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140 Cards in this Set

  • Front
  • Back
Circulatory System: two systems
• Cardiovascular
•Lymphatic system
Cardiovascular – 3 basic components
– Heart – establish pressure gradient
• Dual pump ( right/left systems)
• Atria and ventricles
– Blood vessels – passageway, regulation of distribution
– Blood – transport medium
Cardiovascular subdivisions
• Pulmonary circulation –heart/lungs
• Systemic circulation – heart/other systems
• Functional differences?
• Anatomical differences?
Lymphatic system
– accessory route
– unidirectional vessels
Cardiac system Anatomy
• Position - between sternum and
vertebrate
• Gross anatomy
– base, apex, pericardial sac
– atria atop ventricles, septum
– Right/ left sides =two separate pumps
Atrioventricular (AV) valves
– Prevent backflow \from ventricles into atria
– Right AV/tricuspid valve
– Left AV valve (bicuspid/mitral)
– Chordae tendinae
• Fibrous cords prevent valve eversion
• Papillary muscles
Semilunar valves
– Aortic and pulmonary valves
– Lie at juncture where major arteries leave ventricles
Cardiac Layers
– Endothelium – thin/inner, lies entire CV
– Myocardium – middle/muscle
• myocytes - autonomic innervation
• intercalated discs (gap junctions and desmosomes)
– Epicardium – thin/external
• squamous mesothelium/basal lamina
• blood/nerve supply within CT network
Pericardium
– fluid filled sac

– Fibrous outer layer
– Inner secretory lining – pericardial fluid
tunica intima
(inner layer)
– endothelial lining with basement membrane
– some connective tissue (CT)
tunica media
(middle)
– variable muscular elements – regulate diameter
– variable elastin – “elastic lamina”
tunica adventitia
or
externa
(outer)
– variable connective tissue
– extensive blood and nerve supply
Cardiac muscle
• Similar to skeletal
muscles
– sarcomeres
– actin/ myosin

• Differences from skeletal
muscle
– mononucleated
– branched
– connect through
intercalated disks
(gap junctions,
desmosomes)
Cardiac muscle fibers
• Interconnected by intercalated discs, form functional
syncytia
• Within discs – two kinds of membrane junctions
– Desmosomes
– Gap junctions
T-tubules
larger than
in skeletal muscle, are
aligned with Z-disks
(one per sarcomere)`
SR is juxtaposed with
T-tubules at very small
terminal bulbs, rather
than large cisternae.
SR structure/size
thin and lacy, with
much smaller volume
than skeletal SR
Contractile cells
(99% cardiac cells)
• Do mechanical work of pumping
• Normally do not initiate own APs
Autorhythmic cells
• Send electrical signals to the contractile cells
• Specialized for initiating and conducting action potentials
responsible for contraction of working cells
• Locations:
– Sinoatrial node (SA node)
– Atrioventricular node (AV node)
– Bundle of His (atrioventricular bundle)
– Purkinje fibers
SA node
– right atrial wall near superior vena cava
– Pacemaker of the heart
AV node
– base right atrium
– only connection to ventricles
Bundle of His
(AV bundle)
– at AV node towards interventricular septum
– Form R and L bundle branches down septum
Purkinje fibers
extend
from Bundle of His through
ventricles
Cardiac APs originate
at SA
node
– spread through atria
APs to AV node
– only point of electrical contact
between chambers
– delay ensures atrial contraction
precedes ventricular
contraction (allow complete
filling
APs down interventricular
septum
via bundle of His
Disperses via
Purkinje fibers,
spread via gap junctions
Pacemaker cells
• Pacemaker potential
– small Na+ leak (If) -"funny"
channels
– open at Vm more negative
than ~ -50 mV
– plus some T- Ca2+
channels)

• Threshold
– depolarization at ~ -40 mV
– L - Ca channels open
,
• Repolarization
– Slow K+ channels open
– close Ca2+ channels
Electrical Conduction – Contractile cells
• No pacemaker potentials
–driven by pacemaker cells

• Threshold/depolarization
-classic fast Na+ channels

• Plateau phase
– elevated L-type Ca2+
channels (dihydropyridines)

