Cardiac Evaluation:

Normal Values: Arterial Blood Gases

pH : 7.35 7.45
PaO2
95-100 mm Hg
PaCO2
35-42 mm Hg
Bicarbonate (HCO3-)
22-26 mEq/L
Base Excess
-2.4 to 2.3 mEq/L
Arterial O2 Saturation ( SaO2) 96-98%
Assessment:
Acidosis = respiratory or metabolic = increase in CO2, decrease in
bicarbonate
Alkalosis = Respiratory or metabolic = decrease in CO2, increase in
bicarbonate
Respiratory = CO2
Metabolic = bicarbonate
Kidneys or lungs.
Cardiac output: CO = HR x SV
Cardiac output: The amount of blood pumped by each ventricle in 1
minute.
Average: 4900-5000mL
Heart Rate: The number of contractions of the ventricles each minute
Average : 70 beats
Stroke Volume: The amount of blood ejected from each ventricle with
each contraction
Average: 70 mL
Factors affecting Cardiac output:
Sympathetic nervous system = epinephrine = HR
Venous return ( preload) blood volume = SV
Blood volume = SV
Sympathetic nervous system ( contractility) = SV
Peripheral resistance ( afterload) = SV
Conduction System:

Impulses to initiate cardiac contractions are conducted along specialized

myocardial fibers. NO NERVES are present in the cardiac muscle.
Cardiac muscle has intercalated discs at the junction between cardiac fibers.
These discs contain desmosomes, connectors to prevent muscle cells from
separating during contraction and gap junctions which allow ions to pass
from cell to cell = rapid transmission of impulses.
This specialized structure allows then all of the fibers of the two atria
to contract together and then the two ventricles to contract together. A
coordinated effort. A rhythm established = fills and empties with enough
force to sustain blood flow throughout the body.
ALL cardiac muscle can initiate impulses, but normally the conduction
pathway. originates at the SA sinoatrial node = the pacemaker located in the
right atrium.
You have a base rate called a sinus rhythm = 70 beats per minute.
Affected by the autonomic nervous system that innervate the SA node
and by circulating hormones such as epinephrine.
From the SA node, impulses then spread through the atrial conduction
pathways which results in contraction of both atria.
The impulses then collect at the AV node located in the floor of the right
atrium near the septum. There is a slight pause as the ventricles fill and them
the impulse continues though the bundle of His ( AV bundle). The right and
left bundle branches and the Purkinje network of fibers stimulates the
simultaneous contraction of the two ventricles.
Electrocardiogram.
Control of the heart:
Heat rate and force of contraction are controlled by the cardiac control
center in the medulla of the brain. Cardiac center is composed of two neural
pools. A cardioacceleratory center = sympathetic cardiac nerves to the SA
node AV node and myocardium. These nerves secrete norepinepherine ,
binds to beta-adrenergic receptors in the heart and increases the heart rate.
Peak is at 160-180 bpm SA node can not go any faster. At a high rate though
the ventircles dont fill
A cardioinhibitory center via the parasympathetic fibers in the vagas nerve to
the SA and AV nodes. The vagus nerve secretes acetylcholine which binds to
muscarinic receptors and opens K+ channels in the nodal cells. As K+ leaves
the cells the cells become hyper polarized and fire less frequently, so the

heart rate slows down. As low as 20 bpm. Heart on its own would go 100
bpm, but vegas nerve keeps it at about 70 bpm.
Think of all the things besides that that can affect love, lust, hate,
emotions, fear, fever, anxiety, breathing.
The baroreceptors in the walls of the aorta and internal carotid arteries detect
changes in blood pressure and alert the cardiac center. That then responds
through the stimulation of the sympathetic nervous system (SNS) or the
parasympathetic nervous system (PNS) to alter the rate and force of cardiac
contractions appropriately.
Proprioceptors in the muscle and joints = changes in physical activity. Heart
rate responds even before the metabolic demands of the muscles require it.
Chemoreceptors sensitive to blood pH, carbon dioxide, and oxygen are
found in the aortic arch, carotid arteries and medulla oblongata. Respiratory
control why do you breathe Oxygen = NO.
SNS, innervation increases heart rate ( Tachycardia) and contractility > 100
bpm
PNS or vagus nerve stimulation slow the heart rate ( Bradycardia) < 60 bpm
Factors that raise the heart rate are called positive chronotropic agents and
factors that lower it are negative chronotropic agents
Heart rate is affected by many chemicals. Epinephrine and norepinephrine =
cardiac nerves and adrenal medulla. These first bind to beta-adrenergic
receptors on the myocytes and trigger the intracellular production of the
second messenger cAMP , cyclic adenosine monophosphate
The sympathetic or beta, adrenergic receptors in the heart are an important
site of action for some drugs ( beta blockers).
CLASSES OF DRUGS:
ACE Inhibitors
Angiotensin-Converting Enzyme Inhibitors
These enzymes help the body to convert angiotensin I into angiotensin
II. ACE inhibitors are non-habit forming medications that block the effects

