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CardioResp > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the 4 things that occur in atherosclerosis?

  • What forms?
  • What happens to the vessel wall?
    What occurs to the elasticity?
  • What happens to the size of the lumen and what does that lead to?
A
  • Atherosclerosis
    • Formation of fibro-calcific plaques
    • Hardening of the vessel wall
    • Decreased elasticity and strength of vascular wall
    • Decrease in vascular lumen (stenosis) leading to hypertension
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2
Q

How do aneurysms occur? Lay out the pathway.

A
  • Atherosclerosis → decrease in elasticity and strength of vascular wall AND increase in hypertension → bulging of vascular wall proximal to stenosis → aneurysm
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3
Q

What are the two types of aneurysms? One of the types has two subtypes. What are those? Have a picture in your mind.

A
  • True Aneurysm – has all three layers of arterial wall involved
    • Saccular – one side of vessel bulging
    • Fusiform – both sides of vessel bulging
  • Pseudoaneurysm – bulging with only tunica adventitia involved – interruption in vascular wall
    • Bleeding into layers
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4
Q

List 6 genetic or inflammatory conditions that can lead to a aneurysm and list the mutated genes in each (if applicable).

A
  • Genetic and inflammatory diseases
    • Marfan Syndrome Type I – defect in fibrillin-1 leads to lack of elasticity in vascular wall
    • Marfan Syndrome Type II – defect in gene encoding transforming growth factor beta receptor 2 (TGFBR2)
    • Ehlers-Danlos Syndrome – defect in COL3A1
    • Loeys-Dietz Syndrome – defect in TGFBR1 and TGFBR2
    • Giant Cell Aortitis – vasculitis that is positive for eosinophilic granulomas
    • Infectious aneurysms – syphilis infection can be etiological agent beginning with tunica adventitia involving vasa vasorum
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5
Q

In what age group and gender group is aortic dissection most common?

A

Males from ages 40-60 y/o

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6
Q

What is an aortic dissection and what is one particular reason it is dangerous?

A
  • Tear in the tunica intima that causes blood to dissect the vessel layers
    • Dangerous because flap can block artery or false lumen can collapse true lumen
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7
Q

What is the role of high blood pressure in aortic dissection?

A
  • High blood pressure and turbulent flow leads to initial tear
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8
Q

What are the clinical symptoms associated with aortic dissection?

How is it diagnosed?

A
  • Clinical symptoms
    • Sudden and severe tearing or crushing pain between the shoulder blades
    • Mimics MI pain except that there no relief with antacids or nitroglycerin
    • Associated with very high BP until rupture
  • Diagnosed with CXR, which prompts for a chest CT
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9
Q

What are the two types of aortic dissection?

  • Where does the disection occur?
  • What can it lead to?
  • What are the treatments for each?
A
  • Types of Dissection
    • Type A – a for anything involving ascending aorta
      • Cardiac tamponade – rupture into pericardium leads to blood squeezing the heart, making circulation impossible
      • Rupture leads to fast death due to acute catastrophic hemorrhage
      • Treatment: straight to OR
    • Type B – b for anything beyond the aortic arch
      • Treatment: medication to treat hypertension
      • Malperfusion
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10
Q

What are the two principal heart sounds and why do they occur?

A
  • S1: closing of the AV valves; “lub”
  • S2: closing of the SL valves; “dub”
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11
Q
  • What sound is associated with the physiologic splitting of the second sound?
  • Why does it occur?
  • How often doesit occur in the cardiac cycle?
A
  • “Lub-didub”
  • Splitting is heard near end-inspiration around every 4th cardiac cycle depending RR
  • Respiration causes variation in RV filling volume, because it requires the pulmonic valve to stay open for longer to get the increased RV blood out into the pulmonary trunk
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12
Q
  • Define persistent splitting.
  • What does it indicate and what is the mechanism?
  • At what stage of breathing does it occur?
A
  • Persistent splitting (A2 before P2): RBBB and pulmonary stenosis
    • Happens at every stage of breathing (not just inspiration)
    • RBBB: delay in RV contraction/emptying leads to later pulmonic valve closure
    • PS: delay in RV contraction/emptying leads to later pulmonic valve closure
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13
Q
  • Define paradoxical splitting.
  • What does it indicate and what is the mechanism?
  • At what stage of breathing does it occur?
A
  • Paradoxical splitting (P2 before A2): LBBB, aortic stenosis, R ventricular pacing
    • Happens at expiration
    • LBBB: delay in LV contraction/emptying leads to later aortic valve closure
    • AS: delay in LV contraction/emptying leads to later aortic valve closure
    • R ventricular pacing: if RV contracts before LV
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14
Q

