Ch 20 Cardiovascular System Questions

Front 1

CHAPTER 20 CARDIOVASCULAR REVIEW QUESTIONS

Back 1

CHAPTER 20 CARDIOVASCULAR REVIEW

Front 2

WHAT IS THE STUDY OF THE HEART CALLED?

Back 2

CARDIOLOGY

Front 3

THE HEART HAS TWO PUMPS IN ONE. WHAT ARE THEY?

Back 3

1. PULMONARY CIRCULATION
2. SYSTEMIC CIRCULATION

Front 4

HOW MUCH BLOOD DOES THE HEART PUMP:
PER DAY?
PER MIN?
DURING EXERCISE?

Back 4

7200L PER DAY
AT 5L PER MINUTE
DURING EXERCISE INCREASES SEVERALFOLD.

Front 5

WHAT ARE THE 4 FUNCTIONS OF THE HEART?

Back 5

1. GENERATING BLOOD PRESSURE
2. ROUTING BLOOD
3. ENSURING ONE-WAY BLOOD FLOW
4. REGULATING BLOOD SUPPLY

Front 6

WHAT ARE THE LAYERS OF THE HEART?

Back 6

PERICARDIUM->FIBROUS
->SEROUS->PARIETAL
->VISCERAL

-PERICARDIAL CAVITY

Front 7

WHAT HAPPENS WHEN THE SEROUS PERICARDIUM BECOMES INFLAMED?

Back 7

PERICARDITIS
STAGE 1 __ SEROUS FLUID->FRICTION
STATE 2 __ SEROUS FLUID->HEART COMPRESSION

Front 8

WHAT ARE THE LAYERS OF THE HEART WALL?

Back 8

EPICARDIUM
MYOCARDIUM
ENDOCARDIUM

Front 9

BE ABLE TO IDENTIFY AND DESCRIBE THE ATRIA, VENTRICLES, AND VESSELS OF THE HEART.

Back 9

1.ATRIA-UPPER THIN WALLED;
-INTERATRIAL SEPTUM (SEPARATES LEFT & RIGHT)
2.VENTRICLES- LOWER CHAMPBERS OF THE HEART,THICK, LEFT THICKER THAN THE RIGHT,INTRAVENTRICULAR SEPTUM(SEPARATES THE LEFT FROM RIGHT)
-PAPILLARY MUSCLES CAUSE VENTRICULAR CONTRACTION
3. VALVES- TRICUSPID (RIGHT AV)
- BICUSPID (MITRAL LEFT AV)
4. VESSELS-
-PULMONARY VEIN- CARIES BLOOD FROM LUNGS TO HEART *ONLY VEIN THAT CARRIES O2 RICH BLOOD.
-PULMONARY ARTERY-HEART TO LUNGS
-SUPERIOR VENA CAVA- COLLECTS IN HEAD AND NECK
-INFERIOR VENA CAVA-COLLECTS BLOOD FROM LOWER REGIONS OF THE BODY.

Front 10

WHAT ARE THE LAYERS OF AN ARTERY?

Back 10

1. TUNICA INTIMA
- INNER MOST LAYER
- SIMPLE SQUAMOUS
- RESTS ON BASEMENT MEMBRANE
- ELASTIC PROPERTIES (LAMINA)
2. TUNICA MEDIA
-MIDDLE LAYER
-RESTS ON BASEMENT MEMBRANE
-THICKEST
-CIRCULAR SMOOTH MUSCLE & ELASTIN
-VASODILATED (INCREASE BLOOD VESSEL DIAMETER)
-VASOCONSTRICTION (DECREASE BLOOD VESSEL DIAMETER)
3. TUNICA ADVENTITIA- OUTER MOST; COLLAGEN

Front 11

WHAT ARE THE LAYERS OF A CAPILLARY?

Back 11

-LINING OF SIMPLE SQUAMOUS ENDOTHELIUM
-WALLS CONSISTS PRIMARILY OF ENDOTHELIAL CELLS WHICH REST ON A BASEMENT MEMBRANE
-OUTSIDE OF MEMBRANE DELICATE LAYER OF LOOSE CONNETIVE TISSUE
-PRECAPILLARY CELLS

Front 12

WHAT IS THE CAPILLARY NETWORK?

