WEEK 2 Cardiac Muscle Dysfunc & Failure Flashcards
1
Q
What is the term for a common cause of congestive heart failure that is usually asymptomatic but progresses to symptoms of heart failure?
A
cardiac muscle dysfunction
2
Q
What are 3 symptoms of heart failure?
A
- dyspnea
- fluid buildup
- fatigue @ rest and/or activity
3
Q
What is the most common cause of pulmonary congestion & edema?
A
heart failure
4
Q
Why does hypertension lead to necrosis over time?
A
no increase in vascularity to feed thickened tissue
5
Q
Hypertension leads to increased risk of macro & microvascular damage to major organs, which 3 in particular?
A
- heart
- kidney
- brain
6
Q
What measures ejection fraction?
A
ECG
7
Q
What is the 2nd most common cause of cardiac muscle dysfunction?
A
coronary artery disease
8
Q
What causes ischemia in coronary artery disease?
A
- lipid deposits
- endothelial inflammation (lining damage, leukocytes, plaque deposits)
9
Q
What occurs as a result of scar formation at the ischemic areas of the ventricle?
A
- poor compliance
- decreased filling
- decreased contractility –> decreased ejection fraction
- possible development of cardiac arrhythmia due to increased Ca2+ release
10
Q
How does coronary artery disease present in men vs women?
A
- men: chest pain
- women: stomach pain, back pain, GI upset
11
Q
What is the term for irreversible myocardial necrosis that can be acute or chronic?
A
MI
12
Q
What is most commonly affected in a MI?
A
left ventricular myocardium
13
Q
Which enzyme represents muscle damage?
A
CK-MB (Creatine Kinase)
14
Q
What can be seen during an EKG if there’s an acute MI?
A
ST elevation
15
Q
Cardiac arrhythmias lead to (increased/decreased) CO?
A
decreased
16
Q
What is sick sinus node syndrome?
A
- heart block
- bradycardia
- tachycardia
17
Q
Describe prolonged supraventricular tachycardia.
A
- originates in the atria
- not as life threatening
18
Q
True or False: ventricular tachycardia/fibrillation is life threatening.
A
T
19
Q
How does renal insufficiency contribute to cardiac muscle dysfunction?
A
fluid overload
20
Q
What is the principal treatment of renal insufficiency?
A
reduce reabsorption of fluid @ kidneys
21
Q
Which electrolytes must be balanced to prevent muscle weakness & cardiac arrhythmias?
A
Na+ & K+
22
Q
Describe the chain of events that occurs with the kidney if BP falls.
A
- renin (produced by kidney) is released
- renin converts angiotensinogen (produced by liver) to angiotensin I
- angiotensin I –> angiotensin II by angiotensin-converting enzyme (produced by lung)
- angiotensin II vasoconstricts to raise BP & sends signal to adrenal gland
- BP rises & adrenal gland (cortex) secretes aldosterone
- salt retention occurs also helping BP rise
23
Q
What is the term for high blood content of nitrogen compounds?
A
azotemia
24
Q
What is severe renal insufficiency caused by?
A
- decreased glomerular filtration rates
- decreased blood flow
25
What 3 things are released as a result of low BP signaling to baroreceptors?
- aldosterone
- renin-angiotensin
- ADH
26
Why is sympathetic NS activity increased in severe renal insufficiency?
to increase BP
27
What is the term for disease of heart muscle itself leading to heart failure?
cardiomyopathy
28
Distinguish between primary & secondary cardiomyopathy.
- primary: idiopathic mechanism
- secondary: prolonged HTN, MI, metabolic diseases (DM, thyroid), heart valve problems, cardiac arrhythmias
29
What are the 3 types of cardiomyopathies?
- dilated
- hypertrophic
- restrictive
30
Which type of cardiomyopathy is HFrEF (heart failure reduced ejection fraction - less than 40%)?
dilated
31
What is dilated cardiomyopathy a result of?
- metabolic
- toxic (alcohol abuse)
- infections
- genetic predisposition
32
Dilated cardiomyopathy has decreased energy production of myocytes due to myocardial __________ dysfunction.
mitochondria
33
Dilated cardiomyopathy is (systolic/diastolic) dysfunction. What does this mean?
- systolic
- heart less effective pump
- decreased ejection fraction
34
How is left ventricular end-diastolic volume affected in dilated cardiomyopathy? What does this lead to?
- increased
- dilates & stretches cardiac muscle fibers --> decreased contractility
- impaired frank starling mechanism
35
How is dilated cardiomyopathy treated?
- meds
- pacemaker/implantable defibrillator
- surgery (LVAD & heart transplantation)
36
How do muscle cells present in hypertrophic cardiomyopathy?
- disorganized
- maligned
- inefficient pump
37
Describe what HFpEF for hypertrophic cardiomyopathy means.
