Cardio Flashcards Preview

Pathophysiology > Cardio > Flashcards

Flashcards in Cardio Deck (117)
Loading flashcards...
0
Q

What are the major risk factors for MI?

A
increasing age
male gender
hypercholesterolemia
diabetes
HTN
cigarette smoking
positive family history
1
Q

What are the causes of myocardial ischemia?

A

narrowing of coronary arteries due to atherosclerosis(decreases supply)
severe HTN or tachycardia (increases demand)
coronary artery vasospasm (decreases supply)
severe hypotension (decreases supply)
hypoxia (decreases supply)
anemia (decreases supply)
severe AI or AS

2
Q

What are some other risk factors for MI?

A
obesity
cerebrovascular disease
peripheral vascular disease
menopause
use of high-estrogen contraceptives
sedentary life style
psychosocial characteristics (ex. high stress)
3
Q

What is the problem with persistent myocardial ischemia and necrosis?

A

myocardial remodeling which creates fibrotic muscle with akinetic or dyskinetic movement

4
Q

Describe the structure of an unstable atherosclerotic plaques?

A

lipid rich core and a thin fibrous cap
not uniform
rich in macrophages and T cells with interferon-Y
metalloproteinases that degrade the cap

very unstable!

5
Q

What are some factors that contribute to the rupture of a plaque

A

shear forces
inflammation
macrophage-derived degradative enzymes
apoptosis

6
Q

What is the physiologic response to a ruptured coronary plaque?

A

increased inflammation with release of cytokines, platelet activation with formation of thrombus over the lesion, vasoconstriction of the affected vessel

7
Q

Where are plaques the weakest?

A

at the point where the lipid rich core meets the vessel wall

8
Q

How can acute mental stress precipitate a MI?

A

activation of central and autonomic nervous system
increased catecholamines, HR, BP, platelet activity
decreased plasma volume

all these factors lead to an imbalance between supply and demand, and when compounded with pre-existing risk factors can cause dysrhythmias, plaque rupture, and coronary thrombosis

9
Q

What are abnormal EKG changes that would lead you to believe the patient was having an MI?

A

ST segment depression
T wave inversion
ST segment elevation

10
Q

What are the characteristics of stable angina?

A

no change in precipitating factors for 90 days, including the frequency of pain and the duration of the pain

11
Q

What are the characteristics of unstable angina?

A

caused by less than normal activity
persists for a long time
occurring more frequently
crescendo of pain

occurs with acute plaque changes

12
Q

How is stable angina relieved?

A

rest, reduced demand, vasodilator like nitroglycerin

13
Q

What is Prinzmetal (variant) angina?

A

coronary spasms that can occur at rest in an area with or without plaque

often associated with other vasospastic diseases such as Raynaud’s

14
Q

Where does infarction typically begin?

A

in the subendocardial region of the heart

15
Q

size of a myocardial infarction depends on ______ & ______

A

proximity of the lesion & collateral circulation

16
Q

What is an infarction?

A

necrosis that typically occurs after 20-30 minutes of ischemia

17
Q

When does an infarction usually reach full size?

A

after 3-6 hours

18
Q

What are the complications of a myocardial infarction?

A

papillary muscle dysfunction – valvular disease
external rupture of infarct in 4-7 days (fatal)
mural thrombi which can lead to stroke
acute pericarditis r/t thrombus formation after 2-4 days
ventricular aneurysm in the anteroapical region
arrhythmias
LV failure +/- pulm edema
cardiogenic shock
thromboembolism
rupture of papillary muscle or ventricular wall

19
Q

Which leads will give you the best view of the LV?

A

Leads 2 and V5 will best show ischemia in the LV

20
Q

Occlusion of the RCA leads to _____ MI

A

posterior/inferior MI

21
Q

Occlusion of the LCA leads to ____

A

massive anterolateral MI

22
Q

Occlusion of LAD leads to ____

A

anteroseptal MI

23
Q

Occlusion of the LCX leads to ____

A

lateral MI

24
Q

How is vascular HTN defined?

A

sustained diastolic > 90 mmHg

sustained systolic > 140 mmHg

25
Q

HTN is the most important risk factor in the development of which diseases?

