Cardio Exam 1 Flashcards
1
Q
Talk through Wigger’s diagram
A
Do it
2
Q
What does CVP (central venous pressure) measure?
A
Ability of heart to pump blood out of RA - determined by tricuspid valve function, RV function, pulmonary arterial function etc.
3
Q
Common causes of increased CVP
A
- Heart failure 2. Tricuspid valve disorders 3. Pulmonary arterial HTN
4
Q
Cause of decreased CVP
A
Low blood volume
5
Q
Discuss JVP wafeforms
A
A: Atrial systole X: fall in RA pressure after a wave peak C: ventricular contraction, tricuspid valve Closure X’: descent of cardia base after atrial relaXation V: venous filling of RA Y: rapid ventricular filling - right atrium is emptYing H: continued filling of right atrium during diastole that is inte4r
6
Q
Which jugular vein is more directly related to changes in RA pressure/heart?
A
RIJ REJ is more superficial
7
Q
What does high A wave from jugular pressure waveform indicate?
A
- Stenosis of tricuspid - Closure of tricuspid valve - Right ventricular failure
8
Q
What does distension of jugular vein indicate?
A
severe congestion
9
Q
What does S1 reflect?
A
mitral and tricuspid closure
10
Q
What does S2 reflect?
A
aortic and pulmonic valve closure
11
Q
Between S1 and S2 heart sounds, which sound varies with respiration?
A
S2
12
Q
What cardiac event occurs between S1 and S2? Between S2 and the next S1?
A
Systole between S1 and S2 Diastole between S2 and the next S1
13
Q
Describe physiologic splitting of S2
A
With inspiration, there is increase venous return to RV = increased RV EDV = increased time to expel blood from RV = pulmonic valve stays open longer
14
Q
Common causes of widened S2 splitting? Not the physiologic splitting.
A
- RBBB (delay in RV contraction = delay in closure) - Pulmonic stenosis (more time to open, delay in closing) - Also COPD: increased back pressure into RV
15
Q
Most common cause of fixed splitting of S2?
A
ASD Pulmonary side of heart has low resistance, so volume overload in right heart results in delayed closure of pulmonic valve. These individuals don’t have physiologic splitting with respiration. It is just fixed.
16
Q
Common causes of paradoxical splitting?
A
This just means that pulmonic closes before aortic and this occurs during expiration, not inspiration. LBBB (delay in LV contraction = delay in aortic valve closure) Aortic stenosis (more time open, delay in closure)
17
Q
What sound is heard during mitral stenosis? When does sound occur?
A
Opening snap Why? Calcification and stiffening valve. Note: sound is fixed and occurs at the start of diastole (before S1). No change with respiration.
18
Q
Is S3 pathologic? Why and when does it occur?
A
Produced by tension of chordae tendinae during rapid filling of diastole. Can be seen in young with thin chest wall and supple ventricle - also in athletes. No pathology here. Can be seen in pathology - volume overload or advanced regurg.
19
Q
What is 4th heart sound? Why and when does it occur?
A
Occurs in late diastole and coincides with atrial contraction. It is a pre-systolic sound produced when trying to fill a stiff ventricle. Heard in cases of low ventricular compliance, hypertrophy and acute MI.
20
Q
Murmurs heard in aortic area
A
Ejection type murmurs such as: Aortic stenosis Flow murmur?
21
Q
Murmurs heard in pulmonic area
A
Ejection type murmurs such as: Pulmonic stenosis Flow murmur?
22
Q
Murmurs heard in tricuspid area
A
Pansystolic murmurs such as: Tricuspid regurg VSD Also mid-to-late diastolic murmurs such as Tricuspid stenosis ASD
23
Q
Murmurs heard in mitral area
A
Pansystolic murmurs such as Mitral regurg Also mid-to-late diastolic murmurs such as Mitral stenosis
24
Q
Types of systolic murmurs
A
- Ejection type: aortic stenosis, pulmonic stenosis. Sound here = crescendo, decrescendo 2. Pansystolic (holosystolic): mitral regurg, tricuspid regurg, VSD Sound here = non-crescendo/decrescendo sound 3. Late systolic: MVP Sound here = mid-systolic click with non-crescendo/decrescendo sound
25
Murmurs heard at left-sternal border (Erb's point)
Early diastolic murmurs: Aortic regurg Pulmonic regurg
26
CO calculation. What is normal value in resting adult?
