Term
| What does the right heart pump to? |
|
Definition
It pumps through the lungs (pulmonary circulation) |
|
|
Term
| Where does the left heart pump to? |
|
Definition
| It pumpst through all the body exept the lungs (systemic circulation) |
|
|
Term
Heart
Where is the mediastinum? |
|
Definition
above the diaphragm and between the lungs |
|
|
Term
| What is the cardiac wall? |
|
Definition
-Pericardium: Parietal (outer) and visceral (inner; epicardium)
-Pericardial cavity and fluid; lubricates membrane that line the cavity.
-Myocardium
-Endocardium: CT and layer of squamous cells; continuous with endothelium of arteries. |
|
|
Term
The cambers of the Heart
Thickness |
|
Definition
| The thickness of chamber depends on pressure it must overcome to eject blood ( 14 mm Hg/ pulmonary; 120 mm Hg aortic) |
|
|
Term
Valves of The Heart
Atrioventricular Valves
|
|
Definition
-Cusps attatched to the papillary muscles by chordae tendonae
tricuspid valve (RIGHT) and the bicuspid valve (LEFT atrium and L Ventricle) |
|
|
Term
The Valves of the Heart
What and where are the semilunar Valves? |
|
Definition
-Pulmonic semilunar valve (Right)
-Aortic Semilunar Valve (Left) |
|
|
Term
| What is the cardiac cycle of the heart? |
|
Definition
1. Atrial systol: heart is relaxed, blood flowing from the R & L atriums into the Ventricles
2. Isovolumetric ventricular contraction: Tricuspid and Bicusbid valves close
3. Ejection: semilunar valves open and blood flows out of L & R ventricle and into the lungs and systemic circulation.
4. Isovolumeric ventricular relaxation: Both tricuspid and bicuspid valves are closed and blood is let into the atrium
5.Passive Ventricular filling: tricuspid and bicuspid valves open and allow blood into the ventricles. |
|
|
Term
Conduction System
What does the SA Node do? |
|
Definition
it is the pacemaker, it is innervated by the SNS and PSN; 75 APs/min |
|
|
Term
Conduction System
Atrioventricular Node (AV) |
|
Definition
PNS ganglia receptors for vagus nerve; slows impulse conduction.
-Then proceed down to the Bundle of His (AV bundle)
-Right and left bundle branches
-Perkinke fibers
|
|
|
Term
Electrocardiogram
The sum of all cardiac action potential
P-wave |
|
Definition
|
|
Term
Electrocardiogram
The sum of all cardiac action potential
PR interval |
|
Definition
The time from the onset of the atrial activation to the onset of ventricular activation. The time necessary to tracel from the sinus node through the atrium, AV node, and His-Purkinke system to activate ventricular myocardial cells |
|
|
Term
Electrocardiogram
The sum of all cardiac action potential
QRS complex |
|
Definition
sum of all ventricular depolarizations |
|
|
Term
Electrocardiogram
The sum of all cardiac action potential
ST interval |
|
Definition
ventricular myocardium depolarized |
|
|
Term
Electrocardiogram
The sum of all cardiac action potential
QT interval |
|
Definition
"electrical systole" of the ventricles. Varies inversly with heart rate |
|
|
Term
Cardiac Excitation
Automaticity |
|
Definition
-Spontaneous depolarization to threshold potential; allows generation of AP without stimulus
-By "automatic cells"
-Membrane potential does not "rest" during phase 4; diastolic depolarization |
|
|
Term
Cardiac Exctability
Rhymicity |
|
Definition
-Regular generation of AP
-SA node sets pace; fastest rate of depolarization; 60-100 spontanous depolarizations/minute; natural pacemaker
-AV node takes over if SA damaged; 40-60 per minute
-Purkinje fibers 30-40 beats/minute |
|
|
Term
Cardiac Innervation
ANS influences |
|
Definition
-rate of impulse generation, depolarization and repolarization and strength of atrial and ventricular contracitons
-Important for rapid changes (vs. oxygen, glucose, hormones or other blood borne factors) |
|
|
Term
Cardiac Innervation
What do the SNS and PNS do? |
|
Definition
They innervate all parts of the atria, ventricles SA and AV nodes. |
|
|
Term
| What are efferent sympathetic fibers? |
|
Definition
-orriginate in the thoracic SC
-Branch into superior, middle and inferior cardiac nerves.
