Term
|
Definition
Pressure reservoir of circulation
Conductance vessels; highly elastic and muscular |
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Term
|
Definition
| Resistance vessels; main site of control of blood flow to tissues |
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Term
|
Definition
| Capacitance vessels; volume reservoir of the circulatory system |
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Term
| The pressure gradient which acts as the driving force for blood flow is measured between which two points... |
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Definition
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Term
|
Definition
| Circumflex & anterior interventricular |
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Term
|
Definition
| Marginal, posterior interventricular |
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Term
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Definition
| Volume expansion into pericardial sac; makes it difficult for heart to pump |
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Term
| Properties of cardiomyocytes: |
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Definition
| Striated, t-tubule network, arrangement into sarcomeres, many mitochondria |
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Term
| Non-Cardiomyocyte Cells in the heart |
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Definition
| Fibroblasts, Endothelial/Smooth muscle, Neural Cells |
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Term
| What makes up the structural matrix of the heart? |
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Definition
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Term
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Definition
Desmosomes - physically connect cells
Gap Junctions - electrically connect cells; allows for synchronous depolarization |
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Term
| Nerve AP vs. Pacemaker AP |
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Definition
Nerve: resting membrane potential at -70, depol due to Na influx, repol due to K efflux
Pacemaker: no resting potential (pacemaker potential = slow depol), depol due to Ca influx, repol due to K efflux |
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Term
| Why is the long refractory period important in cardiac muscle cells? |
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Definition
| Allows for complete ventricular filling (prevents tetanus) |
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Term
|
Definition
| Atrial contraction and depolarization |
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Term
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Definition
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Term
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Definition
| Ventricular depolarization and contraction |
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Term
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Definition
| Entire time to depol, then repol ventricles |
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Term
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Definition
| Ventricular repolarization & relaxation |
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Term
| Where do changes in HR normally manifest? |
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Definition
Change in the length of the DIASTOLIC INTERVAL
Tachycardia = shorter
Bradycardia = longer |
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Term
| What two things can control of the heart be related to |
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Definition
Chronotropy - control of rate
Inotropy - control of force of contraction |
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Term
| What 4 mechanisms control heart function? |
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Definition
| Autonomic innervation, hormone levels, drugs, intrinsic mechanisms (Frank-Starling) |
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Term
| Where do SNS and PNS innervation act on and with which NTs? |
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Definition
SNS = B-adrenergic receptors w/ NE
PNS = muscarinic receptors w/ Ach |
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Term
| Difference between SNS and PNS innvervation |
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Definition
SNS = + chronotropy AND inotropy
PNS = - chronotropy |
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Term
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Definition
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Term
| Normal parameters for CO, SV, and HR |
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Definition
CO = 5 L/min
SV = 70 mL/beat
HR = 72 bpm |
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Term
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Definition
| Blood returned to heart from venous circulation |
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Term
|
Definition
| Force required to eject blood from ventricles |
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Term
| SV is dependent on 3 factors: |
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Definition
Preload
Afterload
Contractility (force of contraction) |
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Term
| Vasoconstriction is caused by... |
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Definition
Increased O2/decreased CO2
Endothelin
Cold
Increase in myogenic activity
Increase in SNS
Increase in ANGII/vasopressin |
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Term
| Vasodilation is caused by... |
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Definition