CO = SV.HR Normal ~5L/min in resting adult
27
Define cardiac index
Volume of blood ejected from heart per unit time per unit of body surface area eg. 3L/min/m^2 This is more realistic parameter of cardiac function as it takes into account the size of the human
28
How much of the SV is attributed to rapid filling phase? How about atrial kick/contraction?
~ 80% by rapid filling - passive ~ 20% by atrial contraction
29
Define preload Define afterload
Preload: Tension exerted on the cardiac ventricular muscle when it begins to contract Afterload: pressure that ventricle has to win to produce a stroke volume
30
What happens to SV as preload increases if all other factors are equal? How can this principle be used in patient with heart failure? What must you be careful of?
SV increase within certain limits. Pt with heart failure can have decreased CO. If you want to increase it, you can IV bolus them especially if dehydrated. As you do, BP should go up. Too much can cause patient to go into pulmonary edema.
31
Describe Frank-Starling relationship and mechanism
Relationship: force of ventricular contraction is function of ventricular end diastolic length. If you increase pre-load, contractility and ultimately SV increases. Mechanism: length of sarcomere determines sensitivity to Ca. There is optimum. Within limits.
32
What happens to SV with increasing afterload if all else is equal?
Increase afterload results in decrease in SV.
33
What is the ANREP relationship and mechanism? Why do I care?
Relationship: increase in aortic pressure abruptly = positive inotropic (FOC) effect. Mechanism: increase LV wall tension = increase cytosolic Na level, increase myocardial cytosolic Ca level = increase myocardial contraction. Why do I care? If I want to hear a particularly soft murmur, I can apply a torniquet or have someone make fist to increase work of heart and therefore sound of murmur.
34
What happens to SV when ventricular contractility goes up with all other factors being equal?
Increased contractility = increased SV
35
Review SV vs preload, afterload, contractility graphs
do it
36
Review contractile status, ventricular performance graph
do it
37
What is Bowditch effect/phenomenon?
Increased HR progressively enhances FOC. If too rapid, force decreases. CO is rate-dependent. Makes sense if you remember CO = SV.HR
38
Clinical method of measuring CO
Pulmonary artery catheterization (PAC): thermodilution with bolus injection of cold fluid.
39
The cardiac AP contour looks the same as skeletal muscle AP contour?
Falsch
40
Describe the cardiac myocyte AP curve. Include the phases, ions/channels responsible for the changes
Depolarization = phase 0 - Opening of fast Na = rapid depolarizing Early repolarization = phase 1 - Na channels close, some K channels open, incomplete repolarization Plateau = phase 2 - Membrane potential ~ 0 mV (ECG!!). Slow Ca channels open = Ca in, balanced by opening of K channels allowing K out Rapid repolarization = phase 3 - Ca channels close, opening or more K channels = K out RMP = phase 4 - Only K channels and maintenance Na/K ATPases open allowing for maintenance of RMP until next stimulus
41
Describe cardiac nodal tissue AP
\* note: only phases 0, 3 and 4; no 1, 2 Phase 0: Threshold met = opening of Ca channels slowly Phase 3: After depolarization occurs, K channels open, K out Phase 4: HCN/funny current channels slowly depolarizes cell - progressive reduction in K efflux and progressive increase in calcium influx
42
What is the difference between channels responsible for depolarization in cardiac myocytes and cardiac nodal tissue?
Cardiac myocytes: Fast Na channels Cardiac nodal tissue: Ca channels
43
Describe sequence of depolarization in heart. Note the order of depolarization within the ventricles.
SA node Atria AV node Bundle of His Bundle branches Purkinje fibers Ventricles: Septum, apex and ventricular free walls
44
Approximate rates of conducting tissue in heart
SA node: 60-100 AV: 40-55 Bundle of His, Bundle branches, Purkinje: 25-40 Note: atrial and ventricular myocardium don't have pacemaker rates
45
Which lead on ECG shows greatest net depolarization of heart?
Lead II - greatest deflection 60 degrees
46
The refractory period of the AP in cardiac myocytes is related to which of the following ion channels: a. Sodium channels b. calcium channels c. potassium channels d. chloride channels
- Answer = A. Fast Na channels
47
What are the two refractory periods seen in cardio myocyte AP cycle? What is happening to cause these periods? Can additional stimulus elicit AP during each of these periods?