- Join the cardiac plexus at the root of the aorta. |
|
|
Term
Catecholamines (EPI>NE)
What do they do?
|
|
Definition
-They increase the HR (dromotomic)
-Decrease conduncion time
-Increase rhytmicity of AV node
-Binds with beta receptors to increase Ca influx and force contraction. |
|
|
Term
| Efferent parasympathetic fibers |
|
Definition
Originate in medulla and travel by way of vagus to join sympatheic fibers in cardiac plexus |
|
|
Term
|
Definition
-Decreases HR
- Slows condunction via AV |
|
|
Term
|
Definition
- More beta than alpha receptors; stimulates all 4 types of receptors strongly; NE stimulates them weakly or not at all |
|
|
Term
Adrenergic Receptors
Beta 1 |
|
Definition
mostly heart; SA, AV and myocardial cells of the atria and ventricles
B1 + epinephrine= increase of impulse generation and conduction and strength of contraction. |
|
|
Term
Adrenergic Receptors
Beta 2 |
|
Definition
mostly blood vessel smooth muscle
B2 + epinephrine= dilation of arterioles in coronary, liver, skeletal muscle; vasoconstriction in most vascular beds
(GI, Urinary) |
|
|
Term
Adrenergic Receptors
Alpha 1 |
|
Definition
Mostly blood vessel smooth muscle
-Alpha 1 and NE= vasoconstriction |
|
|
Term
Adrenergic Receptors
Alpha 2 |
|
Definition
Sympathetic ganglia and nerve terminals
-alpha2 and NE inhibits NE, allowing vasodilatiion |
|
|
Term
FRANK-STARLING LAW OF THE HEART
What determines the force of contractility? |
|
Definition
STRETCH
-Length-tension relationship based on cross bridge theory
-More stretch= increased force of contraction
-End diastolic volume (EDV)
LENGTH-TENSION CURVES
-SNS curve A high CO or SV with same EDV
-Heart Failure Curve C; is over stretched |
|
|
Term
|
Definition
T=(P x R)/mu
Relationship between the transmural pressure (P) difference and the tension (T), radius (R), and thickness (mu) of the vessel wall.
-The higher the pressure difference the more tension
-The larger the radius the more tension
-The thicker the wall the less tension |
|
|
Term
Application of Laplace's Law
Dilated CM
T=(P x R)/mu |
|
Definition
Heart distended and the readius increased; to create the same pressure during ejection of blood, much larger wall tension needs to be developed; dilated heart required more energy to pump the same amount of blood as compared to the heart of a normal size. |
|
|
Term
Application Of Laplace's Law
Aneurysm
T=(P x R)/mu |
|
Definition
-As diameter increases, wall tension increases, which contributes to more increase in diameter and risk of rupture. Increased BP (systemic HTN) and increased aneurysm size increase arterial wall tension and therefore increase the risk for rupture. |
|
|
Term
|
Definition
-Pressure generated at the end of diastole (LVEDP)
-LVEDP=Left Ventricular End Diastolic Volume
-Determinded by LVEDV
-Think Starling's Law, when preload exceeds physiologic range further muscle stretch results in decreased CO
-Determined by 2 factors:
1. Amount of venous return
2. ESV; depndent on strength of contraction and resistance to emptying
-Monitor EDP
-Treatment goals: maintain EDV and EDP that will maintain cardiac output |
|
|
Term
|
Definition
-Resistance to ejection during systole.
-Aortic systolic pressure is a good indicator; also affected by aortic valvular function.
-High afterload higher workload against which heart has to work; ejects less blood
-EDV-ESV=stroke volume, blood moved with each beat
-SV/EDV= EFx (ejection fraction)
-HTN chronically evevated TPR, chronic high afterload, high workload of the heart, hypertrophy of the myocardium (LVH) |
|
|
Term
Myocardial Contractility
STROKE VOLUME (=EDV-ESV)
What are the 3 factors that determine force of contraction? |
|
Definition
-Depens on force of contraction and thus myocardial contractility. 3 factors determine force of contraction.
1. Changes in stretching related to changes on preload
2. Alterations in SNS
3. Adequate oxygen supply |
|
|
Term
Myocardial Contractility
INOTROPIC AGENTS
What agents are a positve ionotrope?
