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ABC > Cardio > Flashcards

Cardio Flashcards

1
Q

Non-modifiable Risk Factors for coronary heart disease?

A
  • Men over 45
  • Postmenopausal women
  • Family hx of CVD for males over 55 and females over 65
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2
Q

Modifiable Risk Factors for coronary heart disease?

A
  • Hypertension
  • Smoking
  • Dyslipidemia (low HDL or elevates LDL)
  • Diabetes Mellitus
  • Obesity
  • Left ventricular hypertrophy
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3
Q

Is hyperlipidemia common?

A

Yes! in 40% of pop

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4
Q

What is hyperlipidemia?

A
  • Elevated cholesterol, phospholipids, + triglycerides in blood
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5
Q

Components of a lipoprotein?
How are lipoproteins classified?
Classifications?

A

= Lipid + Apoprotein
- Classified based on density
LDL, HDL, VHDL

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6
Q

What is an apoprotein?

A

Proteins that transport lipids

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7
Q

As nurse, will be given what regarding pt lipid diagnostics?

A

a Lipid Profile

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8
Q

Which lipoprotein causes problems if elevated?

A

LDL’s

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9
Q

Arrange kinds of lipoproteins in ascending order in terms of density.
Which contain greatest percentage of proteins? And which contain more cholesterol/triglycerides?
(Fig. 22-2 p. 461)

A

Chylomicrons - lowest density, 2% protein
VLDL - 5-10% protein
LDL - 25% protein
HDL - 50% protein

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10
Q

Are proteins are fats more dense? Which is heavier?

A

Proteins most dense, are heavier

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11
Q

What is a chylomicron?

A

Fx to transport fat absorbed in small intestines
- Have lowest density of all lipoproteins
(made up 80-90% triglycerides, 2% protein)

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12
Q

What % of LDL’s is cholesterol?

A

50% - high!

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13
Q

General structure of a lipoprotein?

A

Cholesterol esters + tryglycerides located in hydrophobic core of macromolecule, surrounded by phosphlipids + apoproteins

(Fig 22-3 p. 461)

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14
Q

Suffix “sclerosis” refers to?

Prefix “athero” refers to?

A

Hardening (in many cases)

Soft paste

  • Therefore, atherosclerosis = formation and deposition of soft pasty material + hardening
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15
Q

What size of arteries does atherosclerosis typically occur in?

A

larger arteries

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16
Q

What is an “atheroma”

Where does this form in atherosclerosis

A

Fibrofatty lesion - forms in intima of larger arteries

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17
Q

Layers of a blood vessel?

A

Tunica intima: composed of a thin layer of endothelial cells and lines the entire circulatory system

Tunica media: middle layer of smooth muscle + elastic fibres

Tunica externa/adventitia: outermost, loosely woven collagen + elastic fibers (reinforce + anchor vessels) & contains nerves, lymphatic vessels, vasa vasorum

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18
Q

Effect of development of atheroma in atherosclerosis? Ultimate potential outcomes?

A

Affects perfusion –> ischemia –> stroke, MI, PVD

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19
Q

What is ischemia?

A

Restricted blood flow at LOCAL level d/t obstruction in blood vessel

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20
Q

What is infarction?

A

Death of tissue d/t ischemia

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21
Q

PVD = ?

Is this life-threatening?

A

Peripheral Vascular Disease - not immediately life threatening

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22
Q

Are a large amount of deaths d/t issues that arise from atherosclerosis?

A

~32% of all deaths in Canada

d/t MI, stroke

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23
Q

3 Stages of lesion that develops in Atherosclerosis?

A

1) Fatty Streak
- Discoloration of intima
- Lesion contains variety of defence cells
- Is insidious (not yet clinical)

2) Fibrous Atheromatous plaque
- Is basic clinical manifestation
- Pt now experiencing symptoms (?)
- Plaque now has lipids, defence cells, scar tissue + Smooth muscle cells (should NOT be found in intima!)

