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Preclerkship > Cardio > Flashcards

Cardio Flashcards

1
Q

4 phases of cardiomyocyte AP

A
  1. RMP (-90)
  2. Na+ enters, threshold reached @ -70 mV –> rapid/brief depolarization to +10 (L-type Ca channels slowly begin to open)
  3. Brief repolarization (transiently activated K+ channels–>efflux) –> 0 mV
  4. Plateau: Outward K+ and inward Ca2+ are balanced; Ca here is not enough to cause contraction triggers Ca-induced-Ca-release
  5. Repolarization via continued K+ efflux as Ca channels close; Ca efflux through Na/Ca exhanger and Ca-ATPase
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2
Q

Refractory period of cardiomyoctes based on what?

A

Resetting of Na+ channels (need to move from inactivated –> resting state (different gates)

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3
Q

Explain Ca-induced Ca release

A

Ca influx in sarcolemma including T-tubules (invaginations close to sarcoplasmic reticulum)

Ca binds RYR receptors on SR –> Ca release

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4
Q

How does a cardiomyocyte return to rest (ionically)

A

Ca moved back into SR and out of cell

SERCA = Sarco(endo)plasmic reticulum Ca ATPase

Na/Ca secondary active transport

Out of cell via active transport

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5
Q

Why do cardiac muscles have long repolarization phase?

A

So that the AP (and its refractory period) last most of the contraction time to prevent tetanus/arrhythmia

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6
Q

Gap junctions allow the heart muscle cells to act as a…

A

Fuctional syncytium

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7
Q

Explain troponin and tropomyosin

A

Tropomyosin covers myosin-binding sites on actin (thin filaments)

Troponin binds tropomyosin and actin, when Ca binds it releases actin to allow myosin heads to bind

3 subunits of troponin:

TnC - calcium

TnI - actin

TnT - tropomyosin

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8
Q

CO =

A

SV x HR

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9
Q

BP =

A

TPR x CO

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10
Q

Impact of catecholarmines on nodal cells

A

Bind B1AR

G protein cascade –> pKa activation –> phosphorylates and opens Ca channels –> depol, ^ HR

POSITIVE CHRONOTROPIC ACTION

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11
Q

Acetylcholine (Vagus Nerve) impact on cardiac nodal cells

A

Binds M2 receptors

–> Gi cascade –> K+ channel opening and efflux –> hyperpol/decreased HR

Also inhibits AC/pKa/Ca entry

Negative chronotropic action

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12
Q

Catecholamine impact on cardiomyocytes

A

Bind B1AR –> pKa activation (G cascade)

Phosphorylates Phospholamban on SR membrane –> Ca influx into SR –> ^ rate of relaxation

(phospholamban inhibits SERCA when dephosphorylated)

Phosphorylation of L-type Ca channels in sarcolemma as well

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13
Q

Term for the fact that the nodal cells can spontaneously trigger themselves

A

Automaticity

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14
Q

List various pacemaker cells and their spontaneous depolarization rates (4)

A

SA node = 60-100 bpm

Atria < 60

AV node ~50 (40-60)

Ventricles 20-40

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15
Q

Cardiomyocytes are connected by

A

Intercalated disks = gap junctions (connexons) + desmosomes (cadherins + plaque proteins, keratin)

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16
Q

3 things that make pacemaker APs unique

A

1) Phase 4 positive slope (pacemaker current)
2) Maximum diastolic potential =60 mV
3) Phase 0 upstroke is less rapid, lower amplitude (Ca influx not fast Na channels)

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17
Q

Purpose and mechanism of 0.1 sec delay at AV node?

A

Atrial contraction before ventricular contraction

Fewer gap junctions and smaller diameter fibres

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18
Q

Bundle of His branching

A

Bundle of His –> RBB and LBB

LBB –> anterior/posterior fascicles

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19
Q

What anchors the AV valves?

