Ch. 8 (cardiovascular system) Flashcards
(130 cards)
1
Q
Layers of the heart
A
Pericardium: double-walled sac surrounding the heart
Epicardium (outer): CT, coronary arteries
Myocardium (middle): thick muscle
Endocardium (inner): smooth endothelium lining chambers
2
Q
Right side of heart
A
RA, RV
pulmonary pump
circulates blood into pulmonary arteries and lungs
3
Q
Left side of heart
A
LA, LV
systemic pump
circulates blood into aorta, organs, tissues
4
Q
Atrioventricular valves
A
Tricuspid and Bicuspid (mitral) valves
flap-like, between atria and ventricles, prevents black-flow to atria when ventricles contract
5
Q
Semilunar valves
A
pulmonary and aortic valve
cup-shaped, surround orifices of aorta and pulmonary artery, free margins of valves face upward, prevent back-flow into ventricles during diastole
6
Q
pulmonary valve
A
directs blood flow from RV to pulmonary trunk
7
Q
aortic valve
A
directs blood flow from LV to aorta
8
Q
Describe the blood flow through the heart including valves that are encountered.
A
Pulmonary circulation Oxygen-poor blood enters Right Atrium --> Tricuspid valve --> Pulmonary arteries --> Lungs
Systemic circulation Oxygenated blood in lungs --> Pulmonary veins --> Left Atrium --> Mitral valve --> Aorta --> Rest of body
9
Q
What is the purpose of the coronary circulation?
A
main blood supply of the heart
- Aorta branches to right and left coronary arteries carry arterial blood to the heart when relaxed
- Blood passes through capillary beds of myocardium
- Venous blood collected by cardiac veins
- Cardiac veins join together and form the coronary sinus that empties blood into the RA
10
Q
Right coronary artery (RCA)
A
Supplies posterior wall and posterior part of interventricular septum
11
Q
Left anterior descending artery (LAD)
A
Supplies anterior wall, anterior part of interventricular septum
12
Q
Left circumflex artery (LCA)
A
supplies lateral walls
13
Q
LCA branches
A
LAD and LCA
14
Q
Does adult cardiac muscle proliferate to replace damaged or destroyed muscle fibers?
A
NO
Most areas of cell death are repaired with non-contractile scar tissue
15
Q
In what order does current flow through the cardiac conduction system?
A
ORDER:
- Sinoatrial node (SA node)
- Atrioventricular node (AV node)
- Bundle of His (AV bundle)
- Right and left bundle branches
- Purkinje fibers
16
Q
How does the cardiac conduction system work?
A
- A group of specialized muscle cells that initiate electrical impulses
- Impulses are initiated in the SA (sinoatrial node) in RA near opening of the superior vena cava
- Ability of cardiac muscle to depolarize and contract is intrinsic; does not depend on the nervous system
17
Q
systole
A
contraction
18
Q
diastole
A
relaxation
atria fill
all valves closed
19
Q
atrial systole
A
increased atrial pressure causes atrial contraction, forcing blood into ventricles
20
Q
atrial diastole / ventricular systole
A
- AV valves close as pressure rises in ventricles
- Atria relax
- SL valves open when intraventricular pressures exceed pressure in aorta and pulmonary artery
- Blood from LV enter pulmonary trunk
- Blood from RV enters Aorta
21
Q
ventricular diastole
A
- Semilunar (SL) valves closed
- Venous blood returning to atria, flows into ventricles through open atrioventricular (AV) valves
- Additional blood pumped into ventricles during atrial systole
22
Q
different types of blood vessels
A
Large elastic arteries: conduct the blood to various locations throughout the body.
Arterioles: smaller vessels with muscular walls that regulate flow from the large arteries into the capillaries.
Capillaries: thin endothelium-lined channels that deliver nutrients to cells and remove waste products.
Veins: return blood to the heart under low pressure and usually travel with the arteries.