3) Complicated Lesion
- Now close to death

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24
Q

Can you reverse the changes of blood vessels that take place in atherosclerosis?
Is it possible to remove the obstruction?

A

No, and cannot remove obstruction because has developed inside vessel wall

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25
Q

Name for macrophages that have engulfed oxidized lipids in atherosclerosis?

What kind of lipids are engulfed primarily?

A

Foam Cells

LDL’s

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26
Q

How and when does atherosclosis begin?

A

In 20’s
Begins with subtle injury to endothelium
- Is insidious, with no manifestations until later in life
- Takes decades to develop

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27
Q

How is CRP involved in early detection of the development of atherosclerosis?

A

With initial endothelial injury, inflammation occurs –> CRP released.
Will see chronic elevated CPR levels…indicating possible vessel damage

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28
Q

Outline development of Atherosclerosis

A
  • Early in development of lesion, endothelial cells begin to express selective adhesion molecules that bind monocytes + other inflammatory cells that initiate atherosclerotic lesions
  • Monocytes enter intima –> become macrophages + oxidize and engulf LDL’s (now foam cells)
  • Free radicals produced when lipids oxidized by macrophages, which cause more injury + inflm (begins cycle)
  • Foam cells release growth factor, causing proliferation of smooth muscle cells
  • Atheroma forms
  • Adherence and entry of leukocytes + adherence and aggregation of platelets occurs at the atheroma
  • Rupture, ulceration, or erosion of unstable or vulnerable fibrous cap may lead to hemorrhage into the plaque or thrombotic occlusion of vessel lumen (hemorraging initiates clotting…thrombus forms…possible MI)
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29
Q

Risk factors that increase chance of endothelial damage leading to atherosclerosis?

A

High LDL’s
Smoking
Immune mechanisms
Mechanical stress associated with hypertension

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30
Q

Detailed structure of atheroma (p. 471)

A
  • bulge of lipids, fibres, defence cells, smooth muscle cells, etc.);
  • has fibrous cap (of smooth muscle cells and extracellular matrix)
  • Beneath + to side of fibrous cap = shoulder = macrophages, SMCs, and lymphocytes
  • lipid core (lipid-laden foam cells + fatty debris)
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31
Q

T/F: One MI predisposes a person to more MI’s?

A

T

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32
Q

Name the sites of severe atherosclerosis in order of frequency (fig 22-6 p. 466)

A

1) Abdominal aorta and iliac arteries
2) Proximal coronary arteries
3) Thoracic aorta, femoral and popliteal arteries
4) Internal carotid arteries
5) Vertebral, basilar, and middle cerebral arteries

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33
Q

What is occurring in heart during systole + diastole?

A 
Systole = heart contraction
Diastole = heart filling (relaxation of ventricles)
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34
Q

Four major control systems of BP?

see fig 23-2 on p. 487

A

1) Arterial baroreceptors
2) RAA system
3) Vascular autoregulation
4) Regulation of Fluid Volume

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35
Q

Arterial baroreceptors in BP regulation?

A
  • Rapid + short-term response
  • P sensitive receptors located in walls of blood vessels + heart (carotic + aortic baroreceptors located in heart + brain)
  • Respond to changes in P by sending impulse to cardiovascular centres in brain stem to effect changes in HR and vascular smooth muscle tone
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36
Q

Outline RAA system in BP control

A
  • Renin produced by kidneys in response to dec in arterial BP, sympathetic system,
  • Renin converts Angiotensinogen to Angiotensin I
  • ACE from lungs converts to Angiotensin II
  • A II causes :
    1) vasoconstriction of systemic arterioles (inc arterial BP)
    2) adrenal cortex to release more Aldosterone –> insertion of Na+ channels–> inc Na+ reabsorption …water follows = inc vascular vol + inc arterial BP
    3) release of ADH –> H2O channels inserted into DCT + CD, more vasoconstriction
    4) Stimulates thirst
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37
Q

ADH produced and released by?