A
CAD
CVD
cardiac hypertrophy
renal failure
aortic dissection
26
Q

What are some of the causes of secondary HTN?

A

renal
cardiac
neurological
endocrine (thyroid disease)

27
Q

What two factors contribute to cardiac output?

A

blood volume and Frank-Starling factors

28
Q

What factors influence peripheral resistance?

A
humoral factors (constrictors and dilators)
local factors
neural factors (stress)
29
Q

What factors influence the development of essential HTN?

A
genetic factors
stress
obesity
smoking
salt consumption
sedentary lifestyle
30
Q

Describe the theory of renal retention of excess sodium to explain essential HTN.

A

existence of genetic factors&raquo_space; decreased sodium excretion&raquo_space; increased fluid volume and CO&raquo_space; autoregulatory vasoconstriction occurs and BP increases

*continues in cyclical fashion

31
Q

Describe the vasoconstriction and vascular hypertrophy theory of essential HTN.

A

functional vasoconstriction is influenced by neurogenic factors, release of vasocontrictor agents, and a genetic defect in the transport of Na+ and Ca++

AND/OR

stimuli induce structural changes in the vascular walls

32
Q

What are some specific known causes of secondary hypertension?

A
oral contraceptives
renal parenchymal disease
renin-secreting tumors
primary aldosteronism
cushing's syndrome
pheocromocytoma
33
Q

What are some non-pharmacological treatments for HTN?

A
limiting ETOH
reducing sodium in the diet
exercise
weight loss
smoking cessation
relaxation techniques
34
Q

What is hypertensive crisis?

A

sudden increase in DBP >130, due to activity of the RAA system on top of normal HTN

35
Q

What is the treatment for hypertensive crisis?

A

prompt but controlled reduction in BP with nipride&raquo_space;> goal is to decrease DBP to 100-110 over several minutes

monitor urine output
monitor IABP

36
Q

What is the most frequent cause of mitral stenosis?

A

fusion of the mitral valve leaflets during the healing process of acute rheumatic fever

37
Q

Describe the progression of mitral stenosis.

A

when mitral valve area decreases to 1 cm2, an increase in pressure is required to open it (LAP = 25 mmHg), LA becomes enlarged, a-fib can occur when SA node stretches, stasis of blood in the LA predisposes to thrombi

38
Q

What are the symptoms of mitral stenosis?

A

DOE when CO is increased

progression to CHF

39
Q

How can mitral stenosis cause RV failure?

A

decreased LA emptying&raquo_space; increased LA preload&raquo_space; pulmonary edema&raquo_space; increased PVR and decreased O2 supply&raquo_space; RV failure

40
Q

How can mitral stenosis cause LV failure?

A

decreased LA emptying = increased LA preload&raquo_space; decreased force of LA contraction&raquo_space; decreased blood getting to LV&raquo_space; decreased O2 supply from pulm edema&raquo_space; decreased LV output&raquo_space; LV failure

41
Q

What are the main causes of aortic stenosis?

A
  1. progressive calcification and stenosis of congenitally abnormal aortic valve
  2. rheumatic fever (often occurs with MVS too)
42
Q

When does aortic stenosis become significant?

A

transvalvular pressure gradient >50 mmHg

aortic valve orifice area <1 cm2

43
Q

What is a normal aortic valve orifice area?

A

2.5-3.5 cm2

44
Q

What are the characteristic triad of symptoms for aortic stenosis?

A

angina pectoris
DOE
syncope (because of low SV)

45
Q

What is the problem with really ACUTE aortic stenosis?

A

they haven’t had time to compensate by developing hypertrophy or atrial kicks, so they can experience severe symptoms

46
Q

Describe the progression of aortic stenosis in the early stage?

A

obstruction to LV ejection, pressure overload, increased LV mass, decreased LV compliance, increasing preload, increase in atrial kick…

STROKE VOLUME MAINTAINED

47
Q

Describe the progression of aortic stenosis in the late stage?

A

obstruction to LV outflow, increased pressure in LV, increased LV mass, decreased contractility and formation of fibrotic tissue, LV dilation…

DECREASED STROKE VOLUME

48
Q

How does concentric hypertrophy occur? What are the consequences?