A

Chordae tendinae

Connected to papillary muscles

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20
Q

RMP of cardiomyocytes

A

-90 mV

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21
Q

Movement of Na/K ATPase

A

2 K in, 3 Na+ out (hyperpolarizing)

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22
Q

The RMP of cardiomyocytes is approximately the equilibrium potential of…

A

Potassium (rectifier potasium channels open at rest, pretty much only thing membrane is permeable to)

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23
Q

Explain AP in cardiac nodal cells

A
  1. Na+ leaking in through funny channels; RMP -60
  2. Threshold at -40 mV -> L-type Ca channels open –> depol
  3. Ca channels shut, K channels open –> repolarization to -60 (no plateau)
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24
Q

Upward inflections on JVP waveform (3)

A

a = atrial contraction

c = AV valve closure (very small)

v = passive filling during systole

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25
Q

Descents on JVP waveform (2)

A

x = pressure decline after atrial contraction and tricuspid valve closure

y = opening of tricuspid –> blood empties into ventricle

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26
Q

Describe the hepatojugular reflux

A

Press on liver -> ^ venous return -> ^RH volume -> if RH dysfunction, visible JV distention (seen via JVP) lasts a few seconds

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27
Q

Stethoscope: bell vs diaphragm for what freqs

A

Bell for low (lightly)

Diaphragm for high (firm against skin)

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28
Q

Name the 4 heart auscultation areas

A

Aortic, pulmonic, tricuspid, mitral (apex)

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29
Q

What is a condition that could separate the 2 sounds during S1?

A

RBBB

Delayed R ventricular contraction/tricuspid closure

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30
Q

Explain how leaflet drifting impacts S1 sound

A

The leaflets passively drift throughout ventricular filling. The less drift –> louder sound when forced closed by V > A pressure

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31
Q

What might increase S1 sound? (3)

A

Short PR interval (less drifting)

Mild mitral stenosis (reduced flow means prolonged diastolic dP which keeps valves more open)

Rapid HR (short diasole, less drifting)

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32
Q

What might decrease S1 sound (4)

A

1st-degree AV block (prolonged PR interval, ^ drifting)

Mitral regurgitation (leaflets don’t fully contact on closure)

Severe mitral stenosis (leaflets never open much)

“Stiff” L ventricle (high ventricular pressure at end of diastole ^ drift)

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33
Q

S1 and S2 are high or low sounds? Best heart with what part of stethoscope?

A

Both high, diaphragm

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34
Q

S1 and S2 best heard in what auscultation areas?

A

Apex (mitral) and pulmonic repectively

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35
Q

S2 insensity is impacted by what? Examples? (2)

A

Velocity of blood coursing back twd SL valve after ventricle contracts (hypertension –> LOUDER)

Suddenness of closure (stenosis –> valves don’t move much –> softer)

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36
Q

What is physiological splitting of S2?

A

A2 and P2

On inspiration, pulmonary vascular capacitance is increased, resulting in less pressure on the pulmonary valve –> late P2

A1 is earlier because less venous return from pulmonary circulation reduces ventricular pressure and emptying time

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37
Q

S2: Widened splitting

A

A2 and P2 separate during exp and even more during insp

Delayed closure of pulmonic valve (RBBB, stenosis)

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38
Q

S2: Fixed splitting

A

Abnormally wide interval thorughout resp cycle due to chronically increased pulmonary circulation capacitance (e.g. chronic R volume overload)

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39
Q

Paradoxical splitting (S2)

A

P2 before A2 on exp and single sound on insp

Delayed AV closure (LBBB, aortic stenosis)

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40
Q

2 types of extra systolic heart sounds

A

1) Early ejection clicks: opening of SL valves after S1 (e.g. valve stenosis)
2) Mid/Late: systolic prolapse of AV valves into atrium –> regurgitation

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41
Q

Extra diasolic heart sound:

Opening snap

A

AV valve (usually mitral) stenosis –> “snaps” when opening

(third sound on inspiration! Comes after P2)

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42
Q

S3 sound

AKA?

A

Early diastole after AV valves open

Tensing of chordae tendinae due to rapid ventricular filling/expansion

Ventricular gallop when pathological (can be normal in children)

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43
Q

Ventricular gallop can be caused by what?

What is the “word” representing the sound

A

Dilated ventricle (systolic HF), AV valve regurgitation increasing flow

Ken-TuCky

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44
Q

S4

AKA?