What is a negative ionotrope? |
|
Definition
-EPI or NE are the most important positive ionotropes (increases force of contraction)
-Acetylcholine negative ionotrope |
|
|
Term
Myocardial Contractility
OXYGEN AND CARBON DIOXIDE LEVELS
What happens to contractility with MILD hypoxemia?
What happens to contractility with SEVERE hypoxemia? |
|
Definition
-Mild hypoxemia may increase contractility by increaseing myocardial response to catecholamines
-Severe hypoxemia contractility is depressed |
|
|
Term
HEART RATE
Cardiovascular control Center (CCC)
Where is it located?
What controls the HR at rest? |
|
Definition
-Brain stem in the medulla with secondary ares in the hypothalamus, cerebral cortex and thalmus; internernerons
-Nerve Fivers from CCC synapse with autonomic neurons
-Carioexcitatory (parasympathetic excitation/sympathetic inhibition
-Cardioinhibitory (parasympathetic excitation/sympathetic inhibition); HR at rest controlled by parasympathetic override effect of sympathetic on SA node |
|
|
Term
HR
NEURAL REFLEXES
Bainbridge Reflex
In what setting is this reflex seen?
|
|
Definition
change HR after infusions of blood/fluid; mediated by volume receptros in the atria; HR change depends on initial HR (if slow it will increase; if fast it will be slowed down) |
|
|
Term
HR
Neural Reflexes
BARORECEPTOR REFLEX
Where are the receptors located? |
|
Definition
-facilitates HR and BP; mediated by pressure receptors in the aortic arch and carotid bodies; critical to maintaining contant tissue perfusion.
DECREASES HR |
|
|
Term
HR
ATRIAL RECEPTORS
What is stimulated to be released when there is increased level of volume in the Atria? |
|
Definition
-In both atria
-Distention as a result of increased volume results in release of Atrial Natriuric Peptide (ANP); powerful diuretic and natriuretic to decrease BP and blood volume |
|
|
Term
HR
HORMONES AND BIOCHEMICALS
What is affected?
What does EPI do?
What does NE do?
What does TH do?
What is decreased and what does that result in? |
|
Definition
-Affects arteries, arterioles, venules, capillaries and contractility of myocardium
-EPI dilates blood vessels of liver and skeletal muscle and increases myocardial contractility
-NE increases HR, contractility and constricts BV
-Thyroid hormone enhance sympathetic activity to increase CO
-decrease in GH, TH, adrenal hormones results in Bradycardia, reduced CO and low BP
|
|
|
Term
VEINS
What they have to help? |
|
Definition
| muscles to pump towards the help and valves to prevent back flow |
|
|
Term
|
Definition
-It is a life support tissue
-Enables growth, promotes contraction or relaxation (vasomotion) and involved in repair, antithrombogenesis and fibronolysis
-performs functions via synthesis and release of vasoactive chemicals |
|
|
Term
endothelium-dependent vasocontriction
What are factors that cause vascontriction in the endothelium? |
|
Definition
-Thromboxane A2 (which is what ASA inhibits)
-Endothelin: located in the endothelium tissue
--ACE Converts angiotensin I into angiotensin angiotensin II that metabolizes bradykinin which is a vasodilator. |
|
|
Term
Endothelium Dependent Vasodilation
What factors cause dilation in the Endothelium? |
|
Definition
-A variety of exogenous pharmacologic substances, platelet-derived factors, and shear stress can promote the release of nitric oxide synthase (NOS).
-Prostacyclin (PGi2) causes relaxation of vascular smooth muscle cells by cyclic adenosine monophosphate (cAMP)- dependent mechanism, and both nitric oxide and PGI2 inhibit platelet aggregation.5-HT, serotonin; ADP, adenosine diphosphate; ATP, adenosine triphosphate |
|
|
Term
What are factors that affect blood flow?
|
|
Definition
F=P/R
(flow proportional to pressure but inversily proportional to resistance.)