• Repolarization
- Slow ("delayed
rectifier") K+
channels open/ close
Ca+channels; close to restart
cycle.
Electrical Activity of Heart
• Long refractory period with prolonged plateau phase
– limits summation/tetanus of cardiac muscle
– Ensures alternate periods of contraction/relaxation
Modulation of Cardiac Excitation/
Contraction
• Epi/NE – sympathetic - Depolarize V
mat baseline, increases
“funny” current

• Ach – parasympathetic – Hyperpolarize Vm, decreases “funny”
Epinephrine
sympathetic
–beta 1/increase cAMP
– increase Ca 2+ channel
Conductance (permeability)
Ach
parasympathetic
– Muscarinic –
decrease cAMP
– decreasing Ca2+
entry
Electrocardiogram (ECG)
• Record of overall spread of electrical activity through heart
– part of activity in body fluids
by APs that reaches body surface
– not direct cardiac recording
• Overall spread throughout heart during depolarization
and repolarization/not single Aps
• Comparing V differences
on body surface
– not actual potential
– no potential recorded
with heart completely
depolarized/
repolarized
P wave
atrial depolarization
PR segment
AV nodal delay
QRS complex
ventricular depolarization (atria repolarizing simultaneously)
ST segment
time during which ventricles are contracting and emptying
T wave
ventricular repolarization
TP interval
time during which ventricles are relaxing and filling
Heart rate
Normal ~
70 beats/min (SA note
similar)
– Tachycardia >100 bpm
– Bradycardia < 60 bpm
Rhythm –
regularity/spacing
– “sinus” –(SA node) P
same direction/ before
QRS
– Normal intervals
• PR - 0.20 sec
• QRS - 0.08 – 0.10 sec
• QT- 450 ms in men, 460
ms in women
Electrical Abnormalities
• Arrhythmia - Variation from normal rhythm
and abnormal sequence of excitation
– Atrial flutter (200-300 BPM) vs fibrillation
(irregular)
– Ventricular fibrillation
– Premature Ventricular Contraction (PVC)
– Heart block
• 1
st
degree – PR fixed > 0.2 sec
• 2
nd
degree (two types)
– PR gradually lengthened, then drop
QRS
– PR fixed, drop QRS randomly
- 3rddegree block - PR and QRS
dissociated
Mechanical
Events
• Systole = period of contraction
• Diastole = period of relaxation
• Cardiac Cycle = alternating periods
of systole and
diastole
Phase of Cardiac Cycle
1. Rest
(atria/ventricles in diastole – filling with low pressures)
2. Atrial Systole
– completes ventricular filling
3.Isovolumetric Ventricular Contraction
– Increased pressure in the ventricles
causes the AV valves to close…
why? (1st
heart sound)
– Atria go back to diastole
– No blood flow as semilunar valves are closed as well
4. Ventricular Ejection
– interventricular > aortic pressure
(semilumar valves open)
5. Isovolumetric Ventricular Relaxation
- interventricular < aortic
pressure (Semilunar values close – 2
nd heart sound)
Cardiac Output
• Volume of blood ejected by
each ventricle each minute
• Cardiac output = heart rate
(HR) x stroke volume (SV)
– SV ~ 70 ml
– HR ~ 70 beats/min
– Output about 5 L/min at rest
– Increase to 30-40 L/min during
high intensity exercise
Stroke volume
Determined by extent of venous return
and by contractility/afterload
Venous return
end-diastolic volume (EDV)

