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cardiovascular system Flashcards

1
Q

define cardiac output

A

volume of blood ejected from the left ventricle into the aorta each minute

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2
Q

what is the equation for cardiac output

A

cardiac output = stroke volume x heart rate

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3
Q

what is stroke volume

A

the volume of blood ejected by the ventricle after each contraction

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4
Q

what are the 3 factors that regulate stroke volume

A

preload - degree of stretch before contraction
contactility - forcfullness of contractions
afterload - the pressure that must be exceeded for the ventricles to eject blood

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5
Q

what is preload

A

filling pressure detected by stretch receptors in myocytes
roughly equates to end diastolic pressure/volume

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6
Q

what is afterload

A

peripheral resistance

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7
Q

what are the two main forces in fluid balance across a capillary

A

hydrostatic pressure
colloid osmotic pressure

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8
Q

in oedma, what are the changes to the capillary

A

decreased colloid osmotic pressure (low albumin)
damage to alveolar membrane
lymphatic blockage (cancer)
increasedhyfrostatic pressure

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9
Q

what causes pulmonary oedema in heart failuer

A

increased filling pressure due to higher preload causes hydrostatic pressure in pulmonary capillaries to go so high that fluid leaks out faster than lymphatics can take it away

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10
Q

what are some compensatory mechanisms that are devloped to cope with mitral stenosis

A

thickened alveolar capillary membrane
increased drainage

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11
Q

two main effects of heart failure

A

not enough blood is getting to the body which can cause fatigue
ongestion/fluid accumulation

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12
Q

heart failure can be classified into two groups

A

acute and chronic

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13
Q

what are the three main courses of heart failure

A

patient remains stable on meds
gradually deterioates
patient sufferes repeated insults in stepwise fashion slowly losing LV function

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14
Q

describe acute heart failure

A

Acute heart failure is the sudden worsening of the signs and symptoms of heart failure,
typically includes difficulty breathing (dyspnea), raised JVP, leg or feet swelling, and fatigue.

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15
Q

what is anasarca

A

gross fluid retention and oedema everywhere

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16
Q

what is cardiogenic shock

A

an extreme version of heart failure, where somebody has e.g. had a
very large MI and killed so much of their heart that they can’t survive

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17
Q

what is the bodies response to acute heart failure

A

similar to acute blood loss-
 Sympathetic outflow
 -Raises BP, heart rate
 -Preserve flow to vital organs at expense of limbs
 Salt and water conservation
 -Thirst, ADH
 -Shut down kidneys

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18
Q

symptoms of pulmonary oedema

A

 Breathlessness
 Difficulty talking
 Orthopnoeia - Lying down may kill them (flood
all the alveoli)
 Frightening - Experience ‘angor animi’ (fear of
certain impending death)
 Use of accessory breathing muscles
 Pink, frothy sputum - Alveolar fluid with blood
 Sweating
 Cold, clammy

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19
Q

what are the models of progression for chronic heart failure

A

haemodynamic
neurohormonal
peripheral
metabolic

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20
Q

what is law of laplace equation

A

Tension within wall of the LV (T) = [Pressure inside ventricles (P) x Radius of the ventricle (R)]
/Ventricle wall thickness (h

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21
Q

what is the effect on RAAS in heart failure and why

A

activation of RAAS
as kidney perfusion/blood pressure is low
causes vasoconstriction and water /salt retention

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22
Q

what is ergoreflex

A

Reflex generated by exercising muscles - With exercise, muscle being exercised sends signals
to the brain to breath more.
The ergoreflex increases as exercise capacity falls and increases as ventilatory response to
exercise increases.

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23
Q

which reflexes are inhanced and which are poor in those with heart failure

A

enhanced chemo /ergo - increase ventilation
poor baro/cardio reflexes

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24
Q

what are the two types of left sided heart failure

A

systolic - left chamber lacks the force to push blood into circulation

diastolic - left chamber fails to relax normally as muscles have become stiffer

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25
Q

what are the symptoms of left sided heart failure

A

Increased rate of breathing
 Increased work of breathing
 Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
 Fatigue
 Rales or crackles heard in the lung bases (in severe cases, if heard throughout the
lung this indicated pulmonary oedema)
 Cyanosis
 Laterally displaced apex beat (occurs if the heart is enlarged)
 Gallop rhythm
 Heart murmurs may indicate the presence of valvular heart disease as either a cause
(e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure

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26
Q

what are the causes of right sided heart failure

A

muscle injury, such as a heart attack localised to the right ventricle,
damage to the valves in the right side of the heart or elevated pressure in the lungs.