Absolute refractory period Relative refractory period These are a result of the gating kinetics of the fast Na channel found in cardiac myocytes that exist in 3 states: a. Resting: no Na entering cell as inner pore is closed, intracellular gate is open. b. Activated: stimulus lead to VG change and opening of VG sensitive inner pore. Na enters cell. c. Inactivated: intracellular gate closes and Na ceases to enter cell even though inner pore is open. ARP: cannot illicit another AP regardless of strength of stimulus as intracellular gate is closed, despite inner pore being open RRP: can illicit another AP is strength of stimulus is sufficient
48
Why is there a time delay between electrical events in cardiac myocytes and mechanical response in the tissue?
Takes some time for Ca channels to open. This causes the delay
49
Describe events of cardiac myocyte contraction and relaxation
Contraction: - Calcium entry through VOCC - Calcium release from SR (through ryanodine receptor) - Calcium interacts w/trop = contractile shortening Relaxation: - Calcium dissociates from trop - Ca taken back up into SR via SERCA (atpase) - Ca becomes bound to proteins within SR (calcisequestrin) - CA pumped out of cell at cell membrane via NCX (Na/Ca exchanger atpases)
50
Types of arrhythmogeneses
1. Active a. Automaticity b. Triggered activity: Early afterdepolarizations, After depolarizations d. Re-entrant circuits 2. Passive a. Cardiac remodeling
51
Describe arrhythmias from automaticity
These are arrhythmias from cells with phase 4 depolarization. SA node can lead to sinus tachy (via SNS increases automaticity) and sinus brady (via PSNS decreasing automaticity). These are obviously physiologic arrhythmias. Subsidiary or latent pacemakers can be found in atria, AV junction, ventricles. This is abnormal.
52
Diastolic depolarization underlies a major difference in channel expression between nodal and non-nodal cells. What ion channels are not present in non-nodal tissue? a. Calcium ATP-ases b. Na-K ATPases c. Na-Ca exchanger d. Hyperpolarization-activated cyclic nucleotide-gated channels e. Beta-adrenergic receptors
Answer = D. HCN/funny current channel active during phase 4 depolarizations seen in cardiac nodal tissue.
53
Effect of Ach on phase 4
Increases K efflux = reducing slope of phase 4
54
Effect of NE on phase 4
Increase Ca and funny current = increase slope of phase 4
55
Effect of hypokalemic on phase 4
Decrease K current = increase in slope of phase 4
56
Effect if ischemia on phase 4
Decrease K current = increase in slope of phase 4
57
Effect of mild hyperkalemia on phase 4. Severe hyperkalemia?
Mild hyperkalemia = increase in max diastolic potential = increase in slope of phase 4 Severe hyperkalemia = significantly depolarized membrane potential, cells become inexcitable
58
Describe how triggered activity leads to development of arrhythmogenesis? What ions are responsible for DAD and EAD? Which is exacerbated by low HR? Which by high HR?
This refers to eliciting AP changes in cells without phase 4 depolarization, ie. myocytes. DAD: cytosol and / or SR becomes Ca overloaded resulting in change in membrane potential leading to AP. Exacerbated by high HR. Why? Interrupts ability to recycle Ca. EAD: any alterations in any ion flux during plateau phase (2) or phase 3 leading to prolonged AP duration and generation of AP. Specifically: reduced K current, increased Ca, increased Na/Ca exchange activity, increased late Na current. Exacerbated by low HR. Why? APs tend to be long at low HRs.
59
Types of re-entrant circuits. Which are harder to tx? Which have worse prognosis?
Anatomically: WPW syndrome, AVNRT, atrial flutter, PSVT. Tx with ablation. More easier to tx, better prognosis. Functionally: absence of defined pathway. Harder to tx. Worse prognosis.
60
Describe how cardiac remodeling leads to arrhythmogenesis
Changes in gap junctions Changes in cell structure: fibrosis, fat, nerve endings, cell hypertrophy Strength of impulse now acts on smaller amount of tissue = length of AP increased now.
61
Effect of PSNS on blood vessels, heart and coronary arteries
BV: no innervation by PSNS Heart: decrease HR and contractility Coronary arteries: constrict Cranial: 10, 9, 7, 3 Sacral: S2-4
62
Effect of SNS on blood vessels, heart and coronary arteries
BV: constriction (except skeletal) Heart: increase HR and contractility Coronary arteries: dilate Ganglia: T1-L2 Cervical ganglia Lumbar splanchnic
63
Result of flattened diaphragm on CO
Decreased CO
64
Viscero-somatic reflexes for heart
SNS: T1-5 left PSNS: OA (vagus)
65
How do somatic dysfunctions lead to cardiac dysfunction?
