Cardiac Review- Dr E ppt Flashcards
Right atrium of heart?
Systemic veins empty into R Atrium via:
- The superior vena cava (SVC)
- The inferior vena cava (IVC)
* The Eustachian valve protects the lVC - Coronary veins empty into R Atrium via: The coronary sinus
* The Thesibian valve protects the coronary sinus
Characteristics of right ventricle?
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
Characteristics of left atirum
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
Characteristics of left ventricle
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
What are the AV valves
- Tricuspid
- Within the R AV orifice
- 3 leaflets-anterior, posterior, septal
- Tricuspid pays TAPS (tricuspid, anterior, posterior, septal)
- Valve area: 7cm2, symptoms occur at area <1.5cm2
- Mitral valve
- Within the L AV orifice
- 2 leaflets-anteromedial, posterolateral
- Mitral MAP (mitral, anteromedial, posterolateral)
- Valve area: 4-6cm2, symptoms occur at 2-3 cm
What are the semilunar valves?
- Aortic valve:
- Out flow tract of the aorta and the LV
- Has 3cusps
- APLR
- Aortic= posterior, left and right cusps
- APLR
- 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
- PALR
- Pulmonary=anterior, left, right cusps
- PALR
- Valve area: 4cm2 area <1/2 or 1/3 symptomatic
What provides coronary circulation?
- Epicardial
- Subendocardial
- 2 Epicardial Coronaries originate from the sinuses of Valsalva
- Left Coronary Artery (LCA)
- Right Coronary Artery (RCA)
*
Branches of LCA?
- 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)
- LAD
Branches of RCA?
Branches into:
- Sinus node artery- feeds SA node and RA Branch-feeds the RA
- Av node artery-feeds AV node (in 90% of population)
- Anterior RV Branches-feed the RV
- PDA-feeds the posterior 1/3 of the interventicular septum
Leads II, III and aVf
How is coronary dominance determined?
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
What percent of CO goes to coaronaries?
What determines flow in coronaries?
- 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%)
What is coronary autoregulation?
- 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
What composes the cardiac conduction system?
Consists of:
SA node
Internodal tracts
AV node
AV bundle (bundle of His)
Purkinje system
What composes the SA node?
- 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
What composes the internodal tract?
- Within the atria
- Conduction pathways b/w the SA & AV
- Also contain P cells and transitional cells
- 3 Major tracts:
- Anterior (Buchmann’s bundle)-septum
- Middle (Wenckebach’s tract)-SVC
- Posterior (Thorel’s tract)-septum
What composes the AV node?
- 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
What composes the AV Bundle?
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
What is the purkinje system?
- 2 systems: Left and Right
- Left:
* Spreads under the endocardium
* Forms several fascicles-branch over the left ventricle
- Left:
- Right:
* Travels under the endocardium
* Base of the anterior papillary muscle
- Right:
What determines the resting membrane potential of the heart?
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
What are the phases of action potential for ventirular myocte?
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
What is the absolute and refractory phase in ventricular myocte?
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
What composes the sympathetic nervous system for heart?
- 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
WHat provides parasympathetic innervation to heart?
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
What are the vagal receptors and sympathetic fibers for cardiac receptors?
- 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
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
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
What does a pressure volume loop of the heart show?
From pressure-volume loop picture-
- closing of mitral valve
- aortic valve opening
- aortic valve closure
- mitral valve opening
a. diastolic filling
b isovolumetric contraction
c. ventricular ejection
d. isovolumetric relaxation
Volume for 1-4= SV
- SV= EDV-ESV
What determines cardiac output?
CO= Volume of blood pumped by the heart each minute
Determined by:
- Preload
- Afterload
- Heart rate
- Contractility
- Ventricular compliance
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
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
- Can be raised only by increasing coronary blood flow
- Demand
- Wall tension
- Preload
- Afterload
- Contractility
- HR
- More important to address-easier
- Wall tension
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
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
What is aortic stenosis? What does it cause? s/s?
- 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)
Pathophysiology of AS?
- Narrowing of aortic valve causes obstruciton to forward flow
- typically due to rheumatic fever, valve calficiation, or bicuspid valve
- 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
- fibrosis caues
- compensated
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
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!
What is Aortic insufficiency?
- Dilation of aortic root
-
Pathophys-
-
acute-
- infective endocarditis
- trauma
- dissection of thoracic aneurysm
-
chronic
- prior rheumatic fever
- persistent systemic hypertension
-
acute-
-
Pathophys-
- 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
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
*
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
- -Leads to LA enlargement
- -Instead, LA pressures rise
- -DOE occurs when CO is increased
- -Severe MS leads to CHF
- Pathophys- typically due to rheumatic fever
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
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
What is mitral regurgitation?
- -Portion of systolic ventricular flow regurgitates back to the LA
- pathophys- usually due to rheumatic fever and associated with mitral stenosis
- -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
MR Hemodynamic goals?
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
