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Pathophysiology > Exam 3: Cardiovascular > Flashcards

Exam 3: Cardiovascular Flashcards

1
Q

The pulmonary circulation is:

A

blood in the heart and lungs

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2
Q

The systemic circulation is:

A

blood to the rest of the body

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3
Q

Central circulation includes which organs?

A
  • heart

- lungs

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4
Q

What is peripheral circulation?

A

outside of the heart and lungs

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5
Q

What is coronary circulation?

A

circulation in the coronary arteries and veins supplying the heart itself with blood

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6
Q

Blood flow moves from a _________ arterial system to a __________

A

high pressure; low pressure

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7
Q

What role does the left ventricle play in the heart?

A

it is systolic pressure and maintains that pressure throughout the arterial system

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8
Q

What is the normal pressure of the right atrium and why is it so low?

A

4 mm/Hg; to allow the blood to make the complete circuit

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9
Q

How much blood supply does the venous system carry?

A

2/3

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10
Q

What are some characteristics of the venous system?

A

○ Can stretch and expand to hold heavy volumes of static blood
○ Contain valves to prevent backflow of the low pressure blood

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11
Q

This structure provides protection for the heart from infections and consists of parietal and visceral layers

A

Pericardium

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12
Q

This structure is the muscle of the heart and is the muscle layer affected during a myocardial infarction

A

Myocardium

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13
Q

This structure consists of three layers which include the heart valves

A

Endocardium

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14
Q

________ has infected the valves

A

Endocarditis

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15
Q

Cardiac muscle contraction is involuntary but how long is the duration and what is it dependent on?

A
  • duration of contraction is much longer than skeletal muscle and dependent on calcium, potassium and sodium movement
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16
Q

What are the primary electrons for cardiac muscle contraction?

A

sodium and potassium

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17
Q

What is the pathway for electrical conduction?

A

RA > the SA node > AV node >
L/R Bundle of His (contains Na and K b/w cell membranes) > Purkinge fibers (innervates and depolarizes the myocardial cells)

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18
Q

The movement of electrolytes during contraction is __________

A

Depolarization (w/o Na, K, Ca and Mg this cant occur which is bad)

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19
Q

Muscle cells are arranged as intercalated disks that allow what functions to occur?

A
  • Serves as pathways for ions and electrical impulses

- Allows the heart to contract as a SINGLE UNIT

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20
Q

What are the different valves of the heart? What happens if they do not open/close properly?

A
  • Aortic, Pulmonic, Tricuspid, Mitral

- Stenosis or regurgitation will occur

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21
Q

Which valves are the AV valves and what are they supported by?

A
  • mitral (bicuspid) and tricuspid

- supported by the chordae tendineae

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22
Q

Which valves are the SL valves and what shape do they have?

A
  • pulmonic and aortic and are shaped like half-moons
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23
Q

What causes murmurs?

A

the flow of blood across a diseased valve or the narrowing (stenosis) of the valve produces turbulence and rapid blood flow (ex: severe anemia).

a decreased viscosity of blood increases blood flow

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24
Q

What sounds are emitted by the valves when opening is impaired?

A

clicks

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25
Q

What occurs during S1 and where can it be best heard?

A

AV valves are closing and it is best heard at the apex of the heart

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26
Q

What occurs during S2 and where can it be best heard?

A

SL valves are closing and it is best heard at the base of the heart

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27
Q

This condition is rare but has significant mortality. It may evolve over years/months or very quickly

A

Infective Endocarditis

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28
Q

What are some risk factors for Infective Endocarditis?

A

○ Strep throat- Under- treated as a child
○ Drug abuse
○ Congenital heart defects
○ Mitral valve prolapse

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29
Q

What are some causes of Infective Endocarditis?

A

○ Streptococcal with childhood strep
○ Congenital disorders
○ Staph infections in drug abusers
○ Other bacterial, fungal infxn

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30
Q

What is the patho for Infective Endocarditis?

A

Vegetative lesions form on the valves which releases bacteria into bloodstream causing the lesions to break off and form an obstruction. As the lesions grow larger, they weight down the valves and cause regurgitation and stenosis

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31
Q

What are the s/sx of Infective Endocarditis?

A

○ Fever, cough, dyspnea
○ New heart murmur develops when they’re older adults
○ Petechieae, splinter hemorrhage (due to obstruction in small vessels)

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32
Q

What is the treatment for Infective Endocarditis?