Word rhythm?

Examples?

A

Late diastole before S1. Ejecting blood into a stiff ventricle

Atrial gallop

Tenne-ssee

Ventricular hypertrophy, myocardial ischemia

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45
Q

Quarduple rhythm

A

S1 + S2 + S3 + S4

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46
Q

Summation gallop

A

Quadruple rhythm + tachycardia –> S3/4 overlap (short diastole) so becomes a long middiastolic low/loud sound

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47
Q

S3 and S4 frequencies

A

Dull/low (bell!)

Contrast with high freq S1/S2

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48
Q

Murmurs are caused by ____?

5 mechanisms

A

Turbulent blood flow

  1. Flow across partial obstruction
  2. Increased flow through normal structures
  3. Ejection into dilated chamber
  4. Valve regurgitation
  5. Blood shunting into lower-pressure chamber
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49
Q

How to describe murmurs? (7)

A
  1. Timing (systole, diastole, continuous)
  2. Intensity (grading systems)
  3. Pitch
  4. Shape (intensity changes, cresc/decrsc)
  5. Location (loudest)
  6. Radiation (direction!)
  7. Response to maneuvers
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50
Q

Grading scales for murmur intensity

A

Systole: 1/6 –> 6/6

Diastole: 1/4 –> 4/4

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51
Q

Define systolic ejection murmur

2 types?

A

After S1 until before/during S2

Crescendo-decrescendo

Delay after S1 (isovolumetric contraction of L ventricle)

Pulmonary or aortic valve stenoses

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52
Q

Pansystolic (holosystolic) murmur

A

Regurgitation across incompetent AV valve or through VSD

Uniform intensity throughout systole, directly connected to S1 (as soon as pV > pA backflow occurs)

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53
Q

Murmur intensity in VSD is greater in smaller or bigger hole?

A

Smaller

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54
Q

Late systolic murmur: when is it heard and what causes it?

A

Mid/late systole to S2

Caused by mitral valve prolapse into atrium

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55
Q

2 ways to do echocardiography

(bonus points for examples of why you’d use echo)

A

Transthoriacic (TTE)

Transesophageal (TEE)

Evaluate murmurs, valve function, myocardial contractility, septal defects, aneurysms, thrombi…

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56
Q

What causes a continuous murmur?

A

Presistent pressure gradient

Patent ductus arteriosus = abnormal communication b/w aorta and pulmonary artery; aortic pressure always higher

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57
Q

Early diastolic murmur =

A

Regurgitant flow through SL valve (aortic or pulmonic)

Descrescendo because pressure gradient reduces as blood backflows and the aortic/pulmonic pressure decreases

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58
Q

Mid-to-late rumbling diastolic murmurs

2 reasons and describe (including shape)

A

Across AV valves (stenotic or increased flow)

  • Stenosis* –> OS then descrescendo-crescendo (lowering gradient then atrial contraction)
  • Flow* –> fever, anemia, hyperthyroidism, exercise
59
Q

4 main parameters of CO

A

Heart rate

Preload

Afterload

Contractility

(Co = HR x SV, and SV determined by the latter 3)

60
Q

Cardiomyopathy

Definition + 2 risk factors

A

Disease in the heart muscle

Alcohol (dilated cardiomyopathy)

Diabetes mellitus (diabetic cardiomypoathy or via CAD/atherosclerosis)

61
Q

Isometric vs isotonic contractions

Relations to preload/afterload?

A

Isometric: staying same length; preload = ventricular V (stretch) at end of diastole

Isotonic: staying same tension; afterload = fixed load, determines final length

62
Q

Preload impacts are represented through what curve?

Preload approximated via?

A

Frank-Starling

Ventricular EDV or EDP

63
Q

Afterload =

Proxy?

A

Ventricular wall tension during contraction (force that must be overcome for ventricle to eject contents = wall stress)

~systolic ventricular (or arterial) pressure

64
Q

Ventricular wall stress (afterload) is proportional to what?R

A

Ventricular pressure

Ventricular radius (dilated chamber ^ stress)

1/thickness of wall (distribution over greater area)

65
Q

What shifts the Frank-Starling curve?

