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Anatomy and Phyisology > HLTH cardio system review > Flashcards

HLTH cardio system review Flashcards

1
Q

heart location

A

located within the mediastinum and the double walled pericardial sac

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2
Q

3 layers of the heart

A

endocardium, myocardium, and epicardium

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3
Q

atrioventricular valves

A

bicuspid or mitral valve (left side) and tricuspid valve (right side)

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4
Q

where does the heart conduction pathway begin?

A

the SA node

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5
Q

sinus rhythm

A

rhythm established by the SA node

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6
Q

order of flow of heart conduction

A

SA node > AV node > bundle of His > right and left bundle branches > purkinje fibres

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7
Q

P wave of ECG

A

is the atrial depolarization

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8
Q

QRS wave

A

ventricular contraction (and atrial relaxation but this is masked)

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9
Q

T wave

A

represents repolarization of the ventricles

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10
Q

what detects changes in BP?

A

the baroreceptors in the aorta and carotid arteries

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11
Q

sympathetic receptors in the heart

A

beta1-adrenergic receptors

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12
Q

two arteries branching off the aorta

A

left and right coronary arteries

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13
Q

what does the left coronary artery branch into?

A

the left anterior descending artery and the left circumflex artery

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14
Q

what does the right coronary artery branch into?

A

the right marginal artery and the posterior interventricular artery

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15
Q

when is blood flow to the heart the greatest?

A

during diastole or relaxation

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16
Q

collateral channels

A

exist between vessels and are important if one gets obstructed; more develop with aerobic exercise

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17
Q

what does the right coronary artery supply?

A

the right side of the heart, the posterior left ventricle, and the posterior interventricular septum

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18
Q

what does the left coronary artery supply?

A

the anterior sides of the ventricles, the anterior septum, and the left atrium

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19
Q

lubb sounds

A

closing of the AV valves

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20
Q

dubb sounds

A

closing of the semilunar valves

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21
Q

what causes heart murmurs?

A

defective valves that don’t close completely or a hole in the heart septum

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22
Q

apical pulse

A

refers to pulse measured at the heart itself

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23
Q

pulse deficit

A

difference between the radial pulse and the apical pulse

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24
Q

cardiac output

A

the volume of blood ejected by a ventricle in one minute; SV x HR

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25
Q

cardiac reserve

A

refers to the heart’s ability to increase output in response to increased demand

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26
Q

preload

A

refers to the heart at the end of diastole with ventricles at their maximum volume

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27
Q

afterload

A

the force required to eject blood from the ventricles

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28
Q

blood pressure

A

refers to pressure against the systemic arterial walls

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29
Q

systolic pressure

A

is the pressure exerted by the blood during systole of the left ventricle

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30
Q

diastolic pressure

A

refers to pressure that is sustained during diastole

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31
Q

pulse pressure

A

difference between systolic pressure and diastolic pressure

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32
Q

peripheral resistance

A

forces opposing blood flow such as friction

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33
Q

2 ways BP is elevated by the sympathetic system

A

beta1-andregenic receptors increase HR and vasoconstriction occurs

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34
Q

what is an ECG useful for?

A

myocardial infarction, infections, and arrhythmias

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35
Q

echocardiography

A

ultrasound is used to record images of the heart and valve movements; useful for valve defects and congenital defects

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36
Q

nuclear imaging

A

is done with thallium and can asses the size of an infarction

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37
Q

single-photon emission

A

can assess cardiac ischemia at rest

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38
Q

troponin blood tests

A

can measure the level of blood proteins called troponins that are released when the myometrium is damaged

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39
Q

doppler studies

A

a microphone that assess blood flow or obstruction of a vessel

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40
Q

benefits of exercise for the heart

A

decreases serum lipid levels, increases high-density lipoprotein levels, and reduces stress

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41
Q

smoking effects on the heart

A

increases vasoconstriction and heart rate, increases platelet adhesion and thrombus formation, and increases serum lipid levels

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42
Q

vasodilators example and function

A

decrease peripheral resistance, but may also decrease blood pressure; ex. nitroglycerin or isosorbide