Head and neck = T1-4 SNS ganglia are from T1-L2 with close relationships to rib heads SNS cervical ganglia superior at C2/3, middle at C6 and inferior at C7. These target head, heart, neck etc. PSNS is primary vagus which emeres from jugular foramen located between occiput and temporal bones. Ultimately: pain stimulates the SNS nervous system = heightened response on something already potentially overstressed.
66
What are the somatic presentations of visceral problems at heart?
Left-sided chest, left shoulder and arm, jaw, neck, epigastric, back and rib pain.
67
Left SNS fibers to heart innervate what? What does hyperactivity of these fibers lead to?
- innervate deep cardiac plexus and AV node - ectopic foci and v fib
68
Right SNS fibers to heart innervate what? What does hyperactivity of these fibers lead to?
- innervated deep cardiac plexus and SA node - supraventricular tachyarrhythmias
69
Left vagus innervates what in the heart? What does hyperactivity of these fibers lead to?
- AV node - AV block
70
Right vagus innervates what in the heart? What does hyperactivity of these fibers lead to?
- SA node - Sinus bradyarrhythmias
71
Lymphatic drainage from the heart and lungs is carried by what? Impaired drainage could lead to what conditions?
Left thoracic duct Conditions: reduction in collateral circulation (ischemia and infection), atherosclerosis, HTN, CHF, electrolyte imbalance
72
At what angle of scoliosis does cardiac function deteriorate
\> 75%
73
What are the spinal levels/viscero-somatic relationships for: - ventricles - atria - anterior MI - posterior/inferior MI
Do we need to know? - Ventricles: C8-T3 - Atrial: T4-T6 - Anterior MI: left T1-4 - Posterior/inferior MI: C2 and cranial base (OA)
74
For CHF, what OMM treatments should be emphasized?
Lymphatic treatments
75
OMM treatment for essential HTN
Tx kidneys and adrenals to decrease hydrostatic pressure gradient across filtration membranes of glomerula of kidneys. This is T10-12.
76
Anterior LV MIs are best viewed in what leads?
Precordial leads, I and aVL
77
Inferior LV MIs are best viewed in what leads?
Leads II, III and aVF
78
The heart is perfused primary during what phase of cardiac cycle? a. ventricular systole b. ventricular diastole c. isovolumic contraction d. isovolumic relaxation
Answer = B - rapid filling during ventricular diastole
79
What happens to coronary blood flow as LV pressure increases?
Sharp decrease because BVs are squashed
80
Systolic compression of coronary blood vessels is worst in which side of heart?
Left heart \> right heart. Why? left has to generate more pressure to overcome systemic pressures.
81
Flow equation. Using this, how does coronary perfusion/flow remain constant given changes in pressure?
Flow = delta P / R Blood flow maintained through changes to R. Think mathematics and physics here. If decrease in pressure, flow is maintained through reducing resistance within coronary vessels. They change in same direction.
82
What is coronary reserve? Why do I care?
It is the different between passive movement (capacity of vessels) due the pressure of blood and the autoregulatory curve (BV maintaining tension). This is related to how well vessels can vasodilate. Why care? If there is impaired vasodilation to vessels (eg. endothelial dysfunction leads to inability to produce NO) then coronary reserve decreases. Individuals cannot exert themselves as vasodilation isn't functioning properly.
83
What is the relationship between myocardial o2 consumption and blood flow?
As coronary blood increases, o2 consumption increases.
84
Describe how coronary circulation is regulated by metabolism?
Increase in metabolism = Increase in hypoxia (not pathologic yet) = Increase in ATP turnover (use outpaces production) = Increase in cellular adenosine accumulation = Adenosine diffuses out of cell and acts on vascular adenosine receptor = Vasodilation
85
Does hypoxia induce vasodilation or vasoconstriction in cardiac blood vessels? What mediates this?
Vasodilation. Mediated by adenosine.