23
Q
systolic BP
A
pressure during ventricle contraction (highest BP)
24
Q
diastolic BP
A
pressure during ventricular relaxation (lowest BP)
25
ECG and uses
measures electrical activity of heart; used as a diagnostic tool; detects disturbances in rate, rhythm, conduction, muscle injury, extent of muscle damage
26
P wave
atrial depolarization by SA node
27
PQ segment
delay at AV node when atrial depolarization is complete
28
QRS complex
ventricle depolarization and atrial repolarization
29
ST segment
ventricle depolarization is complete
30
T wave
ventricular repolarization
31
depolarization
contraction, systole
32
repolarization
relaxation, diastole
33
Arrhythmia
any deviation from the normal heartbeat, i.e., the normal sinus rhythm
34
signs / symptoms of arrhythmias
- Palpitations
- Tachycardia
- Bradycardia
- Skipped heartbeats
- Syncope
- Fatigue
35
Etiology of arrhythmias
- Results when there is interference within the conduction system of the heart
- Ischemia and drugs cause many arrhythmias
36
normal sinus rhythm
- ECG that is within normal limits with a heart rate between 60-100 bpm
37
sinus bradycardia
A regular rhythm with a heart rate of <60 bpm
This may be normal in an athlete
38
sinus tachycardia
A regular rhythm with a heart rate of >100 bpm
39
atrial fibrillation (A-fib)
- Multiple areas of atrial depolarization
- extremely rapid, incomplete atrial contractions of 400-500 bpm
- Only some of these impulses reach the ventricles
- Causes ventricles to beat irregularly at 140-160 bpm
- Atria quiver
- seen in older people and those with CVD, COPD, hyperthyroidism
40
A-fib ECG
small, irregular, and uncoordinated P waves that cannot be distinguished; ventricular contraction also occurs at irregular intervals
41
A-fib treatment
* Slow down heart rate
* electrical cardioversion or pharmacologic therapy
* Anticoagulation
* Left atrial appendage occlusion device (Watchman device)
42
Premature Ventricular Contractions (PVCs) and causes
one of the most common and least harmful arryhthmias
causes:
- Lack of Sleep
- Caffeine
- Nicotine
- Alcohol
- Anxiety/Stress
43
Premature Ventricular Contractions (PVCs) ECG
- Characterized by a beat that comes early in the cycle, has no P wave, a wide QRS complex, and a different T wave
- The PVC is followed by a pause before the occurrence of the next normal cycle
44
Ventricular tachycardia (V-tach)
- Seen in patients with cardiac disease
| - life threatening and can rapidly deteriorate into ventricular fibrillation and cardiac arrest
45
Ventricular tachycardia (V-tach) ECG
- Characterized by 3 or more PVCs that occur at a rate of 150-250 bpm
- There are no P waves and the QRS complexes are distorted
46
Ventricular Fibrillation (V-fib) and ECG
- One of the more serious arrhythmias
- Rapid and uncoordinated ventricular beat
- Heart cells are contracting spontaneously and the heart just quivers
- It is totally ineffective for pumping blood and will quickly lead to death if not corrected
47
Cardiac arrest, symptoms, etiology, and treatment
Sudden, unexpected cessation of cardiac activity
Symptoms: patient is unresponsive, with no respiratory effort and no palpable pulse
Etiology: results from anoxia or interruption of the electrical stimuli to the heart
Treatment:
- CPR must be initiated within 4-6 minutes
- Defibrillation
- Epinephrine or dobutamine to stimulate the heart
- Antiarrhythmic drugs (lidocaine, amiodarone)
48
treatments for arrhythmias
Depends on the cause:
- Anti-arrhythmic drugs
- Anticoagulants
- oxygen
- Cardioversion (defibrillation)
49
who invented the defibrillator
Dr. Bernard Lown, MD
| nobel prize in 1985
50
What are the 2 types of valvular malfunction?
