Test 3

Front 1

In atrial ES the

Back 1

P wave is deformed but the QRS complex is normal.

Front 2

In nodal extrasystole,

Back 2

the P wave is thus negative and is either masked by the QRS wave or appears shortly after it. Because in supraventricular extrasystole the sinus nodes often also depolarize.

Front 3

Ventricular premature complexes (VPCs)

Back 3

are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular
In this case the QRS complex of the ES is deformed.

Front 4

Two common mechanisms exist for VPCs,

Back 4

1. Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium.2. Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. The slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI.

Front 5

Premature ventricular contraction causes

Back 5

List of possible causes:

Ischemia
Certain medicines such as digoxin, which increases heart contraction
Myocarditis
Cardiomyopathy hypertrophic or dilated
Hypoxia
Hypercapnia (CO2 poisoning)
Mitral valve prolapse
Smoking
Alcohol
Drugs such as cocaine
Caffeine
Magnesium and potassium deficiency
Calcium excess
Thyroid problems
Heart attack

Front 6

Premature ventricular contraction symptoms

Back 6

Chest pain Faint feeling FatigueHyperventilation (after exercise)

Front 7

Frequent episodes of continuous PVCs becomes a form of

Back 7

ventricular tachycardia (VT), which is a rapid heartbeat, because there is an extra electrical impulse, causing an extra ventricular contraction.

Front 8

Treatment of Ventricular extrasystole (premature Ventricular Contraction (PVC)

Back 8

1. restoring the balance of magnesium, calcium and potassium within the body. 2. Pharmacological agents

Front 9

Pharmacological agents class I

Back 9

Sodium channel blockers . Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials. Lidocaine, Phenytoin.

Front 10

Class II agents

Back 10

Beta blockers. They act by blocking the effects of catecholamines at the β1-adrenergic receptors, thereby decreasing sympathetic activity on the heart. They decrease conduction through the AV node.Class II agents include atenolol, propranolol, and metoprolol.

Front 11

Class III agents

Back 11

Block the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. Sotalol

Front 12

Class IV agents

Back 12

Calcium channel blockers. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.Class IV agents include verapamil and diltiazem.

Front 13

Atrial Tachycardia

Back 13

Atrial tachycardia is a rhythm disturbance that arises in the atria. Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular.

Front 14

Ventricular Tachycardia

Back 14

It results from a rapid sequence of ectopic ventricular impulses. Beginning with ES. Ventricular filling and cardiac output decrease and ventricular fibrillation can even ensue, that is a high frequency uncoordinated twitching of the myocardium. Unless treated the failure to eject blood can be just as dangerous as cardiac arrest.with a rate between 120 and 250 beats per minute.

Front 15

First degree AV node block

Back 15

PR interval exceeds 0.20 second

Front 16

Second degree AV node block

Back 16

occurs when the AV node is damaged so severely that only one out of every two, three, or four atrial electrical waves can pass through to the ventricles.
ECG: P waves without associated QRS waves.

Front 17

Third-degree, or complete, AV node block,

Back 17

non of the atrial waves can pass through the AV node to the ventricles. Result is bradycardia.

Front 18

There are two principal types of myocardial cells

Back 18

contractile, and nodal/conducting cells

Front 19

contractile cells

Back 19

which have similar features to skeletal muscle cells

The contractile cells of the heart contain the same contractile proteins actin and myosin arranged in bundles of myofibrils surrounded by a sarcoplasmic reticulum.
They differ from skeletal muscle by having only one nucleus but far more mitochondria. These cells are extremely efficient at extracting oxygen; they extract roughly 80% of the oxygen from the passing blood

Front 20

nodal/conducting cells

Back 20

that have features similar to nerve cells

Front 21

Steps in excitation-contraction coupling

Back 21

PP C slide 17

Front 22

contractility

Back 22

-is the intrinsic ability of the cardiac muscle to develop force at a given muscle length. It is also called inotropism.
-is related to the intracellular Ca2+ concentration.
-can be estimated by the ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%).

-Positive inotropic agents produce an increase in contractility.
-Negative inotropic agents produce a decrease in contractility.

