Module 6: Cardiovascular Flashcards Preview

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Flashcards in Module 6: Cardiovascular Deck (237)
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31

EFFECT OF RESPIRATION ON HEART RATE

Inspiration → ↑ heart rate
Expiration → ↓ heart rate

32

Inspiration → ↓ Intrathoracic Pressure → ↑ venous return (right atrium) → ↑atrial volume → (+) atrial stretch receptors → ↑ heart rate

- the stretched right atrium initiates a nervous reflex called the __, passing first to the vasomotor center of the brain and then back to the heart by way of the sympathetic nerves and vagi, also to increase the heart rate.

Bainbridge Reflex

33

This law states that when increased quantities of blood flow into the heart, the increased blood stretches the walls of the heart chambers. As a result of the stretch, the cardiac muscle contracts with increased force, and this empties the extra blood that has entered from the systemic circulation. Therefore, the blood that flows into the heart is automatically pumped without delay into the aorta and flows again through the circulation.

Frank-Starling law of the heart

34

Factors Affecting Stroke Volume

1. PRELOAD
- The load that stretches the cardiac muscle before contraction
- The degree of tension on the muscle when it begins to contract.
- Considered to be the end diastolic pressure, when the ventricle has been filled

2. AFTERLOAD
- Degree of vascular resistance to ventricular contraction
- The load against which the muscle exerts its contractile force

3. Inotropic State – Myocardial Contractility

35

FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM)

Increased heart rate
- more Action Potential per unit time
- more Ca++ enters myocardial cell during plateau of Action Potential
- more Ca++ released from Sarcoplasmic Reticulum
- greater tension produced during contraction

36

Control of Stroke Volume

A) HETEROMETRIC
- regulation of Stroke Volume as a result of changes in cardiac muscle fiber length (Frank Starlings Principle)
B) HOMEOMETRIC (includes nervous and hormonal control)
- not dependent on muscle length

37

HOMEOMETRIC REGULATION: Nervous Control (autonomic nervous system)

sympathetic → ↑ distensibility and force of ventricular contraction
parasympathetic → ↓ atrial force of contraction

38

HOMEOMETRIC REGULATION: Hormonal Control

1. catecholamines → ↑ distensibility and force of ventricular contraction (cAMP on B1 adrenergic receptors)

2. acetylcholine → ↓ atrial force of contraction (acting on muscarinic receptors )
3. thyroxine
4. glucagon → increases cAMP

39

Other Factors that increases stroke volume

- respiration agents
- caffeine
- theophylline (↑ cAMP)
- digitalis
- temperature

40

Factors that determine an adequate End Diastolic Volume:

1. Filling time of Ventricle - dependent on cardiac rate
2. Distensibility of Ventricle (Vent Compliance)
3. Stronger Atrial Contraction
4. INTRAPERICARDIAL PRESSURE
5. Adequate Venous Return

41

- Increase in ventricular stiffness produced by Myocardial Infarction
- in heart failure, there must be a greater stretch of myocardium to achieve the needed Cardiac Ouput
- attained by administration of + inotropes

Distensibility of Ventricle (Vent Compliance)

42

- a minor factor
- not very essential for ventricular filling WHY:
- adequate filling is often observed in patients with atrial fibrillation, despite absence of atrial contraction
- severe Tachycardia period of ventricular systole becomes markedly shortened ventricular filling is seriously impaired despite the contribution of atrial contraction

Stronger Atrial Contraction

43

Contribution of Atrial Contraction is governed by:

1. Heart rate - Moderate Tachy diastasis shortened therefore atrial contraction becomes substantial

2. Stenotic AV Valve - Atrial contraction is important in ventricular filling

44

- when increased, limits the extent in which the ventricle can fill >> decreased EDV >> decreased CO
ex. Pericardial effusion – heart muscle
- cannot stretch enough to receive blood from the atrium

INTRAPERICARDIAL PRESSURE

45

- flow of blood from periphery back to right atrium
- main determinant of cardiac output
- The degree of myocardial stretch created by venous return is called the PRE-LOAD on the heart

Adequate Venous Return (VR)

46

Factors that influences Venous Return

1. Total Blood Volume

2. Increased Venous Tone (constriction of veins)(Sympathetic Tone)
- venoconstriction
- reduces the size of venous reservoir
- decreases venous pooling
- increases VR

3. Posture
- gravitational force causes pooling of blood in the legs (venous pooling)
- standing decreases VR
- decrease CO because of pooling of blood in lower limbs