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43
Q

beta-blockers function and example

A

prescribed for hypertension and dysrhythmias and act on beta1-adrengenic receptors; ex. metoprolol or atenolol

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44
Q

calcium channel blockers

A

block the movement of calcium into the smooth muscle, thus decreasing contractions

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45
Q

digoxin

A

slows conduction of heart rate (less frequent but more powerful) and used for atrial dysrhythmias

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46
Q

side effects of antihypertensive drugs

A

orthostatic hypotension

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47
Q

anticoagulant drugs

A

aspirin or warfarin, however, hemorrhage can be a risk

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48
Q

cholesterol or lipid lowering drugs

A

are prescribed when exercise and diet are ineffective and are the statin drugs, ex. simvastatin

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49
Q

what does coronary heart disease include?

A

angina pectoris or an MI

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50
Q

dangers of coronary heart disease

A

decreased O2 delivery to the myocardium

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51
Q

cause of angina

A

a deficit of O2 to the myocardium which can be caused by obstructions, spasms, or hypertrophy of the heart

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52
Q

variant angina

A

when vasospasm occurs at rest

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53
Q

unstable angina

A

refers to prolonged pain at rest, perhaps the result of a break of an atheroma

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54
Q

what usually precedes angina?

A

an increased demand for O2; can be exercise, getting angry, following an infection, or eating a large meal

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55
Q

signs of angina

A

chest pain that can radiate to the neck or left arm, followed by pallor, diaphoresis (excessive sweating), or nausea

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56
Q

treatment for angina

A

usually vasodilators like nitroglycerin

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57
Q

myocardial infarction

A

is a heart attack due to death of myocardial tissue due to ischemia

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58
Q

risk for those surviving an MI

A

recurrent MI, CHF, or stroke

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59
Q

2 broad types of MIs

A

ST elevation or non-ST elevation

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60
Q

most common cause of an MI

A

atherosclerosis with thrombus attached

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61
Q

3 causes of an infarction

A

thrombus in an artery grows, vasospasm + partial obstruction, or thrombus breaks away and lodges in a smaller artery

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62
Q

what happens to the heart tissue following infarction?

A

necrosis, inflammation, and fibrous tissue develop, as well enzymes are released

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63
Q

warning signs of an MI

A

persistent chest pain radiating to the left arm, pallor, and rapid, weak pulse

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64
Q

what treatment can prevent permanent heart tissue damage before an MI?

A

thrombolytic therapy

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65
Q

what enzymes are elevated during an MI?

A

LDH-1, aspartate aminotransferase, and creatine phosphokinase with M and B subunits

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66
Q

what causes death during an MI?

A

ventricular arrhythmias and fibrillation

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67
Q

Cardiogenic shock

A

occurs if the pumping capability of the left ventricle is greatly impaired

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68
Q

silent MI

A

no pain is present but gastric discomfort may indicate the infarction

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69
Q

heart block

A

occurs when conduction fibres in the infarcted area can no longer function due to problems in the AV node or bundle of His

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70
Q

what are major causes interfering with the heart conduction cycle?

A

damage to the system or electrolyte imbalances (resulting from stress, fever, hypoxia, infection, or drug toxicity)

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71
Q

major problems with irregular heart contractions?

A

they interfere with normal filling and emptying cycles of the heart

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72
Q

a very rapid heart rate reduces cardiac output because

A

it reduces ventricular filling

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73
Q

brachycardia rate and cause

A

less than 60 bpm and is often an issue with the vagus nerve and the PNS; can cause increased SV

74
Q

tachycardia rate

A

100-160 bpm

75
Q

sick sinus syndrome

A

is alternating bradycardia and tachycardia

76
Q

most common dysrhythmias

A

atrial conduction abnormalities

77
Q

extra contractions name

A

ectopic beats

78
Q

premature atrial contractions

A

are extra contractions or ectopic beats usually resulting from irritable muscle cells outside of the conduction pathway

79
Q

palpitations

A

rapid or irregular heart beats resulting from excessive caffeine intake, smoking, or stress

80
Q

atrial flutter

A

rate of 160-350 bpm and is due to the AV node delaying conduction

81
Q

atrial fibrillation

A

more than 350 bpm and causes pooling of blood in the atria

82
Q

what is atrial fibrillation treated with?

