Module 6: Cardiovascular Flashcards Preview

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Flashcards in Module 6: Cardiovascular Deck (237)
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61

a progressive and sustained enlargement of the heart

Cardiac Hypertrophy

62

- an acute change in cardiac pressure
- Condition in which bleeding occurs between ventricle and pericardium due to puncture of coronary vessels during cardiac catheterization
- Bleeding compresses ventricles

Cardiac Tamponade

63

a slow progressive increase in pericardial fluid

Pericardial Effusion

64

scar tissue following __ in which inflamed pericardium eventually adheres to the epicardial tissues

Pericarditis

65

- condition that leads to irreversible changes and death of cardiac muscle cells.
- occurs when the blood supply to the myocardium is interrupted.
- manifested by chest pain that usually radiates to the lower jaw and shoulder.

Myocardial Infarction

66

FOR CONTRACTION
- normally non automatic
- main bulk of cardiac muscle
- examples: atrial muscle fiber; ventricular muscle fiber

FOR IMPULSE CONDUCTION
- automatic cells
- less abundant
- examples: SA node; AV node; Bundle of His; Purkinje fibers

Myocardial Cells

67

Physiologic Properties of the Heart

- Chronotropism / Autorhythmicity
- Dromotropism / Conductivity
- Bathmotropism / Excitability
- Inotropism / Contractility

68

- Spontaneously generates impulse without neural input
- Has an unstable RMP
- Has no sustained plateau

Action Potential of SA and AV Node

69

- Aka maximum diastolic potential
- The longest portion of the nodal Action Potential (AP)
- Accounts for the automaticity of nodal cells
- Slow depolarization produced by the opening of sodium channels → inward Na current
- Sodium current called If – f stands for funny
- Turned ON by repolarization from the preceding AP, ensuring that each AP is followed by another AP
- As threshold is reached (-40 mV), the T-type calcium channels open for the upstroke

Phase 4 (Pacemaker Potential)

70

- Increased calcium conductance
- Increased inward calcium current
- Calcium influx is carried by T-type calcium channels
- Not inhibited by calcium channel blockers like verapamil

Phase 0 (Upstroke)

71

Specialized Conduction System of the Heart

- SA Node (Node of Keith and Flack)
- AV Node
- Bundle of His: 0.12 m/s
- Bundle branches – right and left
- Purkinje system – spread throughout subendocardial region of ventricle
- Conduction velocity is 1.5 – 4 m/s
- Ventricular muscle fibers: 0.5 m/s

72

- 0.8 m/s

- Anterior interatrial tract
*Atrial muscle fiber: 0.3 m/s

- Internodal tracts
*Preferential pathway: 1.0 m/s
Anterior internodal tract of Bachman
Middle internodal tract of Wenckebach
Posterior internodal tract of Thorel

SA Node (Node of Keith and Flack)

73

- Node of Kent and Tawara: 0.05 m/s
- AN region (atrionodal) – site of principal delay
- N region (nodal/middle nodal) - where AV block most likely to occur
- NH (nodal His) – assumes pacemaker function is SA node is depressed
- Ensures that ventricles have sufficient to fill with blood before they are activated and eventually contract
- Slow conducting velocity is attributed to the small diameter of the nodal cells

AV Node

74

- Are irritable/excitable cells (able to respond to stimulus)
- Can be stimulated by:
Electrical energy – electrical current, defibrillator
Mechanical energy – blood stretching the heart
Chemical energy – epinephrine and norepinephrine

- Can respond by:
Generating impulses / AP
Conducting impulses
Contracting

- Their contraction requires
AP generated from SA node
ATP
Ca2+ from ECF (main source) and ICF/sarcoplasmic reticulum

Excitability: Myocardial cells

75

- Presents striations of dark and light bands
- Has the sarcomere as contractile
*Runs from Z line to Z line
*Contains thick filament (myosin) and thin filaments (actin, troponin & tropomyosin)
- Has sarcotubular system

THE MYOCARDIAL CELL STRUCTURE

76

Shortening occurs according to sliding filament model

- Skeletal Muscles – one sarcomere has 2 T-tubule system
- Cardiac Muscles – a sarcomere has only 1 T-tubule, located at Z line rather than at junction of A and I band
- T-tubule in cardiac muscle well developed, wider diameter, stores calcium also, form DIADS with the SR
- SR in cardiac muscle less developed, store less calcium, small diameter
- T-tubule have a diameter 5x as great as that of the skeletal muscles T-tubule (volume of 25x as great)
- Inside the T-tubules are mucopolysaccharides which are electronegatively charged and bind an abundant store of calcium

77

- Cardiac muscle functions as a __
- A stimulus applied to any one part of the cardiac muscle results in the contraction of the entire muscles
- 2 Syncytiums
1. Atrial Syncytium
2. Ventricular Syncytium

SYNCYTIUM

78

Other features of cardiac muscles

- Slow muscle - Cardiac muscle contracts repetitively for a lifetime thus requires continuous oxygen supply and so dependent on oxidative metabolism
- Very rich in mitochondria which contain the enzymes needed for oxidative Phosphorylation (sustains the myocardial energy requirements)
- Endowed with a rich capillary supply (one capillary per fiber) to provide adequate oxygen
- High content of MYOGLOBIN – a pigment which functions as an oxygen storage mechanism

79

Two different proteins are phosphorylated to produce the increase in contractility

1. Phosphorylation of the sarcolemmal calcium channels that carry inward calcium current during Plateau phase.
2. Phosphorylation of Phospholamban – a protein that stimulates calcium ATPase, resulting in greater uptake and storage of calcium by the SR.

