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AP III Test 1 > Cardiac Review- Dr E ppt > Flashcards

Cardiac Review- Dr E ppt Flashcards

1
Q

Right atrium of heart?

A

Systemic veins empty into R Atrium via:

  1. The superior vena cava (SVC)
  2. The inferior vena cava (IVC)
    * The Eustachian valve protects the lVC
  3. Coronary veins empty into R Atrium via: The coronary sinus
    * The Thesibian valve protects the coronary sinus
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2
Q

Characteristics of right ventricle?

A

Propels blood to the pulmonary vessels via the pulmonary orifice: infundibulum

Communicates with R atrium via the tricuspid orifice: chordae tendineae

Has several muscle bundles: trabeculae carneae-one of which carries the right branch of the AV bundle

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3
Q

Characteristics of left atirum

A

Larger than R atrium

Superior and posterior to the other chambers

Receives pulmonary veins

  • Reservoir for oxygenated blood
  • Provides the “atrial kick” in LVEDV-important in certain conditions

Communicates with the left vetricle via the AV orifice-mitral valve

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4
Q

Characteristics of left ventricle

A

Receives oxygenated blood from the LA

Pumps blood to the body via the Aorta

Ventricular septum: R and L ventricles

Upper 1/3 of the septum is smooth

Lower 2/3 is muscular and covered with trabeculae carneae

2 large papillary muscles-chordae tendineae-cusps of the mitral valve

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5
Q

What are the AV valves

A
  • Tricuspid
    • Within the R AV orifice
    • 3 leaflets-anterior, posterior, septal
    • Valve area: 7cm2, symptoms occur at area <1.5cm2
  • Mitral valve
    • Within the L AV orifice
    • 2 leaflets-anteromedial, posterolateral
    • Valve area: 4-6cm2, symptoms occur at 2-3 cm
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6
Q

What are the semilunar valves?

A
  • Aortic valve:
    • Out flow tract of the aorta and the LV
    • Has 3cusps
    • Sinus of Valsalva
    • Valve Area: 1-3cm2 area <1/2 or 1/3 symptomatic
  • Pulmonic valve:
    • Outflow tract of the pulmonary artery and RV
    • Has 3 cusps
    • Valve area: 4cm2 area <1/2 or 1/3 symptomatic
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7
Q

What provides coronary circulation?

A
  • Epicardial
  • Subendocardial
  • 2 Epicardial Coronaries originate from the sinuses of Valsalva
    • Left Coronary Artery (LCA)
    • Right Coronary Artery (RCA)
      *
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8
Q

Branches of LCA?

A
  • Short left main-ant. inf. & left.
  • Bifurcates into the:
    • LAD
      • `diagonal branch
      • septal perforating branch-feeds the anterior of LV, and the interventricular groove (leads V3-V5)
    • Circumflex-obtuse margin-feeds the posterior LV and part of RV (lead I)
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9
Q

Branches of RCA?

A

Branches into:

  1. Sinus node artery- feeds SA node and RA Branch-feeds the RA
  2. Av node artery-feeds AV node (in 90% of population)
  3. Anterior RV Branches-feed the RV
  4. PDA-feeds the posterior 1/3 of the interventicular septum

Leads II, III and aVf

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10
Q

How is coronary dominance determined?

A

Which artery crosses the crux (junction between the atria and ventricles) to feed the posterior descending coronary branch

In 50% it is the RC

In 20% it is the LC

In 30% a balanced pattern exists

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11
Q

What percent of CO goes to coaronaries?

What determines flow in coronaries?

A
  • 5% of CO or 250ml/min perfusion
  • Flow is determined by:
    • Duration of diastole
    • CPP=Diastolic pressure-LVEDP
  • LCA: flow occurs mostly during diastole
  • RCA: flow occurs in both systole and diastole
  • Myocardial O2 consumption is high with cardiac venous sat. lowest in the body (30%)
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12
Q

What is coronary autoregulation?

A
  • CPP usually autoregulated at 50-120 mmHg
  • Pressure dependent changes
  • Myocardial oxygen demand alters autoregulation: O2 tension acting thru mediators, ie adenosine
  • Greatest dilation occurs in smallest vessels LCA>RCA in autoregulation
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13
Q

What composes the cardiac conduction system?