A

Contractility (inotropic state)

Impacted by hormones/chemicals –> change cross-bridge cycling rate

66
Q

Cardiac output denominator

A

min

67
Q

Define ejection fraction

Normal range?

A

Fraction of EDV ejected during systole

= SV/EDV

Usually 55-75%

68
Q

Describe the ventricular P-V loop

Which part represents the afterload?

A

c-d = afterload

69
Q

Continue at page 3 HF

A
70
Q

Atropine

A

Anticholinergic, ^HR

71
Q

Define Arteriosclerosis + 2 subtypes

A

Hardening of arterial walls

Atherosclerosis = hardening due to atheromatous plaque formation in endothelium

Arteriolosclerosis = hardening of artioles

72
Q

3 tunics of blood vessel walls

A
  1. Tunica intima = endotheium + subendothelium
  2. Tunica medica = SM + elastic fibres
  3. Tunica externa = collage, vasa vasorum (large BVs)
73
Q

Basic steps of atherosclerosis plaque formation

A
  1. Endothelial damage
  2. LDL buildup in intima
  3. LDL oxidation –> inflammatino
  4. Recruitment of monocytes, differentiate into macrophages
  5. Macrophages eat lipids –> foam cells –> fatty streak
  6. Foam cells –> inflammation –> SM (media) proliferation and migration into intima
  7. Formation of lipid core + fibrous cap (CT) –> atheroma
  8. May calcify, may rupture
74
Q

What common hormone is a protective factor for atherosclerosis?

A

Estrogen

75
Q

Prognosis/phenotype of atherosclerosis is highly dependent on

A

Plaque stability (bursting = bad)

76
Q

Risk factors for atherosclerosis

A

Dyslipidemia, Smoking, Hypertension, Diabetes Mellitus

77
Q

Smoking doubles the risk of ___ in patients with CAD

A

Stroke

78
Q

Serum measure associated with atherosclerosis

A

CRP (inflammation)

79
Q

Why do atheromas tend to form in bifurcated vessels (e.g. common carotid, L conary arteries)?

A

Laminar flow –> superoxide dismutase (antioxidant), NO production (vasodilation, platelet inhib, anti-inflamm)

80
Q

Name 5 ways that physical/chemical stressors impact endothelial function and predipose to atheroma formation

A
  1. ^cell-surface adhesion molecules
  2. Impairement of permeability barrier
  3. Inflammatory cytokines
  4. Altered release of vasoactive substances (NO, prostacyclin)
  5. Interference with antithrombotic properties
81
Q

Does early atherosclerotic plaque formation narrow the artery?

A

No - compensatory outward remodelling of the arterial wall preserves diameter (no ischemic symptoms).

Later that isn’t enough, vessel restricted –> ischemia, anging/claudication

82
Q

How does atherosclerosis typically beget acute coronary syndrome?

A

Fibrous cap of plaque ruptures –> prothrombotic molecules exposured –> acute thrombus

83
Q

What is a consequences of atheroma calcification?

A

Increases rigidity/fragility –> bursting

84
Q

What happens when an atherosclerotic plaque ruptures?

A

Thrombogenic materials in core exposed –> thrombus formation –> vessel occulation –> infarction (tissue death due to obstructed bloodflow)

85
Q

Do atherosclerotic symptoms correlate with disease severity?

A

Not consistently

86
Q

What are bruits?

A

Sounds indicating turbulant bloodflow

87
Q

Summarize treatment of CAD

A

Risk factor control (smoking!!!)

Restore perfusion or decrease O2-demand by heart

Stents, CABG

Thrombolytic/anti-platelet/anti-coagulant drugs

Most patients given drugs that reduce myocardial oxygen demand (via reducing HR, contractility, preload/afterload) - Beta/Ca-blockers, nitrodilators

For variant angina treat with drugs to prevent vasospasm

88
Q

What is the “widow-maker”?

A

Anterior interventricular artery (commonly occluded by atherosclerosis plaques)

AKA Left anterior descending artery = LAD

89
Q

Ischemic heart disease

A

Imbalance in myocardial O2 supply/demand

90
Q

Angina pectoris

A

Uncomfortable sensation in the chest (may radiate) due to myocardial ischemia

91
Q

Stable angina

A

Chronic pattern of transient angina pectoris

Precipiated by physical activity or emotional upset. relieved by rest in a few min

Temporary ST depression but no permanent myocardial damage

92
Q

Variant angina

ECG?

