Cardiac Review- Dr E ppt Flashcards

(42 cards)

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
What happens during diastole?
* 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
What occurs during systole?
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
What does a pressure volume loop of the heart show?
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
What determines cardiac output?
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
What is a frank-starling curve?
* 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
What influences coronary supply and demand?
* 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
What are hemodynamic goals in pt with CAD?
* 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
How do treat intraop ishcemia?
* 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
What is aortic stenosis? What does it cause? s/s?
* Narrowing of the valve * At **0.8cm2 s**ymptoms 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
Pathophysiology of AS?
* 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
What are some implications of decreased ventricular compliance?
* 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
Hemodynamic goals of/ AS? preload? afterload? HR? contractiliy? rhythm? o2 depmand balance?
**_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
What is Aortic insufficiency?
* 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
Hemodynamic goals for AI?
**_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
What is mitral stenosis? what occurs?
* -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
MS Hemodynamic goals?
**_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
What is mitral regurgitation?
* -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
MR Hemodynamic goals?
Fa**_st, 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**