A

constant high pressures required to get blood past stenotic valves causes global cardiac muscle enlargement.

can lead to a decrease in chamber size or dilation of the chamber over time

49
Q

What is the most frequent cause of mitral regurg?

A

rheumatic fever – it often accompanies mitral stenosis

50
Q

What is the principal physiologic change in mitral regurg?

A

LA volume overload because of retrograde flow of the LV stroke volume

51
Q

How can you monitor for mitral regurg?

A

it will show up as the V wave on a PAOP swan cath reading…

size of the V wave correlates with the magnitude of regurgitant flow

52
Q

How does mitral valve prolapse contribute to mitral regurg?

A

prolapse permits the valve leaflets to billow back into the LA during systole. when this happens the leaflets separate slightly and blood can flow backwards into the LA

53
Q

What kind of hypertrophy results from mitral regurg?

A

eccentric hypertrophy (dilated)

54
Q

How can problems with the mitral valve cause tricuspid dysfunction?

A

mitral regurg and mitral stenosis increase LA pressure&raquo_space; causes increased LA size and pulm HTN&raquo_space; can cause A-fib&raquo_space; can cause RV dilatation and dysfunction&raquo_space; causes leaflet tethering of the tricuspid valve with annular dilatation&raquo_space; TRICUSPID REGURG

55
Q

What are some causes of acute aortic regurg?

A

trauma
infective endocarditis
dissection of thoracic aortic aneurysm

56
Q

What are some causes of chronic aortic regurg?

A

prior rheumatic fever

persistent systemic HTN

57
Q

What is the problem with aortic regurg?

A

the ejected stroke volume flows backwards into the LV

you have a decrease in forward stroke volume to perfuse the organs

58
Q

How does the body attempt to compensate for aortic regurg?

A

kidneys sense low blood pressure because of decreased stroke volume and activate the RAA system to increase BP, but this creates an even higher afterload that the LV has to pump against and worsens the problem

59
Q

Describe the progression of aortic regurg/aortic insufficiency.

A

aortic insufficiency&raquo_space; LV volume overload&raquo_space; increase in fiber length and LV volume to maintain ejection fraction… the problem progresses…

increased velocity of ejection&raquo_space; higher oxygen costs and increased wall tension with increased mass&raquo_space; increased stiffness and contractility&raquo_space; increases in LA pressure and a decrease in stroke volume&raquo_space; ultimately leading to a change in the cardiac function curve

60
Q

Describe dilated cardiomyopathy.

A

heart has a globular shape and the largest circumference of the LV is not at the base anymore but is not between the apex and the base

61
Q

Describe hypertrophic cardiomyopathy.

A

LV wall is greatly thickened and the LV cavity is made smaller

LA may also be dilated because of poor diastolic relaxation of the LV

62
Q

Describe restrictive cardiomyopathy.

A

LV cavity is the normal size but the LA is dilated because of reduced diastolic compliance of the LV

63
Q

What are the early symptoms of inflammatory myocarditis?

A

fatigue
dyspnea
palpitations

64
Q

What are the two types of dilated cardiomyopathies?

A

inflammatory and non-inflammatory

65
Q

What is the most common cause of inflammatory myocarditis?

A

infection

66
Q

What are the late symptoms of inflammatory myocarditis?

A

CHF symptoms like DOE, syncope, etc.
pulsus alternans
tachycardia
pulm edema

67
Q

What is pulsus alternans?

A

each heart beat isn’t associated with a good blood pressure. Some beats have adequate BPs and some don’t.

68
Q

What is the treatment and prognosis for inflammatory myocarditis?

A

long-term IV antiobiotics and home antibiotics to treat the underlying infective endocarditis

usually results in a complete recovery

69
Q

What are the symptoms of non-inflammatory dilated cardiomyopathy?

A
toxicity (alcohol, drugs)
idiopathic process
degenerative process
infiltrative process (an old infection that results in fibrosis and dilation)
post-MI (necrotic areas become dilated)
70
Q

What are the symptoms of non-inflammatory dilated cardiomyopathies?

A

manifests as CHF symptoms like DOE, pulm edema, syncope, etc.

71
Q

what are the 3 physiologic changes associated with non-inflammatory dilated cardiomyopathy?