Heat
Decreased myogenic activity
Decreased SNS innervation
Increased levels of NO, Histamine
Decreased O2/Increased CO2 |
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Term
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Definition
| Triad of HTN, hyperlipidemia, and insulin resistance (DM II) |
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Term
| Majority of deaths due to CVD are due to? |
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Definition
| CAD (then CVAs, then PVD) |
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Term
|
Definition
Hardening of the arteries; degenerative changes in small arteries
Associated w/ HTN, DM |
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Term
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Definition
| Formation of atheromas in large arteries; INFLAMMATORY process in the vessel wall |
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Term
| What is needed to precipitate athersclerosis? |
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Definition
| Need some sort of endothelial injury |
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Term
| Consequences of Endothelial Injury |
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Definition
Increased vasoconstrictors, less vasodilators
Less antithrombotic and anti-coagulative substances
Increased immune cell adhesion |
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Term
| Basic Process of Atherosclerosis (4 steps) |
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Definition
Endothelial Injury
LDL Retention/Fatty Streak
Formation of Stable Plaque (Atheroma)
Complicated Lesion (Unstable Plaque) |
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Term
| Fatty Streak/LDL Accumulation |
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Definition
Excess LDL accumulates under endothelium and CT (b/c of lesion) -> macrophages enter and take in chol and LDL (become FOAM CELLS)
Fatty streak increases in size and makes vessel lumen smaller |
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Term
|
Definition
Fatty streak forms a lipid core; CT forms around core to form a fibrous cap
Smooth muscle proliferates around and thickens wall (further occludes lumen) |
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Term
| Complicated Lesion (Unstable Plaque) |
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Definition
| If plaque becomes calcified, may weaken & rupture - ruptured plaques can throw clots to smaller vessels |
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Term
| Thrombosis in different areas of the body can cause: |
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Definition
In the coronary circulation -> MI
In the cerebral/carotid arteries -> CVA
In the iliac arteries -> PVD
In the aorta -> aneurysm |
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Term
| Coronary Blood supply to LV, RV, and AV/SA nodes |
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Definition
LV = LCA & circumflex
RV = RCA
SA + AV nodes = RCA |
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Term
| Examples of lipid lowering drugs |
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Definition
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Term
|
Definition
Due to atherosclerosis of coronary arteries - leads to myocardial ischemia (less O2 perfusion)
Can lead to angina pectoris |
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Term
|
Definition
| Chest pain radiating to the left arm triggered by sudden increase in O2 demand |
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Term
|
Definition
| Predictably occurring; relieved w/ rest and or < 3 doses of nitro |
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Term
|
Definition
Occurs at a new onset; can be due to acute coronary syndrome (unstable plaque)
Crescendo pattern
Pain @ rest or minimal exertion |
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Term
|
Definition
Rest - reduce O2 demand of myocardium
Nitroglycerine - 3 doses 5 mins apart
Nitroacts as a VASODILATOR |
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Term
|
Definition
CABG - vascular tissue taken from left internal mammary artery/saphenous vein and grafted onto coronary circulation to reroute flow
Transluminal ballon angioplasty/stent - opens the occluded vessel |
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Term
| Most common cause of MI's |
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Definition
| CAD (with the CAD being precipitated by some sort of athersclerosis) |
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Term
| Blockage of artery in MI occurs by... |
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Definition
| Thrombus forms on atheroma which embolizes a smaller branch of the artery; vasospasm may cause occlusion |
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Term
| Most common chamber affected in MI's |
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Definition
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Term
| What is myocardial damage from the infarct proportional to? |
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Definition
| Proportional to the size of the occluded vessel -> bigger = more damage |
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Term
|
Definition
Radiating chest pain to L arm (not relieved by rest or nitro; most telling symptom)
Pallor, diaphoresis
Hypotension - from cardiogenic shock (increased HR) |
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Term
|
Definition
EKG - akinesis of infarct
ECG - elevated ST segment
Isoenzyme tests in blood -> increased CK-MB, TnT/I, AST, LDH, CRP |
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|
Term