-Pressure difference; high to low
-Resistance: diameter and length |
|
|
Term
Factors Affecting Blood Flow
Poiseuille's law |
|
Definition
R= 8 (viscosity) (length)/pi (v^4)
-Very smal changes in vessel radius result in big changes in resistance. |
|
|
Term
Factors Affecting Blood Flow
What items have Neural control of total peripheral resistance? |
|
Definition
-Change in diameter of the vessles
-Baroreceptors
-Arterial chemoreceptors |
|
|
Term
Factors Affecting Blood Flow
How do hormones affect blood movement? |
|
Definition
EPI, NE, antidiuretic hormone, renin-angiotensin-aldosterone system, natriuretic peptides, adrenomedullin insulin, and others |
|
|
Term
Factors Affecting Blood Flow
VELOCITY |
|
Definition
distance traveled/unit of time (cm/min); directly related to blood flow (ml/min) and indirectly related to cross sectional area (decreased area increased velocity vs. increased area dereases; as vessels cross sectional are increases flow decreases) |
|
|
Term
Factors Affecting Blood Flow
LAMINAR VS. TURBULENT FLOW |
|
Definition
concentric layers of flow at different velocities; less velocity near the wall related to cohesive attraction between fluid and wall |
|
|
Term
Factors Affecting Blood Flow
VASCULAR COMPLIANCE
|
|
Definition
C=VP
-Related to ratio of elastic muscle fibers (veins>arteries; elastic>muscular); compliance determines a vessels response to pressure changes; eg. In the venous system for a small increase in pressure a large volume of blood can accommodate
(*veins are very compliant and will easily expand) |
|
|
Term
|
Definition
|
|
Term
| How do baroreceptors control blood pressure? |
|
Definition
-Located on aortic arch and corotid sinue.
-Action potentials are conducted to the cardioregulatory and vsomotor center.
-The HR can be decreased by the parasympathetic system
-The HR and SV can be increased by sympathetic system
-Sympathetic system can also constrict or dilate blood vessels |
|
|
Term
| How do chemoreceptors regulate BP? |
|
Definition
-They are located in the medulla oblongata and the carotid and aortic bodies detect changes in blood oxygen, carbon dioxide and pH.
-Action potentials are conducted to the medulla oblongata. in response the vasomotor center can cause vasoconstriction or dilation of blood vessels by the sympathetic system and the cardioregulatory center can cause changes in pumping activity of the heart through the parasympathetic and sympathetic systems. |
|
|
Term
| What are the three mechanisms that influence total plasma volume? |
|
Definition
-Antidiuretic Hormone (ADH) and renin-angiotensin and aldosterone tend to increase water retention and thus increase plasma volume.
-The natriuretic peptides antagonize these mechanisms by promoting water loss and sodium loss, thus promoting a decrease in total plasma volume. NPs, ACE angiotensin converting enzyme |
|
|
Term
What are the effects of hormones?
ANGIOTENSIN II |
|
Definition
-Vasoconstriction
-It stimulates the relaese of aldosterone
-Growth promoter; myocyte and vascular hypertrophy and progression of HTN and HF
-Stimulates thirst
- Release of ADH
-Increase SNS output |
|
|
Term
Effects of Hormones
Angiotensin II Receptors
AT1
Where are they located? |
|
Definition
-heart, vascular smooth muscle, andothelial cells, nerve endings adrenal cortex, liver, kidney brain.
-Majoirty of II activity (growth promotion, vasoconstriction, aldosterone secretion inhibition of renin, sypathetic outflow, stimulate inflammation)
-ACE-1 and ARB for preventative and reparative strategies
|
|
|
Term
Effects of Hormones
Angiottensin II
AT2 |
|
Definition
BLOCKS the effect of angiotensin II and its ability for AT1 to have effect on vascular, cardiac and renal
fetal tissue, adrenal medulla, renal tubules, vasculature, uterus, ovaries
-Opposes At1 receptors
-Induces vasodilation
-Mediated by NO |
|
|
Term
Regulation of Coronary Circulation
CORONARY PERFUSION PRESSURE
(F=P/R) |
|
Definition
-Differnce between pressure in the aorta and pressure in coronary vessels; aortic pressure is the driver
-During systole: aortic valves cusps obstruct coronary artery blood flow; coronary arteries compressed by ventricular contraction; most oxygen provided by myoglobin
-Most coronary blood flow occurs during diastole |
|
|
Term
Regularton of Coronary Circulation
AUTOREGULATION |
|
Definition
individual vessels regulate blood flow.
