UNIT 4 EXAM Flashcards
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
Afterload
tension required to cause the contraction;
how hard the heart must work to contract
Effects of Vasodilators
decreased BP, decreased preload and afterload;
decreased blood flow through the heart and body;
decreased work on the heart and oxygen consumption;
increased cardiac output with less effort
Vasodilators
Nitrates
Nitrates
vasodilators;
MOA: dilate blood vessels, decrease blood pressure, decrease venous return (preload and afterload); decreases cardiac work and oxygen consumption
USES: HF, angina, CAD, HTN, MI
DRUGS:
1. nitroglycerin (Nitro-Bid, Transderm Nitro, Nitrostat) - sublingual, tabs, transdermal, IV
do not expose to air or light (drug loses its potency)
2. isosorbide (Isordil or Ismo)
PATIENT CAUSE/SIDE EFFECTS: HA, lightheadedness, tachycardia, orthostatic hypotension - be careful with position changes, no ED meds
Inadequate Oxygenation
brain: dizziness, drowsiness, less alert
lungs: SOB, cough
kidneys: try to compensate; hold on to H2O and electrolytes ->
edema everywhere and in lungs; must give diuretics to eliminate fluid
Beta Blockers
(non-selective beta-1 and beta-2)
MOA: block beta-1 receptors;
decrease HR, FOC and oxygen consumption;
reverse excessive sympathetic activation (compensatory CHF)
USE: CAD, angina, HTN, CHF, arrhythmias - tachycardia, glaucoma, migraines
DRUGS:
Non-Selective Beta Blockers:
propranolol (Inderal)
nadolol (Corgard)
nebivolol (Bystolic)
Selective Beta-1 Blockers:
atenolol (Tenormin)
metoprolol (Lopressor)
Non-selective beta blockers, alpha-1 blocker:
carvedilol (Coreg)
PATIENT TEACHING/SIDE EFFECTS: drowsiness, GI upset, CNS depression, bradycardia, monitor serum lipid levels, mental depression, monitor glucose levels in diabetic patients, avoid using non-selective BBs with asthma patients - bronchoconstriction
Coronary Arteries
blood flows to heart muscle
CAD (Coronary Artery Disease)
blockage -> ischemia occurs
02 demand exceeds the supply
(coronary arteries only)
Arteriosclerosis
hardening or narrowing of coronary arteries due to an aging process
Atherosclerosis
buildup of fatty deposits/plaque that has accumulated in walls of arteries
Angina Pectoris
chest pain caused by reduced/restricted blood flow to the heart caused by arteriosclerosis or atherosclerosis
3 Types of Angina
- Exertional/Stable Classic Angina
- Unstable Angina
- Prinzmetal/Vasopasm of Coronary Artery
Exertional/Stable Classic Angina
chest pain/discomfort that occurs with activity or stress; is usually resolved with rest/meds
Unstable Angina
unpredictable bouts of chest pain, usually occurring at rest; MI is soon to follow; doesn’t respond to rest
Prinzmetal/Vasospasm of Coronary Artery (Angina)
sudden constriction of the coronary artery; decreased O2 to cardiac muscle; chest pain
CAD and Antianginal Drug Therapy
Vasodilators/Nitrates - nitroglycerin;
Beta Blockers (BB) - -olol
Calcium Channel Blockers (CCB)
Calcium Channel Blockers (CCB)
Calcium Antagonists;
Calcium: FOC;
USES: CAD, angina, HTN, tachyarrhythmias
CAUTION: do not use on patients with CHF; already have ineffective pumping
2 Categories: dihydropyridines & nondihydropyridines
Calcium Channel Blockers/Antagonists
Dihydropyridines
have a vasodilating effect;
MOA: 1. block entry of calcium into cardiac muscle to decrease the FOC; demand for O2 decreases
2. block of entry of calcium into smooth muscle; vessels relax, BP decreases
DRUGS:
1. nifedipine (Procardia)
2. amlodipine (Norvasc)
3. nisoldipine (Sular)
USES: angina, HTN
Calcium Channel Blockers/Antagonists
Nondihydropyridines
act on cardiac muscle, heart’s conduction cells, and smooth muscle
vasodilators and antiarrhythmics
MOA: 1. block entry of calcium into cardiac muscle; decreased force of contraction; decreased demand for O2
2. block entry of calcium into smooth muscle cells; vessels relax; vasodilation; decreased BP
3. decreased SA node and AV node conduction; decreased conduction velocity of each (Tx: tachyarrhythmias)
DRUGS:
1. verapamil (Cadan)
2. diltiazem (Cardizem)
USES: angina, HTN, tachyarrhythmias
Calcium Channel Blockers/Antagonists Side Effects
HA, facial flushing (vasodilation), reflex tachycardia, dizziness, hypotension, constipation, xerostomia
Calcium Channel Blockers Drug Interactions
CCB and BB
slows HR and depresses cardiac activity leading to CHF
Myocardial Infarction (MI)
1 killer in the US
heart cells - ischemia
necrosis
to follow are CHF and arrhythmias
infarct
every 20 seconds: MI
every minute: 1 MI death
about 697,000 deaths in the US due to MI (1 in every 5 deaths)
