externa is thick: – Contain collagen fibers and elastic networks * Large lumen and thin walls make veins good storage vessels – Called capacitance vessels (blood reservoirs) because they contain up to 65% of blood supply Blood pressure lower than in arteries, so adaptations ensure return of blood to heart: – Large-diameter lumens offer little resistance
80
venous valves
Prevent backflow of blood * Most abundant in veins of limbs
81
venous sinuses
Flattened veins with extremely thin walls * Composed only of endothelium * Examples: coronary sinus of the heart and dural sinuses of the brain
82
muscular pump
contraction of skeletal muscles “milks” blood back toward heart; valves prevent backflow
83
respiratory pump
pressure changes during breathing move blood toward heart by squeezing abdominal veins as thoracic veins expand
84
sympathetic venoconstriction
under sympathetic control, smooth muscles constrict, pushing blood back toward heart
85
VR
the quantity of blood flowing from large veins into the right atrium each minute
86
factors affecting VR
1. Skeletal muscle pump: increases VR 2. Pressure drop on inhalation: increases VR 3. Valsalva maneuver: decreases VR 4. Increase blood volume: increases VR 5. Increase venous pressure: increases VR 6. Gravity: decreases VR
87
varicose veins
dilated and painful veins due to incompetent (leaky) valves * Factors that contribute include heredity and conditions that hinder venous return: – Example: prolonged standing in one position, obesity, or pregnancy; blood pools in lower limbs, weakening valves; affects more than 15% of adults * Elevated venous pressure can cause varicose veins: – Example: straining to deliver a baby or have a bowel movement raises intra-abdominal pressure, resulting in varicosities in anal veins called hemorrhoids
88
vascular anastomoses
interconnections of blood vessels
89
arterial anastomoses
provide alternate pathways (collateral channels) to ensure continuous flow, even if one artery is blocked: – Common in joints, abdominal organs, brain, and heart none in retina, kidneys, spleen
90
arteriovenous anastomoses
shunts in capillaries example: metarteriole–thoroughfare channel
91
venous anastomoses
so abundant that occluded veins rarely block blood flow
92
BF
volume of blood flowing through vessel, organ, or entire circulation in given period: – Measured in ml/min it is equivalent to cardiac output (CO) for entire vascular system directly proportional to blood pressure gradient (ΔP): – If ΔP increases, blood flow speeds up * Blood flow is inversely proportional to peripheral resistance (R): – If R increases, blood flow decreases
93
BP
force per unit area exerted on wall of blood vessel by blood: – Expressed in mm Hg – Measured as systemic arterial BP in large arteries near heart – Pressure gradient provides driving force that keeps blood moving from higher- to lower-pressure areas
94
resistance (peripheral resistance)
opposition to flow – Measurement of amount of friction blood encounters with vessel walls, generally in peripheral (systemic) circulation more important in influencing local blood flow because it is easily changed by altering blood vessel diameter
95
factors that contribute to resistance
1. Blood viscosity 2. Total blood vessel length 3. Blood vessel diameter
96
blood viscosity
The thickness or “stickiness” of blood due to formed elements and plasma proteins: * The greater the viscosity, the less easily molecules are able to slide past each other * Increased viscosity equals increased resistance
97
total BV length
The longer the blood vessel, the greater the resistance encountered
98
BV diameter
Has greatest influence on resistance * Resistance varies inversely with fourth power of vessel radius: – If radius increases, resistance decreases, and vice-versa – Example: if radius is doubled, resistance drops to 1/16 as much
99
small diameter arterioles
are major determinants of peripheral resistance: * Radius changes frequently, in contrast to larger arteries that do not change often
100
increased resistance
Abrupt changes in vessel diameter or obstacles such as fatty plaques from atherosclerosis * Laminar flow is disrupted and becomes turbulent flow, irregular flow that causes increased resistance
101
laminar flow
Fluid close to walls moves more slowly than in middle of tube
102
cardiac plexus
derived from Autonomic Nervous System – sympathetic and parasympathetic nerve fibers