-With decrease in perfusion pressure or increase in metabolic needs, myocardial cells release CO2, H, K, adenosine that promotes vasodilation
|
|
|
Term
Regulation of Coronary Circulation
Autonomic Regulation |
|
Definition
-Sympathetic nerves cause increased coronary flow despite vascocontriction because of increased myocradial metabolism (because of SNS stimulation of HR and contracitlity); metabolic autoregulation overrides neurogenic influences. |
|
|
Term
|
Definition
-Capillary outflow exceeds venous reabsorption (3L/day)
-Special vascular system that picks up excess tissue fluid and returns it to the blood.
-Consists of lymphatic vessels and nodes; one way valves with closed ends; fluids back to venous system and heart via lymphatic duct and thoracic duct and thoracic duct into right and left subclavian veins. |
|
|
Term
Cardiography and Holter Monitoring
|
|
Definition
-typically 12 lead electrocardiogram
-info about HR and rhythm, the effects of electrolytes and drugs on the heart, and electrical orientation of the cardiac muscle
-detect disturbances in impulse generation condunction |
|
|
Term
|
Definition
elicit clinical manifestations of cardiovascular disease that might not be present at rest |
|
|
Term
| How can the sensitivity of a stress test be improved? |
|
Definition
the use of a radiotracer imaging technique such as SPECT |
|
|
Term
|
Definition
-detects structural and functional cardiac abnormalities over time |
|
|
Term
|
Definition
-Is used to measure the oxygen content and pressure of blood in the heart's chambers and to inject contrast media for x-ray examination of the size and shape of the chambers and valves.
-Injection of contrast medium into cardiac arteries (coronary angiogram), on the other hand permits visualization of the coronary circulation and every tissue perfused by the coronary arteries. |
|
|
Term
Varicose Veins
Mechanism of Action |
|
Definition
-A vein in which blood is pooled
-Trauma
-Gradual venous distention |
|
|
Term
Varicose Vein
clinincal manifestation |
|
Definition
- distended, torturous, and palpable veins |
|
|
Term
Chronic Venous insufficiency
Mechanism of Action |
|
Definition
| - inadequate venous return over a long period due to varicose veins and valvular incompetence |
|
|
Term
Chronic Venous insufficiency
Clinical Manifestations
|
|
Definition
|
venous stasis
venous HTN
circulatory stasis
- tissue hypoxia
|
|
All lead to inflammation fibroscleorotic remodeling and ulceration
|
|
|
|
Term
|
Definition
Obstruction of venous flow leading to increased venous pressure |
|
|
Term
|
Definition
|
- varicose veins and venous insufficiency
- venous statis
- venous endothelial damage
|
hypercoagulable states |
|
|
Term
DVT
Clinical Manifestation |
|
Definition
|
Edema with redness and warmth
|
Increased risk for clots |
|
|
Term
Thrombus Formation in Veins
Mechanism of Action |
|
Definition
|
Thrombus: blood clot that remains attatched to the vessel wall
|
Thromboembolus: detached thrombus |
|
|
Term
Thrombus Formation in Veins
Patho |
|
Definition
|
1. venous stasis
2. venous endothelial damage
3. hypercoag states
-genetic: factor V Leiden, prothrombin mutations
4. accumulation of clotting factors and platelets
|
inflammation |
|
|
Term
Thrombus Formation in the Veins
Clinical Manifestations |
|
Definition
|
Most will dissolve on own, but if left untreated, high risk for pulmonary embolism
|
|
|
|
Term
Aneurysm
Mechanism of Action |
|
Definition
|
Local dilation or outpouching of a vessel wall or cardiac chamber
Most common in thoracic and abdominal aorta
|
|
|
|
Term
|
Definition
|
Intravascular tension stretches non-contracting infracted muscle; stretching produces infarct expansion a weak thin layer of necrotic muscle and fibrous tissue that expands with each systole
Arteriosclerosis
Infection
|
|
|
|
Term
Aneursym
Clinical Manifestations |
|
Definition
|
Heart: dysrhythmias, heart failure, embolism of clots to brain or other vital organs
|
Aortic: often asymptomatic, dyspnea, pain, dysphagia, decreased blood flow to an extremity |
|
|
Term
Embolism
Mechanism of Action
|
|
Definition
| Obstruction of a vessel by an embolus |
|
|
Term
|
Definition
|
Consists of dislodged DVT, air bubble, amniotic fluid, aggregate of fat, bacteria, cancer cells, or a foreign substance
Most come from heart
|
|
|
|
Term
Embolism
Clinical Manifestations |
|
Definition
|
Causes ischemia or infarction distal to obstruction, can be threat to life
|
Embolism of central origin causes dysfunction and pain |
|
|
Term
Peripheral Artery Disease
Mechanism of Action |
|
Definition
|
Atherosclerotic disease of arteries that perfuse the limbs, especially lower limbs
|
Increased O2 demand that could not be supplied |
|
|
Term
Peripheral Artery Disease
Patho |
|
Definition
|
Obstruction of arterial blood flow in the iliofemoral vessels resulting in pain with ambulation
|
Also called intermittent claudcaion |
|
|
Term
Peripheral Artery Disease
Clinical Manifestations |
|
Definition
|
Pain with ambulation that stops when stops ambulating
Claudication
|
|
|
Term
Thromboangiitis Obliterans (Buerger Disease)
Mechanism of Action
|
|
Definition
|
Obliterates small and medium sized arteries
Symptoms are caused by slow, sluggish blood flow
|
Can often lead to gangrenous lesions |
|
|
Term
Thromboangiitis Obliterans (Buerger disease)
Patho |
|
Definition
| Inflammatory disease of peripheral arteries resulting in non-atheroscerotic lesions; T-cell and autoimmunity involved |
|
|
Term
Thromboangiitis Oblinterans (Buerger disease)