AKA?

A

Anginal discomfort at rest due to coronary artery spasm

Causes ST elevation

AKA Prinzmetal angina

93
Q

Unstable angina

A

Increasing freq/duration produced by less exertion –> commonly progresses to MI

94
Q

Myocardial infarction

A

Prolonged lack of blood supply –> myocardial necrosis

(usually due to acute thrombus at site of atherosclerotic stenosis)

95
Q

Describe myocardial oxygen supply (2 main components) & demand (3)

A

Supply:

1) O2 content of blood
2) Coronary blood flow (perfusion pressure + vascular resistance; Q = P/R)

Demand:

1) Wall stress
2) HR
3) Contractility

96
Q

Coronary perfusion pressure is estimated how?

A

Aortic diastolic pressure (coronary vessels not perfused during systole!)

97
Q

Name the main intrinsic mediators of coronary artery tone (3 categories + examples)

A

1) Metabolic: adenosine –> vasodilation
2) Endothelial factors: NO, prostacyclin, EDHF (all dilation), Endothelin 1 (constriction)
3) Neural factors: SNS –> constriction via alpha receptors, dilation via beta receptors

98
Q

Explain why endothelial changes lead to ischemia

A
  1. Loss of antithrombotic properties (NO/prostacyclin)
  2. No longer secrete vasodilatory mediators in response to Ach, sheer stress, serotonin, thrombin. SNS effects not opposited. Impacts of metabolites (adenosine) reduced)
99
Q

__ vessels in heart tend to get plaques, while ____ ones acts as what?

A

Proximal

Distal –> reserves (“resistances vessels”, modulate tone)

100
Q

Explain levels of diameter restriction and their impacts on coronary flow

A

<60% -> no impairment at rest and compensate during exertion

60-~80% –> max flow reduced even with full resistance vessel dilation (exertional ischemia)

>90 –> ischemia even at rest

101
Q

What impacts do Ach, sheer stress, platelet products (serotonin/thrombin) have on vascular diameter?

A

Direct –> SM contraction

Indirect –> release of endothelial factors –> SM dilatino

102
Q

What might you see in patients with cardiac risk factors before plaques form?

A

Endothelial dysfunction

103
Q

Consequences of anaerobic metabolism during ischemia

A

Low ATP –> less systolic contraction & diastolic relaxation –> ^LV pressure –> pulmonary congestion

Metabolic product buildup –> pain and arrhythmia

104
Q

Differentiate stunned vs hibernating vs infarcted myocardium

What is the clinical significance of this?

A

Stunned: prolonged systolic dysfunction after blood returns

Hibernating: prolonged low blood supply and ventricular contractile dysfunction

Infarction: necrotized tissue (permanent)

Former 2 can regain function, latter would not. E.g. don’t do coronary revascularization on necrotized myocardial tissue

105
Q

2 types of stable angina

A

1) Fixed threshold: mostly due to stenosis, constant level of activity required to precip symptoms

2) Variable-threshold: vasoconstriction; diff levels of exertion @ diff times trigger discomfort

106
Q

Unstable angina is a type of ____ and is usually due to ____

A

Acute coronary syndrome

Rupture of an unstable atherosclerotic plaque

107
Q

Why does variant angina frequently cause symptoms at rest?

A

Issue with supply not demand

108
Q

Silent angina is more common in what populations?

A

Women

Elderly

Diabetics

109
Q

How long does an angina attack usually last?

A

More than a few seconds, less than 5-10 min

110
Q

Name some symptoms that may accompany angina

Whare are “anginal equivalents”?

A

Tachycardia, diaphoresis, nausea

Dyspnea (LV dysfunction –> pulmonary congestion)

Fatigue, weakness

“Anginal equivalents” if no chest discomfort but just these symptoms during ischemia

111
Q

How long should angina take to relief after stopping the aggravating activity?