A

Produced by hypothalamus

Released by post. pituitary

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38
Q

Outline vascular autoregulation with regard to BP control

A
  • Local, controls diameter to change resistance

More details?

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39
Q

aldosterone released from?

A

Adrenal cortex of adrenal gland

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40
Q

Regulation of fluid volume in maintaining BP?

A

???

  • Long term regulation of fluid volume primarily done by kidneys (humoral + neural both relatively short term)
  • Kidneys regulate extracellular fluid volume

Intrinsic controls of kidneys:

1) Myogenic mechanism: afferent arteriole in kidney (brining blood to glomerulus) responds to stretching or not, constricts or relaxes to maintain NFP, GFR
2) Tuboglomerular feedback: rate of filtrate flow in DCT triggers release of vasoconstrictors or vasodilators to afferent arteriole

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41
Q

Hypertension =

A

Persistant BP > 140/90 at rest

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42
Q

Categories of Hypertension?

A

Category Systole Diastole
Normal 180 or >110
(Severe hypertension)

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43
Q

Is systolic or diastolic pressure more important in BP?

A

Equally important

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44
Q

When overlap in categories of BP occur, how to classify?

A

Put in higher category to err on side of caution

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45
Q

What is primary hypertension?
AKA?
Common?

A

> 140/90
Aka ESSENTIAL or IDIOPATHIC HTN
- Do not know cause…can bring back to normal but can’t address underlying issue
- Etiology is multifactorial
- Kidney is implicated in all primary hypertension (does not mean kidney is cause but is affected by all compensatory mechanisms and regulates them)

~90% of cases

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46
Q

What is secondary HTN?

Common?

A 
>140/90
Secondary = d/t other problem
Identifiable etiology (ex: renal disease)
- Just because know underlying cause doesn't mean can always fix it
~10% of cases
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47
Q

2 classifications of HTN based on cause?

A

Primary + Secondary

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48
Q

Systolic HTN

A

Systolic >140
Mostly after age 50
Change in vessel compliance: vessels do not accommodate with less elasticity –> inc resistance –>inc systolic P but nomal diastolic

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49
Q

White coat hypertension?

A
  • BP elevate in healthcare setting only

- Reasons not entirely known, not as simple as anxiety…may be vasovagal

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50
Q

Gestation Hypertension

A
  • During pregnancy, does not always go away after pregnancy
  • AKA eclampsia
  • don’t need to know details
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51
Q

Malignant hypertension

A

When diastolic P > 120 and systolic is relatively normal

- Very severe, cause not entirely understood

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52
Q

Manifestation of Hypertension? Complications

A

Elevated BP!

Later complications arise: dizziness, fatigue, palpitations, AM headaches, blurred vision
- Those of progressive organ organ damage (heart, kidneys, eyes, vessels)

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53
Q

Why is BP considered silent killer?

A

If don’t have appropriate technology to monitor, won’t see it until is serious issue

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54
Q

What are palpitations?

A

The sensation of rapid, forceful heart beat

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55
Q

Why do AM headaches occur as complication to HTN?

A

BP has circadian rhythm - is normally highest in morning

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56
Q

Why does blurred vision occur as complication to HTN?

A

Elevated BP causes aneurysms + rupture of blood vessels in retina

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57
Q

Why does dizziness and fatigue result from HTN?

A

??

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58
Q

Why do you see progressive organ damage in HTN? (heart, kidneys, eyes, vessels)

A
  • Damage to capillaries of kidneys and eyes

- Vessels deteriorate when continually bombarded by high BP

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59
Q

Treatement of HTN?

A

1) Will try modification of life-style first (3-6 month trial) - execise, diet, weight; monitored monthly
2) If trial not effective, will try meds: 1st line is diuretics –> inc fluid (H2O + electrolyte) loss from kidneys
3) Then if required, will add one of more of following:
- Ca+ Channel Blockers –> heart contracts less and less forcefully
- Angiotensin II receptor blocker –> less vasoconstriction, reduces BP by mechanisms of A II (via aldosterone, ADH, etc)
- ACE inhibitor (ACE I) –> Angiotensin I no longer catalyzed to Angiotensin II

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60
Q

What occurs in PVD?

