Questions and CORRECT Answers
Cardiac output = stroke volume x heart rate
SNS effect on HR Increases HR
stress, anxiety, acute pain, catecholamines, hypotension,
SNS stimulation
+chronotropic drugs
PNS effect on HR Decreases HR
vagus nerve, cardiac conduction abnormalities, drugs with -
PNS stimulation
chronotropic effect
amount of blood ejected from each ventricle per contraction,
stroke volume mm/beat
positively influenced by preload and contractility (strength)
strength of each myocardial contraction, contributes to cardiac
contractility
output
volume of blood results in pressure or strength during diastole,
affected by amount of venous return to heart
preload
INCREASED by constriction
DECREASED by decreased volume, vasodilators
resistance to ventricular emptying during systole
afterload INCREASED with construction or obstruction of flow
DECREASED with hyperthermia, distributive shocks, vasodilators
Toddler HR 80-130 bpm
School age HR 75-100 bpm
Infant HR 80-160 bpm
Neonate HR 70-170 bpm
Child BP older than 1 year SBP = (agex2) + 90
BP 0-1 month above 60 mmHg
BP 1-12 month above 70 mmHg
Mean arterial pressure average pressure over entire cardiac cycle
, Pulse pressure difference between systolic and diastolic
decreased left ventricular stroke volume, blood loss due to
Low pulse pressure (narrowing)
trauma, low stroke volume (shock, tamponade)
can be transient and normal, chronic conditions (atherosclerosis),
High pulse pressure (widening)
aortic dissection, endocarditis, anxiety, fever
ICP!
widening pulse pressure (or hypertension)
Cushings triad
bradycardia
irregular breathing patterns
drugs that affect the HR, at SA node
chronotropes
adrenaline (positive), digoxin (negative)
Inotropes Drugs that affect contractility, force of contraction of the heart.
drugs that affect automaticity (electrical impulse velocity) of the
Dromotropes
heart at the AV node
Alpha (1) stimulation causes peripheral vascular CONSTRICTION
__________
Beta (2) stimulation causes bronchial smooth muscle DILATION
_________
ACE inhibitors (-prils), Angiotensin receptor blockers (ARBs, -
Vasodilators
sartans), Calcium channel blockers (-dipine), beta-blockers (-lol)
reduces blood pressure in HTN, reduces after load associated
Angiotensin-converting enzyme with HF
inhibitors (aka ACE) (-pril) decreases preload and after load by vasodilation and diuresis
Sx: dry cough, rash, renal impairment
vasodilation and decreased aldosterone levels, increases sodium
Angiotensin receptor blockers
and sparing of K+; HTN and HF
(ARBs) (-sartan)
Sx: hypo-t, dizziness, h/a, hyper-K
calcium channel blockers (- negative inotropic (reduces contractility), chronotropic (reduces
dipine) HR), dromotropic (reduces impulse) effects
negative inotropic (reduces contractility), chronotropic (reduces
beta blockers (-lol) HR), dromotropic (reduces impulse) effects
works on beta receptors
in the heart
Decrease HR
B1 blockers affect: Decrease contractility
Decrease BP
... also work with kidneys to reduce BP through RAAS system
in the lungs
B2 blockers affect: bronchial smooth muscle relaxation
dilation of airways
vasodilator
Nicardipine CCB
coronary, peripheral vasodilator
vasodilator
labetalol slows HR, decreases CO, CP
GRADUALLY lower to reduce ischemia/infarcts