Cardiac Review

1) What are some non-pathological reasons for bradycardia? Pathological?

Non-pathological:
Athlete, Beta-blockers, Sleeping, Vagal response (bearing down)
Pathological:
Fluid overload, late hypoxia, Vagal stimulation
2) What are some non-pathological reasons for tachycardia? Pathological?
Non-pathological:
Exercise, Nicotine, Caffeine, Anxiety
Pathological:
Hypoxia, Respiratory distress, Fever
3) Cardiac Output = Heart Rate x Stroke Volume
a) HR x SV = __ CO
b) HR x SV = __ CO
c) HR x SV = __ CO
NOTE: Think about when the heart is beating WAAAY too fast. Does the heart have time to refill between each beat?
d)Normal CO is = 5 Liters/minute
4) You already know many factors that affect Heart Rate. What are the 3 factors that affect SV?
1. Preload: Amount of blood returning to heart and filling the atria
2. Afterload: Systemic vascular resistance
3. Contractility: How hard the heart can squeeze. (Ventricular compliance & filling pressures influence this)
5) Think about and describe some examples of how the 3 factors that determine SV would affect CO.
- Increased Preload, increased CO
- Increased Afterload, decreased CO
- Decreased Contractility, decreased CO (Contractility decreases with age)
- Increased Contractility, increased CO (more stretch in heart chambers, more contractility)

CARDIAC CONDUCTION SYSTEM (helps you understand some dysrhythmias)
How many bpm is the base rate for each node?

Sinoatrial (SA) node Atrioventricular (AV) node Bundle of His Purkinje fibers

ADULT CARDIAC ISSUES (PRIMARILY ACQUIRED)
6) Whats the difference between Atherosclerosis and Arteriosclerosis? What can be a resulting symptom or problem of
each?
Atherosclerosis: fatty build up of blockages within arteries
Arteriosclerosis: Hardening or thickening of arterial walls.
7) Cardiac Ischemia
Partial/temporary loss of blood flow
If it is severe enough to cause PAIN, it is Angina
If it is severe enough to cause CELL DEATH, it is Myocardial Infarction (Heart Attack)
NOTE: Chest pains are caused by build-up of lactic acid, just like when you are doing strenuous exercise and your
skeletal muscles are working so hard theyre using up the oxygen.
8) Heart Failure
Left Failure: Where is the blood backing up? So what are the symptoms? What is causing the blood to back up? So
what are some causes?
- Respiratory symptoms (Pink-tinged sputum, Difficulty breathing, Pulmonary hypertension, pulmonary edema,
crackles, orthopnea, nocturia)
- Hypertension , MI
Right Failure: Where is the blood backing up? So what are the symptoms? What is causing the blood to back up? So
what are some causes?
- Systemic symptoms (Ascites, Hepatomegaly, Edema, Increased Venous Pressure (jugular venous distention))
- Pulmonary diseases (Pulmonary hypertension, Emphysema); LEFT SIDED FAILURE
NOTE: Notice that some of the causes of one are possible symptoms of the other. Often, Left-sided failure can lead to
Right-sided failure.
9) What are some treatments for Angina? MI? Heart Failure?
Angina: aspirin therapy, Nitroglycerin, rest, oxygen, cholesterol-lowering drugs. Basically, anything that will increase
oxygen supply, decrease oxygen demand, and/or improve the underlying cause (arterial blockages usually!).
MI: Similar as for Angina, but also insert IV line and medicate for pain.
Heart Failure: Diuretics, vasodilators, ACE inhibitors, b-adrenergic blockers, Angiotensin II Receptor Blockers, Oxygen,
rest, pacemaker, heart transplant

Heart Failure
In the latest textbooks, the terminology has changed. It used to be called Congestive Heart Failure (CHF), but the new
term is just Heart Failure (HF). In this study guide we will use the term heart failure.