A
  • Exactly like atherosclerosis but occurs in peripheral vessels
  • Also affects veins + lymphatics
  • Changes similar to coronary a. and cerebral a. in that produce ischemia, pain, impaired fx. infarction, tissue necrosis
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61
Q

2 kinds of PVD?

A

1) Acute arterial occlusion –> results from either thrombus or embolism (clot from other location)
2) Atherosclerotic occlusive disease –> develops gradually in lower extremities

62
Q

Is Acute arterial occlusion easy to fix?

A

Relatively easy because isolated acute event

63
Q

Atherosclerotic Occlusive Disease

1) What population does this occur in and why?

A

1) Elderly and DM
–> elderly more likely to experience results of atheroschlerosis;
vessel damage d/t diabetes mellitus creates potential for thrombus

64
Q

Manifestations of PVD

A

1) Intermittent claudication –> vessel obstruction causes muscle ischemia (by impeding perfusion), causing pain
2) Causes venous and/or lymphatic stasis –> arteriole pressure not strong enough to maintain venous return –> venous stasis –> fluid collects –> lymphatic system overload –> wastes accumulate

65
Q

Intermittent claudication =

A

Pain when walking

66
Q

Compensatory mechanisms used with PVD?

A

1) Fast compensatory response = vasodilation –> an artherosclerotic vessel cannot dilate adequately so problem is not fixed

2) Anaerobic metabolism –> cannot return to aerobic resp so have build up of lactic acid
- -> causes systemic metabolic acidosis, impacts whole body

3) Collateralization (?)

** All of these mechanisms have limited benefit

67
Q

How occluded does a vessel have to become before pain is felt?

A

?

68
Q

Possible outcome if no treatment given for PVD?

A

Ulceration + gangrene ==> possible amputation

69
Q

What is an aneurysm?

A

Very localized, permanent vasodilation

- D/t degenerative change in vessel wall

70
Q

Where in an artery is an aneurysm likely to occur and why?

A

Points at which vessel bends + bifurcate subject to highest pressure –> deterioration of vessel –> bulge forms

71
Q

Risk factors for aneurysm?

A

HTN, atherosclerosis, congenital defects

72
Q

3 types of aneurysms?

A

1) Saccular - comes off one side
2) Fusiform - extends around both sides
3) Dissecting - An aneurysm in which the wall of an artery rips (dissects) longitudinally. This occurs because bleeding into the weakened wall splits the wall.

73
Q

Common sites for aneurysm?

A

Abdominal + Thoracic Aorta, femoral, iliac, popliteal arteries

74
Q 
Difference between complications and manifestations? 
 What are the 3 Points emphasized regularly in class on complications?
A
  • Complications need not develop (only potential); Manifestations always occur when condition is present
  • Be aware of what complications are + try to avoid them
  • Deal with complications as they develop
75
Q

Difference between thrombosis + thrombus?

A 
Thrombosis = process
Thombus = result
76
Q

Complications of aneurysm?

A
  • Pressure on adjoining structures (vessels, brain, etc.)
  • Most serious = rupture
  • Thrombosis –> blood in enlarged area flows slower so has opportunity to clot
  • Distal embolization (clot lodges distal from aneurysm)
77
Q

CAD =

Is it specific to the coronary artery?

A

Coronary Artery Disease

  • Has modifiable + non-modifiable risk factors
  • Major cause of death
  • Almost all d/t atherosclerosis

No, involves other organs in coronary circuit as well

78
Q

2 Types of CAD?

A

1) Acute Coronary Syndromes (ACS)

2) Chronic ischemia Heart Disease

79
Q

Acute Coronary Syndromes (ACS) include?

Chronic Ischemic Heart Disease includes?