What is a gallop and what side of your stethoscope should be used to hear them? Where are they most often heard?

A
  • Gallops = rushing of blood
    • Low-pitched (requires use of bell) and only heard in mitral and tricuspid areas
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15
Q
  • What does an S3 gallop sound like?
  • Why does it occur?
  • What is the prognosis?
  • What is it associated with?
A
  • S3 = Rapid ventricular filling of LV with a high filling pressures
    • “Ken-tuck-y”; S1 → S2 → S3
    • Poor prognosis
    • Associated with
      • Heart failure, high EDP
      • Volume overload –MR, AI, TR
      • Can be normal in young people
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16
Q
  • What does an S4 gallop sound like?
  • Why does it occur?
  • What is it associated with?
A
  • S4 = Atrial contraction against a stiff LV in late diastole
    • “Tenn-ess-ee”; S4 → S1 → S2
    • Associated with
      • Pressure overload – HTN, AS, PS, etc.
      • LVH/RVH
      • Ischemia
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17
Q
  • What does a murmur mean?
  • Is it physiologic or pathologic?
  • What is the grade of the murmur determined by?
A
  • Audible flow
  • May be physiologic or pathologic
  • Grade can be determined using location, quality, shape, radiation, thrills (palpable turbulent flow on surface of skin), and loudness
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18
Q
  • What are 4 physiological changes that could cause a high pitch murmur?
  • What are 3 cardiac conditions that could cause a high pitch murmur?
A
  • High Pitch Murmurs
    • Large pressure difference
    • Small defects/holes
    • High velocity
    • Typically systolic
    • Examples:
      • Aortic stenosis
      • Mitral regurgitation
      • Aortic insufficiency (only high pitch murmur that is diastolic)
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19
Q

What are 4 physiological changes that could cause a low pitch murmur?

What is 1 cardiac condition that could cause a low pitch murmur?

A
  • Low pressure difference
  • Large defects/holes
  • Low velocity
  • Typically diastolic
  • Examples
    • Mitral stenosis (classic example caused by rheumatic fever)
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20
Q

What is the grading scale of systolic and diastolic murmurs? WHich is harder to hear and which has thrills?

A
  • Grading Scale
    • Systolic: graded 1 to 6 out of 6
      • Palpable thrills associated with high grades
    • Diastolic: graded 1 to 4 out of 4
      • Harder to hear and thrills unusual
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21
Q

What are the 4 types of murmurs?

A
  • Systolic ejection murmur
  • Holosytolic murmur
  • Diastolic murmur
  • Continuous murmur
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22
Q

For systolic ejection murmur:

  • What condition is it most commonly associated with?
  • What kind of noise pattern do you hear?
  • Is S1 and S2 heard?
  • Is it high or low pitch?
  • Is S4 heard?
A
  • Systolic ejection murmur – aortic stenosis
    • “diamond-shaped” noise; crescendo-decrescendo
    • S1 and S2 are heard
    • High pitch
    • S4 is heard
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23
Q

For holosystolic murmur:

  • What condition is it most commonly associated with?
  • What kind of noise pattern do you hear?
  • Is S1 and S2 heard?
  • Is it high or low pitch?
A
  • Holosystolic murmur – mitral regurgitation
    • “Plateau” or uniform sound/noise
    • Engulfs S1 and S2
    • High pitch
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24
Q