of angiotensin-converting enzymes, leading a reduced level of angiotensin II

in the body. Angiotensin II causes the constriction of blood vessels. Lower
levels = opposite effect = blood vessels relax and blood requires less force or
pressure to flow through ACE inhibitors are a type of vasodilator. These
lower blood pressure and reduce the workload of the heart.
Indications: Hypertension, heart failure and after heart attack. Affects
are within on hour if pill or liquid = almost immediately if IV.
Alone or in combination ( diuretics, other calcium channel blockers,
beta blockers etc. ) NSAIDS may reduce effect. Can end up with an
increased K+ level.
Angiotensin II receptor Blockers (ARBs)
These are different from ACE inhibitors..
These work specifically on the receptors. Not the conversion. Different.
Same effect, but different point of actionrelatively new.
These act directly buy inhibiting the action of A-II by blocking it from
entering the angiotensin II receptors in the smooth muscle of the heart and
blood vessels. Again a vasodilator.
They are NOT interchangeable with ACE inhibitors. ARBs are more reliable
for consistency. COST $$$$$$$$ do not have the dry cough side effect.
Not the first drug of choice.
Beta Blockers
First used in the 1960s used on the stress response. Blocks the
actions of the sympathetic nervous system. They block the beta receptors.
Pretty mellow people. Stress for talks.. Beta blockers relieve cardiac
stress by slowing the heart rate and reducing the force of heart muscle
contractions. They also reduce blood vessel constriction in the heart, body
and brain.
Two types beta receptor I, beta receptor 2.
Selective beta antagonists only block beta 1 receptors, more
commonly used for treating cardiac conditions.
Non-selective beta antagonists block beta 1 and beta 2 receptors. Have
the potential to worsen bronchoconstriction ( asthma) and peripheral
vascular disease.
Dosing plays a major role in how they will affect in the body. Affect
1-4 hours.
Begin low and work your way up . Light headedness, heart failure.
Cough and cold medication.!!! Big deal, dramatic rise in blood pressure.
NSAIDS conflict.

Calcium Channel Blockers

Wide use by 1980s, ( CCBs or calcium antagonists) are non-habit
forming and used to treat high blood pressure and reduce the workload on
the heart. Calcium is considered an excitatory element, with its entry into
certain kinds of cells, it causes them to contract.
Arterial smooth muscle cells and cardiac muscle cells are sensitive to
calcium. During a normal heartbeat, voltage sensitive channels open in the
heart allowing calcium ions to flow into cells, which causes them to contact.
By blocking this flow of calcium ions, it is possible to reduce the contractile
force of the heart and arteries. This relaxes them, reducing blood pressure
and increasing the supply of oxygen-rich blood to the heart. Calcium
channel blockers are considered a kind of vasodilator.
Dosage by capsule usually and effect within 1-2 hours. More widely
used in the past. Newer drugs now in use, but still effectie.
Organized into four categories
a. Dihydopyridines most potent, most side effects.
b. Virapamil dont sue with a beta blocker makes heart failure
worse. Weakest of them all.
c. Diltiazem, in between vasodilation, best tolerated.
d. Bepridil not used in US.
Again can be prescribed in combination with others.
Inotropes
Inotropes are non-habit forming medications that strengthen the contractions
of the heart so the heart can pump more blood with fewer beats. As a result
the heart does less work with more demands of the body. Dosage may take
up to a week for effect. So we use a loading dose to help that out. Several
health food herbs contain this. FOXGLOVE.
Digitalis and Digoxin.
Diuretics
Non-habit forming medication that stimulates the kidneys to produce more
urine, flushing excess fluids and minerals ( sodium) from the body.
Edema, Loop diuretics, produces the greatest increase in urine flow.
More sodium to be absorbed. Heart failure
Thiazide increase sodium and chloride. Heart patients . High blood
pressure medication.

Osmotic diuretics they draw fluid from the cells of the brain and eyes.
And toxins, clears them.
Potassium sparing diuretic, liver function testing.
Action is within hours, you will see increased urine flow. Other solutes fom
the body: Sodium , potassium, calcium, magnesium, chloride, phosphorus,
uric acid and of course water to make the urine.
Nitrates = Nitroglycerine
Used for more than 100 years. They are commonly used to prevent
and relieve angina, a type of chest pain. The main symptom of coronary
artery disease is chest pain, pressure or discomfort. Nitrates deal with this by
addressing the lack of oxygen-rich blood to the heart (cardiac ischemia).
They widen the blood vessels, by relaxing the smooth muscles , most
notably the muscles of the heart and blood vessels. As a result, pressure on
blood vessel walls is reduced, which allows more blood to circulate with less
effort by the heart. Nitrates affect veins as well as arteries, but less
pronounced.
Lots of delivery methods. Spray under the tongue, tablets, patches,
IV.
Heart attack = myocardial infarction.
Heart failure
After stenting
Pulmonary hypertension.
Pharmacogenetics your own specific DNA genetic code with your
specific receptors a specific medication that will work on just those
areas as opposed to systemic dosing.