A

1) MI
2) Unstable Angina
3) Sudden cardiac death
* all happen + cause death quickly

1) Stable angina
2) CHF (Congestive Heart Failure) - not talking about coronary circuit here

80
Q

Most common cause of CAD?

A

Atherosclerosis (by far)

81
Q

Stable vs. unstable angina?

A

STABLE is stable because:

1) Plaque is stable
2) Chest pain ONLY on exertion (not at rest)

UNSTABLE

  • Chest pain at rest + with exertion
  • Lesion + plaque prone to disruption, can rupture and cause platelet adhesion + thrombus formation
82
Q

Non-ST Segment elevation MI (NSTEMI)

vs. ST-segment elevation MI (STEMI)

A

Both are acute coronary syndromes

  • Unstable angina worsens to NSTEMI with development of thrombus but only partial occlusion (won’t see ST segment elevated on ECG)
  • NSTEMI worsens to STEMI when thrombus fully occludes coronary vessel (will see ST segment elevated on ECG)
83
Q

Is Angina Pectoris a manifestation or its own condition?

A
  • Is manifestation but treated as own condition in class discussion
84
Q

Angina Pectoris means?

A

“angina” = pain
“pectoris” = chest
In latin “squeezing of the chest”

85
Q

3 causes (etiology) of angina pectoris?

A

1) Mostly atherosclerosis (ischemia will cause pain)
2) Vasospam - prolonged constriction of vessel
2) Thrombosis –> independent of atherosclerosis

86
Q

Pathophysiology of angina pectoris?

A
  • Inadequate perfusion –> myocardial ischemia –> chest pain (angina)

(normally arteries dilate on demand to provide nutrients for more energy but with atherosclerosis unable to dilate…inadequate flow = ischemia)

87
Q

Manifestation of angina pectoris?
- Triggers?

  • Is this a non-reversible condition?
A

Chest pain triggered by exertion, emotion, cold

  • Can be reversed, doesn’t have to become big issue
88
Q

Why does cold cause angina pectoris?

A

Vasoconstriction –> dec blood flow –> inc ischemia

89
Q

Stable angina

  • Plaque fixed?
  • Occurs when?
  • Will the pain continue?
A
  • Fixed plaque
  • Impeded perfusion
  • Only occurs with exertion (different level of exertion depends on person)
  • TRANSIENT PAIN (lasts minutes) –> Pain subsides when activity stopped (because metabolic requirements reduced so O2 no longer inadequate) or removed from cold..
90
Q

Unstable angina

  • What is it?
  • How does it result in vasospasm?
A
  • Unstable plaque
  • Plaque collects platelets, fibrin, cellular debris
  • If ruptures, thrombosis –> platelets aggregate –> prostaglandin release –> causes VASOSPASM (locked in constricted state)
  • Note: in caps, prostaglandin causes inc perm and vasodilation….now in arteries, causes vasoconstrictriction
91
Q

Quality and duration of pain in stable vs. unstable angina?

A 
Stable = minutes
Unstable = severe, longer, at rest and/or nocturnal

…is ACS….generally lead to MI

92
Q

Variant/Vasospastic/Prinzmetal’s Angina?

Does it involve atherosclerosis?
Easy to diagnose? Why or why not?
When does it occur?

A
  • Does NOT involve atherosclerosis
  • is tricky diagnostically b/c have to look at ECG when pain and vasospasm are occurring or will not see abnormalities
  • treadmill will not induce vasospasm
  • Can occur at any time (nocturnal, at rest)
93
Q

Likely qualities of pain with angina?

How does this prevent people from seeking medical attn?

A
  • Squeezing, burning
  • Transient, mild to moderate pain
  • Burning similar to indigestion…same location as reflux - may take TUMS and then subsides, so misunderstood to be digestive issue
  • Each period of chest pain puts person at greater risk of MI
  • Likely to see migratory (pain only now in secondary locatioN) or radiating pain in angina
  • Can radiate
94
Q

Why is it important to manage angina?

A

More angina = greater risk of MI!

95
Q

Tx of angina?