For diastolic murmur:

  • What condition is it most commonly associated with?
  • What kind of noise pattern do you hear?
  • Is S1 and S2 heard?
  • Is it high or low pitch?
A
  • Diastolic murmur – mitral stenosis
    • Starts with S2
    • High pitch
    • Pitch and and amplitude decline as diastole progresses
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25
Q

For continuous murmur:

  • What condition is it most commonly associated with?
  • Low or high pitch?
  • Diastolic or systolic?
A
  • Continuous murmur – patent ductus arteriosus
    • Low-pitched, diastolic murmurs
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26
Q

What equation is it associated with oxygen demand of the heart? Is it used to compare consumption in one individual or used to compare different individuals?

A
  • Rate Pressure Product (RPP) = HR x Systolic BP
    • Correlates with oxygen consumption
    • Is very dependent on the individual
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27
Q

What are the 5 charactersitics associated with cardiac demand?

A
  • Wall stress
  • Myocardial mass
  • HR
  • Contractility
  • Resting cardiac metabolism and ionic fluxes – small O2 required even at resting
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28
Q

What is the equation for wall stress?

A

Wall stress = (Pressure * radius) / (2 * wall thickness)

  • So, a thinner wall, larger radius or higher ventricular pressure will cause an increase in wall stress and therefore increase demand
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29
Q

What is the equation for the full pressure volume area?

A
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30
Q

Is HR proportional to O2 consumption?

What is the relationship between contractility and demand?

A
  • O2 consumption is proportional with HR
  • Higher contractility will increase demand
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31
Q

Supply of the heart is dependent on what two main characteristics?

A
  • Oxygen content
  • Coronary blood flow (predominantly important during diastole
    • Coronary blood flow = Pressure/Resistance
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32
Q

What two things affect oxygen content?

What 4 things affect coronary blood flow?

A
  • Oxygen content
    • Hgb content
    • Hgb saturation
  • Coronary Blood Flow
    • Coronary perfusion pressure
    • Coronary vascular resistance
    • HR
    • External compression
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33
Q

What is the most important factor in altering coronary blood flow and what 4 things can it be controlled by?

A
  • Coronary vascular resistance – most important factor is altering coronary blood flow
    • Controlled by
      • Metabolic factors
      • Endothelial factors
      • Neural factors
      • Mechanical factors
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34
Q

How does HR affect coronary blood flow?

A
  • HR (indirect)
    • Decreasing time of diastole (due to higher HR) decreases the blood flow
      • LV is able to compensate for this by dilating the coronary arteries 4x basal flow
35
Q

What are the mediators of metabolic coronary vasodilation?

A
  • Coronary Vasodilation
    • Metabolic
      • Adenosine
      • Lactate
      • Acetate
      • H+ ions
      • CO2
      • Hypoxia
36
Q

What are the mediators of endothelial coronary vasodilation?

What are the mediators of parasympathetic coronary vasodilation?

What are the mediators of sympathetic coronary vasodilation?

A
  • Endothelial
    • NO
    • Prostacyclin
  • Parasympathetic Activity (muscarinic)
    • Ach binding
      • At endothelial cells → NO release → vasodilation
      • At smooth muscle → vasoconstriction
        • Due to damage to endothelial cells that usually cover smooth muscle
  • Sympathetic Activity (beta adrenergic)
37
Q

What are the mediators of endothelial coronary vasoconstriction?

What are the mediators of sympathetic coronary vasoconstriction?

A
  • Endothelial
    • Endothelin-1
    • Angiotensin-2
  • Sympathetic Activity (alpha adrenergic)
38
Q

What fuels do myocardium tissue use and in what progression?

A
  • 60% of O2 consumption in the fasting state is due to oxidation of fatty acids
    • The heart ultimately wants energy so it can switch to other forms of energy like carbohydrates (i.e. lactate, pyruvate and its own glycogen)
    • In starvation, it can also use anaerobic respiration via breakdown of ketone bodies
39
Q

How does the heart react to exercise?