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27
Q

what are some causes of heart failure

A

Past heart attacks
 CHD
 High blood pressure
 Heart valve disease
 Heart muscle disease or inflammation of the heart
 Congenital heart defects
 Lung conditions
 Alcohol/drug abuse

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28
Q

what medications are used to treat pulmonary oedema

A

oxygen!
diuretic (furosemide)
vasodilator (nitrate/GTN)
IONOTROPIC SUPPORT if blood pressure is low - dobutamine

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29
Q

how is anasarca treated

A

induce diuresis
bed rest
fluid restriction
catheter
diuretics
heparin - to prevent DVT

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30
Q

example of loop diuretics

A

bumetanide
furosemide

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31
Q

what is the mechanism for loop diuretics

A

block na/k 2cl transporter in loop of henle

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32
Q

what is the mechanism for EDCT diuretics

A

block na/cl/co transporter

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33
Q

what is an example of EDCT diuretics

A

thiazide

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34
Q

what may a larger P wave indicate

A

enlargment of atrium

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35
Q

what may a larger Q wave indicate

A

myocardial infarction

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36
Q

what may a large R wave indicate

A

enlarged ventricles

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37
Q

what may a flat T wave indicate

A

heart muscle recieving insuffecient oxygen

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38
Q

what is atrial fibrillation

A

muscle fibres are a synchrinous - atrial pumping may cease all together

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39
Q

describe a fib in ECG

A

typically no clearly defined P wave + irregularly spaced qrs complexes

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40
Q

what is atrial extrasystole

A

Atrial extrasystole is where the stimulus is thought to arise in the atrium elsewhere than at the SA node

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41
Q

what is ventricular extrasystole

A

Atrial extrasystole is where the stimulus is thought to arise in the atrium elsewhere than at the SA node

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42
Q

what are the cardiac effects of digoxin

A
  • Cardiac slowing and reduced rate of conduction through AV node, due to increased vagal activity
  • Increased force of contraction
  • Disturbances of rhythm, especially block of AV conduction and increased ectopic pacemaker activity
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43
Q

what are the mechanisms of digoxin

A

Digoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. The sodium calcium exchanger tries to extrude the sodium and in so doing pumps in more calcium. Increased intracellular concentrations of calcium may promote activation of contractile proteins (actin and myosin). This strengthens ventricular contractions so that the heart is able to pump more blood with each beat. It also helps to slow the heart rate by blocking the number of electrical impulses that pass through the AVN into the ventricles.

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44
Q

what family of medication is digoxin

A

glycosides

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45
Q

what are some draw backs of digoxin

A

Adverse effects are common and can be severe. One of the main drawbacks of glycosides, such as digoxin, in clinical use is the narrow margin between effectiveness and toxicity.

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46
Q

what are the cardiac effects of adrenaline

A
  • Increases heart rate
  • Direct stimulation of cardiac muscle which increases the strength of ventricular contraction
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47
Q

what is the mechanism of adrenaline

A

nonselective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, β3, to produce a ‘fight or flight’ response. Its mechanism of action is via membrane receptors, which trigger a second messenger response. Action on the β1 receptors increases the heart rate and contractility of the heart.

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48
Q

What are the 4 main components of vascular walls

A

a. Endothelial cells
b. Elastic fibres
c. Collagen fibres
d. Smooth muscle cells

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49
Q
  1. What are the three layers of blood vessel walls
A

a. Intima
b. Media
c. Adventitia

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50
Q

What blood vessel has the most collagen fibres

A

a. Vena cava

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51
Q

which blood vessel has the most smooth muscle

A

a. Medium arteries /vena cava

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52
Q

Why are arteries elastic

A

a. High compliance to allow for peak ejection flows
b. Recoil forces blood to move on

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53
Q

What causes varicose veins

A

a. Leaky valves allowing black flow

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54
Q

What is the function for the precapillary sphincter

A

a. Redirects blood to deficit region

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55
Q

Where are precapillary sphincters found

A

a. Mesenteric and cerebral circulations

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56
Q

What is a met arteriole

A

a. Short microvessel that links arterioles to capillaries

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57
Q

What are the three groups of capillaries and where are they found

A

a. Continuous capillary – skin, muscle (intercellular clefts)
b. Fenestrated capillaries – glands, villi, kidney glomeruli
c. Sinusoidal (discontinuous) capillaries – liver bone marrow

