Pain in chest, neck, back, jaw, arms and shoulders

Dyspnea

Palpitations

Syncope

Edema

Which structure in the body has all these functions:

Blood tissue interchange

Control of coagulation and clotting

Vessel repair

Modulation of blood flow

Inflammation regulation

Cell growth regulation 

Oxidation of LDL

Right Coronary artery

Left Coronary artery

Mitral and Tricuspid valves

Systole is when the heart emptys, so think MT =Mitral and tricuspid

Ventricle walls relax

Atrial walls fill with blood and then contract, forcing it into the ventricles.

The mitral and tricuspid valves are open during diastole,

the pulmonary and aortic valves are closed

If there is lots of venous return the ventricles will be stretched more. 

This causes more forceful and rapid ventricular contraction

Arterial pressure

Blood thickness

Vessel elasticity

Calcium

B1 system

The SA node is the primary 'pacemaker,' but if necessary the AV node can depolarize spontaneously

Also, the ventricles can depolarize spontaneously

SA node

to

Atria and AV node

to

Bundle of His

to

Purkinje fibers

to 

Ventricles

1. Stimulates B-1 receptors of SA and AV node to increase heart rate

2. Shortens conduction time thru AV node

3. Increases calcium which in turn increases contractility

Name 2 ways that the parasympathetic affects cardiac output.

1. Decreased heart rate thru nodes

2. Increased conduction time

Resulting in decreased cardiac output

Inside=negative charge

Outside=Postive charge

The pump pulls 3 Na+ out for every 2 K+ it puts in. 

In addition to this K leaks out of the cell

Net removal of positive charge, making the inside negative. 

Na channels close

K channels open

K rushes OUT of the cell, making the inside of the cell excessively negative. 

K gates close

Cell equalizes to resting potential via pumps and permability

Natural leakiness of cell membrane to Na and Ca, 

eventually enough Na gets in to start the depolarization

The Ca enters the cell slowly and it's channels close slowly.

Thus even when the K leaves, Ca is still there so cell is still depolarized.

Cell repolarizes when both Ca and K channels close

Cells are smaller than skeletal muscle

Cell membranes are fused together

1. It makes depolarization last longer

2. It increases contractility

The influx of Ca causes the release of even more Ca from the sarcoplasmic reticulum and mitochondria.

The increased concentration of unbound Ca causes increased contraction

It causes slower conduction through the AV node, thereby decreasing heart rate

Also increases intracellular concentration of Ca, thereby increasing contractility

1. Blurred vision

2. Altered color perception

3. Haloes on dark object

Interfere with sodium-potassium pump

Block calcium channels

Interfere with autonomic nervous system

1. Delays influx of calcium into smooth muscle cells of vascular system

2. Decreases contractility

3. Delays removal of calcium from pacemaker cells

Decreased heart rate

decreased contractility

slower conduction time

Creatine phosphokinase

Lactate dehydrogenase

Troponin I

Creatine phosphokinase

Troponin I

Detect pressures

Detect patterns of blood flow

Dye is injected into the bloodstream/heart chamber

X rays are taken to evaluate blood flow

Coronary Calcium scans show deposits of Ca in the heart which can be markers for atherosclerosis.

The scoring indicates the pt's risk for developing coronary artery disease (>100)

1. Scan only picks up Ca, no cholesterol deposits

2. Involves high doses of radiation

Pt exercises on treadmill while being monitored with ECG, BP and pulse monitors.

Changes in the feedback indicate presence and severity of ischemia. 

MUGA scan

Multiple Gated Acquisition Scan

Radioactive Thallium is injected into veins

Scans are used to measure the concentrations of thallium in the heart

Damaged heart tissue does not take up the isotope-"cold spot"

Regular refers to simply a timing issue, like too fast or too slow.

Irregular refers to missed beats, the rhythm is disrupted. These are more concerning since they have a greater effect on cardiac output

Sinus tachycardia

Atrial fibrillation

Paroxysmal supraventricular tachycardia

Exercise

Enhanced catecholamine release (fear, flight, fight etc.)

Anemia

Hyperthyroidism

Heart failure

Beta Blockers

Calcium channel blockers

Atrial fibrillation is:

a. Regular Irregularity

b. Irregular Regularity

c. Irregular Irregularity

c. an Irregular Irregularity

The vessels signal the depolarization with  no rhythm, thus the atria contract with no pattern and the ventricles do so as well.