Clinical Manifestations |
|
Definition
|
Causes pain, tenderness, and hair loss in the affected area
|
Young men who smoke |
|
|
Term
Raynaud's Disease
Mechanism of Action |
|
Definition
|
Phenomenon is secondary to other systemic diseases or condition
|
Disease is primary vasospastic disorder of unknown origin |
|
|
Term
Raynauds Phenomenon and Disease
Patho
|
|
Definition
|
Episodic vasopasm (ischemia) in arteries and arterioles of the fingers, less commonly the toes
|
Changes in skin color and sensation |
|
|
Term
Raynauds
Clinical Manifestations
|
|
Definition
changes in skin color
painful
pallor
numbness
cold sensation in digits
rubor often accompanies throbbing and paresthesias |
|
|
Term
Hypertension (Primary)
Mechanism of Action |
|
Definition
|
Essential or idiopathic
Genetic and environmental factors
|
|
|
|
Term
Hypertension (Primary)
Patho |
|
Definition
| Genetics & Environment cause insulin resistance, inflammation, and dysfunction of the SNS, RAAS, adducin, and natriuretic hormones with cause vasoconstriction and renal salt and water retention with cause increased peripheral resistance and increased blood volume which causes sustained hypertention |
|
|
Term
Hypertension (Primary)
Clinical Manifestations |
|
Definition
|
Stage :140-159 or 90-99
Stage 2
|
>160 or >100 |
|
|
Term
Hypertension (secondary)
Mechanism of Action |
|
Definition
| Caused by systemic disease or medications that raises peripheral vascular/cardiac output |
|
|
Term
|
Definition
See page 1153
-Renal parenchymal disease, renovascular disease, renin-producing tumors, Renal failure, Primary sodim retention
-Endocrine: acromegaly, hypothyroidism, hyercalemia, hyperthyroidism, adrenal disorders, coritcal disorders, cushings syndrome, primary aldosteronism
-Vascular Disorders: Coarction of the aorta |
|
|
Term
HTN (secondary)
Clinical manifestation |
|
Definition
|
Primary aldosteronism
Renal artery stenosis
Chronic kidney disease
|
Obstruction sleep apnea |
|
|
Term
Complicated HTN
Mechanism of Action |
|
Definition
|
Chronic hypertensive damage to the walls of systemic blood vessels
Results in reduced blood flow to organ and dysfunction
|
Kidney, brain, heart, extremities, and eyes |
|
|
Term
|
Definition
|
1. smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media
|
endothelia dysfunction, AngII catecholamines, IR and inflammation contribute |
|
|
Term
Complicated HTN
Clinical Manifestations |
|
Definition
| LVH, angina, CHF, CAD, MI, sudden death, aneurysms, claudication, renal complications |
|
|
Term
Malignant Hypertension
Mechanism of Action |
|
Definition
|
Rapidly progressive hypertension
|
EMERGENCY
Diastolic BP over 160
|
|
|
Term
Malignant HTN
Clinical Manifestations |
|
Definition
| Can cause encephalopathy, high pressures, increased capillary permeability, cerebral edema, and dysfunction |
|
|
Term
Orthostatic HTN
Mechanism of Action |
|
Definition
|
-Decrease in systolic by 20 or more and diastolic by 10 or more on standing
-Acute orthostatic: normal regulatory mechanisms are sluggich
|
-Chronic: secondary to disease or idiopathic |
|
|
Term
|
Definition
|
-Lack of normal blood pressure compensation in response to gravitational changes on the circulation
-Baroreceptor response which usually increases HR and constriction of systemic arterioles is not effective
|
|
|
|
Term
Orthostatic HTN
Clinical Manifestations |
|
Definition
| Blurred vision, presyncopy, syncopy, dizziness |
|
|
Term
Atherosclerosis
Mechanism of Action |
|
Definition
|
Form of arterosclerosis
Plaque development
|
Occurs throughout body |
|
|
Term
|
Definition
Thickening and hardening caused by accumulation of lipid-laden marcrophages in the arterial wall
|
Inflammation of endothelium
Cellular proliferation
Macrophage migration
LDL oxidation
Fatty streak
Fibrous plaque
|
Complixated plaque
|
|
|
Term
atheroscelorosis
Clinical Manifestation |
|
Definition
TIA's often associated with exercise stress
Leading cause of stroke |
|
|
Term
Coronary Artery Disease
Mechanism of Action |
|
Definition
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Any vascular disorder that narrows or occludes the coronary arteries
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Atheroscloerosis is most common cause |
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Term
Coronary Artery Disease
Patho |
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Definition
Local, temporary deprivation of the coronary blood supply; coronary blood cannot meet the demand of the myocardium for oxygen (MI)
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Myocardial cells become ischemic within 19 sec; lactic acid build up; remain viable for 20 min |
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Term
Coronary Artery Disease
Clinical Manifestations |
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Definition
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Stable angina
Prinzmetal angina(unpredicatable, pain that comes and goes, r/t spasm)
Silent ischemia
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Angina pectoris |
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Term
Acute Coronary Syndrome
Mechanism of Action |
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Definition
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Unstable angina: recurrent unpredictable chest pain; result of a revercible myocardial ischemia and is a harbinger of impending doom
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Myocardial Infarction: prolonged ischemia causing irreversible damage to heart muscles |