86
Describe two phases of SNS regulation of coronary circulation
1st phase: transient vasoconstriction (d/t direct effect of NE on alpha-1 receptors) 2nd phase: SNS drives increase HR and FOC = hypoxic vasodilation
87
Describe pulmonary circulation in terms of resistance and capacitance
High capacitance (can hold a lot of blood) Low resistance (compared to systemic)
88
Compare resistance between right outflow and left outflow of heart
Right side = low resistance Left side = high resistance
89
Between the apex and the base of the heart, describe in terms of pressure "cost" - where is it easier to get blood? What is the implication in terms of lymphatic drainage?
Zone 1 (apex): higher pressure cost Zone 3 (base): lower pressure cost Ultimately easier to perfuse base of lungs. Increase in capillary hydrostatic pressure higher at base. Requires lymphatics to function well. If fluid in lungs, crackles heard in lower part first.
90
Hypoxia leads to what response in pulmonary vasculature?
Vasoconstriction.
91
Why alter pulmonary circulation?
Match VQ
92
Describe passive regulation of pulmonary circulation
Recruitment: opening of previously closed capillaries through higher perfusion pressure Distension: accommodation of increased blood volume in capillaries Gravity, body position, lung volume etc.
93
What are the causes and responses to alveolar hypoxia?
Causes: airway obstruction, high altitude, acute lung damage, COPD Low o2 alveolar partial pressure = ? signal = constriction of adjacent blood vessels that are hypoventilated = blood diverted = decreased wasted ventilation areas.
94
Results of chronic hypoxemia in lungs
Hypoxic vasoconstriction = increased resistance to flow, hypoxia stimulates vascular SMC hypertrophy = increased pulmonary pressure = (pulmonary arterial HTN) RVH = RV dilation, valve damage = RV failure
95
Commonly used classification system of anti-arrhythmic drugs
Vaughn-Williams system
96
Describe Vaughn-Williams classification system - list class, MOA and drugs
IA: quinidine, procainamide, disopyramide MOA: moderate Na channel blocking IB: lidocaine, mexilitene MOA: mild Na channel blocking IC: flecinide, propafenone MOA: marked Na blocking II: metoprolol, atenolol MOA: beta-blocking III: sotolol, amiodarone, ibutililde MOA: K blocking. Amiodarone has Na, Ca, K and beta-blocking effect IV: verapamil, diltiazem MOA: CCB
97
Quinidine. Use, MOA, adverse effects
- Use: old drug, previously used for ventricular arrhythmias - MOA: class IA, Na channel blocker - Adverse effects: AV block, Torsades (prolong QT), GI upset, Cinchonism
98
Procainamide. Use, MOA, adverse effects, what is important about pharmacokinetics
- Use: previously used for ventricular arrhythmias - MOA: class IA, Na channel blocker - Adverse: QT prolongation, lupus - Pharmacokinetics: NAPA = active metabolite (ability to make is pharmacogenetically determined)
99
What is common adverse effect of class IA antiarrhythmic drugs?
QT prolongation
100
Disopyramide. Use, MOA, adverse effects, what is important about pharmacokinetics
- Use: previously used for ventricular arrhythmias, may be more effective in atrial arrhythmias - MOA: class IA, Na channel blocker - Adverse: potent anticholinergic effects - Pharmacokinetics: renal and hepatic excretion, must watch dose in kidney failure patients
101
Lidocaine. Use, MOA, adverse effects, what is important about pharmacokinetics of this drug?
- Use: prevention/tx of VT / VF especially during ischemia - effective in preventing re-entrant rhythms (not first line in ACLS) - MOA: class IB, Na channel blocking - Adverse effects: CNS effects at toxic levels, Can give to patients allergic to procaine as this is amide, not ester, AV block rare - Pharmacokinetics: can monitor for toxicity
102
Flecainide. Use, MOA, adverse effects
- Use: SVTs in patients with normal cardiac function (never in ischemic heart dz, CAD or heart failure) - MOA: class IC, Na channel blocking (potent) - Adverse: drugs caused increased mortality in those with post-MI arrhythmias, well tolerated generally
103
Propafenone. Use, MOA, adverse effects
- Use: prevent/convert SVT, VT, VF (in pt without underlying heart disease) - MOA: class IC, Na channel blocking (potent), some beta-blocking - Adverse: fairly well tolerated, not for use in pt without underlying heart disease, can cause torsades, AV block, CHF. Must reduce dose of digoxin or warfarin when using this.
104
Which class of anti-arrhythmic drugs cause increase in mortality?
All class I. Can use class IC in patients with arrhythmia provided they don't have underlying heart disease. Rare to use these drugs. This includes flecainide and propafenone.