4. Skeletal Muscle Pump

5. Respiratory / Thoraco – Abdominal Pump Practical Application : Cardiac patients refrain from Valsalva’s maneuver

47

- determined primarily by the balance between the force of contraction of the ventricle and aortic pressure.
a) force of myocardial contraction
b) aortic pressure load ( afterload )

END SYSTOLIC VOLUME

48

End Systolic Volume Determined by:

1. AFTER LOAD
- In the left ventricle, afterload is equal to all the forces the muscle must overcome to eject at given volume of blood
- Dependent upon:
*Aortic pressure – the major contributor to afterload in the heart
*State of semilunar valves

2. CONTRACTILITY
- Increased myocardial contraction – decreased ESV
- Severely dilated heart (heart failure) – ESV can become much greater than SV

49

- Decreased by increases in myocardial contractility and heart rate
- Increased whenever heart is weakened (heart failure)
- Increased with increased outflow resistance (aortic valve stenosis, increased aortic pressure)
- Examination of ESV is clinically useful as an indicator of conditions affecting the heart

END SYSTOLIC VOLUME

50

Cardiac Output Varies According to:

1. Level of activity of the body
- Strenuous exercise: Cardiac Outpu = 35 L/min
- Entire blood volume pumped around the circuit seven times per minute
- Cardiac Reserve

2. Size of Body (Surface Area)
- Cardiac Output increases in proportion to the surface area of the body, stated in terms of CARDIAC INDEX
- The amount of blood pumped out of the ventricle per minute per square meter of body surface area
- Cardiac Index = CO divided by body surface area
*Normal adults = 3 L/min/ sq.m.
*10 yrs age = 4 L/min/ sq.m.
*80 yrs age = 2.4 L/min/ sq.m.

51

- the difference between Cardiac Ouput at rest and the maximum volume of blood the heart is capable of pumping per minute
- The maximum amount of blood that can be pumped out by the heart above normal value
- Essential to withstand the stress of exercise
- Expressed in percentage
*Normal Young Adult = 300 - 400%
*Old Age = 200 – 250%
*Athletes = 500 – 600%
*Cardiac diseases = minimum or nil

CARDIAC RESERVE

52

- Work the heart performs on each beat
- Is equal force (aortic pressure) x Distance (SV)
- SW = AP x SV
- Cardiac work = ABP x SV
- amount of work done by right heart

STROKE WORK

53

Variations in Cardiac Output: Physiological Variations

- Sleep- no change
- Age
- Sex
- Body build
- Diurnal condition – low early morning
- Environmental conditions - Temperature above 37 degrees centigrade raises CO
- Emotional conditions – anxiety, excitement increases CO to 50%
- After meals – increased during first hour after meal to 30%
- Exercise – increases up to 700%
- Pregnancy – increased by 45 to 60 % during later pregnancy
- Posture – recumbent to upright, decreases CO because of pooling of blood in the lower limb

54

PATHOLOGICAL VARIATIONS: Cardiac Output increased in

- Fever due to oxidative process
- Anemia due to hypoxia
- Hyperthyroidism – increased basal metab

55

PATHOLOGICAL VARIATIONS: Cardiac Output decreased in

- Hypothyroidism
- Atrial fibrillation
- Congestive heart failure
- Heart block
- Hemorrhage
- Valvular lesions (insufficiency)

56

Measurement of Cardiac Output

1. Direct Method
a. Use of cardiometer
b. Use of flowmeter
- Mechanical flowmeter
- Electromagnetic flowmeter
- Ultrasonic doppler flowmeter

2. Indirect Method
- Using FICK’s principle
- CO = O² consumed (in ml/min) / Arteriovenous O² difference

57

The heart rests upon the diaphragm and its apex is directed downward, forward and to the left. Strictly speaking, it is only the apical portion of the heart that goes beyond the sternum and occupies the left side of the chest.

Physiologic Anatomy of the Heart

58

- Normally heard / palpated at the the 5th ICS, LMCL
- Caused by ventricular contraction which rotates the heart, giving rise to a tap by the tip of the ventricle

Apex Beat

59

Enclosed in a 2-layered serous membrane, the PERICARDIUM, forming the pericardial sac

Visceral Layer - adheres to the surface of heart
Parietal Layer - attached to heart only at point of entrance of big vessels

60

Sac composed of fibrous connective tissue, not very distensible

- Helps prevent sudden overdistention of the heart chambers
- Congenital absence is NOT fatal
- Contains thin layer of serous fluid (30 mL) for lubrication