Front 23

Factors that increase contractility (positive inotropism)

Back 23

1. Increased heart rate
2. sympathetic stimulation
3. Cardiac glycoides (digitalis)

Front 24

Factors that decrease contractility (negative inotropism

Back 24

Parasympathetic (Ach) via muscarinic receptors

-decrease the force of concentration in the atria by decreasing the inward Ca2+ current during the plateau of the cardiac action potential.

Front 25

preload

Back 25

the volume of blood in the ventricle at the end of diastole phase (relax) before it contracts. End diastolic Volume. Is about 140 mL

Front 26

afterload

Back 26

the pressure that exists in the aorta or pulmonary trunk

Front 27

End Systolic volume

Back 27

the volume of blood that remains in the ventricle after ejection. Approximately 70 mL

Front 28

stroke volume

Back 28

the volume of blood ejected into the aorta by ventricular contraction. Approximately 70 mL
Stroke volume= EDV-ESV

Front 29

sarcomere length

Back 29

determines the maximum number of cross-bridges that can form between actin and myosin.
-determines the maximum tension, or force of contraction.

Front 30

Velocity of contraction at a fixed muscle length

Back 30

Velocity of contraction is maximal when the afterload is zero.
- Velocity of contraction is decreased by increases in afterload.

Front 31

Length-tension relationship in the ventricles

Back 31

1. Preload
2. afterload
3. sarcomere length
4. Velocity of contraction at a fixed muscle length
5. Frank-Starling relationship

Front 32

Frank-Starling relationship

Back 32

PP C slide 21

Front 33

Steps 1-2

Back 33

(isovolumetric contraction)

Front 34

Steps 2-3

Back 34

ventricular ejection

Front 35

Steps 3-4

Back 35

isovolumetric relaxation

Front 36

Steps 4-1

Back 36

ventricular filling

Front 37

Increased preload (use pictures)

Back 37

refers to an increase in end-diastolic volume and is the result of increased venous return.
-causes an increase in stroke volume based on the Frank-Starling relationship.
-The increase in stroke volume is reflected in increased width of the pressure-volume loop.

Front 38

Increased afterload

Back 38

refers to an increase in aortic pressure.
-The ventricle must eject blood against a higher pressure, resulting in a decrease in stroke volume.
-The decrease in stroke volume is reflected in decreased width of the pressure-volume loop.
-The decrease in stroke volume results in an increase in end-systolic volume.

Front 39

Increased contractility

Back 39

-The ventricle develops greater tension than usual during systole, causing an increase in stroke volume.
-The increase in SV results in a decrease in end-systolic volume.

Front 40

stroke volume

Back 40

is the volume ejected from the ventricle on each beat.

Stroke volume= End-diastolic volume - End-systolic volume

Front 41

cardiac output

Back 41

CO= Stroke volume x Heart rate

Front 42

ejection fraction

Back 42

is the fraction of the end-diastolic volume ejected in each stroke volume.
-is related to contractility.
-is normally 0.55, or 55%.

EF = Stroke volume
End-diastolic volume

Front 43

Cardiac O2 consumption

Back 43

is directly related to the amount of tension developed by the ventricles

Front 44

Cardiac O2 consumption is increased by

Back 44

Increased afterload (increased aortic pressure)
Increased size of the heart
Increased contractility
Increased heart rate

Front 45

cardiac cycle ejection

Back 45

In order for blood to be ejected from the heart, the pressure in the ventricles must be greater than the pressure in the aorta. When the pressure in the left ventricle rises above 80 mmHg (which is the pressure in the aorta), the aortic valve opens.Immediately, blood pours out of the ventricles, while the pressure continues to increase to 120 mmHg. The period during which the ventricles empty blood into the aorta is known as the ejection period.

Front 46

The first heart sound is produced

Back 46

indirectly) by the closure of the AV valves; it is of low pitch and of relatively long duration.

Front 47

The second heart sound is produced

Back 47

indirectly) by the closing of the aortic and pulmonary semilunar valves; this is of high pitch and of relatively smaller duration.

Front 48

A third heart sound

Back 48

sometimes occurs in the middle of diastole. This is caused by blood flowing with rumbling motion into the almost filled ventricles; it is difficult to hear with a stethoscope.