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58
Q

What type of junctions do capillaries in the blood brain barrier have

A

a. Tight junctions

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59
Q

What maintains the shape of erythrocytes

A

a. Glycophorin
b. Band 3 cl HCO3 exchanger

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60
Q

Examples of granulocytes

A

a. Neutrophils
b. Eosinophils
c. Basophils

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61
Q

Examples of non granular

A

a. Lymphocytes
b. Monocytes

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62
Q

What cells do platelets bud off from

A

megakaryocytes

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63
Q

What structures are found in platelets

A

a. Mitochondria
b. Lysosomes
c. Peroxisomes
d. Alpha granules
i. Van willebrans factor
ii. Clotting factor
iii. Fibrinogen

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64
Q

What is the function of platelets having serotonin

A

a. Cause recruitment of other platelets

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65
Q

What is blood viscosity dependent on

A

a. Haematocrit
b. Fibrinogen
c. Vessel radius
d. Linear velocity
e. Temperature

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66
Q

When does blood vessel turbulence occur

A

a. When the radius is large
b. When the velocity is high
c. Local stenosis

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67
Q

What is transmural pressure

A

c. Difference between intravascular pressure and tissue pressure

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68
Q

What factors cause van Willebrand release

A

a. Shear high forces
b. Cytokines
c. Hypoxia

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69
Q

What structures make up a blood clot

A

a. Erythrocytes
b. Leukocytes
c. Serum
d. Mesh of fibrin

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70
Q

When is the intrinsic pathway activated

A

a. Through surface contact activation
b. Membrane of activated platelets

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71
Q

When is the extrinsic pathway activated

A

a. In response to an outside trauma and blood leaving the vascular system

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72
Q

Describe the intrinsic pathway

A

a. Initiated due to blood exposure to negative surface
b. This activates factor 12 into factor 12a
c. Factor 11a cleaves prekallikrien to form kallikrein
d. Factor 11a converts 9 to 9 a
e. Factor 8to 8a
f. 10 to 10a
g. 10a with co factor 5a converts prothrombin to thrombin

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73
Q

Describe the extrinsic pathway

A

a. Platelet plug formed due to tissue injury
b. This causes expression of tissue factor
c. Tissue factor and factor 7a activate factor10
d. 10a and factor 5a convert prothrombin into thrombin

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74
Q

What is the importance of thrombin

A

a. Cleaves fibrinogen into fibrin

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75
Q

What 2 layers make up the pericardium

A

a. The parietal pericardia
b. The visceral pericardia

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76
Q

What is the name for the right atrioventricular valve

A

a. the tricuspid

77
Q

what is the name for the left atrioventricular valve

A

a. the mitral valve

78
Q

what heart wall layer produces pericardium fluid

A

epicardium

79
Q

what type of cells make up the heart

A

a. contractile cells
b. conducting cells

80
Q

what 2 types of cell junctions link cardiac cells

A

a. desmosomes anchor fibres together
b. intercalated disc gap junctions form channels

81
Q

What is the P wave represent

A

a. The depolarisation of the atrium

82
Q

What does the PQ region represent

A

a. The time the impulse travels from the SA node to the AV node

83
Q

What does the QRS complex represent

A

a. The firing of the AV node and ventricular depolarization

84
Q

What does the Q wave represent

A

a. Depolarization of interventricular septum

85
Q

What does the R wave represent

A

a. Depolarization of the main mass of the ventricles

86
Q

What does the S wave represent

A

a. The last phase of the ventricles depolarizing

87
Q

What signal is obscured by the QRS wave

A

a. Repolarization of the atrium

88
Q

What does the ST segment represent

A

a. The myocardial contraction

89
Q

What does the T wave represent

A

a. Ventricular repolarization

90
Q

When does atrial contraction occur on the ECG

A

a. About 0.1 milliseconds after the P wave

91
Q

What is the dicrotic notch

A

a. A blip when aortic valve closes

92
Q

How is pulse pressure calculated

A

a. Systolic pressure – diastolic pressure

93
Q

In the short term how is blood pressure regulated

A

a. Baroreceptors in carotid and aortic sinuses
b. Nucleus tractus solitarius in the brain stem