105
Which is the only class of antiarrhythmic drugs that have been found to reduce mortality in arrhythmia patients?
Beta-blockers (class II)
106
Sotolol. Use, MOA, adverse effects
- Use: prevention of AF and sustained VT/VF - MOA: beta-adrenergic blocking with class III properties - Adverse: Torsades! (prolongs QT in dose dependent fashion - monitor), Bronchospasm
107
What is the typical first drug used by cardiologists for patients to prevent AF and sustained VT/VF?
Sotolol
108
Amiodarone. Use, MOA, adverse effects, what is unique about pharmacokinetics for this drug
Must know!!! - Use: prevention of SVT esp Afib, VT and VF (1st line in ACLS) - MOA: Na, Ca, K and beta-blocking effect. Class III - prolongs AP duration and ERP - Adverse effects: a. Pulmonary fibrosis (most feared side effects, but takes years) b. Thyroid (hypo mostly, but also hyper) - drug is largely composed of iodine. Give L-thyroxine if hypothyroidism develops. If hyper, switch to different drug. c. Ocular d. Neurologic: tremor, seizures, etc. e. Derm: irreversible blue-green discoloration (smurf-drug), photosensitivity f. Hepatic and GI g. Basically interacts with all drugs until proven otherwise! \*\* Must monitor via CXR, EKG, LFTs, TFTs, etc. - Pharmacokinetics: has high Vd (60L/kg!) and gets into most everywhere in the body. Has long half life up to 120 days.
109
What is the 1st line ACLS drug to prevent SVT (aF), VT and VF?
Amiodarone
110
Can amiodarone be used in CHF patients? Dronaderone.
Can use amiodarone in CHF patients. Dronaderone is contraindicated.
111
Dronaderone. Use, MOA, adverse effects
\*Class III derivative of amiodarone with replacement of iodine - Use: AF (not as effective as amiodarone) - MOA: class III, all channel blocking? - Adverse effects: contraindicated in severe CHF. Milder than amiodarone (no serious skin, pulmonary, thyroid problems).
112
Dofetilide. Use, MOA, adverse effects
- Use: conversion and maintenance of AF, option for pts with LV dysfunction, relatively safe in CHF - MOA: ? - Adverse effects: high incidence of Torsades (even higher than sotalol)! Newer drug: 3 day inpatient stay with initiation of drug, only registered physicians may prescribe, only 1 mail-order pharmacy authorized to dispense
113
What is the standard treatment for most ventricular arrhythmias?
ICD: implantable cardioverter defibrillator. Much better than drugs.
114
What drugs are used to tx Afib in the following patients: a. A fib with no other heart dz? b. A fib with hx of CAD, but normal EF? c. A fib with CHF?
a. Flecainide, propafenone b. Sotolol c. amiodarone or defetilide
115
Rate-control drugs
Beta-blockers, diltiazem, digoxin
116
Define atherosclerosis
Progressive, chronic inflammatory disease of large arteries that starts in childhood and progresses rapidly in third decade or later in life. Involves intima of vessels.
117
Pathogenesis and various hypotheses of atherogenesis
Current hypothesis: - Endothelial cell injury induced by hypercholesterolemia, disturbed flow, or other factors - ECs over-expression VCAM which increase cellular adhesion & recruit inflammatory cells - Macrophages arrive: plasma LDL undergoes modification or oxidation by them. Oxidized is cytotoxic. - MCP-1 (monocyte chemo-attractant protein-1) recruits monocytes - Proliferation of SM cells - Activated macrophages release additional cytokines. - Foam cells: macrophages and SM cells packed with droplets of cholesterol esters. These secrete many factors contributing to the inflammatory process. know cell players: endothelial cells, smooth muscle cells, macrophages, also platelets
118
Histology of atherosclerosis
Histology (same as any chronic inflammation): infiltration by macrophages and lymphocytes, mesenchymal cell proliferation, fibrosis, cell necrosis, neovascularization. KEY: SM proliferation, accumulation of CT elements, lipid deposition
119
Risk factors for atherosclerosis. Why are multiple risk factors bad?
Non-modifiable: increasing age, male, family hx, genetic abnormalities (hyperlipidemia etc.), chronic renal dz Modifiable: hyperlipidemia, HTN, CIGARETTE SMOKING (200% by smoking, cessation halves the increased risk), DM, CRP, inactivity, stress, obesity, maybe homocysteine? Multiple risk factors may impose more than additive effect, they are synergistic.