A

anticoagulants

83
Q

first-degree block

A

the time between atrial and ventricular contractions is delayed

84
Q

second-degree block

A

when a conduction delay at the AV node results in intermittent missed ventricular
contractions

85
Q

total or third degree block

A

occurs when there is no transmission from the atria to the ventricles, causing the ventricles to contract at a rate of 30-45 bpm; the ventricles are totally independent of the atria

86
Q

bundle branch block

A

occurs as a result of a problem in one of the bundle branches; does not alter CO but does show up on a ECG as a prolonged QRS wave

87
Q

ventricular tachycardia

A

reduces CO because ventricular filling is reduced

88
Q

ventricular fibrillation

A

muscles are contracting independently and rapidly and this is ineffective is ejecting blood, causing hypoxia to the myocardium

89
Q

PVCs

A

are additional beats from a ventricular muscle cell and usually are no concern, but if occur frequently this can cause ventricular fibrillation and CHF

90
Q

stroke volume

A

ESP - EDP

91
Q

problem with bradycardia

A

can cause increased SV

92
Q

problem with tachycardia

A

can decrease CO

93
Q

treatment for arrhythmias

A

changing medication (potassium sparing diuretics or beta-blockers), beta-adrenergic blockers, calcium blockers, digoxin (atrial), or pacemakers

94
Q

cardiac arrest

A

cessation of all heart activity causes no oxygen delivered to the body

95
Q

congestive heart failure

A

occurs when the heart is unable to pump blood to meet the metabolic needs of the body; usually one side of the heart fails first, followed by the other side

96
Q

how do the body’s compensation mechanisms make CHF worse?

A

reduced blood flow causes aldosterone secretion, but vasoconstriction adds to the heart’s workload; SNS response also increases HR; and the heart chambers dilate and then hypertrophy

97
Q

2 basics effects resulting from CHF

A

CO decreases (causes lethargy, fatigue, and acidosis) and backup congestion occurs

98
Q

left-sided CHF

A

the left ventricle pumping is impaired, causing systemic circulation volume to decrease and for blood to be backed up returning to the left ventricle; pulmonary edema occurs

99
Q

right-sided CHF

A

the right ventricle pumping is impaired, causing congestion in the systemic circulation, apparent in the feet, legs, and hepatic circulation

100
Q

leading cause of CHF

A

coronary artery disease

101
Q

cor pulmonale

A

is right-sided CHF due to pulmonary disease

102
Q

forward effects of CHF

A

same for both left and right sided; are fatigue, weakness, dyspnea, exercise intolerance, cold intolerance, and dizziness

103
Q

backup effects of left-sided CHF

A

dyspnea (when lying down), cough, and paroxysmal nocturnal dyspnea

104
Q

paroxysmal nocturnal dyspnea

A

occurs when sleeping and waking up short of breath and possibly hemoptysis; due to pulmonary edema

105
Q

backup effects of right-sided CHF

A

edema in the lower limbs, hepatomegaly, splenomegaly, ascites, flushed face, distended neck veins, headache, and visual disturbances

106
Q

signs of CHF in children

A

feeding difficulties, delayed growth, sleep problems, and cough

107
Q

congenital heart defects

A

are valve, septal, shunt, or vessel problems developing in the first 8 weeks of embryonic life; can be environmental or genetic

108
Q

left-to-right shunt

A

blood from the left side of the heart goes to the right side, leading to increased volume in the pulmonary circulation and decreased CO

109
Q

right-to-left shunt

A

blood from the right side of the heart goes to the left side, causing the lungs to be bypassed

110
Q

acyanotic conditions

A

result when systemic blood consists of oxygenated blood

111
Q

cyanotic conditions

A

venous blood mixes with arterial blood, permitting significant amounts of unoxygenated blood to bypass the lungs and enter the systemic circulation; causes bluish colour of the lips and nails

112
Q

signs of a minor heart defect

A

heart murmur

113
Q

signs of a major heart defect

A

pallor, cyanosis, dyspnea, clubbed fingers, delayed growth, cold and exercise intolerance, tachycardia, and squatting position

114
Q

most common congenital heart defect

A

ventricular septal defect

115
Q

ventricular septal defect

A

is a hole in the interventricular septum, causing a left-to-right shunt of blood; this results in more blood entering the pulmonary circuit (causes pulmonary hypertension) and less in the systemic

116
Q

what valves are most often defected?