HTN

HF

Rheumatic heart disease

Excessive alcohol

Thyrotoxicosis

Which of these is NOT listed as a cause of Atrial fibrillation?

a. Rheumatic heart disease

b. Hypertension

c. Diabetes

d. Cigarette smoking

e. Thyrotoxicosis

1. Severe Ischemic stroke

2. Embolization

3. Dementia, even w/o stroke

The blood is not sent out from the heart effectively. Thus embolisms can occur due to blood pooling in the heart chambers.

Dementia can occur as a result of poor oxygen supply to the brain due to disrupted cardiac output

1. Meds to slow ventricular contractions

2. Meds to prolong action potentials

3. Anti-coagulative therapy

Amiodarone (Cordarone)

Dronedarone (Multaq)

Vernakalant is under investigation

Warfarin (Coumadin)

Dabigatran (Pradaxa)

1. Corneal microdeposits (whorl keratopathy) 90%

2. Disc edema

3. Optic neuritis

4. Lens opacities

Perform a baseline exam, careful recording of all structures

Recheck every 6 months for whorl keratopathy, neuritis , edema and opacities in the lens

Amiodarone

Acetaminophen

T/F

Optic Neuritis due to amiodarone happens to many patients and will resolve once the drug is discontinued

False

Optic neuritis is rare but permanent

T/F

The lens opacities that result from Amiodarone generally do not affect vision

Subconjunctival hemorrhage

Spontaneous hyphema

Retinal/vitreous hemorrhage

Cerebral hemorrhage

Send them for clotting studies

Contact their PCP or cardiologist to monitor for cerebral hemorrhage

There are two functionally different paths through the AV node. 

One is a slow pathway with a short refractory period. The other is a faster pathway (faster conduction) with a longer refractory period, atrial impulse usually conducts thru this one. 

However, if the atrial impulse happens too soon the normal, fast pathway is still in refractory period. 

Then the slow pathway will propogate the impulse. By the time it reaches the ventricles the fast pathway has recovered so the impulse travels back through it. 

Their target is to stimulate the vagus nerve

1. Carotid sinus massage - increase parasympathetic

2. Valsalva maneuver

3. Head immersion in cold water

Age

Alcohol

Emotional Stress

Caffeine

Infection 

Tobacco

Sustained Ventricular tachycardia

Ventricular fibrillation

There is no order to the contraction of the ventricles, causing a rapid and irregular heart rate.

Results in virtually no cardiac output, which can cause death without resolution

Inadequate SA node activity

Blocked conduction

Age 

Medications (like beta blockers and calcium channel blockers)

1st- longer conduction time, but impulse does make it to ventricles-no symptoms or tx

2nd-sometimes the impulse does not make it to the ventricles -->Pacemaker

Virtually no atrial impulses reach the ventricles.

The ventricles may contract spontaneously, but at a very slow rate

Treated with pacemaker

Hypertensive retinopathy

Retinal Artery emboli

Anterior Ischemic Optic neuropathy

Retinal Vein/Artery Occulsion

Time of Day

Level of anxiety (white coat)

Recent activity

Caffeine intake

What systolic measure of BP puts a pt in the category

"Stage 2 Hypertension"?

What diastolic measure of BP puts a pt in the category

"pre-hypertension"

What diastolic measure of BP puts a pt in the category

"Stage 2 Hypertension"

BP of 163/102

Category?

BP of 125/98

Category?

Atherosclerosis

Coronary artery disease

Heart failure

Left Ventricular HYpertrophy

MI

Could cause

Stroke

Alzheimer's disease

Peripheral Resistance

Cardiac output

Vessel size

Vessel elasticity

Blood viscosity

Juxtaglomerular cells

Systemic Baroreceptors (in aortic arch, carotid, pulmonary vessels)

How does the body interpret increased Co2 and H in the blood?

How does it respond?

Interprets high levels as inadequate tissue perfusion

Responds by increasing sympathetic brain stem activity

The removal of salt from the body, 

impairment can cause hypertension

1. defective renal excretion of salt

2. Altered renin-angiotensin-aldosterone system

3. adrenal or pituitary tumor

4. Thyroid disease

5. Sleep apnea

6. Sleep deprivation

7. Medications

Oral Contraceptives

Steroids

NSAIDs (except ASA)

Cold remedies

Appetite suppressants

Tricyclic antidepressants

Reduced cardio risk

Decreased stroke incidence

Decresed MI incidence

Decreased heart failure incidence

Smoking cessation

Dietary restriction/regulation of things like sodium, potassium, calcium, magnesium, vitamins etc. 

Weight loss and exercise

Limitation of alcohol intake

Dark Chocolate

Laughter