120
Clinical features of atherosclerosis
Clinical features: MI, ischemic stroke, peripheral arterial dz, visceral infarction, atherosclerotic aneurysms
121
What is the most important serum cholesterol component that increases risk for atherosclerosis?
LDL. Note: lipoprotein a is a significant risk factor independent of LDL
122
Which dyslipoproteinemias lead to premature atherosclerosis? Which lead to severe? Which don't lead to premature atherosclerosis?
No premature AS: type I = familial LPL deficiency (increases chylomicrons) Premature AS: - Type IIa: famililal hypercholesterolemia (high LDL) - Type IIb: familial combined hypercholesterolemia (high LDL and VLDL) - Type III: familial type III lipoproteinemia (high IDL) - Type IV: famililal hypertriglyceridemia (high VLDL and high TGs) Severe AS: - Type V: familial AI/CII deficiency - no HDL
123
Characteristics lesions of atherosclerosis
Fatty streaks Proliferative lesions Fibrofatty plaques (aka atheromas)
124
At what locations in vessels is atherogenesis more likely?
Arterial branch points where eddies and circular flow occur. Areas of low shear/and/or disturbed flow.
125
Complications from atherosclerotic lesions
Calcification Hemorrhage Rupture (aneurysm) or ulceration Thrombosis (occlusion, stenosis)
126
Which atherosclerotic plaques are vulnerable?
Soft w/lipid filled core. These are prone to rupture. Those with thick cap have reduced rupture risk.
127
What is the earliest lesion in atherosclerosis?
Fatty streak
128
Which atherosclerotic lesion is the bad guy?
Fibrous plaque
129
What is considered positive family history risk factor for atherosclerosis?
- Family history of premature CAD in a first degree relative (not aunt, uncles, cousin, grandparents). In male
130
Most common cause of death in DM patient
Atherosclerosis and consequences thereof
131
Diagnosis of metabolic syndrome
Requires any 3 of following: a. diabetic dyslipidemia b. primary arterial hypertension c. central abdominal obesity d. insulin resistance e. prevalence in CAD patients
132
What would you tell your patient to encourage them to stop quitting to reduce the risk of atherosclerosis?
~ 50% reduction in year 1 by year 5 after smoking cessation, risk of CAD or MI approximates that of non-smokers
133
Mechanisms of enhanced atherosclerosis due to smoking:
- hemodynamic stress - endothelial injury & dysfunction - atherogenic lipid profile - enhanced coagulability - arrhythmogenesis - relative hypoxia (CO)
134
Outcomes of coronary atherosclerosis
- ACS: unstable angina (ischemia), MI - Sudden death (VT, VF) - Dilated (ischemic) cardiomyopathy - A fib/flutter
135
Primary and secondary preventive therapies for coronary atherosclerosis
Primary: appropriate diet, regular exercise, optimum weight, stop smoking Secondary: tx dyslipidemias (statins), tx DM (goal: HgA1C
136
Determinants of myocardial o2 demand
HR, contractibility, systolic wall tension
137
Symptoms of myocardial ischemia
Chest discomfort referred to jaw, shoulder, ulnar L arm, most often exertional, DOE, nausea, other GI (someone who had intractable diarrhea)
138
Differential diagnosis of chest pain
Costochondritis, GI (esophageal spasm, GERD, biliary colic), aortic dissection, pericarditis
139
Symptoms of angina
heavy pressure, band-like, crushing lasts
140
Stable vs unstable angina
Stable: same pattern, timing, severity, episodes Unstable: new onset, subjectively worse discomfort than with previous, onset with less activity, angina at rest (angina decubitus)
141
PE findings of myocardial ischemia
May be normal Maybe: cardiomegaly, murmurs, S4
142
Diagnosis of myocardial ischemia
Resting ECG Basic labs: lipids, basic chems, exercise stress testing, echo
143
When should stress testing be performed?
Atypical chest discomfort
144
Meds used to do pharm stress testing of heart
Adenosine and dipyridamole: vasodilate, increases HR and work Dobutamine: increase contractility
145
What does ST depression mean?
Subendocardial ischemia
146
What does ST elevation mean?
Full thickness ischemia
147
When is stress testing highly predictive of myocardial ischemia?