Review and define the terms:
Preload is the amount of blood returning to the heart from the body via the Vena Cava.
After load is the amount of resistance the heart must pump against to eject blood from the heart into the body.
Cardiac output = SV X R stroke volume times rate is the amount of blood circulated through the body in a minute.
Stroke volume is the amount of blood pump from each ventricle during contraction
Starlings Law of the Heart reflects the elasticity creating force of cardiac cells to contract. As heart goes into failure the
cells are stretch and dilated and so lose the ability to contract with efficient force. Think of a rubber band, the more it is
stretch and dilated the weaker it is and loses its recoil ability. This is the same physiology seen in heart failure.

How do the baroreceptors in the carotid arch influence hormone secretion in heart failure?
Baroreceptors sense the pressure with which the blood as ejected and fills the aorta. This is reflected in the blood
pressure. If the pressure is low, word is sent out to secrete hormones of the body to contract the arteries, and retain fluid
to fill the arteries thus raising the blood pressure.

Explain the role of these hormones in heart failure:
Adrenalin causes vasoconstriction of blood vessels leading to hypertension
Aldosterone binds with sodium to retain water and cause the symptom of edema
Antidiuretic Hormone closes the epithelial cells in the distal kidney tubule and thereby retains water that adds to the
symptoms of hypertension and edema.
Rennin is secreted by the juxtaglomulerus of the kidney in response to the request of the baroreceptors in the aortic
arch. Rennin then goes to the lungs to initiate the formation of Angiotensin I and II that will add to hypertension.
Angiotensin II goes to the cardiac cells to stimulate remodeling or the formation of immature cardiac cells that are not
able to contract with the force necessary to eject the volume of blood necessary for adequate stroke volume, thus the
cardiac output remains low and the heart continues into failure.

What is the physiology that causes the primary symptoms of dyspnea, edema, and fatigue in heart failure?
Dyspnea comes from lungs trying to compensate for decrease perfusion in alveoli.
Fatigue results from lack of oxygen and build up of carbon dioxide in cells as sluggish circulation cause tissues to not
have normal cleaning and perfusion.
Edema is a safety mechanism to third space fluid and decrease the work load of the heart pumping blood.

Why does PND paroxysmal nocturnal dyspnea occur primarily at night?
Edema fluid held in the legs during the day while a person is sitting, returns to the general circulation when the person is
horizontal in bed. This fluid causes overload and drowning sensation leading to symptoms of severe dyspnea, air hunger
and pulmonary edema.

Contrast the etiology of left and right sided heart failure.
Left sided heart failure occurs after MI, hypertension, or other causes that weaken the pumping ability of the left
ventricle. Occurs in response to resistance of blood pumping in afterload. Low blood flow over the carotid baroreceptors
triggers the compensatory hormone mechanisms or Adrenalin, Aldosterone, ADH and Rennin. Treatment is medication
to reduce afterload or intraortic balloon pump is person goes into shock.
Right sided heart failure deals with preload. The edema fluid is trying to return to the already full distended right
ventricle.
Think about it blood cant be pumped out to the body or lungs so ventricles are full of blood. Where is new blood
trying to ender the heart going to go? It backs up so jugular veins distend and A/V waves can be seen when the heart
contracts. The body employs safety measure of third spacing reducing the flow of blood back to the heart by pushing it
into the tissues by increased hydrostatic pressure. This is similar to when a river is full of water; the water overflows the
banks and seeps into the ground. Same thing in heart failure, the ground is the tissues of the body (pulmonary edema of
lungs, ascites from the liver, and pitting edema in the legs.

Differentiate Cor Pulmonale from right sided heart failure.
Right sided heart failure occurs with MI, Cor Pulmonale occurs from COPD as heart has to pump against the resistance of
lung tissue pathology.