A

Consists of:

SA node

Internodal tracts

AV node

AV bundle (bundle of His)

Purkinje system

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14
Q

What composes the SA node?

A
  • Mass of specialized cells
  • Junction of SVC and RA
  • 2 Cell types
    • I. P cells (pacemaker cells)
    • II. Transitional or intermediate cells- conduct impulses within and away from the node
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15
Q

What composes the internodal tract?

A
  • Within the atria
  • Conduction pathways b/w the SA & AV
  • Also contain P cells and transitional cells
  • 3 Major tracts:
      1. Anterior (Buchmann’s bundle)-septum
      1. Middle (Wenckebach’s tract)-SVC
      1. Posterior (Thorel’s tract)-septum
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16
Q

What composes the AV node?

A
  • Supplied by nerve endings including vagal ganglionic cells.
  • Causes a delay in the transmission of the action potential:
    • Size of cells: smaller
    • Resting memb. potential: more negative
      • (-60 vs -50 for SA node).
    • Gap junctions: very few
    • Resistance to action potential: incr.
  • Rate of about 50bpm
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17
Q

What composes the AV Bundle?

A

Extends from the AV Node

Enters the posterior part of the ventricle and Purkinje system.

Preferential channel for conduction from the atria to the ventricles

18
Q

What is the purkinje system?

A
  • 2 systems: Left and Right
    1. Left:
      * Spreads under the endocardium
      * Forms several fascicles-branch over the left ventricle
    1. Right:
      * Travels under the endocardium
      * Base of the anterior papillary muscle
19
Q

What determines the resting membrane potential of the heart?

A

The cell at rest:

The resting cell is relatively permeable to potassium and much less to either sodium or calcium

Thus the resting membrane potential of the heart is most dependent on potassium

20
Q

What are the phases of action potential for ventirular myocte?

A

Five phases:

Phase 0-depolarization Fast Na+ channels

Phase I- repolarization Na+ influx ends

Phase II-plateau Slow Ca+ channels open allowing an influx of Ca+

Phase III-terminal repolarization Slow Ca+ channels are inactivated and efflux of K+ occurs

Phase IV-diastolic phase Na+ - K+ pump

21
Q

What is the absolute and refractory phase in ventricular myocte?

A

Refractory Pds

Long lasting action potentials prevent premature excitation

Absolute: No response occurs during phase 0- middle of phase III

Relative: Middle of phase III to phase IV when a second stimulus will cause a weaker action potential than the first

22
Q

What composes the sympathetic nervous system for heart?

A
  • Sympathetic:
  • Arise from:
    • Stellate ganglion and caudal cervical fibers
  • Turn into:
    • The right dorsal medial and lateral cardiac nerves
    • They unite to form one large nerve that follows the course of the L main CA
    • They then branch along the ant. descending and circumflex arteries.
  • Cholinergic fibers-ventricle
  • Sympathetic Cnt’d:
    • Release of ACh-post synaptic nicotinic receptors
  • Stimulation of:
    • Norepinephrine activates the β1-adrenergic receptors
23
Q

WHat provides parasympathetic innervation to heart?

A

Parasympathetic:

  • Arise in medulla in dorsal vagal nucleus and the nucleus ambiguus
  • Enter via recurrent laryngeal nerve and thoracic vagal nerves
  • Form plexuses that give rise to the R and L coronary cardiac nerves and the L lateral cardiac nerve

Ganglia occur w/in the heart close to structures innervated by postganglionic neurons

Post ganglionic transmission occurs by stimulation of nicotinic receptors at junctions and activate the muscarinic receptors in the heart

24
Q

What are the vagal receptors and sympathetic fibers for cardiac receptors?

A
  • Vagal receptors
    • Atrial musculature
    • SA and AV nodes
    • Ventricular myocardium
    • Most prevalent in SA node, then AV, RA, LA and ventricles
  • Sympathetic fibers
    • All through the heart
    • RA contains mostly (75%) B1
    • Ventricles contain mostly (85%) B1
25
Q

What happens during diastole?