A

semilunar valves

117
Q

stenosis for valves

A

refers to the narrowing of a valve

118
Q

incompetence for valves

A

refers to a valve not completely closing, causing backflow of blood

119
Q

Mitral valve prolapse

A

refers to abnormally large leaflets that backwards with pressure

120
Q

result of valvular defects

A

the heart has to work harder to maintain pumping and SV, causing the heart to hypertrophy and eventually fail

121
Q

4 defects in the tetralogy of fallot

A

pulmonary valve stenosis, VSD, dextroposition of the aorta, and right ventricle hypertrophy

122
Q

result of the tetralogy of fallot

A

the pulmonary circulation receives low amounts of unoxygenated blood from the right ventricle and the oxygen deficit is great

123
Q

rheumatic fever

A

results from an abnormal immune response occurring a few weeks after an untreated infection; inflammation will affect the heart, skin, and joints, and scar tissue will form in the heart

124
Q

what is the cause of rheumatic fever?

A

a group A beta hemolytic streptococcus

124
Q

what does the preceding infection of rheumatic fever present as?

A

an upper respiratory infection, strep throat, tonsillitis, or pharyngitis

124
Q

problems of pericarditis and rheumatic fever

A

may cause effusion, which impairs filling

125
Q

problems of myocarditis and rheumatic fever

A

may cause aschoff bodies to develop, which interfere with conduction

126
Q

problems of endocarditis and rheumatic fever

A

endocarditis is the most common and the mitral valve is usually affected; valves are affected, causing verrucae to form and can result in stenosis

127
Q

verrucae

A

are wart like vegetations on the outer edge of valves

128
Q

effects of rheumatic fever not in the heart

A

joints are inflamed, skin develops rashes, nontender cutaneous lesions may form on extensor surfaces, and the basal nuclei in the brain are affected, causing rapid, jerky movements

129
Q

antibodies present for rheumatic fever

A

antistreptolysin O antibodies

130
Q

how does rheumatic fever manifest in later years

A

heart murmur and arrhythmias

131
Q

infective endocarditis

A

occurs when organisms invade the endocardium, causing inflammation and vegetations (fibrin, platelets, blood cells, and microbes) to develop around valves; can be acute or subacute

132
Q

example of an organism causing acute infective endocarditis

A

S aureus

133
Q

example of an organism causing subacute infective endocarditis

A

streptococcus viridans

134
Q

risk factors for developing infective endocarditis

A

valve defects, rheumatic fever, mitral prolapse, and those with a depressed immune system

135
Q

subacute endocarditis signs

A

fever, anorexia, splenomegaly, painful red nodes on the fingers, or CHF

136
Q

acute endocarditis signs

A

spiking fever, chills, drowsiness, and impairment of heart function

137
Q

pericarditis

A

is usually secondary to another condition and can be acute or chronic; is large amounts of fluid accumulate, expansion and filling of the heart may be impaired, usually affecting the right side first

138
Q

serous fluid indication

A

inflammation

139
Q

purulent fluid indication

A

infection

140
Q

blood in fluid indication

A

trauma or cancer

141
Q

chronic pericarditis

A

signs are gradual and can cause adhesions between pericardial membranes, causing this to become tough and limiting movement

142
Q

signs of pericarditis

A

chest pain, dyspnea, tachycardia, cough, friction rub may be present, and neck veins may be distended

143
Q

another name for essential hypertension

A

primary

144
Q

secondary hypertension

A

is caused by renal problems, endocrine problems, or an pheochromocytoma

145
Q

pheochromocytoma

A

a benign tumor of the adrenal medulla or SNS ganglion chain

146
Q

malignant hypertension other name

A

resistant

147
Q

malignant hypertension

A

is an emergency and can damage organ damage, including damage to the CNS and renal system