1. stenosis
| 2. insufficiency (incompetence, regurgitation)
51
Stenosis and common causes
- Hardening of cusps of valves that prevents complete opening of valves
- Impedes blood flow into next chamber
- Causes the heart to have to work harder to pump blood forward
Common causes:
- Rheumatic heart disease
- Infective endocarditis
- Congenital malformations
- Calcification of the valve cusps
52
Insufficiency (incompetence, regurgitation)
- Failure of valves to close completely
(Allows blood to be forced back into the previous chamber as the heart contracts)
-This exerts added pressure on that chamber and overloads the heart
(Ultimately the ventricle will dilate and fail)
53
Rheumatic fever
an immunologic reaction that develops weeks after initial streptococcal infection (NOT a bacterial infection)
- Commonly encountered in children
- Complication of group A beta hemolytic streptococcal infection (sore throat and scarlet fever)
- Anti-streptococcal antibodies against strep antigens cross react with similar antigens in tissues
- Antigen-antibody reaction injures connective tissue and causes fever
54
Rheumatic fever signs and symptoms
- Fever
- Inflammation of connective tissue throughout the body, especially heart and joints
- Acute arthritis (multiple joints)
- Inflammation of heart
55
Rheumatic fever clinical outcomes
- Death from severe inflammation and acute heart failure
- Healing with scarring of tissues (heart valves)
- Can recur if another streptococcal infection reactivates hypersensitivity and tissue damage
56
Rheumatic fever treament
After the development of rheumatic fever:
o Antibiotics
o Anti-inflammatory agents (NSAIDs and steroids)
o Antipyretics (fever reducers)
57
Rheumatic heart disease / cause
complication of rheumatic fever; primarily affects mitral and aortic valves
- In acute disease, valves become red, thickened, and swollen
- Inflammatory damage produces scarring causing stenosis or incompetence
58
Rheumatic heart disease prevention
- Treat beta strep infection promptly
- Prophylactic penicillin to prevent strep infections, reduce risk of recurrent rheumatic fever and further heart valve damage
59
mitral stenosis, etiology, treatment
- Most common of all valve diseases
- Impairs the passage of blood from the left atrium to the left ventricle
Etiology: rheumatic heart disease
Treatment:
- Diuretics
- Anticoagulants
- Surgical intervention includes commissurotomy, balloon valvuloplasty, valve replacement
60
two types of non-rheumatic aortic stenosis
Type 1: Aortic stenosis secondary to bicuspid aortic valve
Type 2: Calcific aortic stenosis
61
Type 1: Aortic stenosis secondary to bicuspid aortic valve
- Aortic valve has 2 cusps than usual 3 cusps
- Functions satisfactorily for a time, then becomes thickened, calcified, and rigid from increased strain on valve, leads to heart failure
- Occurs in 2% of population (RARE)
62
Type 2: Calcific aortic stenosis
Common valvular heart disease:
- Normal 3 cusps
- Leaflets undergo connective tissue degenerative changes → fibrotic, calcified, rigid → restricts valve mobility, stenosis
- Recent studies: also occurs with deposits of lipids and macrophages as in coronary atherosclerosis
63
clinical outcomes, of non-rheumatic aortic stenosis
Clinical outcomes:
- increased strain
- left ventricular hypertrophy
- heart failure
64
prevention and treatment of non-rheumatic aortic stenosis
Prevention: Control risk factors (high cholesterol, diabetes, hypertension, smoking)
Treatment:
• Digitalis can be used as an inotropic agent
• Anticoagulants
• Balloon valvuloplasty and valve replacement
65
Mitral valve prolapse
- Fairly common
- One or more of the cusps of the mitral valve protrudes back into the left atrium during ventricular contraction
- Prolapsing leaflets may not fit together tightly → blood leaks back into LA; mitral regurgitation
- Usually a benign, asymptomatic condition and does not require treatment
66
Etiology of mitral valve prolapse
- Abnormally long or short chordae tendineae may not allow the valve to close properly