A
  • Exercise activate the sympathetic nervous system → increasing HR and contractility → increasing O2 demand → coronary blood flow must increase
40
Q

Describe the structure of lipoproteins

A
  • Structure
    • Polar/hydrophilic envelope
      • Apolipoprotein
      • Free cholesterol
      • Phospholipid
    • Neutral lipid core
      • Cholesteryl ester
      • Triglyceride
41
Q

Increasing density of cholesterol and decreasing size

A

Chylomicron → VLDL → IDL → LDL → HDL → HDL2

42
Q

What is the function of LDL?

A
  • LDL
    • Gets cholesterol into tissues
    • Gets TG into circulation
43
Q

What is the function of HDL?

A
  • HDL
    • Gets cholesterol out of tissues
    • Gets TG out of circulation
44
Q

Explain the synthesis, absorption and clearance of cholesterol?

A
  • Intracellular synthesis – HMG CoA Reductase
    • SREBP increases transcription of HMG CoA Reductase
  • Absorption from the intestine
  • Clearance from the bloodstream – LDL receptors
45
Q

Explain the role of bile in cholesterol circulation

A
  • Bile synthesis and enterohepatic circulation
    • Cholesterol is secreted as bile, but can be reabsorbed in the ileum as bile
46
Q

Exogenous Pathway

A

Chylomicrons absorb triglycerides from the gut and put them into bloodstream → stripped of fatty acids/triglycerides by lipoprotein lipase at different tissue sites → chylomicron remnant → travel to the liver

47
Q

Endogenous Pathway

A

Liver produces VLDL → deposits lipids into different tissue sites → IDL (E receptor on liver can reuptake) → deposits lipids into different tissue sites → LDL (B100 receptor on liver can reuptake)

48
Q

HDL Pathway

A

HDL: a naïve molecule that picks up cholesterol via LCAT and takes it to the liver for recycling

49
Q

What does Apolipoprotein E, A, C, B?

A
50
Q

List some exogenous disorders of TG metabolism

A
  • Exogenous
    • Primary (genetic) hyperchylomicronemia
    • Primary (genetic) hypertriglyceridemia
    • Secondary hypertriglyceridemia
51
Q

Familial Hypercholesterolemia

Mechanism

A
  • Receptor synthesis/transport/folding
  • Failed presentation of receptor
  • PCSK-9 gain-of-function mutations
52
Q

What is PCSK-9?

GOF vs. LOF mutations

A

PCSK-9: catalytic enzyme which degrades LDL receptors

Gain of function mutation: Increased LDL receptor degradation → familial hypercholesteremia

Loss of function mutation: Decreased LDL receptor degradation → reduced LDL levels in the blood

53
Q
  • Metabolic syndrome
    • What is it?
    • Criteria
A
  • Central obesity with 2 of the following:
    • high fasting glucose, high BP, high triglycerides, low HDL
  • Its insulin resistance
54
Q

Role of CETP

Effects on LDL and HDL

A
  • CETP exchanges cholesterol from HDL/LDL with triglycerides from VLDL → triglycerides are deposited at different tissue sites via lipase activity → small density HDL/LDL particles form →
    • Small density HDL particles are renally cleared
      • decreases HDL concentration from body
    • Small density LDL particles are very atherogenic!
      • Produces smaller but more LDL molecules
55
Q

Calculation of LDLc

A
  • LDLc = TC – (TG/5 + HDLc)
    • Must be done after fasting to get rid of the chylomicrons
    • Can only be used when TG < 400 mg/dL
    • Key
      • TC: Total Cholesterol
      • TG = triglycerides
56
Q

Explain the importance of assessing ventricular function

A

Important when the following symptoms arise: hypotension, exertional dyspnea, orthopnea, edema, syncope, arrhythmias, or unexplained organ failure