A

A few min

(3-5 min after taking nitroglycerine)

112
Q

Carotid bruits are a sign of

A

Cerebrovascular disease

113
Q

2 signs of peripheraly artery disease on physical exam

A

Femoral bruits

Decreased pulses in lower extremities

114
Q

Name 5 physical exam signs for myocardial ischemia and why they are present

A

Dyskinetic apical impulse (abnormal bulge on palpation) - systolic dysfunction

Rales/Crackes - Pulmonary edema

S4 - Reduced diastolic complicance

Mitral regurgitation - papillary muscle dysfunction

Diaphoresis, elevated HR/BP - SNS tone

115
Q

Name 4 cardinal symptoms of myocardial ischemia (to help with differential)

A
  1. Brought on by exertion, relieved by rest/nitroglycerin
  2. Lasts <10 min
  3. Retrosternal tightness/pressure, radiating to neck/jaw/L shoulder/arm
  4. ECG: transient ST depression/elevation, or flattened/inverted T waves
116
Q

Name 3 possible differentials for chest pain and how to tell them apart from angina

A

Pleuritis –> longer-lasting, worse on inspiration

GI issues (e.g. GERD) –> precipitated by certain foods, may improve with antacids

Musculoskeletal –> more superficial/localized, point with finger!

117
Q

What is the Levine Sign?

A

Clenched fist over sternum when patient describing anginal pain

118
Q

ECGs in angina patients

A

Between attacks: ~50% patients normal, some have chronic changes (e.g. pathological Q waves from past MI)

During attack: transient ST-depression and T-wave flattening/inversion

ST-elevation possible in severe transmural ischemia or Prinzmetal’s angina (similar to STEMI)

119
Q

What tests do you do to look for angina in a patient not in an acute attack? (4 subtypes)

A

Stress tests:

  • Standard exercise testing
  • Nuclear imaging (+exercise)
  • Exercise echocardiography
  • Pharmalogical stress tests
120
Q

What are some signs indicating a positive exercise test for myocardial ischemia? (5)

A

Iscemic ECG changes

Exercise intolerance <2 min for cardiopulmonary reasons

High-grade ventricular arrhythmia

Drop in systolic BP

Replication of chest discomfort

121
Q

Why would nuclear imaging (IV radionuclide injection) be indicated in an exercise stress test for ischemia?

What are “cold spots”?

A

Patient has baseline abnormalities of ST segments (e.g. LBBB)

If standard ex test doesn’t align with clinical suspision

Radionuclide accumulates proportionally to viable myocardial cells; cold spots = ischemic or infarcted (repeat @ rest to see if it fills back in)

122
Q

When is echo-exercise stress testing indicated for ischemic testing?

A

Baseline ST- or T-wave abnormalities

Standard ex test results don’t match clinical suspision

123
Q

Describe pharmacologic stress tests for ischemia (2 types)

When are they indicated?

A

If patient can’t exercise

Coronary vasodilator (e.g. adenosine) - shunts blood away from ischemic regions which are already fully dilated

Inotrope (dobutamine) - if patient took caffeine/theophylline (adenosine antagonists), reactive airway disease (adenosine –> bronchospasm)

Can couple w/ echo or nuclear imaging!

124
Q

What is the gold standard test for CAD diagnosis? Is this used in all patients?

A

Coronary angiography

  • inject radiopaque contrast (invasive)

No - only use in patients who are not responding to meds or very unstable

125
Q

What does coronary angiography show?

(include added possible test)

A

Anatomical issues (not functional consequences which are important to guide treatment!)

Can use catheterization –> functional flow reserve (=Pdistal to stenosis/Paorta)

126
Q

Types of revascularization for treatment of myocardial ischemia (2 + 2 subtypes each)

A

Percutaneous Coronary Intervention (PCI)

  • Percutaneous transluminal coronary angioplasty
  • Coronary stents

Coronary Artery Bypass Graft Surgery

  • Saphenous vein or internal mammary artery
127
Q

Why are coronary stents preferable to percutaneous coronary angioplasty?