80

Two factors determine how much calcium is released from the Sarcoplasmic Reticulum

1. The size of the inward calcium current during the plateau of AP (size of the Trigger calcium)
2. The amount of calcium previously stored in the SR for release.

**The larger the inward calcium current and the larger the intracellular stores, the greater the increase in intracellular calcium concentration and the greater the contractility.

81

The amount of extracellular calcium entering the cell during phase 2 (Plateau) is directly proportional to the:

1. Extracellular calcium concentration
2. Number of open calcium channels
3. Duration of Action Potential
4. Number of action potentials

82

FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM)

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

2. Sympathetic Stimulation (Catecholamines) via B1 receptors increase force of contraction by 2 mechanisms:
- increases the inward Ca++ current during plateau phase
- increases the activity of Ca++ pump of SR by Phosphorylation of Phospholamban. Result is more Ca++ accumulated by SR, thus more Ca++ available in subsequent beats.

3. Xanthines (caffeine & theophylline)
- inhibit breakdown of cAMP

83

FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM) 2

4. Glucagon
- increases formation of cAMP used in some heart disease

5. Cardiac Glycosides (Digitalis)
- Increase force of contraction by inhibiting Na+, K+ - ATPase in the myocardial cell membrane. This increases intracellular Na+ which leads to increased availability of Ca++

6. Length
- tension relationship in the ventricle Frank Starling’s Law of the Heart)
- direct relationship between initial fiber length and total tension developed
- at high degrees of stretch, the developed tension decreases. Not due to a decrease in the number of crossbridges between actin and myosin (skeletal muscle) because cardiac muscles do not reach this state. Severely dilated hearts not stretched to this degree

84

This enhanced contractility helps the heart eject more blood with each contraction and helps compensate for reduced filling time that is associated with tachycardia

a. positive staircase or BODWITCH STAIRCASE
- Increased HR increase the force of contraction in a stepwise fashion as the intracellular calcium increases cumulatively over several beats
- Force-frequency relationship

b. Post - extra systolic potentiation
- the beat after an extra systole has increased force of contraction because extra calcium entered the cells during the extra beat independent of ventricular filling
- due to increased availability of intracellular Ca††

85

FACTORS THAT DECREASE CONTRACTILITY

1. Parasympathetic stimulation (Ach) via muscarinic receptors, decreases force of contraction by decreasing the inward calcium current during plateau phase of AP

2. Calcium blocking agents
Ex. Verapamil - long acting
Nifedipine (Calcibloc) - short acting

- Impedes slow Ca++ channel – reducing the amount of Ca++ ions that enter the myocardial cells during plateau phase, thus diminishing strength of contraction
- Used in treatment of hypertension

3. Hypercapnia
4. Hypoxia
5. Acidosis
6. Drugs – barbiturates (quinidine, procainamide)
7. Heart failure – Myocardial ischemia

86

Optimal concentrations of Na†, K† and Ca†† are necessary for cardiac muscle contraction (Sodium and Potassium)

1. without Sodium - heart not excitable, will not beat
2. reduction in extracellular Potassium
- has little effect on myocardial excitation and contraction
- increases in extracellular Potassium (hyperkalemia)
*loss of excitability of myocardial cells
*cardiac arrest in diastole called
- Potassium Inhibition – heart dilated and flaccid

87

Optimal concentrations of Na†, K† and Ca†† are necessary for cardiac muscle contraction (Calcium)

3. removal of Ca++ from ECF results in
→decreased contractile force
→arrest in diastole

- increase in ECF Ca++ -enhances contractile force
- spastic contraction
-arrest in systole (Calcium Rigor)

The strength of cardiac contraction depends to a great strength on the cone, of Ca++ in the ECF

88

CONDITIONS AND AGENTS THAT CAN ALTER THE INOTROPIC STATE OF THE HEART

1. Myocardial ischemia (lack of oxygen to heart) – results in inhibition of the calcium channels therefore (-) Inotropism
2. Acidosis (increased plasma H+) – inhibits myocardial contractility
3. Cardiac glycosides

89

- Have large amount of elastin in their walls.
- Highly distensible – this serves to dampen the pulsatile blood flow when blood is ejected from the ventricles and converted to a steady flow in the capillaries
- If arterial system not distensible, all blood during systole will flow to the peripheral vessels, no flow will occur during diastole

AORTA AND PULMONARY ARTERY

90

- thick walled with extensive development of elastic tissue, smooth muscle and connective tissue
- Transport blood under HIGH PRESSURE to the tissues.
- The volume of blood contained in the arteries called STRESSED VOLUME (blood volume under high pressure

Arteries