A

○ Must diagnose with blood cultures
○ IV antibiotics for six weeks (a million units of penicillin Q2H intradermal)
▪ High doses of Abx lead to other
microbes growing (vaginal fungal
infection and C. diff)
○ Prophylaxis with certain procedures
○ Valvular replacement may be necessary

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33
Q

What events occur during the cardiac cycle?

A
  • 1st heart sound- closure of AV valves
  • systole- ejection of blood (high ventricular pressure); ventricular depolarization
  • 2nd Heart sound- closure of semilunar valves
  • diastole- ventricular repolarization, (T wave)
    ○ Heart is resting and ventricles are filling
    ○ Ends with atrial contraction
    ▪ 30% more blood volume into
    ventricles for systole
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34
Q

Electrical activity does not equal:

A

pumping activity

* electrical activity PRECEDES mechanical activity *

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35
Q

What is Pulseless Electrical Activity (PEA)?

A

pumping activity of the heart fails but electrical activity continues (DO NOT SHOCK W/ defibrillator…..need V-tach/V-fib to shock)

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36
Q

What does a EKG show and measure?

A

blockages in the conduction of the heart muscles that results in errors in the conduction pathways; measures the electrical activity of the cardiac conduction

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37
Q

P wave =
QRS =
T =

A

Atrial depolarization

V depolarization & A repolarization

V repolarization

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38
Q

What is the SA node innervated by?

A

the sympathetic and parasympathetic nervous system (which is innervated by the Vagus, located in the Medulla)

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39
Q

What type of trauma can cause the heart to stop beating?

A

head trauma to the back of the head can lead to damaged medulla and
cause the heart to stop beating

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40
Q

What allows for cardiac filling?

A

low right atrial pressure

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41
Q

What is venous return affected by?

A

the amount of blood available to come into the heart

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42
Q

If the Ventricular pressure ______ then Atrial pressure _______

A

increases; increases

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43
Q

What is preload?

A

the volume of blood coming into the left ventricle causing muscle stretch and the amount of blood the Right Ventricle will have to push into the pulmonary circuit during
systole

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44
Q

What represents workload of the heart?

A

the stretching of the fibers in systole, resulting in a stronger cardiac output

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45
Q

What is nitroglycerin given for?

A

to decrease preload so the heart doesn’t have to work so hard

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46
Q

What did the Frank-Starling Law state?

A

the more muscles are stretched in diastole the greater the contraction in systole

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47
Q

What does a HR >100 result in?

A

reduced filling time (the faster the HR the worse it gets)

48
Q

What is the normal stretch in diastole and what is a normal stroke volume in adults?

A

its about 2 1/2 times resting length; 70 mL

49
Q

What is the formula for cardiac output and what is the normal CO for adults?

A

CO = (SV X HR)

4-6 L/min

50
Q

When does CO increase and decrease? And what factors cause variations in CO?

A
  • Cardiac output increases with physical activity and decreases with rest
  • CO varies with body size and metabolic needs
51
Q

How can you clinically measure CO?

A

with the pulmonary artery catheter using the Fick temperature method

52
Q

What is afterload (systemic vascular resistance)?

A

the pressure the ventricles works against that directly affects pumping

  • ANYTHING THAT INCREASES SYSTEMIC VASCULAR RESISTANCE INCREASES AFTERLOAD *
53
Q

What factors will result in an increase in afterload?

A

○ Arterial blood pressure = main source of afterload LV
○ Pulmonary pressure = main source of afterload RV
○ Increase in serum lipids
○ Aortic stenosis

54
Q

What are some causes of primary HTN?

A
  • family history
  • age
  • hyperinsulinemia and insulin resistance (T2DM)
55
Q

What are the risk factors for HTN?

A
  • race
  • high salt intake (more blacks)
  • obesity
  • Na and K intake
  • excess alcohol consumption
  • stress
  • OCPs
56
Q

What are some s/sx of HTN?

A
  • asymptomatic
  • headache (late symptom)
  • latent symptoms relate to target organ damage
57
Q

What effects does HTN have target organs?

A

▪ Brain = CVA (#1 organ)
▪ Kidneys- loss of ability to concentrate urine
▪ Heart- Heart failure, CAD, sudden death
▪ Circulatory- peripheral vascular disease

58
Q

What are some treatment options for HTN?

A
  • lifestyle modifications
  • drugs
    > step wise therapy
    > beta blocker/calcium channel blocker
    > ACE inhibitors for DIABETICS
    >Diuretics (i.e. furosemide/Lasix)
    > Thiazide diuretic = best for blacks
    □ Beta-blockers (Metopr-olol)
    □ ACE inhibitors (Lisin-opril)
    □ Alpha1 blockers (Praz-osin)
    □ Calcium channel blockers (Nifed-ipine)
    □ ARB’s (Angiotensin II receptor blockers) = (Los-artan)
59
Q

What is the #1 COD in the U.S. in both men and women?