Back 12

ARTERIOLES -> METARTERIOLE THROUGHFARE= PAPILLARY SPHINCTERS (VASCULAR SHUNT) SMOOTH MUSCLES ACT AS VALVES
EX. EAT!
THE NETWORK FORMS NUMEROUS BRANCHES THAT TRANSPORT BLOOD FROM THE THROUGHFARE CHANNEL AND CAN RETURN TO THE CHANNEL

Front 13

HOW ARE VARICOSE VEINS DEVELOPED?

Back 13

STRETCHING OF THE VEIN WALLS IN THE LOWER LIMBS CAUSING VALVES TO BECOME INCOMPETENT.

Front 14

BE ABLE TO TRACE THE PATHWAY OF BLOOD IN THE PULMONARY CIRCUIT

Back 14

PULMONARY CIRCUIT-
LUNG TISSUE -> PULMONARY VEINS-> LEFT ATRIUM -> BICUSPID VALVE -> LEFT VENTRICLE -> AORTA

Front 15

BE ABLE TO TRACE THE PATHWAY OF BLOOD IN SYSTEMIC CIRCUIT.

Back 15

BODY TISSUES-> SUPERIOR VENA CAVA -> RIGHT ATRIUM -> TRICUSPID VALVE -> RIGHT VENTRICLE-> PULMONARY SEMILUNAR VALVES -> PULMONARY TRUNK-> PULMONARY ARTERIES -> LUNG TISSUE

Front 16

BE ABLE TO TRACE THE PATHWAY OF BLOOD IN THE CORNARY CIRCULATION.

Back 16

AORTA-> LEFT CORONARY ARTERY-> ANTERIOR INTERVENTRICULAR ARTERY-> CIRCUMFLEX ARTERY-> MARGINAL ARTERY-> CORONARY VEINS CONVERGE IN CORONARY SINUS AND DRAIN INTO RIGHT ATRIUM

Front 17

WHAT ARE THE ARTERIES OF THE HEART?

Back 17

RIGHT & LEFT CORONARY ARTERIES
RIGHT & LEFT MARGINAL ARTERIES
CIRCUMFLEX ARTERY
POSTERIOR & ANTERIOR INTERVENTRICULAR ARTERIES

Front 18

BE FAMILIAR WITH HEART HISTOLOGY.

Back 18

HEART SKELETON CONSISTS OF A PLATE OF FIBROUS CT BETWEEN THE ATRIA & VENTRICLES, THIS CT PLATE FORMS FIBROUS RINGS AROUND THE ATRIOVENTRICULAR AND SEMILUNAR VALVES & PROVIDES A SOLID SUPPORT, ALSO SERVES AS ELECTRICAL INSULATION BETWEEN THE ATRIA AND VENTRICLES & PROVIDES RIGID SITE FOR ATTACHMENT OF THE CARDIAC MUSCLES

Front 19

TRACE THE PRODUCTION OF AN ACTION POTENTIAL THROUGH THE CONDUCTING SYSTEM OF THE HEART.

Back 19

-SA INITIATES ACTION POTENTIAL; SPREADS ACROSS ATRIA & CAUSES TO CONTRACT
-AP ARE SLOWED IN AV NODE; ALLOWS ATRIA TIME T O CONTRACT & BLOOD TO MOVE TO VENTRICLES
-AP TRAVELS THROUGH AV NODE & BUNDLE BRANCHES -> PURKINJE FIBERS-CAUSES VENTRICLES TO CONTRACT
SA= PACEMAKER- SPONTANEOUSLY & RHYTHMICALLY GENERATE AP (AUTORHYTHMIC)

Front 20

BE FAMILIAR WITH CARDIAC ACTION POTENTIALS AND HOW THEY ARE PROPAGATED.