| Peak levels of isoenzymes and relative time post-MI |
|
Definition
CPK-MB = 24 hrs
AST = 48 hrs
LDH = 72 hrs |
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Term
|
Definition
Arrythmias (V fib is leading cause of death post-MI)
CHF
Shock
Ventricular rupture |
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Term
|
Definition
| Deviations from a normal cardiac rate/rhythm |
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Term
|
Definition
Bradycardia - lower than 60 bpm
Tachycardia - higher than 100 bpm |
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Term
| Disorders of Heart Rhythm |
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Definition
PVA's/PVC's
Heart Blocks (AV conduction blockage)
A fib/ V fib |
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Term
| Why are dysrhythmias dangerous? |
|
Definition
Decrease in CO (in tachycardia see decreased SV, in bradycardia see decreased HR)
Increase O2 demand - can precipitate angina |
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Term
| Intrinsic Rates of Pacemakers |
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Definition
SA node = 70-80 bpm
AV node = 40-55 bpm
Bundle, branches, Purkinje = 25-40 bpm |
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Term
| Causes of cardiac dysrhythmias |
|
Definition
SA node abnormalities
Atrial conduction abnormalities - PACs, atrial flutter or fib
AV node conduction abnormalities - heart block
Ventricular conduction abnormalities - V fib, bundle branch block |
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Term
| Causes of SA node abnormalities |
|
Definition
SA node ischemia (supplied by RCA)
Electrolyte abnormality
Activated autonomic NS (tachy = SNS, brady = PNS)
Intrinsic disease (sick sinus syndrome - scar tissue at node)
Drugs (B-blockers, cocaine) |
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|
Term
| What typically occurs to HR during SA node abnormalities? |
|
Definition
| Other pacemaker takes over SA function - get a lower intrinsic rate |
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|
Term
| Causes of atrial conduction abnormalities |
|
Definition
| Ischemia, electrolyte abnormalities, infarct, scar tissue |
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Term
|
Definition
| Extra atrial contractions due to contraction of ectopic foci |
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Term
|
Definition
| Atrial HR of 160-350 bpm; b/c AV node delays conduction, ventricular rate is slower |
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Term
|
Definition
Atrial HR > 350 bpm; see pooling of blood in atria (NO P WAVE because no coordinated contraction)
See a variable P/QRS ratio (ventricular rate may be slow or fast) |
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Term
|
Definition
| AV node abnormality; impulses from SA node don't reach ventricles |
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Term
|
Definition
Impulses from SA node are delayed excessively long in AV node
Prolonged PR interval |
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Term
|
Definition
See some "dropped beats" - some SA impulses do not make it past the AV node
Some P waves lack QRS waves (every 2nd to 3rd beat is dropped) |
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Term
|
Definition
NO impulse conducted through AV node; need another pacemaker to maintain ventricular contraction rate
"Atrioventricular dissociation" - contract independent of each other |
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Term
|
Definition
Conduction deficiency in one or both bundle branches
WIDE QRS complex (longer depolarization) |
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Term
|
Definition
MOST serious conduction abnormality
Ventricles "quiver" - no coordinated contractions (no CO)
Need immediate CPR, defib
Caused by = ischemia, drugs, electrolyte deficiency |
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Term
|
Definition
| Anti-Arrythmics = B-blockers (less SNS innervation), Ca channel blockers (less contraction), Digoxin (slows atrial dysrythmia) |
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|
Term
| Treatment for AV/SA nodal disease? |
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Definition
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|
Term
|
Definition
|
|
Term
|
Definition
| Slows rate of conduction through AV node; fix atrial dysrhythmias |
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Term
|
Definition
| Heart cannot meet metabolic needs of body, OR can only do so with compensatory mechanisms |
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Term
|
Definition
Forward decreased output - decreased CO or SV; less perfusion to organs = fatigue & acidosis
Back-up congestion - incomplete emptying of ventricles causes congestion (output < input) |
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Term
|
Definition
CAD (MAIN CAUSE) - decreased coronary flow, heart works harder (hypertrophy), fails
MI - myocyte death = failure; see dilatation and remodeling
Inherited myopathy
Valve defects - stenosis (increased afterload), incompetence (increased preload)
HTN - increases afterload (hypertrophy & failure)
DM
Pulmonary disease (leads to R sided CHF) |
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|
Term
| Progression of L sided CHF |
|
Definition
Less CO to systemic circulation -> activate RAA system to increase BP and volume
See backup in pulmonary circulation - pulmonary congestion and edema |
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Term
| Progression of R sided CHF |
|
Definition
Inadequate CO to pulmonary circulation, leads to less CO to systemic circulation as well -> RAA activates to increase blood pressure and volume