94
Q

How is arterial pressure regulated long term

A

a. Renin angiotensin aldosterone system

95
Q

Where is decreased pressure detected in the renin/angiotensin system

A

a. Decrease in renal perfusion
b. Mechanoreceptors in afferent kidney arterioles

96
Q

What does the reduced renal perfusion stimulate

A

a. Prorenin to be converted to renin
b. Renin converts angiotensinogen to angiotensin
c. ACE catalyses its conversion to angiotensin 2

97
Q

What are the affects of angiotensin 2

A

a. Adrenal cortex synthesize and secrete aldosterone
b. Increase NA absorption
c. Increase thirst
d. Vasoconstriction

98
Q

What is chronic hypertension

A

a. Baroreceptors do not perceive the elevated BP as abnormal
b. Hypertension not corrected

99
Q

Examples of diseases high BP can increase risk

A

a. Heart related
b. Aneurysms
c. Vascular dementia
d. Kidney disease
e. Stroke

100
Q

What are the treatments for CHBP

A

a. ACE inhibitors
b. Angiotensin 2 receptor blockers
c. Diuretics – thiazide
d. Calcium channel blockers – prevents calcium from entering cells of heart and arteries
e. Alpha blockers – relax blood vessels
f. Alpha agonists
g. Renin inhibitors

101
Q

Under which structures of the ribcage is the right side of the heart found

A

a. Between the 3rd and 6th

102
Q

Under which structures of the ribcage is the left side of the heart found

A

a. 2nd costal cartilage and 5th intercostal space

103
Q

What three vessels enter the right atrium

A

a. Superior and inferior venae cavae which together deliver blood to the heart from rest of the body
b. Coronary sinus which returns blood from the walls of the heart

104
Q

What is the name of the outflow tract that leads to the pulmonary trunk

A

a. The conus arteriosus

105
Q

What is the septomarginal trabecula

A

a. Bridge between lower portion of interventricular septum to base of the anterior papillary muscle

106
Q

How do the trabeculae carneae differ in each ventricle

A

a. Finer and more delicate in the left than in the right

107
Q

Which coronary artery provides both ventricles and left atrium with blood

A

a. Left coronary artery

108
Q

Which cardiac vein drains the areas supplied by the LEFT CA

A

a. Great cardiac vein

109
Q

Which cardiac vein drains areas supplied by the posterior interventricular branch of the right coronary artery (left and right ventricles

A

a. Middle cardiac vein

110
Q

What vein drains the right atrium and right ventricle

A

a. Small cardiac vein

111
Q

What vein drains the right atrium and directly empties into the right atrium

A

a. Anterior cardicac veins

112
Q

Name of the tissue that lines the inner heart wall

A

a. Endocardium – squamos epithelium

113
Q

What are the layers of the pericardium

A

a. Fibrous pericardium – tough
b. Serous pericardium
i. Parietal pericardium
ii. Visceral pericardium

114
Q

Pericardial cavity is between which two layers

A

a. Parietal and visceral

115
Q

What is STEMI

A

a. Elevated ST segment myocardial infarction – the artery Is completely blocked off
b. Hump shape

116
Q

What is NSTEMI

A

a. Non-ST elevation myocardial infarction
b. Partial blockage of coronary artery – raised troponin levels

117
Q

What are the cardinal symptoms of acute coronary syndromes

A

a. Chest pain
b. Arm pain
c. Breathlessness
d. Palpitations
e. Syncope

118
Q

What are the differences of symptoms between angina and MI

A

a. Angina is often exercise
b. Angina is worsened by cold
c. MI is 30 minutes +

119
Q

What are the symptoms of pericarditis

A

a. Sharp stabbing pain
b. Worse with inspiration
c. Worse lying flat
d. Eased y sitting up + NSAIDS
e. Hours to days

120
Q

What are the causes of pericarditis

A

a. Infection
b. Pericardial infusion – infection, malignancy, lymphoma

121
Q

What are the changes on the ECG for pericarditis

A

a. Concave scooped ST elevation – U SHAPE

122
Q

What are the symptoms of aortic dissection

A

a. Sudden, tearing, knife-like pain
b. Excruciating
c. Radiated to back
d. Often seen in elderly population with hypertension
e. Seen in people with stressful jobs with hypertension at a young age