A

CAD

60
Q

What causes CAD?

A
  • Atherosclerosis
  • Coronary Circulation
  • RCA
  • Left main coronary artery
61
Q

CAD asymptomatic until:

A

70% occlusion of the artery

62
Q

How is CAD diagnosed?

A
  • EKG
    ▪ Pathological Q wave shows zone of necrosis
    ▪ ST depression in lead II shows zone of injury
    ▪ T wave inversion
  • Treadmill exercise testing with EKG or medication
  • Cardiac Catheterization
63
Q

When are VLDL’s - triglycerides considered high? How do VLDLs work?

A

150+
▪ Contain large amounts of triglycerides
▪ VLDL’s carry their fats to tissue capillaries of fat and muscle

64
Q

What are the main carriers of cholesterol?

A

LDLs (should be below 100; >190 is BAD)

65
Q

What should the range for HDLs be?

A

40-60

66
Q

Where is cholesterol deposited?

A

in the intima layer of the epithelium arteries

□ “fatty streak”.
□ Begins developing at an early age
□ Fatty Streak can progress and regress w/ lifestyle behaviors

67
Q

These are the “Good Guys”, Inhibits cellular uptake of LDL’s and are increased with exercise

A

HDLs

68
Q

What are some risk factors for hyperlipidemia?

A

○ Metabolic Syndrome (need 3/5 of these conditions for this Dx to be the cause: abdominal obesity, HTN, low HDL, insulin resistance, hyperglycemia)
○ Smoking
○ Increased Age
○ C-Reactive Protein (CRP rise in response to inflammation)
○ Increased Homocysteine levels

69
Q

What is Homocysteine?

A

is biosynthesized from methionine and inhibits clotting cascade; is associated with endothelial damage.

70
Q

How do you treat high cholesterol?

A 
○ Limit saturated fat
○ Limit daily intake of cholesterol
○ Lower caloric intake = lower LDL's
○ Drugs to lower cholesterol ("statins")
○ Get tested annually for lipid levels (begin at age 20)
71
Q

What are some examples of statins? What are their function?

A

○ Atorvastatin (Lipitor); fluvastatin; lovastatin; pravastatin; rosuvastatin; simvastatin;
○ Inhibits enzyme for production of cholesterol and increases number of LDL receptors = increasing LDL uptake and catabolism

72
Q

What are the risk factors for Atherosclerosis?

A

○ Hyperlipidemia - Cholesterol > 200
○ Low HDL’s <40 (men lower than women)
○ Increasing age (men 45+; women 55+)
○ FHx of MI/Sudden Death before 55 in men and 65 in women
○ HTN = smaller vessels = inc. resistance
○ Smoking
○ Diabetes Mellitus = sugar is sharp and causes damage
○ Obesity

73
Q

What is the patho for Atherosclerosis?

A
  1. Development of fatty streak (occurs at a young age)
  2. Injury to the intima- inner layer of the artery is damaged and WBC/PLT attach
  3. Accumulation of platelets, lipids, WBC’s, growth factors.
  4. Weakening, and rupture of the unstable plaque causing hemorrhage
  5. More clotting - larger blockage d/t platelets forming a clot over hemorrhage
74
Q

What are the s/sx of Atherosclerosis?

A

pain or angina (only appearing after blood vessel narrows too much due to ischemia. This causes a switch to anaerobic respiration and the lactic acid stims the
nociceptors and causes the pain)

75
Q

Describe s/sx of stable angina and treatment:

A

○ Substernal/radiating chest pain to the left arm (pain is burning, squeezing, and usually doesn’t increase in intensity)
○ Predictable pattern & predictable duration
○ Precipitated by emotion, exercise, or cold.
○ It lasts for a short time <5 minutes and stops with rest; greater than 5 minutes = necrosis

Treatment: rest and Nitroglycerine

76
Q

Describe s/sx of unstable angina and treatment:

A

○ Symptoms of chest pain occurring at rest; Prolonged chest pain >15-20 minutes and non-predictable; pain is persistent even w/ Nitro
○ Patho:
▪ Probably triggered by changes to the unstable Plaque
▪ Plaque is changing in nature/shape/form

Treatment:

  • medical emergency; cardiac catheterization; 12 lead (direction) EKG = ST depression, T wave inversion
  • IV nitroglycerine to relieve pain
  • Antiplatelet drugs (aspirin, Plavix)
  • Calcium channel blockers (-edepines)
  • TPA instantly dissolves the clots
  • Percutaneous Transluminal Coronary Angioplasty (PTCA or PCI)
  • Stents to keep vessel open
  • CABG will have to be done if stents are ineffective
77
Q

What are the 3 zones of a MI damage?

