UNIT 4 EXAM Flashcards
(47 cards)
Blood Flow
Venae Cavae -> Right Atrium -> Tricuspid Valve -> Right Ventricle -> Pulmonary Trunk -> Pulmonary Arteries -> Pulmonary Capillaries (site of exchange) -> Pulmonary Veins -> Left Atrium -> Bicuspid (Mitral) Valve -> Left Ventricle -> Aortic Semilunar Valve -> Aorta
Important Electrolytes
Na+ (sodium): main extracellular electrolyte; fluid balance
K+ (potassium): main intracellular electrolyte; maintains the structure and function of the cell (especially cardiac muscle)
Ca2+ (calcium): mineral associated with bone; aids in muscle contraction and blood coagulation; FOC
Conduction System
SA node fires;
signal spreads through the atria to the atrial myocardium;
signal reaches the AV node;
signal travels down the Bundle of His;
signal travels down bundle branches;
signal travels down Purkinje Fibers;
signal reaches ventricular myocardium
SA node
(RA) pacemaker; impulse starts here;
auto rhythmicity - heart initiates its own impulse
Conduction
coordinates contraction of the heart;
monitored by EKG (ECG)
Phases of Action Potential
Phase 4: RMP (-90 mV)
diastole (Na+ outside the cell; K+ inside the cell)
Phase 0: rapid depolarization; Na+ flows into cell; rapid change in voltage from RMV, generates an action potential
Phase 1,2 and beginning of 3: K+ moves out of cell; repolarization occurs, bringing membrane potential back to resting
refractory period - another contraction cannot occur; cannot receive another action potential; prevents continuous contraction - tetany
Phase 2: plateau phase; balance of Ca2+ moving into cell and K+ moving out of cell; muscle contraction occurs
Phase 3: rapid repolarization; Ca2+ channels close, more K+ channels open
EKG/ECG
P wave - atrial depolarization
PR segment - AV node delay
QRS complex - ventricular depolarization
ST segment - absolute refractory period (another contraction cannot occur; prevents tetany)
T wave - ventricular repolarization
Control of the Heart
Autonomic Nervous System: regulates HR and FOC
SNS: NE
EPI from adrenal medulla
increases HR (chronotropic); increases FOC (inotropic); increases conduction (dromotropic)
PNS: ACH
decrease HR; decrease FOC; decrease conduction (dromotropic)
Normal Sinus Rhythm
Normal Rate and Rhythm
Measurements are Accurate
No Extra Beats
Fibrillation
quivering;
ineffective contractions
Diseases of the Heart
Heart Failure (HF/CHF)
Congestive Heart Failure
Heart Failure (CHF/HF)
occurs with activity or at rest;
heart is unable to pump out blood effectively;
more blood enters the heart than leaves;
less blood reaches the organs;
kidneys compensate, resulting in edema, fluid and electrolyte retention;
hypertrophy;
sympathetic nerves compensate: vasoconstriction, increase in HR & FOC
Tx: cardiac glycosides ( increase FOC); beta-blockers, vasodilators, diuretics
Hypertrophy
increase in volume of a tissue/organ due to enlargement of component cells
Congestive Heart Failure
Left Ventricular Failure - Pulmonary Congestion;
dyspnea, tachypnea, orthopnea, nocturnal dyspnea, pulmonary edema, coughing
Right Ventricular Failure - Venous Congestion
pitting edema; ascites
Possible Actions of Cardiac Drugs
1) Chronotropic: positive/negative HR
positive: EPI, atropine
negative: cardiac glycoside
2) Inotropic: positive/negative FOC
positive: cardiac glycosides
negative: calcium channel blockers
3) Dromotropic: positive/negative conduction
Ascites
a condition in which fluid collects in spaces within your abdomen
Pitting Edema
accumulation of an excessive volume of fluid within the body;
when pressure is applied, a dent is formed
Dyspnea
shortness of breath
Tachypnea
rapid breathing
Orthopnea
shortness of breath that occurs while lying down; is relieved when sitting up or standing up
The Rights
- Right Patient
- Right Drug
- Right Dosage
- Right Route of Administration/Form
- Right Time
- Right Response
- Right Documentation
Cardiac Glycosides
MOA: increase the FOC; accelerate entry of Ca2+ into the cardiac muscle cells; this, in turn, increases kidney fxn; kidneys eliminate excess fluid and electrolytes that cause edema;
decreases HR; slows down AV node conduction
USES: CHF;
arrhythmias: atrial fibrillation and atrial tachycardia
DRUGS: digoxin (Lanoxin)
PATIENT TEACHING/SIDE EFFECTS: interfere with Na+/K+ pump,
hypokalemia occurs that results in arrhythmias, nausea, headache, visual disturbances
check pulse: to administer has to be 60 - 100 bpm
GOAL: increase FOC without increasing oxygen consumption
digoxin (Lanoxin)
digitalization (administration of the drug):
maintenance dose, low TI, must monitor levels
therapeutic serum levels: 0.5 ng/mL - 2.0 ng/mL
toxic: over 2.5 ng/mL
rapid onset and short duration of action
toxicity: cardiac: slow pulse, irregular pulse
CNS: headache, confusion, visual disturbances (halos around dark objects), delirium
GI: N/V/D
toxicity: give K+ to increase heart’s ability to contract; d/c drug, serum levels
antidote: digoxin immune fab (Digibind)
Preload
how stretched the chamber is prior to contraction;
venous blood return to the heart
