Dysrhythmias
valvular disease
peripheral vascular disease
aneurysms
cardiac conduction
myocardial physiology and dysfunction
coronary artery disease
Bachmann's
Wenckebach's
Thorel's
Frank-Starling's
Left atrium
Left ventricle
Right atrium
Right ventricle
The bundle of His
Purkinje fibers
Right bundle branch
Bachmann's bundle
AV node
SA node
Purkinje fibers
Bundle branches
Coronary arteries
Anterior and posterior descending arteries
Left anterior descending and posterior descending arteries
Right and left anterior descending arteries
15-40 times a minute
40-60 times a minute
An average of 70 times a minute
100 times a minute
Phase 0 is the resting membrane potential
Phase 1 is early repolarization
Phase 2 is a platau
Phase 3 is rapid repolarization
Phase 4 is the resting membrane potential
Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
Phase 0
Phase 1
Phase 2
Part of phase 3
Phase 4
The P wave corresponds to atrial depolarization
The P wave corresponds to the action of the SA node
The isoelectric line between P and Q corresponds to AV depolarization
The vertical axis of the EKG is time in seconds
The T line corresponds to ventricular repolarization
Sinus tachycardia
Sinus dysrhythmia
Paroxysmal supraventricular tachycardia
Sick sinus syndrome
Irregular rate
Irregular rhythm
Lack of definitive P waves
A twisting or rotating pattern
Ventricular fibrillation
Ventricular tachycardia
Premature ventricular contractions
Sinus arrest
It can be acquired or inherited
It is linked to cocaine use
It is caused by delayed repolarization of the atria
When inherited it can be triggered by increased sympathetic tone
P wave
PR interval
QRS interval
ST interval
Is the ability of the Purkinje fibers to depolarize during phase 4
Can be increased by acetylcholine
Can be decreased by epinephrine
Is a property in the SA and AV nodes
Atrial septal defects
Rate changes
Lev's and Lenerge's diseases
Aortic valve disease
A first degree AV block
A second degree AV block associated with a prolonged QRS interval
Is seen transiently in inferior myocardial infarction
Has a high incidence of progression to high degree heart block
Originates in the upper descending aorta distal to the left subclavian and extends distally to the bifurcation
Originates in the ascending aorta only
Originates in the ascending aorta above the aortic valve and extends distally to the abdominal aorta
Is an AAA
Hypotension
Turbulent blood flow
Atherosclerosis
Marfan's syndrome
Troponin
Tryopomycin
Actin and myosin
Calcium channels
Is from the formation of cross bridges
Is caused by the activation of troponin and tropomycin
Is caused by blood moving across the gradient
Increases the permeability of sarcolemma to calcium ions
The volume blood ejected by the ventricle per beat
The volume of blood ejected by the left ventricle into the aorta per minute
The volume of blood ejected by the left ventricle into the aorta per minute corrected for body size
The degree of tension on the heart muscle when it begins to contract
The amount of tension needed to open the semilunar valves and eject blood
Preload
Contractility
Afterload
The LaPlace equation
Preload
Afterload
Contractility
Stroke volume
Decreases both heart rate and contractility
Decreases heart rate and increases contractility
Increases both heart rate and contractility
Increases heart rate and decreases contractility
Low output heart failure concerning increased preload
Low output heart failure concerning increased afterload
Low output heart failure concerning decreased contractility
High output heart failure
Hyperthyroidism
Aortic regurgitation
Hypertension
Myocardial infarction
Hypervolemia
States that stretching myocardial fibers during diastole increases force of contraction in systole
Hypothesizes that ventricular hypertrophy decreases afterload
States that increased arterial pressure requires more tension to eject blood
States that if the ventricular wall is thicker, you need less tension to eject blood
Increased preload
Increased afterload
Decreased afterload
Increased contractility
Decreased contractility
Anorexia
Pulmonary edema
Ascites
Cough
Dyspnea
Angiotensin I, a potent vasoconstrictor, is released in response to activity in the kidney
Epinephrine and norepinephrine are released in the sympathetic response
Wall thickness is decreased and the number of sarcomeres is increased
Atrial and brain natriuretic peptides cause an antidiuretic effect
TNF and interleukin 6 increase the nitric oxide vasoconstriction effect
Dilated cardiomyopathy
Congestive cardiomyopathy
Restrictive cardiomathy
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Congestive cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
200 mg/dL
100 mg/dL
40 mg/dL
30mg/dL
40 mg/dL
100 mg/dL
200 mg/dL
300 mg/dL
400 mg/dL
The heart
The kidneys
The brain
The blood vessels
The liver
Mobitz I heart block
Mobitx II heart block
Ischemia
Right bundle branch block
Left bundle branch block
Cardiac enzymes are increased (creatine kinase, creatine phosphokinase, troponin)
ST and Q levels are changed on an EKG
Collateral circulation is a compensatory mechanism
The right coronary artery is the "widowmaker"
Functional changes in the heart are similar to ischemia
Papillary muscle shunting
Venous return decreases
Fall in stroke volume
Decrease in heart rate
Deactivation of the renin-angiotensin-aldosterone system
Ventricular aneurysm
Thromboembolism
Pericarditis
Papillary muscle dysfunction
Cardiac tamponade
Obstructs flow
Increases volume work
Allows backflow
Involves valve leaflets that do not close securely
It often follows streptococcal pharyngitis
A sign of it is Aschoff's bodies
The highest incidence is in the elderly
Patients often have a rash
It follows infection by six months
The bicuspid valve is narrowed to 2 square centimeters
The tricuspid valve is narrowed to 2 square centimeters
The bicuspid valve is narrowed to 1 square centimeter
The tricuspid valve is narrowed to 1 square centimeter
Mitral valve prolapse
Acute mitral regurgitation
Chronic mitral regurgitation
Mitral stenosis
Tricuspid valve stenosis
Tricuspid valve stenosis
Pulmonic regurgitation
Pulmonic stenosis
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Aortic regurgitation
Intermittent claudication
Skin color changes based on posture
Orthopnea
Absent or diminished pulses
Pain at bed time or at rest
Venous stasis
Anemia
Venous injury
Hypercoagulability
Hypovolemia
Deep vein thrombosis
Superficial thrombophlebitis
Thromboembolic venous disease
Valvular insufficiency
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