103
cardiac reflex loops
between the heart and CNS baroreceptors (stretch/pressure) and chemoreceptors (chemical)
104
heartbeat
modified by ANS via cardiac centers in medulla oblongata
105
cardioacceleratory center
sends signals through sympathetic trunk to increase both rate and force ▪ Stimulates SA and AV nodes, heart muscle, and coronary arteries
106
cardioinhibitory system
parasympathetic signals via vagus nerve to decrease rate ▪ Inhibits SA and AV nodes via vagus nerves
107
Ach
(cholinergic/muscarinic) Inhibitory
108
NE
(adrenergic/B1) Excitatory
109
cardiac receptors
are linked to the CNS with afferent fibers of the Vagus nerve present in: -Atria – Ventricles – Carotid bodies – Aorta
110
baroreceptor
* Stretch or pressure receptors * Locations: carotid sinus (via CN IX), aortic arch (via CN X), right atria, left atria * Stimulated: by distension of the vessel where they are located * Results: – Increase discharge rate to reverse the stimulus (negative feedback mechanism) will adapt to long term change in BP – will decrease in response to patients with chronic HTN
111
baroreceptor reflex mechanism
1. Increased pressure in carotid artery and aorta (increase BP) 2. Stimulates baroreceptors in the carotid sinus and aortic bodies 3. Information travels via the glossopharyngeal (IX) and vagus nerves (X) 4. Processed in the medulla 5. Increase parasympathetic tone (inhibits sympathetic tone) 6. Result: – Decrease HR – Decrease SV (and CO) – Vasodilation (decrease in BP)
112
chemoreceptor
Chemoreceptors are sensitive to changes in blood chemistry * Location: carotid bodies, aortic bodies, medulla * Involved in the control of rate and depth of respirations * Main function: – Keep the alveolar pCO2 at a normal level of 40mmHg, which also helps to maintain arterial pO2, PCO2, and pH
113
chemoreceptor reflex mechanism
Increased CO2 (deceased O2) * Detected by carotid sinus (via CN IX) an aortic bodies (CN X) * Information sent to the medulla * Results: – Stimulates respiratory center: increase rate and depth – Stimulates sympathetic tone: vasoconstriction (increased BP) – Indirectly increases NE release from adrenal medulla: same vasoconstriction (and increased BP)
114
systole
period of contraction
115
diastole
period of relaxation
116
cardiac cycle
blood flow through heart during one complete heartbeat – Atrial systole and diastole are followed by ventricular systole and diastole – Cycle represents series of pressure and blood volume changes – Mechanical events follow electrical events seen on EKG * Three phases of the cardiac cycle (following left side, starting with total relaxation) series of events that occur to complete a heartbeat * Electrical impulses start in the SA node, causing the atria and ventricles to contract and relax * In this cycle: * The heart contracts (systole) – expelling blood (70ml with each contraction) * The heart relaxes (diastole) – filling back up with blood (up to about 120ml when relaxed)
117
SL valve closure
dub
118
AV valve closure
lub
119
cardiac muscle contraction
Muscle contraction is preceded by depolarizing action potential – Depolarization wave travels down T tubules; causes sarcoplasmic reticulum (SR) to release Ca2+ (skeletal muscle do not use EC Ca2+) – Excitation-contraction coupling occurs: * Ca2+ binds troponin causing filaments to bind, interact, and slide
120
contractile cells
responsible for contraction
121
pacemaker cells
noncontractile cells that spontaneously depolarize= heartbeat: * Initiate depolarization of entire heart * Do not need nervous system stimulation, in contrast to skeletal muscle fibers
122
cardiomyocytes
contract as unit (functional syncytium), or none contract * Contraction of all cardiac myocytes ensures effective pumping action * Skeletal muscles contract independently
123
aerobic respiration
* Cardiac muscle has more mitochondria than skeletal muscle so has greater dependence on oxygen: * Cannot function without oxygen * Skeletal muscle can go through fermentation when oxygen not present * Both types of tissues can use other fuel sources: * Cardiac is more adaptable to other fuels, including lactic acid, but must have oxygen
124
AP
initiated by pacemaker cells 1. Pacemaker potential: K+ channels are closed, but slow Na+ channels are open, causing interior to become more positive 2. Depolarization: Ca2+ channels open (around −40 mV), allowing huge influx of Ca2+, leading to rising phase of action potential 3. Repolarization: K+ channels open, allowing efflux of K+, and cell becomes more negative