A

elevated filling pressures (needed to fill non-compliant ventricles)

failure of contractile strength (beyond frank-starling stretch curve and muscles have lost the ability to bounce back quickly)

marked inverse relationship between arterial impedance and SV (higher the arterial impedance, the lower the stroke volume)

72
Q

Describe the progression of non-inflammatory dilated cardiomyopathies.

A

decreased contractility&raquo_space; dilated ventricles in an attempt to increase contractility&raquo_space; increased LV radius leads to increased cardiac work&raquo_space; increased O2 consumption&raquo_space; CO falls&raquo_space; attempts to compensate through increases in SNS outflow to raise SVR and HR&raquo_space; stroke volume falls!!!

73
Q

What are the general symptoms of non-inflammatory dilated cardiomyopathies?

A

fatigue
oliguria (r/t low SV to kidneys)
hypotension

74
Q

How does the RAA system respond to dilated cardiomyopathies?

A

reduced renal perfusion = activation of the system which causes the body to hold onto water and sodium and increases the circulating blood volume in an attempt to compensate for low CO

75
Q

What are the results of backward failure during dilated cardiomyopathies?

A

elevated filling pressures required to continue moving blood forward in the failing heart

secondary mitral regurg due to dilation of the ventricle

76
Q

What are the symptoms of L sided CHF?

A

orthopnea
pulm edema
paroxysmal nocturnal dyspnea

77
Q

What are the symptoms of R sided CHF?

A

JVD
peripheral edema
hepatomegaly

78
Q

What are the 4 types of hypertrophic cardiomyopathy?

A

IHSS (idiopathic hypertrophic subaortic stenosis)
asymmetrical septal hypertrophy
hypertrophic obstructive cardiomyopathy
muscular subaortic stenosis

79
Q

What are the symptoms of IHSS?

A

sudden death on exertion
syncope, dyspnea, angina in a more sedentary person

however… the majority of patients are asymptomatic

80
Q

What is the likley cause in IHSS?

A

it is an autosomal dominant trait that causes defects in the contractile tissue of the heart because of an increase in Ca++ channels

81
Q

When do patients with IHSS become symptomatic?

A

in their 20s-30s

82
Q

What are the common rhythms which can cause fatal events for people with IHSS?

A

75% V-tach/V-fib

25% SVTs

83
Q

Describe the physiologic changes in hypertrophic cardiomyopathies

A
  1. asymmetric myocardial hypertrophy
  2. diastolic dysfunction because the ventricle can’t relax properly
  3. disproportionate enlargement of the interventricular septum just below the aortic valve usually
  4. rapid LV ejection (usually most CO in the first part of systole)
  5. really high subaortic pressure gradient but really low pressure after the aortic valve
84
Q

How can the obstruction become worsened in hypertrophic cardiomyopathy?

A

decreased preload/decreased ventricular volume
decreased afterload
increased contractility

85
Q

How can the CRNA modify or modulate the problems associated with hypertrophic cardiomyopathy?

A

give agents to reduce contractility
increase afterload to slow things down for the heart
give LOTS of fluids to increase preload and increase SV

give drugs like beta blockers, neosynephrine, Ca-channel blockers and fluids to treat these people

86
Q

How can vasodilators affect a patient with hypertrophic cardiomyopathy?

A

most of these patients have some degree of mitral regurg and when you administer a vasodilator, it can actually worsen the MR

*vasoconstrictors would attenuate the MR

87
Q

Why do patients with hypertrophic cardiomyopathy require supplemental oxygen?

A

they have such a heavy, dense heart that requires lots of O2 because of the high rate of O2 consumption… could result in angina is demand becomes greater than supply

88
Q

Why are beta blockers used in hypertrophic cardiomyopathy?

A

decrease tachyarrhythmias

blunt the sympathetically mediated increases in subaortic stenosis

89
Q

How do Calcium-channel blockers work in hypertrophic cardiomyopathy?

A

the improve diastolic relaxation of the ventricle to allow for greater filling time

90
Q

What are the echo findings in a patient with hypertrophic cardiomyopathy?

A

thickened intraventricular septum (IVS) from base to apex
poor septal motion
anterior displacement of the mitral valve

91
Q

How can diuretics help patients with CHF (not IHSS type)?