- preserved
- rapid ventricular emptying
38
Hypertrophic cardiomyopathy is a (systolic/diastolic) dysfunction. What does this mean?
- diastolic
- impaired diastolic filling because myocardium doesn't relax (less compliant)
39
In hypertrophic cardiomyopathy, what is increased?
- left end diastolic pressure
- left atrial pulmonary artery, pulmonary capillary pressure
40
What causes hypertrophic cardiomyopathy?
- genetic
- prolonged HTN
41
What is a common cause for sudden cardiac arrest in young athletes?
hypertrophic cardiomyopathy
42
What is the term for myocardial fibrosis leading to defect in myocardial relaxation?
restrictive cardiomyopathy
43
Restrictive cardiomyopathy is (systolic/diastolic) dysfunction.
diastolic
44
What will often develop in restrictive cardiomyopathy?
hypertrophy
45
True or False: restrictive cardiomyopathy is HFrEF.
F (HFpEF)
46
What causes restrictive cardiomyopathy?
- cardiac amyloidosis
- diseases of endocardium
- iron overload
- sarcoidosis
- scarring after radiation or chemo
- scleroderma
- tumors
47
What changes in the heart happen as a result of heart valve abnormalities?
- heart contracts more forcefully
- myocardial hypertrophy
- decreased ventricular distensibility (systolic & diastolic dysfunction)
48
What is the difference between valvular insufficiency & stenosis?
- insufficiency: leaky
- stenosis: narrow
49
How does valvular stenosis impact CO? How about BP?
both decrease
50
How does valvular regurgitation impact CO?
maintains it at first but then decreases
51
What happens as a result of valvular incompetence?
- regurgitant blood fills atria & ventricles forcefully
- myocardial dilation & hypertrophy
- cardiac muscle dysfunction due to impaired relaxation of myocardium
52
Which valves are affected by atrioventricular valve incompetency?
mitral & tricuspid
53
Which structure is dilated if there's mitral valve incompetency? How about tricuspid valve?
- mitral: left atria
- tricuspid: right atria
54
Which valves are affected by ventricular valve incompetency?
aortic & pulmonic
55
Which structure is dilated if there's aortic valve incompetency? How about pulmonic valve?
- aortic: left ventricle
- pulmonic: right ventricle
56
Describe acute valve dysfunction.
- medical emergency
- decreased CO due to regurgitant blood
- produces cardiac muscle dysfunction & pulmonary edema
57
What relieves pericardial effusion pain? What worsens it?
- relieves: sitting up or leaning forward
- worse: when laying down
58
What are the signs & symptoms associated with cardiac tamponade?
- anxiety, restlessness
- chest pain
- difficulty breathing
- discomfort
- fainting, light-headedness
- pale, gray, or blue skin
- palpitations
- rapid breathing
- swelling of abdomen or other areas
59
Where does chest pain radiate to in cardiac tamponade?
- neck
- shoulder
- back
- abdomen
60
How does pulmonary embolism cause lung infarction? Why?
decreased right ventricular blood flow since it's lodged in pulmonary artery branch
61
What does increased pulmonary hypertension with pulmonary embolism lead to?
- RV hypertrophy
- decreased RV stroke volume --> decreased LV stroke volume & CO
62
Cardiac muscle dysfunction can occur with pulmonary embolism due to elevated __________ __________ pressure.
pulmonary artery
63
What is the protein that is released when a blood clot is produced?
d-dimer
64
What value of mPAP is considered primary pulmonary hypertension at rest? How about with exercise?
> or = 25 mmHg @ rest, > or = 30 with exercise
65
For individuals with COPD, what causes pulmonary artery hypertension?
hypoxia
66
Which group of pulmonary hypertension is pulmonary arterial hypertension (PAH)?
1
67
Which group of pulmonary hypertension is due to left-sided heart disease?
2
68
Which group of pulmonary hypertension is due to lung disease and/or hypoxia?
3
69
Which group of pulmonary hypertension is chronic thromboembolic pulmonary hypertension (CTEPH)?
4
70
Which group of pulmonary hypertension is unclear or with multifactorial etiologies?
5
71
What is the term for right-sided heart failure?
cor pulmonale
72
What is the term for pathological decrease in CO?
congestive heart failure
73
Which structure of the heart fails in CHF? What does this lead to?
- left ventricle
- pulmonary congestion
74
What does increased pulmonary capillary pressure lead to in CHF? What caused this?
- pulmonary edema
- increased pressure because LV failing --> LA --> pulmonary vein --> pulmonary circulation as blood backs up
75
What is the enzyme produced by atria or ventricle whenever the ventricle stretches?