- Malfunctioning papillary muscles
67
Infective endocarditis and what it can cause
- Bacterial endocarditis is most common
- Vegetations: build up of large, easily fragmented infective masses
Can cause:
- Erosion of valve leaflets
- Seeding of the blood with infective agent
- Embolization
68
Subacute infective endocarditis and symptoms
Caused by organisms of low virulence
Affects abnormal or damaged (mitral, aortic valves)
Platelets and fibrin may deposit on abnormal or damaged valves; then serve as sites for bacteria to implant or for thrombi to form followed by emboli and tissue infarction
Mild symptoms of infection
69
Prophylactic antibiotics are given prior to dental or surgical procedures to prevent
Subacute and actute infective endocarditis
70
Acute infective endocarditis, symptoms, at risk groups
- Caused by highly pathogenic organisms, commonly staphylococci
- Affects normal heart valves
- Severe symptoms of infection and valve destruction
- at risk groups: intravenous drug
71
treatment and prevention for acute infective endocarditis
- IV anti-infective therapy
- Antipyretics
- Anticoagulants
- surgical repair or replacement of valves
prevention: prophylactic antibiotics given prior to dental or surgical procedures
72
hypertension and how it develops
Elevated blood hydrostatic pressure in the systemic arterial system
Excessive vascoconstrition of small arterioles resulting in:
o Increased peripheral resistance --> increased diastolic blood pressure
o Results in an increased force of ventricular contraction --> Compensatory increase in systolic pressure
73
BP categories:
- normal
- elevated
- hypertension stage 1
- hypertension stage 2
normal: <120/<80 max
elevated: 120-129/<80
stage 1: 130-139/80-89
stage 2: >140/90
74
hypertension treatment goal and symptoms
<130/80 for most people, depending on:
- Calculated 10-year risk for heart disease and stroke
- Other medical conditions of patient
usually asymptomatic
75
risk factors of hypertension
- Genetics
- Race
- Increased age
- Smoking
- Obesity
- Stress
- Sedentary lifestyle
76
Primary/essential Hypertension (HTN)
90-95% of cases
IDIOPATHIC CAUSE
- Thought to be due to some defect in the blood pressure control mechanism
- Has an insidious onset, with few if any symptoms until permanent damage has occurred
77
Secondary Hypertension and examples of causes
some other specific disorder is identified as the cause of elevated BP
Kidneys: chronic kidney disease
excessive hormone levels: pituitary or adrenal tumor, hyperthyroidism
78
Consequences of systemic hypertension (cardiac, vascular, renal)
Cardiac effects: increased peripheral resistance → higher workload → heart enlarges → heart failure
Vascular effects: increased pressure → premature wearing out of vessels; accelerates atherosclerosis; injury to arterioles → weakened areas may rupture and hemorrhage
( linked to strokes and heart attacks)
Renal effects: narrowed renal arterioles → decreased blood supply to kidneys → injury and degenerative changes in glomeruli and tubules → renal failure
79
treatment of hypertension
1. reduce unfavorable factors
2. drugs therapies:
- diuretics
- beta blockers
- ACE inhibitors
- Angiotensin receptor blockers (ARBs)
- calcium channel blockers
- vasodilators
80
diuretics
enhance fluid loss and reduce circulating blood volume
81
beta blockers
block sympathetic nervous system input to heart, slow heartbeat and force of contraction --> reduce cardiac output
82
ACE inhibitors
inhibits the formation of angiotensin II
- Reduces systemic vasoconstriction
- Reduces aldosterone secretion
83
Angiotensin receptor blockers (ARBs)
accomplish the same results as ACE inhibitors by blocking the receptors that angiotensin II work at
84
calcium channel blockers
restrict the available calcium present in the smooth muscles of arterioles
- Produces vasodilation
- Also slows the heart rate
- Reduces cardiac output
85
vasodilators
directly dilate vessels
86
What is myocarditis, what usually causes it, and what is the typical course of the disease?