A
  • Isovolumetric relaxation
  • Blood returns from the periphery
  • Aortic valve closes
  • Ventricular pressure still exceeds atrial pressure for about 0.02-0.04 secs, as the ventricular pressure continues to drop and equalizes and then gets lower than atrial pressure
  • Ventricular filling
  • AV Valve begins to open
  • Then opens completely
  • Ventricular volume rises rapidly, and then slower as pressure rises slightly until the ventricle is filled and the AV valve closes
26
Q

What occurs during systole?

A

SYSTOLE:

  • Isovolumetric contraction
  • The AV valve is closed (atrial diastole)
  • Ventricular pressure continues to rise
  • The semilunar valve opens
  • Ventricular systole occurs
  • Ventricular action
  • Atrial pressure decreases, due to blood now entering the pulmonary artery & aorta
  • Rapid ejection occurs
27
Q

What does a pressure volume loop of the heart show?

A

From pressure-volume loop picture-

  1. closing of mitral valve
  2. aortic valve opening
  3. aortic valve closure
  4. mitral valve opening

a. diastolic filling

b isovolumetric contraction

c. ventricular ejection
d. isovolumetric relaxation

Volume for 1-4= SV

  • SV= EDV-ESV
28
Q

What determines cardiac output?

A

CO= Volume of blood pumped by the heart each minute

Determined by:

  1. Preload
  2. Afterload
  3. Heart rate
  4. Contractility
  5. Ventricular compliance
29
Q

What is a frank-starling curve?

A
  • relationship between SV and LVEDP
    • afterload increases or CO decreases—> frank startling curve downward
    • afterload decreases or increase in CO–> frank starling curve upward
30
Q

What influences coronary supply and demand?

A
  • Supply
    • Can be raised only by increasing coronary blood flow
      • Diastolic time
      • HR
      • CPP
      • Coronary vasc. tone
      • Intramural obstruction
      • Arterial O2 content/extraction
  • Demand
    • Wall tension
      • Preload
      • Afterload
    • Contractility
    • HR
      • More important to address-easier
31
Q

What are hemodynamic goals in pt with CAD?

A
  • Preload
    • Reduce wall tension, increase perf. press
  • Afterload
    • Maintain afterload, hypotension is Undesirable
  • Contractility
    • Depression is desired when LV function is adequate
  • HR
    • Maintain a slow HR, this is of utmost importance
    • Rhythm
    • Usually sinus rhythm
  • Myocardial O2 balance
    • Control of demand is not enough, must monitor for ischemia and increase supply
32
Q

How do treat intraop ishcemia?

A
  • Supply
    • •Decreased BP
    • •Increased PCWP
    • ACTIONS:
      • Vasoconstrictors
      • Decrease depth of anesthesia
      • Phenylephrine + NTG, Inotropes, CCB
  • Demand
    • •Increased BP
    • •Increased PCWP
    • •Increased HR
    • ACTIONS:
      • NTG
      • Increase depth of anesthesia
      • Treat cause
      • β blockers
33
Q

What is aortic stenosis? What does it cause? s/s?

A
  • Narrowing of the valve
    • At 0.8cm2 symptoms are truly evident
  • Chronic obstruction to LV ejection
    • Increased systolic pressure
    • Increased wall tension
  • Concentric hypetrophy
    • Decreased diastolic compliance
  • Myocardial O2 supply&demand compromised
  • Characteristic triad of
    • syncope
    • angina
    • dyspnea on exertion (SAD)
34
Q

Pathophysiology of AS?

A
  • Narrowing of aortic valve causes obstruciton to forward flow
  • this causes pressure overload (stenosis is always pressure overload)
    • pressure overload always causes concentric hypertrophy
  • increase LV mass
    • compensated
      • normal wall tension, normal afterload
      • normal contractility
      • decreased LV compliance
      • decrease early filling, increase in late filling of ventricle–> SV nromal
    • decompensated
      • fibrosis caues
        • increase wall tension: afterload excess
        • decrease contractility
        • decrease LV compliance
      • leads to LV dilation
      • decreased SV
35
Q

What are some implications of decreased ventricular compliance?