Front 49

Cardiac Output

Back 49

the amount of blood each ventricle can pump in one minute. At rest, the cardiac output is roughly 5 liters (1.3 gallons) of blood every minute.

Front 50

stroke volume

Back 50

is the amount of blood pumped by one ventricle during one contraction/heartbeat.

Front 51

At rest the heart rate is ____ and stroke volume is ____

Back 51

70 beats per min and 70mL/beat

Front 52

The Control of Heart Rate

Back 52

PP C slide 32

Front 53

Atherosclerosis

Back 53

is patchy intimal plaques (atheromas) in medium and large arteries; the plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue. This disease happens when the arteries get blocked by fats and cholesterol.

Front 54

Atherosclerosis causes

Back 54

Dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension Smoking The hallmark of atherosclerosis is the atherosclerotic plaque, which contains lipids (intracellular and extracellular cholesterol and phospholipids) inflammatory cells (eg, macrophages, T cells) smooth muscle cellsconnective tissue (eg, collagen, elastic fibers)thrombiCa++ deposits.

Front 55

Atherosclerosis symptoms complications

Back 55

Shortness of breath Tightening pain in the chestComplications: Strokes Damage of muscles, body organs and blood vessels Deficiency of blood supply due to obstruction (angina)

Front 56

Atrial fibrillation and flutter

Back 56

are abnormal heart rhythms in which the atria are out of sync with the ventricles.

Front 57

In atrial flutter, the atria

Back 57

beat regularly and faster than the ventricles.

Front 58

In atrial fibrillation,

Back 58

the heart beat is completely irregular. The atrial muscles contract very quickly and irregularly; the ventricles beat irregularly but not as fast as the atria.

Front 59

Causes of atrial fibrillation and flutter

Back 59

In most cases, the cause of atrial fibrillation and flutter:
many types of heart disease
stress and anxiety
caffeine
alcohol
tobacco
diet pills
open heart surgery

Front 60

Heart murmurs

Back 60

are generated by turbulent flow of blood, which may occur inside or outside the heart. Murmurs may be physiological (benign) or pathological (abnormal).

Front 61

Abnormal murmurs causes

Back 61

Stenosis restricting the opening of a heart valve, causing turbulence as blood flows through it. Valve insufficiency (or regurgitation) allows backflow of blood when the incompetent valve is supposed to be closed.

Front 62

ECG Electrodes

Back 62

They are bipolar (i.e., they detect a change in electric potential between two points) and detect the electrical potential change in the frontal plane.  

Lead I: is between the right arm and left arm electrodes, the left arm being positive.

 Lead II: is between the right arm and left leg electrodes, the left leg being positive.

 Lead III: is between the left arm and left leg electrodes, the left leg again being positive.

Front 63

Chest Electrode Placement

Back 63

V1: Fourth intercostal space to the right of the sternum
.V2: Fourth intercostal space to the Left of the sternum.
V3: Directly between leads V2 and
V4.V4: Fifth intercostal space at midclavicular line
.V5: Level with V4 at left anterior axillary line.
V6: Level with V5 at left midaxillary line. (Directly under the midpoint of the armpit)

Front 64

Chest Leads
a. V1 & V2
b. V3 & V4
c. V5 & V6

Back 64

a. Right Ventricle
b. Septum/Lateral Left Ventricle
c. Anterior/Lateral Left Ventricle

Front 65

Myocardial infarction

Back 65

The blood supply to certain areas of the myocardium is obstructed. The muscle tissue at the center of the infarct dies off.

Front 66

Myocardial infarction diagnostic criteria

Back 66

1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes. 
2. Changes in serial ECG tracings.
3. Rise and fall of serum cardiac biomarkers such as creatine kinase -MB fraction and troponin T and I and myoglobin, Lactate dehydrogenase as they are more specific for myocardial injury. (The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks).
4. If there is a high positive R, there is also a Larger negative Q waves, ST segment elevation or depression, or coronary intervention are diagnostic of MI.

Front 67

Myocardial infarction treatment

Back 67

A MI is a medical emergency which requires immediate medical attention. Oxygen, aspirin, and nitroglycerin.