Active inflammation of heart muscle associated with injury and necrosis of individual muscle fibers
- Usually viral cause
- Abrupt onset may lead to acute heart failure
- Usually complete recovery
87
primary cardiomyopathy
A non-inflammatory disease of the cardiac muscle resulting in enlargement of myocardium and ventricular dysfunction that occurs in the absence of other cardiac conditions
88
Secondary cardiomyopathy
caused by a known medical condition (such as hypertension, valve disease, congenital heart disease, or coronary artery disease)
89
Dilated cardiomyopathy
- Diffuse degeneration of myocardial fibers leading to decreased contractile effort
- Heart becomes enlarged and dilated, impairing ventricular action and leading to chronic heart failure
90
etiology, symptoms, and treatment for dilated cardiomyopathy
Etiology: chronic alcoholism, an autoimmune process, or viral infections
(often idiopathic)
Symptoms: CHF
Treatment:
- Control of the CHF
- Cardiac glycosides
- Diuretics
- Anticoagulants
- Vasodilators
91
Hypertrophic cardiomyopathy
- Disorganized muscle fibers
- The left ventricular wall and interventricular septum hypertrophies / thickens
- impedes flow into aorta
- Thick septum blocks outflow from left ventricle
92
etiology, symptoms, and treatment of Hypertrophic cardiomyopathy
Etiology: idiopathic, hereditary dominant transmission
Symptoms: as with CHF
Treatment (to reduce workload):
- Beta blockers
- Calcium channel blockers
- Surgical resection of septum
93
Fetal circulation: how blood flows through the foramen ovale and ductus arteriosus.
The shunt that bypasses the lungs is called the foramen ovale. This shunt moves blood from the right atrium of the heart to the left atrium. (right to left)
The ductus arteriosus moves blood from the aorta to pulmonary artery
94
Why do congenital heart diseases usually occur, what are some causes, and how are they prevented?
Usually due to persistence of normal fetal blood channels or faulty embryologic development
ex) German measles, Down syndrome
causes: drugs, genetic factors
(over 90% are idiopathic)
Prevention: protect developing fetus from intra-uterine injury
95
Left-to-right shunt
Blood is diverted from systemic circulation to the lungs
Causes pulmonary hypertension and damage lungs
96
Right-to-left shunt
Blood is diverted from pulmonary circulation to systemic circulation
Blood is poorly oxygenated
Results in cyanosis, polycythemia, clubbing of fingers and toes
(immediately obvious after birth)
97
What are the 4 main causes of congenital heart disease?
1. Fetal bypass channels fail to close normally
2. Atrial, ventricular, or combined septal defects
3. Abnormalities obstructing flow
4. Abnormal formation of the aorta and pulmonary artery of abnormal connection of vessels
98
abnormalities obstructing flow examples (3)
- Pulmonary stenosis
- Aortic stenosis
- Coarctation of the aorta
99
Abnormal formation of the aorta and pulmonary artery or abnormal connection of vessels examples (2)
- Tetralogy of Fallot
| - Transposition of great vessels
100
Fetal bypass channels fail to close normally examples (2)
- Patent ductus arteriosus (PDA)
| - Patent foramen ovale (PFO)
101
Patent ductus arteriosus (PDA), type of shunting caused, symptoms, treatment, result of unrepaired)
- The ductus arteriosus does not close after birth
- Blood is shunted from aorta to pulmonary artery
- Often asymptomatic
- causes right-sided heart failure
- PDAs may be surgically repaired w/suture
102
Atrial Septal Defect (ASD), type of shunting caused, symptoms, treatment, result of unrepaired
- Abnormal opening between the right and left atria
- Blood is shunted from the left-to-right side (because left side is stronger)
- Often goes undetected (asymptomatic) in childhood
- Catheter closures with amplatzer
- If unrepaired, will cause right-sided heart failure
103
Ventricular septal defect (VSD), type of shunting caused, symptoms, treatment, result of unrepaired
- Abnormal opening between the right and left ventricles
[more problematic]
- Blood is shunted from the left-to-right in large volumes
- most common congenital defect of infancy
Symptoms:
- Pulmonary congestion
- Dyspnea
- Fatigue
- Susceptibility to pulmonary infections
Treatment:
- Closed surgically with a patch
If unrepaired: will cause right-sided CHF
104
Coarctation of the Aorta
- Narrowing of the aortic lumen causes a partial obstruction of the flow of blood
- Occurs primarily in males
- Large pressure gradient across narrowing