A
  • Sensitivity to volume depletion
  • Depend heavily on atrial “kick” for adequate ventricular filling pressure
  • Wide swings in ventricular filling pressure
  • PCWP underestimates LVEDP
  • ­Increase LVEDP reduces CPP
36
Q

Hemodynamic goals of/ AS?

preload? afterload? HR? contractiliy? rhythm? o2 depmand balance?

A

Slow, tight, full

  • Preload
    • Full, maintain adequate preload
  • Afterload
    • Maintain CPP, already somewhat elevated
  • Contractility
    • In end stage AS might need inotropes especially on induction
  • HR
    • Maintain nml, too slow will DECREASE CO,
    • too fast will cause ischemia
  • Rhythm
    • Must maintain NSR, SVTs will cause hymodynamic instability
  • Myocardial O2 Balance
    • Ischemia is a big risk, must avoid tachycardia and hypotension

ADEQUATE Diastolic TIME and Perfusion Pressure are KEY!

37
Q

What is Aortic insufficiency?

A
  • Dilation of aortic root
  • Leads to chronic volume overload
    • ​Eccentric hypertrophy (chamber enlargement, increased wall thickness)
  • Chamber size increased gradually
  • Increased wall stress
  • Decrease in forward left ventricular SV
  • Increase in chamber diastolic compliance thus maintenance of LVEDP
  • Can be acute or chronic
38
Q

Hemodynamic goals for AI?

A

Fast, Normal, Forward

  • Preload
    • Normal to slightly ­INCREASEd
  • Afterload
    • Reduction will benefit forward flow
  • Contractility
    • Usually adequate
  • Rate
    • Modest tachycardia will reduce ventricular volume, raises aortic diastolic pressure
  • Rhythm
    • Usually sinus, not a problem
  • Myocardial Oxygen Balance
    • Usually not a problem

¨INCREASE PRELOAD AND DECREASE AFTERLOAD-Key

*

39
Q

What is mitral stenosis? what occurs?

A
  • -LV is not subject to pressure or volume overload, actually underloaded
    • -Instead, LA pressures rise
      • -Leads to LA enlargement
        • -Predisposes the pt to have Afib
  • -DOE occurs when CO is increased
  • -Severe MS leads to CHF

Pathophys summary

  • obstruction to LA emptying
  • increase LA Pressure, size–> afib
  • increase in pulm venous pressure
  • increase PA pressure
    • decrease CO
    • Severe pulm HTN
      • RV overload–> TR
  • Perivascular edema
    • reversal pulmonary blood flow
    • decrease pulmonary compliance
    • increase WOB
40
Q

MS Hemodynamic goals?

A

Slow, Tight, Full

  • Preload
    • Enough to maintain flow across stenosis
  • Afterload
    • Avoid ­RV afterload, inotropes for hypotenstion
  • Contractility
    • LV is okay, RV may be impaired
  • Rate
    • Slow to allow time for ventricular filling
  • Rhythm
    • Often have Afib, control ventricular response
  • Myocardial Oxygen Balance
    • Usually not a problem
  • ¨ SLOW heart rate-key
41
Q

What is mitral regurgitation?

A
  • -Portion of systolic ventricular flow regurgitates back to the LA
  • -Regurgitant fraction depends on
    • •Size of the regurgitant valve orifice
    • •Pressure gradient b/w LA & LV
      • Inotropic state of Lv-peak systolic BP
      • Compliance of the LA
      • Compliance of pulmonary veins
    • Time available for regurgitation to occur (systole)
    • Aortic outflow impedence
      • SVR
      • Regurgitation can be significantly influenced by changes in impedance to aortic flow
42
Q

MR Hemodynamic goals?

A

Fast, Full, Forward

  • Preload
    • Pretty full, although reduction may reduce regurgitant flow
  • Afterload
    • Decreases are beneficial, increases augment regurgitant flow
  • Contractility
    • Unrecognized myocardial depression
  • Rate
    • Faster rate decreases LV volume
  • Rhythm
    • Usually Afib, control ventricular response, this rhythm is usually a problem
  • Myocardial Oxygen Balance
    • Problematic only if regurge is due to MI
  • ¨REDUCE AFTERLOAD-KEY

AP III Test 1 (7 decks)

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