A
  • Decrease activity (causing the pain)
  • Nitroglycerine –> systemic vasodilator…will have side effects because dilation occurs in vessels in brain (headache)
  • Prevention (by avoiding trigger) –> dec risk of MI
96
Q

STEMI

  • How to diagnose?
  • What does heart do during ST-segment?
A

ST-Segment Elevated MI

  • Need to look at ECG for ST segment
  • ST segment = no electrical activity..heart is at rest
97
Q

STEMI

Etiology (3)?

A

1) atherosclerosis (mostly)
2) Hemorrhage (from any vessel)
3) Coronary artery spasm (any vessel in coronary circuit)
* All have to do with inadequate blood supply

98
Q

Patho of STEMI?

A

Atherosclerosis –> complicated lesion –> ischemia –> cardiac hypoxia –> anerobic metabolism (compensatory mechanism) –> possible acidosis –> arrythmias –> inability to pump + infarction (part of heart wall dies)

99
Q

Why do arrhythmias result from acidosis?

A

Ability of heart to pump affected by change in pH as acidosis affects ion exchange across cell membranes

100
Q

Is damage of MI reversible?

A

No - muscle cells cannot proliferate

101
Q

Size of myocardial infarction depends on?

A

1) Affected vessel - how much it perfuses will determine amount of tissue affected (larger vessel = more damage because more affected downstream)
2) Extent of occlusion
3) Duration of occlusion
4) Metabolic status of the heart
5) HR, BP, and rhythm (the higher they are…?)
6) Collateral circulation = more than one blood vessel supplying tissue…if exists, tissue will still receive some blood so damage is less

102
Q

2 TYPES OF INFARCTION

A

1) Subendocardial Infarction

2) Tranmural Infarction

103
Q

Subendocardial infarction

  • Affect on ST-segment?
  • What part of heart is affected?
  • Location of occlusion?
A
  • ST-segment depression
  • Affects inner 1/3 to 1/2 of ventricle wall
  • Distal occlusion (farther from aorta) - most commonly will see severe narrowing but not full occlusion of artery
104
Q

Transmural Infarction

  • Affect on ST-segment?
  • What part of heart is affected?
  • Location of occlusion?
A
  • ST-segment elevation
  • Entire ventricle wall affected
  • Occurs at larger, more proximal artery (most commonly occurs with full obstruction of artery)
105
Q

Manifestations of MI

A
  • Chest pain w radiation to left arm, neck, jaw
  • Anxiety + tachycardia
  • Nausea, vomiting, fatigue

Less common = dizziness, SOB, palpitation etc….

106
Q

Why is severe pain often associated with nausea and vomiting?

A

Electrical activity of pain has close anatomic proximity to “vomit reflex centre”…electrical energy of pain emanates to this area

107
Q

How is MI often different in women?

A
  • More often radiates to back more + less common manifestations seen more often
108
Q

Dx of MI?

Is is difficult?

A
  • Not difficult but want to get done as quickly as possible to limit damage
  • ECG: is gold standard
  • Cardiac angiogram
  • Serum markers: Troponin I & Troponin T, myoglobin, CKMB
109
Q

Outline heart activity at each part of ECG

A

??

110
Q

Cardiac angiogram =

  • How does it work + what does it show
  • Is this invasive?
  • Risks?
A
  • Cather inserted into artery + threaded to heart (into coronary system)
  • put in contrast medium, can see blood flow through coronary circuit and where contrast medium is stopped (indicating occlusion)
  • Will fix occlusion if discovered
  • Is very invasive
  • Risk dislodging clot
111
Q

How do serum markers show cardiac damage?

A

When cells damaged, release proteins, which then enter circulation
–> inc in these proteins indicative of damage

112
Q

Serum markers used for detection of MI?

A

1) Troponin T & I
2) Myoglobin
3) CKMB

113
Q

What are troponins?
Which are specific to heart?
Are they time specific?