148
Q

rate for hypertension

A

above 140/90

149
Q

essential hypertension

A

occurs when there is an increase in arterial vasoconstriction and peripheral resistance; this often causes decreased RBF, triggers RAAS system and more vasoconstriction; over time vessels are damaged, become hard and thick

150
Q

complications of hypertension

A

wall may tear, causing an aneurysm, atheroma formation is triggered, and necrosis may develop

151
Q

areas most frequently impacted by hypertension

A

kidneys, brain, and retina

152
Q

signs of hypertension

A

fatigue, malaise, and morning headache

153
Q

shock

A

is caused by decreasing BV, leading to decreased tissue perfusion and general hypoxia, CO is usually low

154
Q

hypovolemic shock

A

is due to loss of circulating blood and can result following hemorrhage, burns, dehydration, or infections like pericarditis or pancreatitis

155
Q

cardiogenic shock

A

is due to decreased pumping capability of the heart and may result following an MI of the left ventricle or arrhythmias

156
Q

vasogenic shock

A

is vasodilation due to a loss of sympathetic and vasomotor tone and can be due to fear or pain, spinal cord injury, or hypoglycemia (insulin shock)

157
Q

anaphylatic shock

A

is vasodilation and increased permeability following an allergic reaction

158
Q

septic shock

A

is vasodilation due to severe infection, usually caused by gram-negative bacteria

159
Q

3 things blood pressure is determined by

A

blood volume, heart contraction, and peripheral resistance

160
Q

result of hypoxia from shock

A

anaerobic metabolism and increased lactic acid production

161
Q

compensation mechanisms for shock

A

SNS activation, adrenal cortex stimulation, RAAS system, ADH secretion, glucocorticoid secretion, and acidosis stimulates respirations

162
Q

does acidosis or alkalosis occur with shock?

A

acidosis

163
Q

signs of shock

A

first signs are thirst, agitation and restlessness; this is followed by cool, pale, moist skin, tachycardia, hyperventilation, and oliguria

164
Q

arteriosclerosis

A

is a general term for all arterial changes; elasticity is lost, walls become thick and hard, and the lumen narrows which all can lead to necrosis and ischemia

165
Q

peripheral vascular disease

A

refers to any vessel abnormality outside of the heart

166
Q

atherosclerosis

A

refers to the presence of a atheroma, which are plaques consisting of lipids, cells, fibrin, and debris, often with attached thrombi

167
Q

where do atheroma’s often form?

A

large arteries, typically at merging points

168
Q

low-density lipoproteins

A

are the bad lipids and have a high lipid content; they transport cholesterol from the liver to cells

169
Q

high-density lipoproteins

A

are the good lipids and have a low lipid content; they transport cholesterol from the peripheral cells to the liver

170
Q

how do thrombus develop?

A

usually following an injury, the inflammatory response causes an accumulation of WBCs and lipids, the smooth muscle proliferates and multiples, and platelets adhere to this; as this develops, prostaglandins are released, causing vasospasm and more inflammation

171
Q

signs of atheroma formation

A

weakness and fatigue in the legs, intermittent claudication, sensory impairment, weak peripheral pulse, and pallor/cyanosis

172
Q

intermittent claudication

A

leg pain associated with exercise due to muscle ischemia

173
Q

aneurysm

A

is a localized weakening and dilation of an arterial wall

174
Q

most common location for aneurysms

A

thoracic or abdominal aorta

175
Q

saccular aneurysm

A

occurs on one side of the vessels

176
Q

fusiform aneurysm

A

occurs on both sides of the vessel and is circumferential

177
Q

dissecting aneurysm

A

is when there is a tear in the tunica intima, causing blood to flow along the length of the vessel between layers

178
Q

causes of an aneurysm

A

atheromas, trauma (car accidents), syphilis, and congenital defects

179
Q

signs of an aneurysm

A

pain and shock symptoms

Anatomy and Phyisology (94 decks)

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