105
symptoms and treatment of Coarctation of the Aorta
Symptoms:
- Hypertension in the head and upper limbs
- Hypotension in the abdomen and lower limbs
- Left ventricular hypertrophy
Treatment:
- Repaired by surgically removing the defective area and reconstructing the aorta
If untreated, will cause left-sided CHF
106
Tetralogy of Fallot, type of shunting caused, symptoms, treatment, result of unrepaired
Is a combination of four defects:
1. Ventricular septal defect
2. Pulmonary stenosis
3. Displacement of the aorta
4. Right ventricular hypertrophy
- causes right-to-left shunting
- Blood is diverted through the VSD to the systemic circulation and bypasses the lungs
- Leads to cyanosis
- Corrected surgically
107
Transposition of the Great Vessels
The aorta and pulmonary arteries are reversed
- aorta connected to RV
- pulmonary valve connected to LV
Results in 2 closed-loop circulatory systems
Treatment: Prostaglandins are administered to keep the ductus arteriosus and the foramen ovale from closing
Blood flow is redirected by surgical correction
108
Aneurysm
weakening of portion of arterial wall
| and resulting local dilation or ballooning out
109
Etiology of aneurysms
- most common = build up of atherosclerotic plaque
| - Congenital (usually the ones in the head)
110
consequences of aneurysms (5)
- Thrombosis
- Thromboemboli
- Pressure on adjacent structures (nerves, brain)
- *Rupture
- *Dissection
111
symptoms of aneurysms
Depend on location and size
| Often asymptomatic
112
Abdominal aortic aneurysms
most common aneurysm
- abdominal or back pain and a pulsating mass in the abdomen
- May rupture leading to massive and fatal hemorrhage
- Hard to detect clinically
- high fatality
113
Dissecting aneurysm of aorta and symptoms
- Degenerative changes (tear) causes middle layer to lose cohesiveness and separate
- Pressure forces blood through a tear and causes separation of the layers
Symptoms: severe chest and back pain
114
How are aneurysms treated?
- Depends on size, location, likelihood of rupture, surgical candidacy
- surgical repair
(May be done by replacing the damaged area with a synthetic graft, by endovascular stenting, or coiling)
- If the aneurysm is small or the patient is not a good surgical candidate, watchful waiting is employed (regular ultrasounds)
115
Thrombophlebitis
inflammation of a vein caused by or associated with the formation of a blood clot,
in the superficial leg veins
causes an interference with blood flow and resulting edema
116
etiology of Thrombophlebitis
- Disruptions in blood flow
- Hypercoagulable state
- Injury or infection to the venous wall
(same as Virchod's triad)
117
symptoms and treatment of Thrombophlebitis
Symptoms;
- Pain, swelling, and warmth in the affected
- Involved area is tender to palpation
- cord like
Treatment:
- RICE /supportive care (if uncomplicated)
- Antibiotic treatment (if sign of infection)
- Anticoagulation (if risk of getting to deep circulation)
- Heparin
118
Varicose veins and etiology and at risk people
- Dilated, tortuous, and knotted veins
- Usually occur in superficial veins of the legs
Etiology: elevated venous pressure; dilation leads to failing of the valves (incompetent) and worsening of the problem
at risk: standing on feet a lot, obese, pregnant women
119
symptoms and treatment of varicose veins
Symptoms:
- fatigue in legs
- dull ache
- leg cramps at night
- swollen ankles
- thickening of veins
- hurt to touch
Treatment:
- rest, elevate legs
- compression stockings
For superficial ones: injection of sclerosing agent
For big ones: vein stripping and ablation (newer)
- surgery (advanced)
120
what comes first, rheumatic fever or rheumatic heart disease?
rheumatic fever
121
joint arthritis, heart inflammation, systemic CT inflammation are symptoms of rheumatic fever of rheumatic heart disease?
rheumatic fever
122
atherosclerosis often leads to the development of
aneurysm
123
orthopnea
difficulty breathing when laying down
124
symptoms of right side heart failure
peripheral edema and hepatosplenomegaly
125
what is digitalis
cardiac glycoside
126
angina is caused by
coronary heart disease
127
most common symptom of hypertension
asymptomatic
128
why is digitalis used to treat CHF?
increase contraction
| raise stroke volume and cardiac output
129
foramen ovale
The shunt/hole that bypasses the lungs
This shunt moves blood from the right atrium to the left atrium.
130
Ductus arteriosus
Moves blood from aorta to the pulmonary artery