A

Regulatory proteins in the heart
The “bosses”
I and T are specific to heart
- Begin to appear 3-4 hrs post MI, peak in about 8-12hrs

114
Q

What is myoglobin?
Is it specific to heart?
When does it peak?

A

Respiratory pigment in muscle (stores O2)

- Appearance early (1-2hrs) after MI BUT NOT SPECIFIC TO HEART

115
Q

CKMB aka?

3 subclasses?

A

CPK (Creatine phosphokinase)

1) CKMB = specific to heart
2) CKMM = in both heart + skeletal muscle
3) CKBB = specific to brain (will see in stroke)

116
Q

Which class of CPK would indicate stroke?

A

CKBB

117
Q

Tx of MI?

A

1) Immediate goal = doing whatever you can to ensure pt survives (provision of O2, etc)
2) Drugs: thrombolytics, anti-arrhythmics, anticoagulants
3) O2 for hypoxia
4) Morphine PRN
5) Post stabilization: will add drugs such as IV diuretic, inotrope + vasodilator
6) Revascularization sx (angioplasty, bypass)

118
Q

How do anticoag and thrombolytics work?

A

Anticoag: addresses thrombosis by minimizing platelet aggregation

Thrombolytics: dissolve clot (ensure no distal embolization that might occur if only broke up clot)

119
Q

Is hypoxia localized or systemic in MI?

A

Starts localized, becomes systemic (with lack of perfusion from loss of CO)

120
Q

Reason for use of diuretic with MI (post-stabilization)?

A

Dec blood volume, dec workload of heart

121
Q

What is an inotrope?

A

Inotrope = drug that affects FORCE of heart contraction (not rate)
- Can be positive inotrope (inc force) or negative inotrope (dec force)

122
Q

What is an angioplasty?

Possible complication?

A

Can be BALLOONING or STENT (metal bracket) put into vessel

  • Done during angiogram when occlusion found
  • Complication: stent can cause initiation of clotting, so inc clot risk (have elutin stents now that release med to prevent this)
123
Q

What is cardiomyopathy?

Types?

A 
Disorder or heart muscle
Several types, put into primary and secondary, but disussed:
1) Hypertrophic
2) Dilated congestive
3) Restrictive
124
Q

Hypertrophic Cardiomyopathy
What is it?
Effect on systole?

A
  • 60% of cardiomyopathy cases
  • Excessive hypertrophy of ventricle –> thick interventricular septum
  • Impeded flow of blood exiting left ventricle d/t IV septum in way
  • Systolic fx usually NORMAL, therefore can be asymptomatic (would think thickened heart wall would mean dec in CO, but systolic not affected)
125
Q

Etiology of Hypertrophic Cardiomyopathy

Manifestations (for those who are symptomatic?

A
  • Genetic (50%) - is AUTOSOMAL DOMINANT
  • Idiopathic (50%)

Manifestations:

  • Dyspnea
  • Angina (simply chest pain, not disorder described before)
  • Syncope: d/t loss of blood to brain
  • Palpitations
  • Sudden death: like SCD, heart pushed beyond limits
126
Q

Why is hypertrophic cardiomyopathy sometimes asymptomatic?

A

Normal systolic fx

127
Q

Why does dyspnea occur with hypertrophic cardiomyopathy?

A

Whenever have systemic hypoxia, dyspnea will be manifestation - not a compensatory mechanism but…?

128
Q

Tx of hypertrophic cardiomyopathy

A
  • Negative inotrope (dec contraction)

- Alcohol septal ablation (to reduce thickened wall)

129
Q

Dilated/Congestive Cardiomyopathy
Primary or secondary?
What happens?

A

Primary

  • Cardiac enlargement (esp ventricles) as overstretching w/o enough elastic to recoil
  • larger ventricles with thinner walls
  • Weak contractions result - decreased ejection fraction
  • Alcohol abuse implicated
130
Q

Restrictive Cardiomyopathy
Primary or secondary?
Common?
What occurs?