See back-up in systemic circulation -> edema in legs and feet, ascites; if severe, distended neck veins & increased ICP |
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Term
|
Definition
Dyspnea, orthopnea
Cough - fluid irritates respiratory passages
IF ACUTE - paraoxysmal nocturnal dyspnea (acute pulmonary edema)
Increases likelihood of lung infections |
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Term
|
Definition
Dependent edema in legs, feet, buttocks
Ascites; splenomegaly, hepatomegaly
Increased BP in jugular veins
If ACUTE - pallor, headache, distended neck veins, blurred vision |
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|
Term
| Adaptive mechanisms for CHF |
|
Definition
| Frank-Starling, Neurohormonal (SNS, RAA), Remodeling Myocardium |
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|
Term
| Frank-Starling adaptation to CHF |
|
Definition
See a DOWNWARD SHIFT in curve (for any given pre-load, SV is less)
Less able to increase SV in response to increased pre-load |
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|
Term
| SNS innervation during CHF |
|
Definition
INCREASE in SNS innervation (increased levels of NE)
Acutely - useful; maintains CO, increases BP
Chronically - increased BP = more work = hypertrophy; increased afterload can cause arrythmias as well |
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|
Term
| How can you reduce SNS compensation in CHF? |
|
Definition
|
|
Term
|
Definition
Less perfusion to kidneys = activate RAA system
Acute - beneficial because of increase in BP and volume
Chronically bad - increased edema because of volume, increased PR = increased afterload, increased pre-load on heart
Develop cardiac fibrosis |
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|
Term
| How to counteract RAA activation in CHF? |
|
Definition
ACE-I - reduce ANGII
ARB - block receptors
Spironolactone - diuretic; aldosterone antagonist |
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|
Term
| Other Hormonal Mechanisms in CHF |
|
Definition
ANP/BNP - both aid in Na/H2O excretion; higher levels = worse prognosis
Endothelin - vasoconstrictor; good short term, bad long term
TNF - weakens heart long term |
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|
Term
| How is the myocardium remodeled in CHF? |
|
Definition
Dilatation - ventricular cavity enlarges
Hypertrophy - ventricular muscle increases in size |
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|
Term
| What causes dilatation and hypertrophy in the ventricles during CHF? |
|
Definition
Dilatation = chronic volume overload (can't fully empty)
Hypertrophy - chronic pressure overload on ventricles |
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|
Term
| Difference in treatment for ACUTE and CHRONIC CHF |
|
Definition
Acute - determine precipitant, administer O2 and diuretics, vasodilators
Chronic - Digitalis (decrease force of contraction), Diuretics, Spironolactone, After-load reducers = ACE-I, ARB's, B-blockers |
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|
Term
| What drugs have been shown to reduce mortality in CHF patients? |
|
Definition
| Spironolactone, ARBs, B-blockers |
|
|
Term
| What is the 1st sign of young children with CHF? |
|
Definition
| Feeding difficulties (cannot gain weight) |
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|
Term
| When do congenital defects arise? |
|
Definition
| First 8-12 weeks of fetal life |
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|
Term
| What is the primary cause of death in the first year of life? |
|
Definition
|
|
Term
| Consequences of Congenital Heart Defects |
|
Definition
| Heart murmurs (most common for valvular defects), Cyanosis (w/ R-to-L shunts), Pulm HTN, Decreased CO |
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|
Term
| Signs of Congenital Heart Defects |
|
Definition
Pallor
Tachycardia (rapid sleeping pulse)
Dyspnea
Squatting position
Clubbed fingers & growth defects |
|
|
Term
| Two main types of congenital defects? |
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Definition
| Septal defects (creating shunts in the heart), valvulopathies (leading to stenosis or incompetence of valves) |
|
|
Term
| What is the most common congenital heart defect? |
|
Definition
| Ventricular septal defects |
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|
Term
|
Definition
1st see L-to-R shunt (because of higher pressure in the L ventricle); this causes decreased CO to systemic circulation
Now see a back-up in pulmonary circulation leading to higher pressures -> causes hypertrophy of RV due to pulmonary HTN, now get a R-to-L shunt leading to cyanosis |
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|
Term
| What valves are most commonly affected in valvulopathies? |
|
Definition
| Aortic and pulmonary valves (semilunar) |
|
|
Term
| Difference between stenosis and incompetence in valvulopathies? |
|
Definition
Stenosis - hardening of the valves; reduces SV (decreaseed flow; increased work on heart)
Incompetence - get regurgitation of blood backwards, see pooling of blood |
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|
Term
| Effects of Valvular Stenosis |
|
Definition
Increased work on heart because of decreased blood flow, hypertrophies heart muscle; also have increased afterload (b/c of Frank-Starling see additional hypertrophy)
Like CHF, get back-up congestion before valve |
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|
Term
| Symptoms seen in Aortic/Mitral valve stenosis vs. Pulmonary/Tricuspid valve stenosis? |
|
Definition
Aortic/Mitral - pulmonary edema
Pulmonary/Tricuspid - systemic edema, ascites |
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|
Term
| Two consequences of Valvular Incompetence |
|
Definition
Chronic volume overload in heart - DILATATION