A

Necrosis
□ Inner zone of dead tissue that was ISCHEMIC for 20-40 min. Will become scar tissue and won’t contract

Area of Injury’
□ Cells will die if the ischemia is not stopped IMMEDIATELY

Ischemia
□ Cells usually doesn’t die…
□ Can recover fully and work like normal

78
Q

How is a MI diagnosed?

A

○ 12 lead EKG- pathologic Q wave and ST elevation
○ Enzymes (Bio-Markers) - released from dead cells due to necrosis; you can assess the extent of necrosis
▪ Elevated Troponin levels >1 is positive in 1-2 hours
▪ CKMB rises (signs of muscle metabolism)

79
Q

How is MI treated?

A 
○ TPA = dissolves the clot
○ Aspirin and other anti-platelet aggregator
○ Heparin - anticoagulant (prevents new clots)
○ Anti-dysrhythmics
○ Beta blockers (decrease HTN)
○ Calcium channel blockers
○ Nitroglycerine IV
Morphine = chest pain
○ Valium = anxiety
○ Stent to keep artery open
○ PTCA
○ CABG
○ Lifestyle modification education
80
Q

What are some causes of CHF?

A

○ #1 Cause = MI
○ Hypertension, volume overload
○ Cardiomyopathies also cause CHF
○ Valvular disorders

81
Q

What is the patho for CHF?

A

○ Reduced ejection fraction, decreased CO and decreased renal blood flow (results in increased sodium and water retention & increased venous return / blood
volume)
○ Poor renal perfusion leads to RENIN secretion
○ Inappropriate myocardial hypertrophy and remodeling (Increase in muscle mass of the Left Ventricle & Chamber dilation, heart tries to compensate but worsens)

82
Q

What are the s/sx of right sided heart failure?

A 
□ Congestion in the liver
□ JVD
□ Dependent edema (legs)
□ Ascites
□ Fatigue
83
Q

What are the s/sx of left sided heart failure?

A 
□ Crackles
□ Dyspnea
□ Cyanosis
□ Tachycardia = compensation
□ Fatigue
84
Q

How is CHF diagnosed?

A

○ Chest X-ray
○ BNP- lab test (100+ = CHF)
○ Echocardiogram used to monitor treatment
○ EKG- will show changes such as atrial and/or ventricular hypertrophy
○ Angiography
○ Cardiac Catheterization

85
Q

How is CHF treated?

A

○ Require continuous monitoring
○ Diuretics- Lasix
○ Digoxin- Increases cardiac contractility
○ Vasodilators to reduce BP (nitro)
○ Mechanical support- used for end-stage heart failure (LVAD)
○ Patient education: restrict Na and increase K intake

86
Q

What is used in the making of steroid hormones?

A

Cholesterol

87
Q

What are excess carbs converted into and where are they carried?

A

converted into triglycerides; carried by the lipoprotein to adipose tissue for storage

88
Q

What is the cause of hyperlipidemia?

A
  • genetics
  • lack of LDL receptors
  • increased dietary sensitivity to cholesterol = increase absorb and increased serum levels
89
Q

Atherosclerosis leads to:

A

CAD = #1 COD in US b/w men and women

90
Q

This is death (necrosis) of cardiac tissue due to prolonged ischemia lasting about 20-40 minutes

A

MI (#1 killer of americans)

91
Q

What is the patho for MI?

A

○ Atherosclerotic plaque disrupts circulation and the blood vessel ruptures or acute coronary thrombosis occurs

92
Q

What are the necrotic areas cleaned out by after a MI and what does it result in?

A

macrophages within the next 48 hours resulting in increased Temperature d/t inflammatory process.

▪ In about 10 days scar tissue begins forming and is complete in 7 weeks. Scar areas cannot contract or conduct action potentials

93
Q

What are the s/sx of a MI?

A 
○ Acute chest pain (radiates to left arm with no relief)
○ EKG changes
○ Nausea and vomiting (d/t chest pain)
○ Weakness
○ Pale, cool skin
○ Fever and leukocytosis
○ ESR rises
○ Dyspnea
○ Symptoms of cardiogenic shock with renal shutdown (most will DIE)
94
Q

______ is the worst prognosis for immediate death in those suffering from a MI

A

LAD occlusion

95
Q

This condition occurs when the heart is unable to compensate for the demands placed on it and the pumping action is impaired resulting in edema

A

CHF

96
Q

Who is CHF most common in and what is the prognosis?