57
Q

List some invasive techniques to access ventricular function

A

pulmonary artery catheter, thermodilution, ventriculography

58
Q

Pulmonary artery catheter

A
  • Description: Catheter balloon is inflated → static column of blood from catheter balloon to the pulmonary vein
    • Gives a good estimate of left atrium pressure (wedge pressure)
59
Q

Thermodilution

A
  • Description: Cold saline is injected and then monitor cardiac function using PA catheter
  • Temperature differences from blood and the injected saline is a function of cardiac output
    • High cardiac output is correlated with fast temperature changes
  • Only used in critical patients
60
Q

Ventriculography

A
  • Ventriculography – second to ECHO for EF analysis
    • Description: Catheter-guided visualization of left ventricle
61
Q

list noninvasive techniques to access ventricular function

A

fick method, cardiac hemodynamic assessment, echocadiography

62
Q

Fick method

A
  • SEE BELOW BC ARSH STILL DOES NOT REALIZE THAT EQUATIONS DO NOT PASTE
  • In the heart, the denominator is flipped to , because of the extremely high venous oxygen content and the low arterial oxygen content
63
Q

Cardiac Hemodynamic Assessment

A
  • Description: No tool or imaging is used. The patient is assessed based on symptoms only
  • If patient is hypotensive, it can be assumed that the patient is hypovolemic
  • Useful when many conditions coexsist
64
Q

Echocardiography

A
  • Echocardiography – most commonly used for EF analysis
    • Description: ultrasound of the heart
65
Q

List and describe the 6 main characteristics which ventricular function is assessed

A
  • Dimensions: Size/volume/shapes → determines preload
  • Global systolic function (EF) – Heart failure can be separated into two types: reduced EF and preserved EF
  • Wall motion abnormalities – common cause for LV dysfunction
  • Hypertrophy – increased LV mass commonly caused by diastolic dysfunction (HF with preserved EF)
  • Septal motional abnormalities: provides info on abnormal ventricular pressure/volume
  • Diastolic function: perturbed diastolic LV pressure-volume relationships
66
Q

concentric vs. eccentric hypertrophy

A

Concentric hypertrophy: thickened wall with same volume

Eccentric hypertrophy: dilation

67
Q

4 clinical risk factors

A
  • Smoking → endothelial damage
  • Diabetes → glycosylation of LDL
  • Hypertension → increases LDL entering into tunica intima
  • Hyperlipidemia → increased LDL
68
Q

what are some other risk factors for CAD

A
  • Traditional risk factors
    • Age
    • Male gender
    • Family history in 1st degree relative → genetic predisposition
  • Other emerging risk factors
    • Greatest to least risk
      • Exercise tolerance: fitness
      • Smoking
      • Systolic BP > 140
      • Cholesterol > 240
      • BMI > 27
69
Q

Diagram the mechanism of progression of CAD.

A
  • Atherosclerotic plaque → further occlusion → plaque rupture → thrombosis
    • Big thrombosis causes a myocardial infarction
    • Small thrombosis causes myocardial ischemia
  • Basically, CAD is the narrowing of the vessels supplying the heart (myocardial oxygen delivery is thereby reduced)
70
Q

Sequence of events for ischemia:

A
  • Inadequate blood flow
  • Metabolic abnormality – reliance on beta-oxidation, which is not sustainable
  • Abnormal wall motion – decreases contractility and wall eventually becomes akinetic
  • EKG – ST depression (a little ischemia) and ST elevations (MI)
  • Chest pain – late event (ischemia is silent; MI can be silent)
    • Stable angina: activities requiring higher oxygen demand reproduces symptoms
    • Unstable angina; less activity (or rest) reproduces symptoms
71
Q

Relate the pathophysiology to methods to detect CAD.