125
cardiac pacemaker cells
have unstable resting membrane potentials called pacemaker potentials or prepotentials – KEY: never fully at rest
126
CCB
decrease HR, decrease contractility, decrease conduction velocity = vascular smooth muscle relaxation vascular smooth muscle relaxation = decrease HR, decrease contractility, decrease conduction velocity
127
malignant hyperthermia
Life-threatening, hypermetabolic reaction to anesthesia (halothane-inhaled or succinylcholine – fast acting muscle relaxant) * Cause: AD inherited gene mutation on the RyR1* (ryanodine receptor) found in the SR of skeletal muscles: (RyR2 found in SR of cardiac muscles): – Causes the voltage gates for Ca2+ to remain open/not close in the presence of anesthesia Signs: unexplained tachycardia, unexplained elevation of CO2, hypoxemia, tachypnea, muscle rigidity, and rapid elevation in temperature * Treatment: d/c triggering agent, hyperventilate with 100% O2, and Dantrolene (a muscle relaxant - found in MH carts in surgery)
128
hypermetabolism
in malignant hyperthermia use up ATP and O2 increased CO2 increased heat
129
dantrolene
mechanism of action: inhibits/closes the RyR1 receptor to prevent the further release of Ca2+ * Key: no Ca2+ = no binding of actin and myosin = no expenditure of energy = reduced O2 levels to normal levels
130
steps of cardiac cycle
1. atrial systole-> atrial contraction pushes blood into ventricles 2. ventricular systole (1st phase)-> ventricular contraction pushes AV valves closed 3. ventricular systole (2nd phase)-> SL valves open; blood is ejected 4. ventricular diastole (early)-> SL valves closed; blood flows into atria 5. ventricular diastole (late)-> blood fills ventricles passively; chambers relax
131
myocytes
2 types: contractile and pacemaker cells
132
refractory period
Tetanic contractions cannot occur in cardiac muscles: ▪ Cardiac muscle fibers have longer absolute refractory period than skeletal muscle fibers: – Absolute refractory period is almost as long as contraction itself – Prevents tetanic contractions – Allows heart to relax and fill as needed to be an efficient pump
133
sequence of excitation
SA node->AV node->bundle of his->right and left bundle branches->purkinje fibers
134
SA node
– Primary pacemaker of heart in right atrial wall: * Depolarizes faster rate than rest of myocardium firing sites, thus referred to as the primary pacemaker * Generates impulses at average of 75×/minute (normal sinus rhythm). * Average firing rate: 60 – 100 bpm * Impulse spreads across right atria to left atria, and to AV node
135
AV node
In inferior interatrial septum – Delays impulses approximately 0.1 second * Because fibers are smaller in diameter, have fewer gap junctions * Allows atrial contraction prior to ventricular contraction * Average firing rate: 40 – 60 bpm * Inherent rate of 50×/minute in absence of SA node input, thus referred to as the secondary pacemaker
136
bundle of his
In superior interventricular septum – Only electrical connection between atria and ventricles: * Atria and ventricles not connected via gap junctions
137
right and left bundle branches
Two pathways in interventricular septum – Carry impulses toward apex of heart
138
purkinje fibers
Complete pathway through interventricular septum into apex and ventricular walls * Average firing rate: 20 – 40 bpm * AV bundle and subendocardial conducting network depolarize 30/minute in absence of AV node input * Ventricular contraction immediately follows from apex toward atria * Process from initiation at SA node to complete contraction takes ~0.22 seconds
139
arrhythmias
irregular heart rhythms * Uncoordinated atrial and ventricular contractions
140
fibrillation
rapid, irregular contractions * Heart becomes useless for pumping blood, causing circulation to cease; may result in brain death * Treatment: defibrillation interrupts chaotic twitching, giving heart “clean slate” to start regular, normal depolarizations
141
ectopic focus
defective SA node abnormal pacemaker that takes over pacing If AV node takes over, it sets junctional rhythm at 40–60 beats/min (inherent firing rate)
142
extrasystole (premature contraction)