A

Primary type

  • Very rigid V walls
  • Incomplete V filling –> dec CO
  • Usually leads to CHF
131
Q

Flow of electrical current through heart?

A

SA node = pacemaker

  • Travels to AV node
  • Through left + right bundle branches
  • To purkinje fibres
132
Q

What systems work on heart to change heart rate from SA node pace to compensate for different needs of the body?

A

Neural + hormonal influences

133
Q

What type of cells are autorhythmic cells?

A

Specialized muscle cells

134
Q

Normal SA rhythm =

A

~70bpm (ave heart rate)

135
Q

Arrhythmia aka?

A

Dysrhythmias

136
Q

What are arrhythmias? Do they occur in normal or diseased hearts? Effect?

A

Abnormality of HR, rhythm, or both

  • In normal or diseased
  • Alters cardiac cycle (filling/emptying) –> CO and perfusion affected
137
Q

Et of arrhythmias?

A
  • Congenital heart defects
  • Myocardial ischemia (can be transient…if ischemia fixed, arrhythmias stop, if not can lead to MI
  • MI
  • Drugs that simulate heart
  • Fluid/electrolyte imbalance
138
Q

4 Types of Arrhythmias?

A

1) Atrial flutter
2) Atrial fibrillation
3) Heart block
4) Ventricular fibrillation

139
Q

Atrial flutter

A
  • Regular, atrial tachycardia (~300bpm)
  • Regular, ventricular tachycardia (~150bpm)
    (about 2:1 ratio of A to V)
  • Disjointed contractions
140
Q

Atrial Fibrillation

A

Irregular, chaotic contractions (400-600bpm)

Irregular rapid V rate (80-180bpm)

141
Q

What does fibrillation refer to?

A

Uncordinated, spontaneous contraction

142
Q

Heart Block
What is it?
Three types?

A

Abn or no impulse conduction from A to V

1) 1st degree = delayed conducting, regular rhythms
2) 2nd degree = intermittent failure of conduction - block only occurs sometimes
3) 3rd degree = no conduction, independent AR and VR (pacing in ventricles kicks in so still contracting, but happens independently so out of sync)

143
Q

Ventricular Fibrillation

A
  • Worst kind of arrhythmia
  • Quivering, no contraction
  • Can cause death in minutes
144
Q

Tx of arrhythmias?

A
  • If not affected heart fx, may not need treatment
  • Tx based on type
  • Drugs
  • Defibrillation: stops all heart activity, then see “sinus rhythm” as SA pacemaker kicks in
  • Pacemaker
  • Ablation: will do if can identify misbehaving section or infarcted area
145
Q

2 kinds of problems that arise from valve damage?

A

1) Valve is open when is not supposed to be –> regurgitation
2) Valve does not close adequately –> stenosis

  • damaged valves = impeded flow + regurgiation
146
Q

Which heart valves are most at risk of damage?

A

Aortic semilunar and left AV (mitral) valves b/c pressure on left side is greatest

147
Q

Blood flow through heart?

A

k

148
Q

Etiology of valvular damage

A

Valve trauma
Degenerative change
Ischemic damage
Congenital defects

149
Q

Stenosis + Incompetent valves?

A

Stenosis = stiff valve with narrow orifice –> impeded flow

Incompetent valve
- Distorted valve –> improper closure –> regurgitation

150
Q

Tx of valvular disease?

A

Maintain/improve fx (prevents failure)

Sx? Replace valve

151
Q

Describe baroreceptors in regulation in BP

A
  • In aortic arch and carotid sinus
  • When stretched, inc frequency of AP’s to the cardiovascular center in medulla
  • Motor commands sent via parasympathetic fibres of vagus nerve
  • Reduces HR, contracilitity + causes veins + arteries to dilate
  • Veins dec venous return –> dec preload –> dec SV, dec CO, dec MAP
152
Q

Is a vasodilator advantageous during an MI?

A

No, body will have already used this compensatory mechanism with thrombus forming, so will not have effect until after (as preventative).

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