123
Q

What are the symptoms of pulmonary embolus

A

a. Over infarcted area
b. Pleuritic pain
c. Associated with SOB
d. Tachycardia/AF
e. Tachypnoea

124
Q

What is an aortic dissection

A

a. a serious condition in which a tear occurs in the inner layer of the body’s main artery

125
Q

what is a pulmonary embolus

A

a. blockage in the lungs

126
Q

what is dyspnoea

A

a. abnormal uncomfortable awareness of breathing

127
Q

what is tachypnoea

A

a. fast breathing

128
Q

what is paroxysmal nocturnal dyspnoea

A

a. Paroxysmal nocturnal dyspnea (PND) causes sudden shortness of breath during sleep. As a result, you wake up gasping for air.
b. PND is caused by the failure of the left ventricle. When this happens, it is unable to pump as much blood as the right ventricle, which is functioning normally. As a result, you experience pulmonary congestion, a condition in which fluid fills the lungs

129
Q

What are the symptoms of paroxysmal nocturnal dyspnoea

A

Wake from sleep (2 to 4 hours)
b. Cough, wheeze
c. Have to sit up while sleeping - Ask how many pillows they sleep with at night
d. Frightening
e. Lasts 15-30 minutes

130
Q

What is syncope

A

a. Transient loss of consciousness (fainting) and postural control (collapse) due to cerebral hypoperfusion

131
Q

What can cause a S3 heart sound

A

a. Occurs with cardiac problems such as a failing left ventricle as in dilated congestive
b. heart failure
c. * Caused by the oscillation of blood back and forth between the walls of the ventricles
d. after the rush of blood from the atria

132
Q

what can cause S4 heart sounds

A

a. Just after atrial contraction/end of diastole before S1 * Produced by the sound of blood being forced into a stiff or hypertrophic ventricle (caused by aortic stenosis, hypertension, hypertrophic cardiomyopathy)

133
Q

What blood pressure would be hypertension

A

a. Systolic blood pressure of 140

134
Q

What do you see in chronic hypertension

A

a. Increased vascular tone
b. Enhanced sympathetic activity
c. Increased levels of angiotensin

135
Q

What is Renal artery stenosis

A

a. he narrowing of one or more arteries that carry blood to your kidneys

136
Q

what causes renal artery stenosis

A

a. caused by atherosclerosis

137
Q

what is atherosclerosis

A

a. build up of plaque in the inner lining of an artery

138
Q

what is Primary hyperaldosteronism (Conn’s syndrome)

A

a. Adrenal tumours (or more commonly hyperplasia) that produces aldosterone.

139
Q

What is pheochromocytoma

A

a. Rare adrenal medullary tumours secreting catecholamines.
b. * α-mediated vasoconstriction
c. * β-mediated cardiac stimulation

140
Q

What is coarction of the aorta

A

a. Rare congenital disease - If the isthmus of the aorta (just after the left subclavian artery) doesn’t develop properly it is stenosed. Narrower than usual

141
Q

What are the affects of hypertension on the aorta

A

a. Atheroma
b. Aneurysm
c. Aortic dissection

142
Q

What are the affects of hypertension on the brain

A

a. Thrombotic
b. Increased carotid atheroma
c. Haemorrhagic

143
Q

What are the affects of hypertension on the kidneys

A

a. Glomerular damage
b. Renal artery stenosis/atheroma

144
Q

What are the affects of hypertension on the eye

A

a. Hypertensive retinopathy
b. Pailloedema

145
Q

what are the 5 types of medications used to treat CHF

A

diuretics
ace inhibitor
angiotensin receptor blocker
beta blockers
mineralocorticoid receptor blockers

146
Q

what is the mechanism for ace inhibitors

A

ACE inhibitors block angiotensin converting enzyme in the lungs, to lower blood pressure

147
Q

what type of medication is ramipril

A

ace inhibitor

148
Q

what is the mechanism of ARBs

A

angiotensin receptor blockers, prevents ang II being converted to aldesterone

149
Q

what type of medication is losartan

A

angiotensin receptor blocker

150
Q

what is coughing a common side of effect of which medication

A

ACE inhibitors

151
Q

what is the mechanism for MRAs

A

Mineralocorticoid receptor agonists are potassium sparing diuretics which block the effects of aldosterone