– Increases “pre-load”
• Amount of stretch within myocardium (‘load’ prior to contraction)
• Length-tension patterns (Frank-Starling Law)
– Determinants
• Skeletal muscle pump
• Respiratory pump
• Cardiac “Suction
Contractility
contributes to ESV
– Stronger contraction =
larger stroke volume
– “inotropic agents”
(epinephrine/NE; Ach
is opposite)
– Increased Ca2+
entry/modulation –
more force per unit
muscle/length
Afterload
contributes to ES
– aortic pressure to overcome to
open semilunar valves
– Higher afterload - reduces
ejection fraction (SV/EDV) ~
normal=52%
– indirect relationship- Higher
aortic pressure = lower stroke
volume
– Causes?
• Elevated blood pressure
• Loss of compliance in aorta
(loss of elasticity)
Cardiac Mechanics (Pressure/Volume Curve)
• Pressure/Volume relation often plotted to indicate
demands on cardiac tissue
– Start at (a) diastole, (b)-(c) systole, (d)-(a) diastole
– Curve runs counter-clockwise
LEFT VENTRICULAR
PRESSURE/VOLUME CURVE
A. mitral valve opens
– Heart relaxation
– vent P < atrial P
B. diastole (filling)
– increase volume in ventricle
– Low pressure-chamber
expanding
C. start of systole
– Mitral valve closes (vent P >
atrial P)
– Rapid increase in pressure
(no change in volume no
valves open)
LEFT VENTRICULAR
PRESSURE/VOLUME CURVE
D. aortic valve opens
– Vent P > aortic P
– Blood starts to be ejected
E. systole (cont)
– Decreased vent volume
with blood ejection
– Maintaining high pressures
F. start of diastole
– Aortic valve closes (vent P
< aortic P)
– Rapid drop in pressure (no
change in volume – no
valves open)
Coronary Circulation
• Supplies oxygen and nutrients to heart (blood received
during systole and diastole)
• Coronary blood flow keep pace with oxygen needs
Coronary Arterial Disease (CAD)
– Primary cause of mortality in US
– Can cause myocardial ischemia or
infarction (3 mechanisms)
• Vascular spasm of coronary arteries
• Formation of atherosclerotic plaques
• Thromboembolism
– Angina Pectoris
• Controlled w/ exertion
• Uncontrolled – vasospasm
?
Outcomes Post-Myocardial Infarction
1. Immediate death
2. Delayed complications/death
3. Full recovery
4. Recovery with impaired function
Immediate death
– heart ineffective in pump function
– fatal ventricular fibrillation 2⁰
damage conducting tissues
Delayed complications/death
– Fatal rupture of dead/degenerating
cardiac wall
– Progressive heart failure
Full recovery
– Replacement of damaged wall with
scar
– Enlargement, compensation of
remaining contractile tissue
Recovery with impaired function
– Permanent functional defects
– bradycardia, conduction blocks
Blood Vessels Function
– Route for transport (arteries – away, veins – towards)
– Exchange (capillaries)
– Control/regulate blood pressure
Structure allows function
– Aorta – absorb pulse pressure (SBP - DBP)
– Large arteries- conduct/distribute blood to
specific regions
– Arterioles – regulate flow and mean arterial pressure (MAP)
– Capillaries – exchange
– Venules – collect/direct blood
to veins
– Veins – return blood to
heart/reservoir
Arterial system
away from heart

Large elastic arteries
(little resistance to flow

Systolic Blood Pressure
~120 mmHg at brachial artery

Diastolic Blood Pressure
– with aortic recoil/closure of aortic
semilunar valves (~80 mmHg at brachial artery)