Front 68

Endocarditis is

Back 68

inflammation of the inside lining of the heart chambers and heart valves (endocardium). Endocarditis is usually a result of a blood infection. Bacteria or other infectious substance can enter the bloodstream during certain medical procedures, including dental procedures, and travel to the heart, where it can settle on damaged heart valves.

Front 69

The following increase chances for developing endocarditis:

Back 69

-Artificial heart valves -Congenital heart disease (atrial septal defect, patent ductus arteriosus)-Heart valve problems (such as mitral insufficiency). -History of rheumatic heart disease.

Front 70

Endocarditis treatment

Back 70

Long-term, high-dose antibiotic treatment is needed to get rid of the bacteria. Treatment is usually given for 4-6 weeks, depending on the specific type of bacteria. Blood tests will help your doctor choose the best antibiotic.Surgery may be needed to replace damage heart valves.

Front 71

Mitral Stenosis

Back 71

Mitral stenosis is a heart valve disorder that involves the mitral valve. Stenosis refers to a condition in which the valve does not open fully, restricting blood flow.

Front 72

Mitral Stenosis causes

Back 72

the valve area becomes smaller, less blood flows to the body. The upper heart chamber swells as pressure builds up. Blood may flow back into the lungs. Fluid then collects in the lung tissue (pulmonary edema), making it hard to breathe.

-Rheumatic fever
-Congenital mitral stenosis

Front 73

Mitral regurgitation

Back 73

is a long-term disorder in which the heart's mitral valve does not close properly, causing blood to flow backward (leak) into the upper heart chamber when the left lower heart chamber contracts. The condition is progressive, which means it gradually gets worse.

Front 74

Cardiac output is distributed among various organs

Back 74

Cerebral=15%

Coronary=5%

Renal=25%

Gastrointestinal=25%

Skeletal muscle=25%

Skin=5%

Front 75

Proximal tubule Na

Back 75

reabsorb 2/3, or 67%, of the filtered Na+ and H2O, more than any other part of the nephron.

Front 76

Thick ascending limb of the loop of Henle

Back 76

reabsorbs 25% of the filtered Na+.

Front 77

Distal tubule and collecting duct

Back 77

together reabsorb 8% of the filtered Na+.

Front 78

Principal cells

Back 78

reabsorb Na+ and H2O.-secrete K+.-Aldosterone increases Na+ reabsorption and increases K+ secretion.-Antidiuretic Hormone increases H2O permeability by directing the in secretion of H2O channels in the luminal membrane. In the absence of ADH, the principal cells are virtually impermeable to water.

Front 79

2. alpha Intercalated cells

Back 79

-secrete H+ by a H+ adenosine triphosphatase (ATP ase), which is stimulated by aldosterone.-reabsorb K+ by a H+, K+-ATPase.

Front 80

Proximal tubule K

Back 80

reabsorbs 67% of the filtered K+ along with Na+ and H2O.

Front 81

Thick ascending limb of the loop of henle

Back 81

reabsorbs 20% of the filtered K+.

Front 82

urea

Back 82

-Fifty percent of the filtered urea is reabsorbed passively in the proximal tubule.Rest are impermeable.-ADH increases the urea permeability of the inner medullary collecting ducts.

Front 83

phosphate

Back 83

Eighty-five percent of the filtered phosphate is reabsorbed in the proximal tubule by Na+-phosphate cotransport. 15% of the filtered load is excreted in urine.-Parathyroid hormone inhibits phosphate reabsorption in the proximal tubule by activating adenylate cyclase, PTH causes phosphaturia and increased urinary cAMP.

Front 84

Calcium

Back 84

Sixty percent of the plasma Ca+ is filtered across the glomerular capillaries.-Together, the proximal tubule and thick ascending limb reabsorb more than 90% of the filtered Ca+ by passive processes that are coupled to Na+ rabsorption.-Together, the distal tubule and collecting duct reabsorb 8% of the filtered Ca+ by an active process.*PTH increases Ca+ reabsorption by activating adenylate cyclase in the distal tubule.

Front 85

magnesium

Back 85

-is reabsorbed in the proximal tubule, thick ascending limb of the loop of Henle, and distal tubule.-In the thick ascending limb, Mg2+ and Ca+ compete for reabsorption; therefore, hypercalcemia causes an increase in Mg2+ excretion (by inhibiting Mg+ reabsorption ).