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Term
Acute Coronay Syndromes
Patho
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Definition
| Atherosclerotic plaque partially obstructs coronary blood flow; causes unstable plaque with ulceration or rupture and thrombosis; causes acute coronary syndromes; causes transient ischemia; causes unstable angina or MI |
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Term
Myocardial Infarction
Mechanism of Action
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Definition
| Plaque progression, disruption, clot formation; thrombus less labile and occludes vessel for a prolonged time, myocyte necrosis and death |
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Term
Myocardial infarction
Patho |
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Definition
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1. cellular injury
2. cellular death and tissue necrosis
3. structural and functional changes in cardiac tissue surrounding area of infarcti
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4. repair |
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Term
Myocardial Infarction
Clinical Manifestation |
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Definition
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EKG changes
Cardiac enzymes
Dysrhythmias, organic brain syndrome, and ventricular aneurysm
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Term
Acute Pericarditis
Mechanism of Action |
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Definition
| Inflammation of the pericardium |
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Term
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Definition
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Idiopathic or viral primarily
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Can result from MI, trauma, neoplasm, surgery, bacterial infection, radiation therapy |
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Term
Acute Pericarditis
Clinical Manifestation |
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Definition
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Pericardial membrane inflamed and roughened
Pericardial effusion
Chest pain worsening with breathing
Fever
Myalgias
malaise
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Term
Dilated Cardiomyophathy
Mechanism of Action |
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Definition
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Most idiopathic (familial origin; cardiac autoantibodies)
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IHD, valvular heart disease, renal failure, ETOH, drugs, DM, nutritional |
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Term
Dilated Cariomyopathy
Patho |
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Definition
| Diminished myocardial contractility, decreased systolic performance, decreased EF |
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Term
Dilated Cardiomyopathy
Clinical Manifestation |
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Definition
| Fatigue and dyspnea; pulmonary congestion, palpitations, dizziness |
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Term
Hypertrophic Cardiomyopathy
Mech of action |
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Definition
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Most common inherited disorder, autosomal dominant
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Serious risk for arrhythmias and sudden death |
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Term
Hypertrophic Cardiomyopathy
Patho |
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Definition
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Thickened septal wall, may cause outflow obstruction to the left ventricular outflow tract
Hyperdynamic state and impaired diastolic relaxation
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Term
Hypertrophic Cardiomyopathy
Clinical manifestations |
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Definition
| Angina, syncope, palpitations |
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Term
Restrictive Cardiomyopathy
Mechanism of Action |
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Definition
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Idiopathic or secondary to systemic disease
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Myocardium rigid and non-compliant |
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Term
Restrictive Cardiomyopathy
Patho |
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Definition
| Restrictive filling and reduced diastolic volume with normal to near normal systolic function and wall thickness |
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Term
Restrictive Cardiomyopathy
Clinical Manifestations |
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Definition
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Right heart failure with systemic venous congestion
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Cardiomegaly and dysrhythmias are common |
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Term
Aortic Stenosis
Mechanism of Action |
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Definition
| Develops gradually; angina, syncope and HF; also reduced SBP, slow HR, poor pulses; cresendo/decresendo systolic heart murmur |
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Term
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Definition