Typical symptoms of angina OR ECG shows horizontal or downsloping of ST depression. With ST depression \> 2mm, the diagnosis is certain!!!
148
3 results of myocardial ischemia
1. Myocardial infarction 2. Chronic ischemia w/o infarction 3. Relief
149
Treatment of myocardial ischemia
1. increase o2 supply: reperfusion (thrombolysis, PCI, CABG) coronary vasdilation (nitrates, dihydropyridines) 2. decrease o2 demand beta blockers (decrease HR, decrease contractility) decrease BP reduce preload (diuretics, nitrates) reduce circulating catecholamines (sit with patient, calm them down)
150
Drug therapies for myocardial ischemia. How do they work in this case?
- nitrates: decrease preload (venodilate), coronary dilations, enhanced endothelial function - beta blockers: decrease HR and contractility = decrease o2 demand, no effect on supply - CCBs: prevent spasm, reduction of afterload (vasodilating), some (verapamil, diltiazem) reduces contractility and / or HR, no change on preload (no venodilating)
151
Functional classification of cardiomyopathies
- Dilated: disorder of myocardial muscle resulting in dilation and weakening of the left ventricle - most common - Hypertrophic: disorders of myocardial muscle resulting in hypertrophy, left ventricular dysfunction and arrhythmias - Restrictive: group of disorders resulting in excessive myocardial stiffening with resultant ventricular dysfunction
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Define cardiomyopathy
group of diseases of varying etiologies in which the main feature is myocardial involvement
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What is meant by etiologic classfication?
inflammatory, metabolic, toxic, infiltrative, fibroplastic, hematologic, hypersensitivity, genetic, misc, idiopathic, physical agents
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Dilated cardiomyopathy. a. Etiologies b. How is it diagnosed? History? Sx? PE findings? Studies? c. Treatment of choice
a. Etiologies: Idiopathic, ischemic, hypertensive, ALCOHOLIC, infectious, metabolic b. Diagnosis - History: relates to etiology (angina, previous MI, HTN, etoh/toxins, foreign travel) - Sx (related to LV failure): fatigue, weakness, dyspnea (exertional, orthopnea, PND) - improves as RV fails, pale, tachy, also: anorexia, early satiety, abdominal fullness - PE: i. Signs of LV failure: tachy, pallor, dyspnea, apical life/thrill (apical), S3 universally present (overload), many different murmurs, P2 may vary ii. Signs of RV failure: elevated JVPs, cardiomegaly, RV life, P2 varies, RV and LV S3 universal (overload), various murmurs, pulsus alternans, hepatomegaly, splenomegaly, ascites, peripheral edema, evidence of poor nutrition - Studies: no specific ECG findings (maybe sinus tachy, voltage for LVH, LBBB, non-specific ST and T changes), CXR, radionuclide studies, cardiac cath, echo (chamber dilation, poor systolic function) c. Tx: reduce activity, restricted Na intake, drug: ACEIs = drug of choice Note: afib common finding with, must stop drinking
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Hypertrophic cardiomyopathy. a. Etiologies, types b. How is it diagnosed? Sx? PE findings? Studies? c. Treatment of choice
a. Etiologies: - Types (macroscopic): Asymmetric septal hypertrophy without obstruction, ASH with obstruction, concentric hypertrophy with obstruction, apical hypertrophy (rare) b. Diagnosis - Sx: young onset (avg 26), sudden death, dyspnea, angina, fatigue, syncope - PE: slight displaced bifid LV impulse (double bump), bisferiens (double bump) carotid pulse, S4 very common (myocardium incompliant), systolic murmur of variable qualities - Studies: ECG (increased voltage in anterior leads, ST and T wave changes, Q waves in inferior lateral, ventricular arrhythmias), echo are diagnostic (LV hypertrophy w/ various other things; chamber normal to small in size and shows nml contractility) c. Tx: reduce physical activity esp vigiours sports, pharm (beta blockers to decrease contractility which is a problem as it obstructs LVOT or: disopyramide, verapamil), myotomy/myectomy
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What is the hallmark of restrictive cardiomyopathy?
Hallmark is diastolic dysfunction
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Etiologies of restrictive cardiomyopathy
Processes that lead to material infiltrating heart tissue: amyloidosis, hemochromatosis, sarcoidosis, Loeffler's endocarditis, endomyocardial fibrosis
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Do L18-19, 20, 23
Do L18-19, 20, 23