Back 20

PERMEABILITY CHANGES DURING AP IN CARDIAC MUSCLE:
1. DEPOLARIZATION PHASE:
* V-GATED Na+ CHANNELS OPEN
* V-GATED K+ CHANNELS CLOSE
* V-GATED Ca2+ CHANNELS BEGIN TO OPEN
2. EARLY REPOLARIZATION & PLATEAU PHASES:
* V-GATED Na+ CHANNELS CLOSE
* SOME V-GATED K+ CHANNELS OPEN, CAUSING EARLY REPOLARIZATION
* V-GATED Ca2+ CHANNELS OPEN, PRODUCING THE PLATEAU BY SLOWING FURTHER REPOLARIZATION
3. FINAL REPOLARIZATION PHASE:
* V-GATED Ca2+ CHANNELS CLOSE
* MANY V-GATED K+ CHANNELS OPEN

Front 21

WHAT DOES AN ECG MEASURE?

Back 21

RECORDS ONLY THE ELECTRICAL ACTIVITIES OF THE HEART.
-DEPOLARIZATION OF THE ATRIA PRODUCES THE P-WAVE
-DEPOLARIZATION OF THE VENTRICLES PRODUCE QRS COMPLEX
-REPOLARIZATION OF THE ATRIA OCCURS DURING THE QRS COMPLEX
-REPOLARIZATION OF THE VENTRICLES PRODUCES THE T-WAVE

Front 22

WHAT ARE P-WAVES, QRS COMPLEX, T-WAVE, AND QT INTERVALS?

Back 22

1. P-WAVES: 1ST COMPLEX OF THE ECG REPRESENTING DEPOLARIZATION OF THE ATRIA.
2. QRS COMPLEX: PRINCIPLE DEFLECTION IN THE ECG, REPRESENTING VENTRICULAR DEPOLARIZATION
3. QT INTERVAL: TIME ELAPSING FROM THE BEGINNING OF THE QRS COMPLEX TO THE END OF THE T-WAVE REPRESENTING THE TOTAL DURATION OF ELECTRICAL ACTIVITY OF THE VENTRICLES.
4. T-WAVE: DEFLECTION IN THE ECG FOLLOWING THE QRS COMPLEX REPRESENTING VENTRICULAR REPOLARIZATION

Front 23

LOOK AT EXAMPLES OF IRREGULAR ECGs. PAGE 686 FIGURE 20.17

Back 23

1. COMPLETE HEART BLOCK (P WAVES AND QRS COMPLEXES ARE NOT COORDINATED)

2. PREMATURE VENTRICULAR CONTRACTION (PVC) (NO P WAVES PRECEDE PVC's)

3. BUNDLE BRANCH BLOCK (PROLONGED QRS COMPLEXES)

4. ATRIAL FIBRILLATION (NO CLEAR P WAVES AND RAPID QRS COMPLEXES)

5. VENTRICULAR FIBRILLATION (NO P, QRS, OR T WAVES)

Front 24

WHAT IS MAP? AND HOW IS IT MEASURED?

Back 24

MAP= MEAN ARTERIAL PRESSURE- IS THE AVERAGE BLOOD PRESSURE BETWEEN SYSTOLIC & DIASTOLIC PRESSURE IN THE AORTA.
MAP=CO x PR=
ITS PROPORTIONAL TO CARDIAC OUTPUT OR MINUTE VOLUME, IS THE AMOUNT OF BLOOD PUMPED BY THE HEART PER MINUTE AND PERIPHERAL RESISTANCE IS THE TOTAL IS THE TOTAL RESISTANCE AGAINST WHICH BLOOD IS PUMPED.

Front 25

BE ABLE TO DETERMINE CARDIAC OUTPUT IF GIVEN A SET OF VALUES FOR HEART RATE AND STROKE VOLUME. BE ABLE TO DETERMINE HEART RATE AND STROKE VOLUME IF GIVEN THE OTHER 2 VALUES.

Back 25

CARDIAC OUTPUT IS EQUAL TO HEART RATE TIMES STROKE VOLUME. HR IS THE NUMBER OF TIMES THE HEART BEATS PER MINUTE. SV WHICH IS THE VOLUME (CARDIAC CYCLE) IS EQUAL TO END DIASTOLIC VOLUME MINUS END SYSTOLIC VOLUME. STROKE VOLUME IS THEREFORE EQUAL TO 70ML.
CO=HR x SV

Front 26

WHAT IS PERIPHERAL RESISTANCE AND HOW DOES IT RELATE TO MAP?