  • Reduced peak blood flow
  • Metabolic abnormality
  • Contractile abnormality
  • Repolarization abnormality
  • Chest Pain
A
  • Reduced peak blood flow
    • Exercise stress test (EST) with myocardial perfusion
  • Metabolic abnormality
    • PET scan
  • Contractile abnormality
    • Echocardiogram post-exercise
  • Repolarization abnormality
    • Standard (EKG) stress testing without imaging
  • Chest Pain
    • Patient says “ouch my chest hurts”
72
Q

Explain basic treatment plan for CAD

4 parts

A
  • Treat the risk factors. Then consider the physiology
    • Ceasing smoking and initiation of exercise reduces of cardiovascular event more than drugs.
  • Beta-blockers
    • Decrease myocardial oxygen consumption by decreasing contractility, HR, and increasing diastole time
  • Nitrates
    • Venous dilation
  • DHP Calcium-channel blockers
    • Arterial dilation
73
Q

Explain the central role of LDL cholesterol in cardiovascular (CV) risk management.

A
  • High levels of LDL are correlated with higher chance of cardiovascular-related risk
  • Low levels of HDL are more correlated with a higher chance of cardiovascular-related risk
74
Q

What are the 4 clinical risk groups CVD and statin therapy options

A
  • Clinical ASCVD (atherosclerotic cardiovascular disease)
    • Tx: High/moderate intensity statin depending on age
  • Hereditary Familial Hypercholesteremia
    • Characteristics
      • LDL-C > 190 mg/dL
      • Age > 21 y/o
    • Tx: High intensity statin
  • Primary prevention – diabetes
    • Characteristics
      • Age 40-75
      • LDL-C of 70-189 mg/dL
    • Tx: High/Moderate intensity statin
  • Primary prevention – no diabetes
    • Characteristics:
      • 10-year ASCVD risk of greater than 7.5%
        • If between 5-7.5%, talk to patient about benefits/risks of statins.
      • Age 40-75
      • LDL-C of 70-189 mg/dL
    • Tx: High/Moderate intensity statin
75
Q

Identify the components of diet that alter CV risk.

A

To reduce cholesterol: eat fruits, vegetables, whole grains, nuts, and fish

Dairy and eggs have a low risk of increasing cholesterol in diet

Red meat and processed meats are high in cholesterol

76
Q

statins vs. diet and exercise

A

Exercise and diet can only lower your LDL by a few percentage points. Therefore, the need for statin therapy is important because it can lower your LDL around 10-15%

77
Q

Statins

MOA

Side effects

Utility

A
  • MOA: HMG-CoA Reductase inhibitor; thereby increasing LDL clearance
  • Adverse effects: Myalgias and rhabdomyolysis (muscle breakdown)
  • Utility: Primary and secondary prevention
78
Q

What is your body’s reflex to long term statin use

A
  • Reflex: compensation for statin therapy
    • GI cholesterol absorption increases
    • Cellular production of HMG CoA reductase increases
    • The PCSK9 gene is activated
79
Q

Ezetimibe

MOA

A
  • MOA: inhibits cholesterol transport into enterocytes
  • When given with statins, Ezetimibe has a better effect on preventing CV events
80
Q

Bile acid sequestrants (i.e. Cholesevalam, Choleystyramine)

MOA?

A
  • MOA: inhibit bile acid reabsorption in the ileum → more bile is secreted → more LDL is secreted → lower LDL
81
Q

Plant stanols/sterols

MOA?

A

MOA: lowers reabsorption of LDL

82
Q

PCSK-9 inhibitors (Evolocumab)

MOA?

Drawbacks?

A

MOA: monoclonal antibodies that bind to PCSK9 → inhibiting LDL receptor degradation → increasing LDL resorption into cells for degradation

Negative: $$$$$

83
Q

Explain Unusual therapies for homozygous FH (HoFH)

  • Lomitapide
  • Mipomersen
  • LDLpheresis
A
  • Lomitapide
    • MOA: blocks the apolipoprotein B from attaching to VLDL
  • Mipomersen
    • MOA: blocks the loading of triglycerides on apolipoprotein B
  • LDLpheresis
    • MOA: dialysis that removes LDL from your blood

CardioResp (14 decks)

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