Pulse Pressure
– SBP - DBP

Mean Arterial Pressure (MAP)
• MAP = DP + 1/3 Pulse Pressure
• Evaluates general health of CV system
Blood Pressure
Measured indirectly using
sphygmomanometer
• Korotkoff sounds
– Sounds heard when determining blood
pressure
– Sounds are distinct from heart sounds
associated with valve closure
Measured indirectly using sphygmomanometer
1. Cuff pressure > SBP -No sound.
2. The first sound is heard at peak SBP.
3. Sounds are heard while cuff pressure < SBP but > DBP
4. Sound disappears when cuff pressure < DBP
Flow dynamics (CO, MAP, Resistance)
• Cardiac output = net flow throughout CV system
• MAP – mean hydrostatic pressure
gradient
driving fluid flow
(depends on blood volume/vessel compliance)
• Resistance – ease of flow through vessels, total peripheral
resistance (TPR) proportional to MAP and CO
– With increased resistance but similar CO, what happens to
MAP?
– With anaphalaxis, what happens to resistance, MAP, CO
Blood Flow/reconditioning
• Blood constantly reconditioned
(composition relatively constant)
• Reconditioning organs receive more
blood than metabolic needs
– Digestive organs, kidneys, skin
– Adjust extra blood for homeostasis
• Blood flow to other organs can be
adjusted according to metabolic needs
• Brain can least tolerate disrupted
supply
Arterioles
• Major resistance vessels
– Radius adjusted independently to
distribute CO
– Help regulate arterial blood pressure
• Histology/function
– Larger arterioles – reduced elastic fibers
from arteries, increased muscle fibers
– Smaller arterioles - relatively greater
smooth muscle
• Adjusting arteriolar resistance
– Vasoconstriction - narrowing a vessel
– Vasodilation – increase vessel radius
– Alter smooth muscle contractions
Smooth Muscle
Characteristics
– Walls of hollow organs/tubes
– No striations (no sarcomeres/
myofibrils)
– Spindle-shaped cells, single
nucleus
• Cells usually arranged in
sheets within muscle
• Have dense bodies containing
same protein found in Z lines
Filaments/structures
– myosin (thick) - Longer than those
in skeletal muscle
– actin (thin) - Contain tropomyosin,
no troponin
– Intermediate - part of
cytoskeleton, not directly related to
contraction
Activation of smooth muscle
– Ca
2+
dependent 2
nd
messenger
– Increased Ca2+
entry from ECF
– Result in phosphorylation of
myosin thick filament
– Actin-myosin interaction
Multi-unit
– Neurogenic
– Discrete units that function independently of one another
– Units must be separately stim
ulated by nerves to contract
– Locations (large blood vessels, large airways, vision (iris/lens),
hair follicles
Single-unit
– Self-excitable (does not always require PNS for contraction)
– Visceral smooth muscle
– Fibers become excited and contract as single unit
– gap junctions/desmosomes interconnecting - “functional
syncytium”
– Slow/energy-efficient contractions - distensible, hollow organs
Opposition to blood flow in
arterioles
– Resistance (R) directly
proportional to:
• vessel length (L),
• blood viscosity(η),
• inversely proportional of
radius (to the 4th power)
R =Lη/r4
– L and η
constant, so R =
1/r4
Vessel diameter controls
are local and systemic
– Enables tissues to control
their own blood flow
– Local controlling
mechanisms include intrinsic
and extrinsic
Intrinsic responses
1. myogenic responses

2. paracrine vasoconsrictors

3. paracrine vasodilators
Myogenic responses
stretch with increased pressure (mech gated Ca2+ channels)
Paracrine vasoconstrictors
• Serotonin – activated platelets
• Endothelin – by endothelium
Paracrine vasodilators
NO – by endothelium
• Bradykinin/histamine/prostaglandins
(inflamm)
• Adenosine – hypoxic cells
•decrease O2,
-increase CO2, 
-increase K+, 
-increase H+, 
-increase temp
Extrinsic responses
-vasoconstrictors

-vasodilators
Vasocontrictors
• NE – sympathetic postganglionic
• Vasopressin (ADH) – post pituitary
(CNS release with low BP)
• NE – sympathetic postganglionic
• Vasopressin (ADH) – post pituitary
(CNS release with low BP)
Vasodilators

-beta 2 Epi (adrenal medulla)
• Ach – parasymp postganglionic
• ANP (atrial natriuretic peptide) –
atrial myocaridum /brain
• VIPs (vasoactive intestinal
peptides) – from neurons
Vascular Control of Blood Flow (hyperemia)
Hyperemia is locally mediated increases in blood
flow (active or reactive)
Vasoconstriction/dilation
depending on demands
– Rest
• Vasodilation – Ach release
(parasymp) at GI/splanchnic
• Vasoconstriction (no NE release,
locally mediated
– Exercise
• Vasodilation – dominated by
metabolic factors at local active
muscle (active hyperemia)
• Vasoconstriction – NE mediated
Medullary Cardiovascular
Control Center
– Receives inputs from carotid and aortic baroreceptors

– Outflow to ANS

• Symp- SA & AV nodes, myocardium, arterioles/veins
• Parasymp- SA Node Neural signals to

**cardiovascular control center in medulla
Cardiovascular Physiology
• Change in flow, velocity, pressures
, resistance throughout CV system

• Flow constant, decrease in
velocity with increased crosssectional
area

• Pressure drop with blood
movement/friction along vessel
length
Capillaries
• Thin-walled, small-radius, extensively branched

• Sites of exchange
What allows for exchange
– Slow velocity – adequate exchange time

– Passive exchanges (diffusion and bulk flow)

• Diffusion (area, permeability, concentration gradient, diffusiondistance)