ectopic focus of small region of heart that triggers impulse before SA node can, causing delay in next impulse: * Heart has longer time to fill, so next contraction is felt as thud as larger volume of blood is being pushed out * Can be from excessive caffeine or nicotine
143
heart block
defective AV node Few impulses (partial block) or no impulses (total block) reach ventricles – Ventricles beat at their own intrinsic rate (20 – 40 bpm) * Too slow to maintain adequate circulation – Treatment: artificial pacemaker, which recouples atria and ventricles
144
enlarged R wave
enlarged ventricles
145
elevated or depressed S-T segments
cardiac ischemia
146
prolonged Q-T intervals
reveals a repolarization abnormality that increases risk of ventricular arrhythmias
147
junctional rhythm
SA node nonfunctional P waves absent AV node paces heart to 40-60 bpm
148
ventricular fibrillation
electrical activities disorganized APs occur randomly throughout ventricles acute HA and electrical shock chaotic, abnormal EKG
149
CO
amount of blood pumped by each ventricle per min HR*SV
150
SV
amount of blood ejected from each ventricle w/ each contraction
151
factors affecting CO
SNS (NE) venous return (preload) BV SNS (contractility) peripheral resistance (afterload)
152
preload
volume of blood that leads to ventricular stretch at the end of diastole (venous return)-> EDV more fluid that returns, more the relaxed muscle stretches prior to contracting, results in stronger contractions
153
afterload
amount of resistance heart must overcome to open the aortic valve and push the BV out into the systemic circulation (peripheral resistance)-> ESV Normal aortic pressure: 80mm Hg (normal SV = 70ml results)
154
EDV
end diastolic volume: when diastole (ventricular relaxation) ends, EDV is the volume of blood that has filled the relaxed left ventricle (120ml)
155
ESV
end systolic volume: the amount of blood remaining in the left ventricle after systole (ventricular contraction) is called the ESV (50ml)
156
SV
EDV-ESV Average SV = 70ml = amount of blood ejected with each beat increased preload=increased SV increased contractility= increased SV increased afterload= decreased SV
157
MAP
average arterial pressure throughout one cardiac cycle = systole, and diastole. * MAP is influenced by cardiac output and systemic vascular resistance, each of which is influenced by several variables
158
systemic vascular resistance
determined primarily by the radius of the blood vessels. Decreasing the radius of the vessels increases vascular resistance. Increasing the radius of the vessels would have the opposite effect
159
blood viscosity
increase in hematocrit will increase blood viscosity and increase systemic vascular resistance
160
dicrotic notch
Closure of the aortic semilunar valve
161
intropic agents
* Positive inotropes can help with heart failure and a slow heart rate * Negative inotropes can help you with high blood pressure and chest pain
162
positive intropes
can help when your heart can’t get enough blood to your body because it is too weak to pump the amount of blood your body needs * Positive inotropes make your heart muscle contractions stronger, raising your cardiac output to a normal level and increasing the amount of blood your heart can pump out * This helps your organs get the blood and oxygen they need to keep working
163
positive intropic meds
Epinephrine (Adrenalin® or Auvi-Q®) *Norepinephrine (Levophed® or Levarterenol®) *Dopamine *Dobutamine *Levosimendan *Milrinone *Digoxin (Cardoxin® or Lanoxin®)
164
digoxin
injection medication that treats heart failure and an irregular heartbeat called AFib (atrial fibrillation). It helps your heart beat stronger. It can also stabilize your heart’s rhythm by slowing down overactive electric signals
165
negative intropes
keep your heart muscles from working too hard by beating with less force * This is helpful when you have high blood pressure, chest pain (angina), an abnormal heart rhythm or a disease like hypertrophic cardiomyopathy
166
negative intropic meds
Flecainide. *Verapamil (Calan® or Verelan®). *Cibenzoline. *Clonidine (Catapres® or Kapvay®). *Atenolol
167
verapamil
a calcium channel blocker that widens your blood vessels and relaxes your heart muscle. This improves blood flow to your heart and helps it pump more easily. Verapamil is for people with high blood pressure or angina (chest pain). Some people with irregular heart rhythms like SVT also take it.