A

elderly; poor with 99-100% dying within 9 years of dx

97
Q

How would you assess for arterial diseases of the extremities?

A

○ Monitoring capillary refill time
○ Peripheral pulses (strength)
○ Auscultation to hear a bruit
○ Doppler ultrasound

98
Q

What are the s/sx of arterial insufficiency?

A

○ Intermittent claudication with walking (gastrocnemius muscle has highest O2
consumption)
○ Cool temperature
○ Limb color blanches with elevation and becomes deep red when leg is in dependent
position
○ Pain becomes more severe at rest (rest pain) and leg must be lowered to gain relief.
○ Diminished or absent peripheral pulses
○ Loss of hair on toes, feet, nails thickened and ridged
○ Arterial ulcers

99
Q

How do arterial ulcers appear and where do they appear?

A

▪ Very painful, deep, and circular with a black base
▪ Tend to be on tips of toes, heel or other pressure areas
▪ Arterial ulcers are CLEAN - but deep and painful

100
Q

How do venous ulcers appear and where do they appear?

A

gross, jagged edges, purulent with minimal pain and irregular borders

101
Q

How is arterial insufficiency treated?

A

○ Femoropopiteal (Fem-Pop) Bypass graft surgery
○ Walking to point of claudication to develop collateral circulation
○ Stop smoking
○ Control diabetes mellitus (#1 cause of arterial insufficiency)

102
Q

This condition results from vasospasm of the hands and is triggered by cold and strong emotional responses; it is more common in women

A

Reynaud’s Disease

103
Q

How is Reynaud’s Disease treated?

A

○ Avoid exposure to cold
○ Vasodilators (Nitro)
○ Calcium channel blockers,

104
Q

What can Reynaud’s Disease cause?

A

gangrene d/t intense vasospasm if left untreated

105
Q

This results from a abnormal dilation of a blood vessel that usually occurs in the aorta and the brain; the area is weakened and grows larger from BP on vessel

A

Aneurysms

106
Q

What is a risk factor for dissection of the aneurysm?

A

HTN (life threatening)

107
Q

How do you treat an aneurysm?

A

surgery & resection of area (prosthetic graft)

108
Q

What occurs during Chronic Venous Insufficiency?

A

○ Usually a result of DVT or valvular incompetence (varicose veins)
○ Valves of the legs are unable to close properly and blood refluxes in the legs; muscle pumps ineffective

109
Q

What are the s/sx of Chronic Venous Insufficiency?

A 
▪ No ischemia as in arterial insufficiency
▪ Tissue congestion, edema,
▪ Varicose veins
▪ Brown discoloration
▪ Lymphatic Insufficiency
▪ Development of venous ulcers 
▪ Moderate to severe non pitting edema
110
Q

How can you educate a patient with venous Insufficiency?

A

▪ Stop and Walk Every Several Hours When Traveling

▪ Long term immobility = worsening symptoms

111
Q

What is Deep Vein Thrombosis?

A

○ Presence of a thrombus in the vein
▪ Venous stasis
▪ Increased blood viscosity
▪ Vessel wall injury

112
Q

What are the r/f for a DVT?

A 
▪ Bedrest (i.e. after surgery)
▪ Prolonged immobility (traveling)
▪ MI, CHF
▪ Pregnancy, childbirth, oral contractives
▪ Dehydration
113
Q

What complications can result from a DVT?

A

Pulmonary embolism

114
Q

What are the s/sx of a DVT?

A 
▪ Asymptomatic if vessel not 100% occluded
▪ Sxs depend on site of DVT
▪ Signs for DVT in legs:
□ Calf pain, deep muscle tenderness
□ Swelling
□ Dorsiflexion causes pain (Homan’s sign)
□ Fever
□ General Malaise
□ Redness
□ Increased WBC, ESR
115
Q

How can you prevent, diagnosis and treat a DVT?

A 
□ Active leg exercises when immobile
□ Keep entire leg elevated at 15-20 to prevent stasis
□ Early Ambulation
□ Support stockings when on bedrest
□ Use of SCD’s
□ Prophylactic anticoagulants 
- Heparin
- Lovenox
- Coumadin (warfarin)
□ Heat to relieve vasospasm

Pathophysiology (10 decks)

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