– Water-filled gaps (pores – aquaporins selective for H20)
– Some capillaries are more “leaky”, less with pericytes
– Lipid-soluble right through
Passive exchanges (diffusion and bulk flow)
• Hydrostatic Pressure (P) and Osmotic (oncotic)
Pressure
Driving forces into blood
– hydrostatic interstitial pressure (PIF)
– osmotic blood pressure
Driving forces out of blood
– hydrostatic blood pressure (PC)
– osmotic interstitial pressure (IF)
Lymphatic System: function
– Return of excess filtered fluid and protein
– Defense – nodes with lymphocyte aggregates
– Transport of absorbed fat
Structures
– Blind-ending capillaries (overlapping endothelial
cells) throughout IF
– Lymphatic vessels - drainage
– Drainage between
Veins: structures
– Capillaries to venules, to small/large veins
– Mostly collagen/little elastin (“valves” in larger veins)
– Variable muscular tissues
– Leaky in venules (inflammatory cells)
functions
– Large radius = little resistance
– “reservoir” – capacitance vessels
Factors which affect/enhance
venous return
– Gravity
– Initial blood pressure, cardiac “suction”
– Venous vasoconstriction
– Skeletal/respiratory muscle activity
(venous valves)
Blood pressure monitored/ regulated
– Provides adequate driving pressure (brain/organs)
– Prevents extra work
Primary determinants
– Cardiac output
– Total peripheral resistance

MAP = CO x TPR
Mean Arterial Pressure
• Constantly monitored by baroreceptors (pressure
sensors) within circulatory system

• Short-term control adjustments (secs)
– Adjustments made by alterations in cardiac output and total peripheral resistance
– Mediated by ANS influences on heart/vasculature

• Long-term control adjustments (minutes/days)
– adjusting total blood volume
– restoring normal salt and water balance via thirst, renal system (aldosterone/ADH)
Additional factors influencing CV function
• Left atrial receptors and hypothalamic osmoreceptors - longterm regulation of BP via plasma volume (ANP)

• Chemoreceptors (carotid/aortic bodies) are sensitive to low O2 or high acid levels in blood –increase respiratory activity

• Associated with certain behaviors and emotions mediated through cerebral-hypothalamic pathway

• Exercise modifies cardiac responses

• Hypothalamus controls skin arterioles for temperatureregulation
Cardiovascular Disease: Epidemiology:
• Over 300 risk factors associated with coronary heart disease, hypertension and stroke

• Approx. 75% CVD attributed to conventional risk factors

• Developing countries: 2X risks (undernutrition, infections+ CVD) Major modifiable
BP Abnormalities - Hypertension
• Definition: > 140/90 mm Hg

• Primary - Catch-all for increased BP by variety of unknown causes (vs single disease entity)
– Defects in renal Na regulation/excessive Na intake
– Diets low in K+ and Ca2+
– Plasma membrane abnormalities (defective Na+-K+ pumps)
– Gene variation for angiotensinogen
– Abnormalities in NO, endothelin, or other local-acting chemicals
– Excess vasopressin

• Secondary hypertension (10% cases) – renal, endocrine, neurogenic
Hypertension - complications
• Cardiac failure
• Atherosclerosis (stroke, heart attack)
• Spontaneous hemorrhage/aneurysm
• Renal failure
• Retinal damage
Cardiac failure:
• adaptive mechanisms to compensate for altered physiology

• deleterious structural changes with increased compensation

• Increased O2 demands of heart vs decreased blood supply

• Mismatch leads to ischemia (may lead to angina)
Congestive heart failure
• heart cannot pump or fill adequately

• division of circulation that requires most work usually the most affected

• where does blood back up?

• what could we expect from such a back-up??
Cardiac failure: causes
• Hypertension

• Myocardial infarction

• Additional causes:
Hypertension –
– Adaptive response to increased stretch (filling) and increased NE release/effects

– Both have immediate and long-lasting (trophic) effects on cardiac function
Myocardial infarction:
– Impaired cardiac muscle function – decrease “pump” capacity

– Damaged, non-regenerative muscle – scar formation leads to loss of tissue distensibility
Additional causes:
– Altered blood flow regulation (regurgitation)
• Valve incompetence
• Oxygenated blood flow to deoxygenated blood sources

– Valve stenosis
Pathophysiology: cardiac failure
• Septal defects
– Atrial (ASD)
– Ventricular (VSD)
– Patent ductus arteriosus

• Valvular diseases
– Mitral valve prolapse
– Aortic stenosis
form of arteriosclerosis (‘hardening’)
– intimal wall thickening