A

help relieve pulmonary congestion

92
Q

How can the combination of nipride and dopamine help a patient in CHF (not IHSS type)?

A

helps the heart move blood along but also improves pump function

93
Q

How can phentolamine be helpful in a CHF patient (except IHSS type)?

A

acts as a potent vasodilator which can decrease the pressure the heart has to pump against

94
Q

In a CHF patient who is losing lots of volume in the OR, what fluid should you treat with?

A

replace blood loss with blood, not crystalloid!

95
Q

What are the three common congenital L to R shunts?

A

Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Patent ductus arteriosus (PDA)

96
Q

When does cyanosis appear in patients with a L to R shunt?

A

later in life (tardive cyanosis) because in the beginning at least some oxygenated blood is getting through… will not appear cyanotic from the outset

97
Q

How does ASD develop and what is the result?

A

foramen ovale does not close properly or close all the way during the first 4-6 weeks in utero and it allows for blood to flow from the LA to the RA

98
Q

What are the clinical features of ASD?

A
  1. cyanosis
  2. eventual pulmonary HTN which can become so severe that it actually switches to a R to L shunt, causing significant CHF and mitral insufficiency
99
Q

When is VSD diagnosed?

A

at birth

100
Q

How does VSD form?

A

septum develops between week 4-8 of embryonic development and simply doesn’t close properly…

this may fix itself spontaneously over time

101
Q

How is severe VSD corrected?

A

surgical intervention for larger VSDs which are not closing on their own

102
Q

What are the clinical results of a VSD?

A

severe L to R shunting of blood resulting in CHF and pulm edema

infective endocarditis can also occur r/t stasis of blood when it flows backwards

103
Q

What is the normal function of the ductus arteriosus in fetal circulation?

A

allows for mixing of oxygenated and unoxygenated blood in the fetus so that it can bypass the lungs, which is actually ok!

but it needs to close once the baby is born!

104
Q

Why does the DA close right after birth normally?

A

increased O2 level
decreased pulmonary resistance
decrease in PGE2

105
Q

What are the clinical results of a PDA?

A

a high pressure L to R shunt resulting in pulm HTN, cyanosis, CHF and infective endocarditis

106
Q

What are the more common congenital R to L shunts?

A

Tetralogy of Fallot

Transposition of great vessels

107
Q

What is the dysfunction in a R to L congential cardiac shunt?

A

unoxygenated blood from the R side of the heart is introduced directly into systemic circulation again without being re-oxygenated by the lungs

108
Q

What is the clinical presentation of a R to L shunt that allows it to be immediately detected at birth?

A

CYANOSIS AT BIRTH

109
Q

What is the cause of tetralogy of Fallot?

A

abnormal division of the truncus arteriosus into a pulmonary trunk and an aortic root

110
Q

What are the 4 components of TOF?

A
  1. VSD
  2. RV hypertrophy
  3. RV outflow obstruction
  4. dextraposed aortic root that overrides the VSD (aorta shifted R!)
111
Q

What are the clinical manifestations of TOF?

A

mostly due to chronic cyanosis:

  1. erythrocytosis
  2. increased blood viscosity
  3. clubbing of fingers and toes
  4. infective endocarditis
  5. systemic emboli
  6. brain abscesses
112
Q

What is transposition of the great vessels?

A

aorta arises from RV and pulm trunk arises from LV

*it must be associated with ASD, VSD or PDA for the baby to survive after birth

113
Q

What is the clinical presentation of a patient with transposition of the great vessels?

A

cyanosis r/t R to L shunting

114
Q

What is coarctation of the aorta?

A

narrowing/stenosis of the aorta, classified on where the narrowing occurs in relation to the ductus arteriosus… either preductal or postductal

115
Q

Describe preductal COA.

A

diagnosed in infancy
presents with weak femoral pulses, cyanosis in legs and CHF
needs surgical correction immediately to survive

116
Q

Describe postductal COA.

A
  • diagnosed in later life/early adulthood because collateral vessels have developed
  • decreased perfusion to the kidneys causes activation of RAA system
  • presents with clubbing in lower extremities, high BPs in upper extremities and low BP in lower extremities, intermittent claudication