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Congenital bicuspid valve; degeneration with age, inflammatory damage cause by RHD
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Causes diminished blood flow from left ventricle to aorta, increases pressure in left ventricle, left ventricular hypertrophy, increased workload, increased oxygen demand, angina |
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Term
Aortic Stenosis
Clinical Manifestations |
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Definition
| If untreated can lead to dysrhythmias, MI, and HF |
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Term
Mitral Stenosis
Mechanism of Action |
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Definition
Impairs flow of blood from left atrium to left ventricle
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Term
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Definition
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-Autoimmunity in response to group A beta strep M protein antigens leads to inflammation and scarring; leads to fibrous and fused leaflets and chordae tendonae become shorter
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-Incomplete emptying of left atria, elevated atrial pressure, dilation and hypertrophy |
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Term
Mitral Stenosis
Clinical Manifestations |
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Definition
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Decrescendo diastolic murmur; opening snap
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Pulmonday congestion and right heart failure |
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Term
Aortic Regurg
mechanism of action |
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Definition
| Inability of leaflets to close properly; abnormalities in leaflets, root, annulus or both; acquired or congenital; blood flow back into left ventricle during diastole |
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Term
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Definition
| Left ventricle volume overload, increased EDV, mycaridal fiber stretch, compensatory dialation to increase SV and maintain CO, hypertrophy, ultimately heart failure |
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Term
Aortic Regurg
Clinical Manifestation |
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Definition
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Diastolic decrescendo murmur, prominent carotid pulsations, bounding pulses
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Dysrhythmias and endocarditis common |
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Term
Mitral Regurg
Mechanism of Action |
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Definition
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Most common cause MVP, RHD, also ineffective endocarditis, CAD, CT disease
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Backflow from left ventricle to left atrium during systole; increased volume of left atrium |
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Term
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Definition
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Left atrium volume incease, atrial dilation, associated with a-fib, may result in pulmonary hypertension and failure of right ventricle
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Left ventricle dilated and hypertrophied to maintain CO; may end in left failure |
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Term
Mitral regurg
Clinical Manifestations
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Definition
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-Well trolerated for years until ventricle failure occurs |
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Term
Tricuspid Regurg
Mechanism of Action |
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Definition
| Associated with cardiac failure and dilation of right ventricle secondary to pulmonary HTN; less common causes RHD and infective endocarditis |
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Term
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Definition
| Volume overload of right ventricle, increased systemic venous BP, right heart failure |
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Term
Mitral Valve Prolapse
Mechanism of Action
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Definition
| Anterior and posterior cusps billow upwards into atrium during systole |
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Term
Mechanism Valve Prolapse
Patho |
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Definition
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Myxomatous degeneration of leaflets in which the cusps are redundant, thickened and scalloped; chordae tendonae elongated
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Autosomal dominant x-linked inheritance |
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Term
Mitral Valve Prolapse
Clinical Manifestations |
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Definition
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Mainly asymptomatic; midsystolic click
Can cause palpitations, lightheadedness, fatigue lethargy, weakness dyspnea chest tightness; vague symptoms
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Some increase risk for endocarditis, cardioembolic stroke, sudden death |
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