168
frank sterling law
a description of cardiac hemodynamics as it relates to myocyte stretch and contractility * The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases * Due to the myocyte stretch causing a more forceful systolic contraction
169
Erb's point
3rd ICS LSB * Clinical significance: where S2 is heard the best * Performed: patient instructed to breath in and hold breath temporarily during auscultation
170
incompetent or insufficient valves
swishing sound
171
stenotic valve
high-pitched sound or clicking
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EF
50-65% can be diagnosed via echo
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causes of CHF
atherosclerosis HT MI DCM
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DCM
dilated cardiomyopathy ventricles stretch and become flabby, and myocardium deteriorates drug toxicity or chronic inflammation may play a role
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PDE-3 inhibitors
increase levels of intracellular cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP), which leads to various physiological effects including smooth muscle relaxation, vasodilation, bronchodilation, and anti-inflammatory effects
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protein kinase A
stimulated by cAMP regulates heart contraction
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protein kinase G
stimulated by cGMP and NO regulates SM
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LSHF
pulmonary congestion tachy fatigue cyanosis exertional dyspnea
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RSHF
"col pulmone" fatigue ascites JVD edema
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aortic valve location
2nd ICS RSB
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tricuspid valve location
5th ICS LSB
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bicuspid/mitral valve location
5th ICS MCL
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pulmonary valve location
2nd ICS LSB
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SA and AV node
supplied by the RCA
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RCA
supplies the inferior portion of the left ventricle
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myoglobin
enzyme elevated very early after MI return to normal after 24 hr (detects recent damage) from muscle breakdown
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angina decubitus
variant of angina pectoris that occurs at night while the patient is recumbent (lying down)
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age risk for MI
males= 45 females= 50 father or brother diagnosed with heart disease before age 55 or a mother or sister diagnosed before age 65
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LDH
peaks 48-72 hrs lactate dehydrogenase
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CABG
If >50% LDA stenosis Multivessel CAD
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HF
most frequent cause of hospitalization in patients older than 65 Rehospitalization rates during the 6 months following discharge are as much as 50%
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high CO failure
chronic underlying medical condition with an unusually high demand for blood circulation Hyperthyroidism Pregnancy
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low CO failure
reduced EF (HFrEF); LVEF 40% or less (valvular disease or ischemic HD) preserved EF (HFpEF); LVEF 50% or more (HT or hypertrophic cardiomyopathy)
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HF tests
CBC: rule in/out comorbidities, thyroid conditions, reversible causes of HF CMP: electrolyte imbalances (low Na+ poor prognosis), BUN/creatinine BNP: core marker and elevated in CHF (>100pg/ml) Troponin: not a core marker but elevated, indicator of poor prognosis Echocardiogram: single best test – assesses ventricles and valves, estimate EF EKG: ventricular hypertrophy, arrhythmias, ischemia, low QRS
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ARNI
sacubritril (inhibits neprilysin enzymes) valsartan (blocks angiotensin II receptors)
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BNP
responsible for salt and water balance neprilysin is an enzyme that breaks BNP down prevents them from doing their job
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AAA
abdominal aorta aneurysm 90% of all AAA occur below the renal arteries >3cm is considered “aneurysmal” Males > females >age of 65 PMH: smoking, hyperlipidemia, obesity, family history
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AAA screening
Ultrasound in men age 65 – 75 who have ever smoked more than 100 cigarettes in their lifetime Once detected, CT or MRI evaluation give you more information
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AAA symptoms
Unruptured AAA: back pain, flank pain Ruptured AAA: hypotension and severe “tearing” abdominal pain radiating into the back
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AAA treatment
Elective repair: when >5.5cm
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thoracic aortic aneurysm
PMH: hypertension, smoking, hyperlipidemia * Imaging: CT is the best choice for imaging * Prevention of growth: use of Betablockers * Surgical repair when: >5.0 – 5.5cm * Two types: * Type A: involves ascending and arch * Type B: descending aorta distal to subclavian artery
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thoracic aortic dissection
Most common condition associated with the degeneration and worsening of the aneurysm that leads dissection is hypertension * Connective tissue disorders can also lead to dissection: 1. Marfan’s Syndrome: genetic disorder of connective tissue, primary problems with heart and aorta 2. Ehler-Danlos Syndrome: genetic disorder of connective tissue, overflexibility of joints, many different types, problems with vessels being thin and small – rupture easily
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HT EKG
Increased QRS = LV hypertrophy * ST segment depression * Asymmetric T wave inversion left atrial enlargement left ventricular hypertrophy
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secondary HT causes
HTN at especially young or old age * Patient with Stage 2 HTN > 140/90 * Abrupt onset of HTN * Drug resistant HTN * Presence of clinical clue (abdominal bruit, low potassium)