– collagen deposition, loss of elastic tissue (think tissue healing and scar formation)
formation of atheroma
– 1st stage - sub-endothelial accumulation of cholesterol (aka fatty streak)

– 2nd stage - smooth muscle migration, division, enlargement

– 3rd stage - plaque formation, calcification
Virchow’s triad
• Abnormality of vessel wall
(endothelium)

• Abnormality of blood flow

• Alterations in blood contents
Atherosclerosis (cont.)
primary cause of mortality, major cause of
morbidity
formation of thrombus
– roughened surface, damaged endothelium,
stagnant blood

– breaking off of thrombus??
will occlude blood flow downstream
– stroke, heart attack, arterial insufficiency

– if have one disease, obvious predisposition for
other
with arterial damage
weakening can lead to aneurysm

– out-pouching, held together by elastic lamina,
adventitia
– rupture – potential for massive blood loss
– other causes?? Genetic? Environmental?
Endothelial injury (heart and arteries)
• Direct injury
– Trauma to cardiac valves
– Hypertension (arteries)
– Cigarette smoking
– Hypercholesterolemia
– Radiation

• Abnormal flow
– Turbulence (heart and arteries)
– Stasis (veins)
Hypotension
Low blood pressure (BP < 100/60 mm Hg)
– There is too little blood to fill the vessels
– Heart is too weak to drive the blood
Orthostatic (postural) hypotension
– Transient (typically)
– insufficient compensatory responses to gravitational
shifts
Circulatory shock – when BP falls
– BP falls, inadequate flow to tissues
– Hypovolemic, cardiogenic, vasogenic, neurogenic
Venous insufficiency
• loss of valve integrity

• external dilations/ contortions of
superficial veins

• varicosites
varicosites
– chronic – genetic component, manifest in legs

– esophagus, anal plexus – secondary to portal hypertension

– hemorrhoids – pregnancy, constipation
Sustained venous hypertension
venous ulceration

10% population with valvular
incompetence, 0.2% with ulceration
Clinical features
• Pitting edema - preceded ulceration, greater later in day

• Hemosiderin pigmentation

• Lipodermatosclerosis – indurate, fibrotic subcutaneous tissue

• Atrophic, sweat gland/hair follicle loss
Atherosclerosis of peripheral
vasculature
arterial ulceration

– Other causes: diabetes, thromboangitis, vasculitis

– Resultant tissue hypoxia and damage
VENOUS insufficiency/ulceration
-Hemodeserin (brown discoloration)
-lipodermatosclerosis
Arterial insufficiency/ulceration
-Punch-out ulceration
-Champagne bottle deformity (can occur in either)
Systemic and localized edema
Regulation of fluid via oncotic vs. hydrostatic
pressures
Hydrostatic
Hydrostatic
• Increased BP
• Fluid accumulation/backup
– “Pump” failure
– Drainage failure
Oncotic
• altered plasma proteins
• albumin production
Diuretics
increase Na excretion (thiazides)
Sympatholytic drugs
–  blockers – vasodilation
–  blockers – decrease HR and contractility
Vasodilator drugs
(hydralazine, minoxidil)
Calcium antagonist drugs
– Verapamil and diltiazem act on heart and vessels to lower BP
– Nifedipine - lower BP only by vasodilation
– also used to treat angina pectoris and cardiac arrhythmias
ACE inhibitors
– inhibit formation of angiotensin II – less vasoconstriction

– decrease aldosterone release - decreased Na, H20 retention
Nitrites and nitrates
amyl nitrate, nitroglycerin

– NO - potent vasodilator of all blood vessels

– Raipdly decreases cardiac work, oxygen consumption

– Decrease BP may cause reflex tachycardia, dizziness, hypotention
Beta blockers
– decreases cardiac work, oxygen demands

– used prophylactically to prevent angina,

– Blunted HR responses to exercsie
Ca channel blockers
act on myocardium or vessels
CHF
• Digoxin and digitoxin
– Main effect: increase myocardial contractile force
• inhibit Na/K ATP pump, more Na inside myocardial cells
• Increased intracellular Na stimulates Na/Ca exchange,
• more Ca entry increases contractility
– Cardiac glycosides also decrease heart rate and
atrioventricular conduction (vagal stimulation)

• Also utilize diuretics, vasodilators to decrease work of heart