Chronic pressure overload - HYPERTROPHY |
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|
Term
| Differences in symptoms between Aortic and Mitral regurgitation? |
|
Definition
Aortic - wide pulse pressure
Mitral - pooling in pulm circulation (pulm edema) |
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|
Term
|
Definition
Pulmonary Valve Stenosis - leads to pooling of blood behind the valve; more work on RV
RV hypertrophy - due to valvular stenosis
VSD - due to RV hypertrophy have increased pressure, get R-to-L shunt
Dextraposition of aorta over VSD - get deoxy blood from RV into systemic circulation (cyanosis) |
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|
Term
| What causes the inflammation in rheumatic fever? |
|
Definition
| Antibodies formed attack collagen in heart (inflammation & scarring) |
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Term
|
Definition
| Seen in endocarditis; small fibrous projections from the valves |
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|
Term
|
Definition
| Fever, Leukocytosis, Tachycardia, Heart murmurs |
|
|
Term
| Effects of inflammation in the various layers of the heart |
|
Definition
Pericardium = effusion (cardiac tamponade)
Myocardium = arrythmias
Endocardium = valvulopathy |
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|
Term
| Acute vs. Sub-Acute Endocarditis |
|
Definition
Acute - infection with very virulent organism (Staph); rapid progression
Sub-Acute - infection with less virulent organism (Strep); longer onset |
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|
Term
|
Definition
| Weakened immune system, bacteremia, pre-existing valve defects |
|
|
Term
|
Definition
| Murmurs, fever, fatigue, splenomegaly, Osler nodes (deposition of antibody-antigen complexes in feet and knuckles) |
|
|
Term
| Pathogens causing myocarditis in NA vs. SA |
|
Definition
NA = coxsakievirus (enterovirus)
SA = parasites |
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|
Term
| Complications of Pericarditis |
|
Definition
Pain, friction rub - due to decrease in pericard fluid
Effusion - accumulation of fluid in pericardial space (decreases CO) |
|
|
Term
| Acute vs Chronic Pericarditis |
|
Definition
Acute = Tamponade -> effusion of fluid compresses heart
Chronic = Constrictive -> prolonged inflammation; get adhesion of membranes & restrict movement |
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|
Term
| What is most susceptible to acute pericarditis (tamponade)? |
|
Definition
|
|
Term
| Symptoms of chronic pericarditis |
|
Definition
Pain, dyspnea, tachycardia, distended neck veins
Pulsus Paradoxus
Abdominal Discomfort |
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|
Term
| Treatment for Chronic Pericarditis |
|
Definition
| Pericardiocentesis - aspirate fluid from sac |
|
|
Term
|
Definition
| Chronically elevated BP > 140/90 on 3 separate visits spaced 2 weeks apart |
|
|
Term
| Systolic vs. Diastolic HTN |
|
Definition
Systolic = increase in Sys BP; wide pulse pressure
Diastolic = increase in Dias BP; increased PR; rarely occurs without systolic HTN |
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|
Term
| Multifactorial etiology of primary HTN |
|
Definition
Salt sensitivity - increased NaCl intake causes increased BP
Membrane ion transport deficiency
Accumulation of Ca in vascular muscle = more tone = vasoconstriction
Insulin resistance - increased insulin = increase Na retention, Ca, muscular hypertrophy |
|
|
Term
| When is secondary HTN most likely to occur? |
|
Definition
|
|
Term
| Common causes of secondary HTN |
|
Definition
Renal disease
Endocrine causes - hyperaldosteronism (increased blood volume), Cushing's (increased glucocorticoids = vasoconstriction, Pheochromocytoma (increased secretion of E and NE)
Oral contraceptives |
|
|
Term
| End organs affected by HTN |
|
Definition
| Heart, Kidneys, Brain, Eyes |
|
|
Term
| End organ effects of HTN on HEART |
|
Definition
Increased PR = increased afterload for heart -> more work = hypertrophy
Later leads to remodeling and dilatation -> CHF
Can also cause angina/MI -> increased O2 requirements |
|
|
Term
| End organ effects of HTN on KIDNEYS |
|
Definition
HTN causes glomerular damage -> DECREASE in GFR (decrease in kidney function)
Vicious cycle - kidneys secrete renin, leads to increased BP and blood volume = more HTN = more damage = more renin secretion |
|
|
Term
| End organ effects of HTN on BRAIN |
|
Definition
Hypertensive encephalopathy - usually due to acute HTN -> altered consciousness, increased ICP, seizures, blurred vision
Often see hemorrhagic CVAs |
|
|
Term
| End organ effects of HTN on EYES |
|
Definition
Hypertensive retinopathy -> **Hallmark of malignant HTN
Scotomata, blurred vision, blindness |
|
|
Term
|
Definition
| Localized dilatation of arterial wall |
|
|
Term
| What can weaken the media to lead to an aneurysm? |
|
Definition
| Turbulent flow from atheroma/thrombus or bifurcation in vessel |
|
|
Term
| Where are aneurysms most common? |
|
Definition
| In the aortic and abdominal aorta |
|
|
Term
|
Definition
Fusiform - circumferential dilatation
Saccular - bulging to one side; see thrombus formation
Dissecting - due to tear in media and intima; blood flows through layers of vessel |
|
|
Term
|
Definition
| Atherosclerosis, trauma, congenital vascular defect, syphilis |
|
|
Term
|
Definition
| Dilated areas in veins due to chronic stretch of wall |
|
|
Term
| What can cause varicose veins? |
|
Definition
| Weakness in vein wall or valvular dysfunction in veins |
|
|
Term
| What can cause varicose veins? |
|
Definition
| Excessive hydrostatic pressure - long periods of standing, pregnancy, thrombophlebitis (vein inflammation) |
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