A

PCA (stretch artery via balloon) –> recurrance common in 6 mo

Coronary stents reduce restonosis

128
Q

Describe 2 problems with coronary stents and how they are dealt with

A
  1. Thrombogenic - must take aspirin + P2Y12 receptor antagonist
  2. Neointimal proliferation (migration of SM cells + ECM production) –> drug-eluting stents w/ antiproliferate med; but also slow protective endotheliazation making anticoagulants all the more important!
129
Q

Why might PCI be preferable over CABG?

A

Less invasive, faster recovery

130
Q

Do PCIs reduce MIs/death in stable CAD?

A

NOPE

131
Q

What medical treatment is essential after CABG?

What BV is preferred for the same reason?

A

Lipid-lowering to prevent atherosclerosis

Internal mammary artery (anastomose it) more resistent than saphenous vein

132
Q

In what patients is the survival benefit of CABG > medical therapy and PCI

A
  • Large amounts of myocardium at ischemic risk (>70% stenosis in all 3 major coronary arteries)
  • >50% stenosis of L main coronary artery
  • Diabetes with multivessel disease
  • Critical narrowing of LAD
133
Q

What are the 4 classes of angina pectoris (Canadian Cardiovascular Society)

A
  • Class I* - Only during strenuous/prologed exertion
  • Class II* - Slight limitation in ordinary activities
  • Class III* - marked limitation in ordinary activities
  • Class IV* - can’t do any activity without angina, inclds angina @ rest

New-onset Class III-IV –> hospitalization indicated

134
Q

Name 4 types of therapies for prevention of acute cardiac events

(not to treat symptoms, but to actually reduce risk of MI/death!!)

Include brief description of treatment plan/goal

A
  1. Antiplatelet therapy (aspirin) - continue indefinitely in all CAD patients unless otherwise indicated
  2. Platelet P2Y12 ADP receptor agonists (clopidogrel) if allergic to aspirin, or use combo) - prevent platelet activation/aggregation
  3. Statins = HMG-CoA reductase inhibitors (goal =50% LDL reduction)
  4. ACE-inhibitors (reduce MI/stroke/death)
135
Q

How do venodilation and arteriodilation impact wall stress?

A

Both reduce it

(veno –> reduces preload; arterio –> reduces afterload)

136
Q

Why wouldn’t you want to combine Beta-blocker and Ca-blocker in a patient? What particular patients should this especially be avoided in?

A

Both are negative inotropes and decrease contractility

Especially avoid in patients with L ventricular dysfunction

137
Q

Name 4 common meds that are used for symptomatic relief in stable angina (no HF or LV dysfunction) but don’t actually reverse atherosclerosis or increase longevity

A

Organic nitrates

Beta-blockers

Ca-channel blockers (dihydropyridines, non-DHP e.g. verapamil)

Ranolazine

138
Q

Mechanism of action of organic nitrates for myocardial ischemia

Side effects?

A

Decrease demand: reduce preload via VENOdilation

Increase supply: ^perfusion, decrease vasospasm

ADR: Headache, reflex tachycardia (combine w/ BB!), hypotension

139
Q

Beta blockers mechanism of action for myocardial ischemia

Side effects?

A

Demand: Decrease O2 demand by decreasing HR and contracility

Supply: Increases time in diastole –> ^coronary perfusion

ARD: Fatigue, bradycardia, reduce LV contraction, bronchoconstriction, hypoglycemic symptom-masking

140
Q

Ca-channel blockers mechanisms of action (overall, although they vary b/w types) and ARDs

A

Decrease demand: reduce proload (venodilation), wall stress/BP, contractility, HR

Increase supply: ^ perfusion and decreased vasospasm

ADRs: headache, decrease LV contraction, bradycardia, edema, constipation

*Use long-acting (once per day) as 2nd line to nitrate and BBs!

141
Q

What does ranolazine do?

A

Decreases late-phase inward Na current (which is enhanced in ischemia leading ot Ca overload and reduced relazxation)

No impacts on HR or BP!

142
Q

Can you use B1-selective BBs in patients with obstructive airway disease?

A

NO! Not fully despective, still can cause bronchospasm

(Recall: B1AR on myocardium, B2AR in bronchial tree/BVs)

143
Q
A

Preclerkship (25 decks)

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