152
Q

what type of medication is eplerenone

A

MRA

153
Q

what type of medication is spironolactone

A

MRA

154
Q

which beta blockers are used in heart failure

A

carvedilol, metaprolol, bisoprolol

155
Q

what is the mechanism of ivabridine

A

IF current is responsible for spontaneous depolarisation in pacemaker cells which
results in heart beating, ivabridine blocks IF so slows down the rate of spontaneous depolarisation which slows the heart rate - This is the only effect it has so very specific (no change in BP
etc)- voltage gated sodium channels

156
Q

what class of drug is ivabradine

A

hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blockers

157
Q

what is the mechanism of sacubitril/valsartan

A
  1. The heart produces natriuretic peptides - Vasodilators that
    make you excrete salt and water in urine
  2. Natriuretic peptides (ANP and BNP) are broken down by neutral endo-peptidase
    (NEP)
  3. sacubitril inhibits NEPs
  4. valsartan
158
Q

why are drugs such as digoxin and amlodopine avoided in heart failure

A

amlodipine - negative inotrope
digoxin - possible toxicity?

159
Q

antihypertensives

A

a - ACE inhibitors
b - beta blockers
c - calcium channel blockers
d - diuretics

160
Q

what is the mechanism of calcium channel antagonists

A

Block calcium entry into smooth muscle cells
 Causes smooth muscle cells to relax (vasodilation)
 Slows heart rate and useful for angina

161
Q

what are the two classes of calcium channel antagonists

A

dihydropiridines/non - dihydropirines

162
Q

what type of medication is amlodipine

A

dihydropiridine calcium channel antogonist

163
Q

what type of medication is nifedipine

A

dihydropiridine calcium channel antagonist

164
Q

what type of medication is verapamil

A

non-dihydropiridine calcium channel antogonist

165
Q

what type of medication is diltiazem

A

non-dihydropiridine calscium channel antagonist

166
Q

what is the mechanism for alpha blockers

A

Mediate sympathetic vasoconstriction

167
Q

what class of drug is doxazosin

A

alpha blocker

168
Q

what is the mechanism for central agents

A

Stimulate central alpha receptors to decrease sympathetic outflow. Side effects include
sedation and dry mouth.

169
Q

what type of medication is clonidine

A

central agent

170
Q

what process forms cardiac cells

A

myogenesis

171
Q

describe pace maker cells

A

autorythmic, contract in the absence of neuronal innervation

172
Q

what are intercolated discs

A

contain gap junctions, provide communication channels between cells, allow waves of depolarization to sweep across cells

173
Q

what actin makes up cardiomyocytes

A

2 strands of alpha globular protein

174
Q

how is the cardiac action potentiol different from normal muscle cells

A

repolarization takes longer to occur and there for cannot be stimulated at high frequency, prevented from going into tetanus - prolonged contraction

175
Q

what is atrial systole

A

lasts 0.1 seconds, atria are contracting, ventricles are relaxed

176
Q

what is ventricular systole

A

0.3 seconds, ventricules are contracted, atria are relaxed

177
Q

which valves are the AV valves

A

tricusbid and mitral

178
Q

what is the first heart sound

A

blood turbulence associated with the turbulence of closure of AV valves

179
Q

what is the second heart sound

A

blood turbulence associated with the closure of SL valves

180
Q

what is cardiac reserve

A

the difference between a person’s maximum cardiac output and their cardiac output at rest

181
Q

where is the cardiovascular system in the brain

A

medulla oblongatat

182
Q

what division of the nervous system is directly responsible for heart rate

A

autonomic division of the peripheral nervous system

183
Q

role of parasympathetic nerous system in heart

A
  • Decreases heart rate
  • Reduces force of contraction
  • Constricts the coronary arteries
    from the right and left vagus nerve
184
Q

role of the sympathetic nervous system

A
  • Increases heart rate
  • Increases the force of contraction
  • Vasoconstriction
    from the sympahtic trunk
185
Q

the effects of adrenaline and noreadrenaline

A

enhance the heart’s pumping effectiveness, they increase both heart rate and contractility.

186
Q

the role of thyroid hormones on heart rate

A

enhance cardiac contractility and increase heart rate.

187
Q

the effect of elevated K or Na

A

decreases heart rate and contractility, na blocks ca inflow decreasing forces of contraction, excess k blocks generation of action potentials

188
Q

excess intistitial ca

A

speeds up heart rate and strnegthens heart beat

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