Back 26

RESISTANCE TO BLOOD FLOW IN ALL THE BLOOD VESSELS.
DEPENDING ON THE PERIPHERAL RESISTANCE, THE MAP OR AVG BLOOD PRESSURE BETWEEN SYSTOLE AND DIASTOLE WILL BE AFFECTED

Front 27

WHAT FACTORS INFLUENCE RESISTANCE?

Back 27

BY INCREASING END-DIASTOLIC VOLUME OR BY DECREASING END-SYSTOLIC VOLUME

Front 28

WHAT IS STARLING'S LAW OF THE HEART AND WHAT DOES IT MEASURE?

Back 28

THE RELATIONSHIP BETWEEN PRELOAD & STROKE VOLUME.
IT MEASURES THE RELATIONSHIP BETWEEN CHANGES IN THE PUMPING EFFECTIVENESS OF THE HEART AND CHANGES IN THE PRELOAD.

Front 29

WHAT IS TACHYCARDIA? BRADYCARDIA?

Back 29

TACHYCARDIA-ABNORMAL HEART RHYTHMS
-SYMPTOM: HEART RATE IN EXCESS OF 100bpm
-CAUSES: ELEVATED BODY TEMP., EXCESSIVE VAGAL STIMULATION, TOXIC CONDITIONS

BRADYCARDIA- HEART RATE LESS THAN 60bpm
-CAUSE: ELEVATED STROKE VOLUME IN ATHLETES, EXCESSIVE VAGAL STIMULATION, CAROTID SINUS SYNDROME

Front 30

HOW IS THE HEART RATE REGULATED?

Back 30

TO MAINTAIN HOMEOSTASIS, THE AMOUNT OF BLOOD PUMPED BY THE HEART VARIES. EITHER INTRINSIC OR EXTRINSIC REGULATORY MECHANISMS CONTROL CARDIAC OUTPUT.
INTRINSIC-FROM NORMAL FUNCTIONAL CHARACTERISTICS OF THE HEART/ DOESN'T DEPEND ON HORMONAL OR NEURAL REGULATION
EXTRINSIC- INVOLVES NEURAL & HORMONAL CONTROL

Front 31

WHAT ARE TH MAJOR EFFECTS OF AGING ON THE HEART? (6)

Back 31

1. AGING RESULTS IN GRADUAL CHANGES IN THE FUNCTION OF THE HEART WHICH ARE MINOR UNDER RESTING CONDITIONS BUT ARE MORE SIGNIFICANT DURING EXERCISE.
2. HYPERTROPHY OF THE LEFT VENTRICLE IS A COMMON AGE-RELATED CONDITION.
3. THE MAXIMUM HEART RATE DECREASES AND BY AGE 85 THE CARDIAC OUTPUT MAY BE DECREASED BY 30-60%.
4. THERE IS AN INCREASED TENDENCY FOR VALVES TO FUNCTION ABNORMALLY AND FOR ARRHYTHMIAS TO OCCUR.
5. AN INCREASED OXYGEN CONSUMPTION, REQUIRED TO PUMP THE SAME AMOUNT OF BLOOD, MAKES AGE-RELATED CORONARY ARTERY DISEASE MORE SEVERE.
6. EXERCISE IMPROVES THE FUNCTIONAL CAPACITY OF THE HEART AT ALL AGES.

Front 32

CARDIAC TAMPONADE

Back 32

BUILDUP OF BLOOD IN THE PERICARDIAL SAC

Front 33

ANGINA PECTORIS

Back 33

-REDUCTION IN BLOOD SUPPLY TO MYOCARDIUM
-PAIN RADIATING IN CHEST, NECK, LOWER JAW, LEFT ARM, AND LEFT SHOULDER

Front 34

MYOCARDIAL INFARCTION

Back 34

-PROLONGED BLOOD DEPRAVATION TO CARDIAC MUSCLE RESULTING IN CELLULAR DEATH
-MOST COMMON CAUSE IS THROMBUS BLOCKING ARTERY
-ALSO CAUSED BY ATHEROSCLEROTIC LESIONS.