Brain Natriuretic Peptide (BNP)
76
If there's right CHF, what happens?
fluid backup into right atrium or periphery
77
If there's left CHF, what happens?
fluid buildup in lungs
78
If there's bilateral CHF, what happens?
fluid backs up into lung --> increases pulmonary artery pressure --> right ventricular failure
79
If there's systolic dysfunction CHF, what happens?
low stroke volume due to decreased ventricular contraction
80
If there's diastolic dysfunction CHF, what happens?
impaired ability for ventricles to accept blood @ rest or activity
81
What is HFmEF?
ejection fraction less than 50 but not 40 (mid range)
82
How do stroke volume & ventricular end-diastolic volume change from normal to heart failure?
- decreased stroke volume
- increased ventricular end-diastolic volume
83
What positively affects myocardial contractility?
- sympathetic nerve impulses
- epinephrine
- frequency of contractions
- use of pharmacological agents (digitalis, lanoxin)
84
What negatively affects myocardial contractility?
- loss of myocardial cells
- pharmacological depressants (e.g., B blockers)
- acidosis
- hypercapnia
- anoxia
85
What senses reduction in blood volume in renal & nonrenal systems?
arterial sensors
86
Explain why there is increased alpha adrenergic neural activity & catecholamine circulation in CHF.
In response to decreased CO, norepinephrine & epinephrine are released & act on adrenergic receptors to increase HR, contractility, & vasoconstriction.
87
Explain why there is increased angiotensin II production in CHF.
vasoconstriction to maintain BP & also triggers release of aldosterone to retain water & sodium.
88
Increased levels of what leads to azotemia?
increased BUN & creatinine
89
What is the renal filtration fraction?
ratio of (glomerular filtration rate) GFR to renal blood flow
90
Which stage of pulmonary fluid accumulation is when there's increased lymph flow without net gain in interstitial fluid & gas exchange improved?
1
91
Which stage of pulmonary fluid accumulation is when liquid buildup compromises small airways of lung, V/Q mismatch, hypoxemia & tachypnea?
2
92
Which stage of pulmonary fluid accumulation is when pulmonary edema increases, increased pulmonary capillary wedge pressure that floods alveoli, gas exchange compromised, & severe hypercapnea & hypoxemia?
3
93
Which receptor is responsible for myocardial inotropy & chronotropy?
B1
94
Which receptor is responsible for vasodilation of capillary beds & bronchodilation?
B2
95
Which receptor is responsible for vasoconstriction of vascular beds of GI, kidney, & brain?
a1
96
Which receptor is responsible for arterial vasodilation & vasoconstriction of coronary arteries?
a2
97
Which receptor gets downregulated when there's too much stimulation from sympathetic NS? What does this lead to?
- B1
- decrease myocardial contractile force & HR
98
What does fluid overload lead to in terms of hepatic function?
- hepatic venous function
- hepatomegaly
- hypoxemia & hypoperfusion --> cardiac cirrhosis of liver
99
Why is increased RBC production from bone marrow not necessarily a good thing during CHF?
polycythemia can make blood thick & increase blood volume which makes heart have to work even harder
100
How is anemia potentially beneficial to CHF? What is the drawback of this?
- decreased blood viscosity --> decreased BP & reduced afterload on ventricles
- but less O2 carrying capacity
101
What is the value of the critical blood O2 concentration point that causes O2 desaturation from hemoglobin?
@ or below 60 mmHg
102
Explain why severe anemia blood transfusions may decrease CO.
decreased HR due to better tissue O2 perfusion so heart doesn't have to work as hard to get O2 there
103
Damage of which organs can lead to decreased thrombin secretion?
liver (mostly) & kidney
104
Which type of function are these meds trying to restore? - heparin - aspirin - corticosteroids - B blockers - antibiotics
hematologic
105
What happens to skeletal muscle when there's CHF without cardiomyopathy?
- decreased type I & II muscle fiber diameter
- decreased normal isometric max voluntary contraction of quads
- increased intracellular lipid accumulation
- increased muscle fatigue (intracellular apoptosis & decreased phosphocreatine)
106
What happens to skeletal muscle when there's CHF with cardiomyopathy?
- normal nerve conduction & motor unit potential
- type I & II muscle fiber atrophy
- mitochondrial abnormalities in type I muscle fibers
- decreased max isometric muscle strength by 50%
- increased muscle fatigue
- increased relative muscle output @ any given workload
107
What happens with the pancreas when there's CHF?
decreased blood flow because splanchnic visceral vasoconstriction due to LV failure
108
What worsens pancreatic function when there's CHF?
sympathetic nerve activity (glycogenolysis & glucose elevation)
109
What does a dysfunctional heart rely on as primary fuel source? How about normally?
- dysfunctional: glucose
- normal: oxidation of fatty acids
110
How is nutrition affected with CHF?
- anorexia
- cachexia
- malnutrition
- GI absorption abnormalities (GI hypoxia)
- decreased protein-calorie intake
- increased excretion
- hypermetabolism
- worsened azotemia as a result