Comparison of heart, kidney, and liver failure symptoms
Symptom heart kidney liver
Ascitesedema ADH, rennin, Aldosterone secretion,
venous congestion into right
ventricleIncreased hydrostatic pressure
ADH, rennin, Aldosterone secretion, venous
congestionLack of output
Decreased albuminPortal
hypertension, increased capillary
pressure, obstruction of venous
flow
hypertension ADH, rennin, Aldosterone secretion,
arterial congestion, edema, arterial
constriction
ADH, rennin, Aldosterone secretion, fluid retention Liver does not metabolize
aldosterone
breath acetone Fetor hepaticus
Change
sensorium
Decreased circulation and oxygen Increased nitrogen and acidosis Ammonia and nitrogen
hepatomegaly Venous engorgement Scar tissue, inflammation
puritis Uric acid crystals, uremic frost Bile salts and jaundice
anemia Low hemoglobin and oxygen carrying
power
Lack of erythropoietin Inability to metabolize
hemoglobin and clotting factors
Diagnostic labs H &H, BNPAldosterone BUN, creatinine, electrolytesCreatinine clearance AST, ALT, PT, BUN, A/G ratio
acidosis Decrease CO, inadequate tissue
perfusion, decrease oxygen exchange in
cells, lactic acidosis
Hydrogen retention
anorexia Venous stasis in the abdominal organs,
ascites
Toxins, ammonia Ascites, toxins
diet DASH, low sodium, cholesterol, low
triglycerides, and fluid restriction
Low sodium, potassium, protein, Giovanetti diet, fluid
restriction, high carbohydrate
High carbohydrate, low protein,
low sodium
hepatomegaly venous engorgement Inflammation, scar tissue
Treatments diuretics dialysis Diuretics, SPA







Dysrhythmias
Arrhythmia Whats wrong on the EKG? Treatment or medication What should the nurse do?
Normal sinus rhythm P,QRS and T normal time and
pattern
none Heart rhythm is stable
impulse is originated in SA
node and following normal
conduction to AV node,
bundle of HIS right and left
bundle branches and into the
perkinjie fibers.
Sinus bradycardia Normal P,QRS and T at slow
rate of 60 or below
Atropinepacemaker Obverse for adequate organ
perfusion
Sinus tachycardia Normal P,QRS and T at slow
rate of 100 or above
Beta blocker, correct the underlying problem Obverse for adequate organ
perfusion
PAC P,QRS and T normal time and
pattern the occur early, then
primary rate continues
None, observe Obverse for adequate organ
perfusion
A trial fibrillation Irregular R to R intervalNo p
wavesWavy baseline between
QRS
Digoxin, Amiodarone, Diltiazem,
Verapamil,Anticoagulant,cardioversion
Monitor for emboli blood
clots causing stroke or other
organ ischemia
Atrial flutter Saw tooth baseline between
QRS complex
Digoxin, Amiodarone, Diltiazem,
Verapamil,Anticoagulant,Cardioversion
observe
First degree heart block Prolong PR interval none Observe for further
progression
Second degree heart block
(Mobitz type II)
2:1 block of 2 or more P
waves before QRS (
Pacemaker if necessary observe
Second degree heart block
(WenckebachMobitz type I)
Lengthening of PR interval
before QRS until a beat is
dropped
Pacemaker if necessary observe
Third degree heart block Atria beat 60 to 100 times per
minute ventricles beat 20 to
40 beats per minute, two are
not related but go at their
own rate.
pacemaker Prepare for pacemaker and
do post operative teaching
PVC Wide bizarre QRS occur early
in cycle with compensatory
pause following T wave
Correct underlying problem,Lidocaine ,
Procainamide, Amiodarone, Magnesium Sulfate
Obverse for adequate organ
perfusion
Ventricular tachycardia Coiled spring QRS LidocaineProcainamideAmiodaroneMagnesium
Sulfate
Cardioversion

Obverse for adequate organ
perfusion
Ventricular fibrillation Bizarre baseline with no QRS Defibrillation and CODE for CPR Follow CODE protocol