Front 35

CALCIUM CHANNEL BLOCKERS

Back 35

-PREVENTS INFLUX OF Ca2+ THROUGH V-GATED Ca2+ CHANNELS
-REDUCE HEART RATE AND PREVENT TACHYCARDIA

Front 36

ABNORMAL HEART SOUNDS

Back 36

-MURMURS
*GURGLING OR SWISHING SOUND
*INCOMPETANT VALVES

-STENOSED
*RUSHING SOUND
*NARROWED BLOOD VESSELS

Front 37

MYOCARDITIS

Back 37

INFLAMMATION OF MYOCARDIUM; CAN LEAD TO HEART FAILURE

Front 38

PERICARDITIS

Back 38

INFLAMMATION OF PERICARDIUM (BACTERIAL OR VIRAL INFECTIONS) THAT CAN BE VERY PAINFUL

Front 39

RHEUMATIC HEART DISEASE

Back 39

STREPTOCOCCAL INFECTION IN YOUNG CAUSES OVER ACTIVE IMMUNE RESPONSE LEADING TO STENOSED OF INCOMPETENT VALVES

Front 40

CORONARY HEART DISEASE

Back 40

INADEQUATE BLOOD FLOW TO THE HEART USUALLY IN OLDER PEOPLE

Front 41

CORONARY THROMBOSIS

Back 41

FORMATION OF BLOOD CLOT IN CORONARY ARTERY DUE TO DEGENERATIVE CHANGES IN ARTERY WALL

Front 42

MYOCARDIAL INFARCT

Back 42

AREA OF DAMAGED TISSUE CAN RESULT IN DEATH IF INFARCT IS LARGE. IF INFARCT IS SMALL, SCAR TISSUE DEVELOPS MAKING HEART FUNCTION DIFFICULT.

Front 43

CONGENITIAL HEART DISEASE

Back 43

*ABNORMAL DEVELOPMENT OF THE HEART RESULTING IN DECREASE IN PUMPING EFFECTIVENESS

Front 44

INCOMPETENT HEART VALVE

Back 44

A LEAKY VALVE

Front 45

CYANOSIS

Back 45

INADEQUATE HEART FUNCTION IN BABIES RESULTS IN LOW BLOOD OXYGEN LEVELS; CAUSES SKIN TO APPEAR BLUE, HENCE THE NAME "BABY BLUE".

Front 46

HYPERTENSION

Back 46

* INCREASES AFTERLOAD ON HEART AND CAN CAUSE THE HEART TO ENLARGE; LEADS TO HEART FAILURE.
* ABNORMALLY HIGH SYSTEMIC BLOOD PRESSURE
* EFFECTS ABOUT 1/5 THE POPULATION IN UNITED STATES
* RECOMMENDED DIET LOW IN FATS AND CHOLESTEROL AS WELL AS LOW IN REFINED SUGAR
* TOBACCO AND ALCOHOL ARE CONTRIBUTING FACTORS ALONG WITH STRESS AND LACK OF EXERCISE.

Front 47

WHAT DOES THIS ECG INDICATE?

Back 47

NORMAL SINUS RHYTHMS

Front 48

WHAT DOES THIS ECG INDICATE?

Back 48

2ND DEGREE HEART BLOCK (BLOCKAGE OF AV NODE) 2 P-WAVES (FAULTY AV NODE)

Front 49

WHAT DOES THIS ECG INDICATE?

Back 49

JUNCTIONAL RHYTHM (IN AV NODE) DEFECTIVE SA NODE OR PACEMAKER

Front 50

WHAT DOES THIS ECG INDICATE?

Back 50

SINUS TACHYCARDIA (FASTER THAN 100 BPM)

Front 51

WHAT DOES THIS ECG INDICATE?

Back 51

PREMATURE VENTRICULAR CONTRACTION (PVC)
(WIDE COMPLEX) ("ECTOPIC FOCUS")

Front 52

WHAT DOES THIS ECG INDICATE?

Back 52

VENTRICULAR FIBRILLATION (NO P,QRS, OR T WAVES)