• chest pain (angina)
• dyspnea
• orthopnea
• paroxysmal nocturnal dyspnea
• edema
• palpitations
• syncope

• Class I: no dyspnea
• Class II: dyspnea on more than usual activities (able to climb 2 flights/walk 2 blocks)
• Class III: dyspnea on less than usual activities (UNable to climb 2 flights/walk 2 blocks)
• Class IV: dyspnea at rest or with any activity

Understand and label each part of this pressure diagram

[image]

• a: left atrial contraction (blood pumped into relaxed left ventricle)
  
• b: mitral valve closes (S1) and ventricular cntx begins
• b-c: isovolumetric contraction
• c: aortic valve opens
• c-e: systolic ejection period
• e: aortic valve closes (S2)
  
• e-f: isovolumetric relaxation
• f: mitral valve opens (blood passively flows into relaxed left ventricle)

pulse that is small and late:

• slow upstroke
• low amplitude
• small pulse pressure
• severe aortic stenosis

• rapid upstroke
• high amplitude
• wide pulse pressure
• severe aortic regurgitation

• >10mmHg fall in systolic BP during inspiration
• classically = pericardial tamponade
• also = pericardial constriction, obstructive lung dz, massive PE, RV infarction
• in severe cases this can be palpated - pulse will obliterate during inspiration

Jugular Venous Pulse & Waveform:

Why and How?

• The right internal jugular vein acts as a manometer for right atrial pressure.
• With pt supine at 45°, measure the vertical height of pulsations above the sternal angle + 5 cm H₂O
• Normal ~ 7 cm H₂O

Describe each point in this jugular venous waveform:

[image]

• A wave: caused by RA cntx -> blood flows to RV, SVC, IVC
• X descent: atrium relaxes
• C wave: tricuspid valve closes
• V wave: passive filling of RA from SVC, IVC, coronary sinus
• Y descent: tricuspid valve opens -> blood flows to RV
• A wave: caused by RA cntx -> blood flows to RV, SVC, IVC

Large V waves on IJV waveform means what?

[image]

• Severe tricuspid regurgitation
• Normal V wave caused by venous return to RA during systole (TV closed)
• With TR extra regurgitated blood comes back into RA in addition to normal venous return
• Additional blood backtracks into IJV and produces large V wave

Cannon A waves on IJV waveform means what?

[image]

• Complete heart block
• Normal A wave caused by RA cntx. When the right atrium contracts against closed tricuspid valve, little/no blood goes thru TV into RV.
• More blood goes back into SVC->IJV to create large A waves

• Gentle sustained pressure over liver causes transient increase in JVP of small magnitude in all pts.
• Increase in JVP is of greater magnitude and longer duration in those with abnormal central venous pressure (fluid overload).

• Abnormal increase (or failure to decrease) in JVP with inspiration.
• Classically = pericardial constriction
• Also in RV infarct, severe RV failure
• Generally, something is wrong with RV filling.

• location: 4th-5th intercostal space in the mid-clavicular line (mitral valve area)
• lateral placement: suggests cardiac dilatation (in the absence of thoracic cage abnormalities)
• prominent: MR/AR (also thin ppl, high flow states)
• sustained: suggests LVH

• heard best at apex
• caused by closure of mitral and tricuspid valves
• may be split (tricuspid component often not heard)
• loud in mitral stenosis (pliable leaflets), short PR, rapid heart rate

• heard best at base (2nd intercostal space)
• caused by aortic & pulmonic valve closure
• normally split into A2 followed by P2, wider in inspiration
• loud P2 in pulmonary HTN

• Left bundle branch block
• P2 then A2, wider on expiration
• (normal = A2 then P2, wider on inspiration)

• Right bundle branch block
• A2 is constant but P2 is persistently delayed, even on expiration

• Rapid ventricular filling
• May be normal in children and young adults
• May be manifestation of ventricular dysfunction and correlates with CHF
• May originate in LV (apex) or RV (left sternal border)
• Can be augmented at bedside with passive leg raising and isotonic exercise

• Originates from atrial cntx into a stiff ventricle (LVH, ischemia, HTN)
  
• Always pathologic!
• Requires atrial cntx (cannot be heard in AFib)
• May originate in LV (apex) or RV (left sternal border)
• May be augmented at bedside with isometric exercise

mitral stenosis

(valve opening usually does not cause sound)

constrictive pericarditis

(at the time of S3, due to myocardium striking the pericardium)

atrial myxoma

(an early diastolic sound)

• flow across structurally abnormal valves
• increased flow across structurally normal valves
• flow across abnormal communications
• flow into a dilated receiving chamber

• May be benign!
• Or states of increased flow: anemia, fever, pregnancy, thyrotoxicosis, etc.
• Or flow through abnormal structures:
  • subvalvular (HCM, subvalvular membrane/tunnel)
  • valvular (aortic sclerosis, aortic/pulmonic stenosis)
  • supravalvular
• Originates from LV or RV outflow tracts

• Begins after S1 and terminates before S2.
• Crescendo-decrescendo pattern (diamond pattern)
• Duration and timing of peak intensity varies with severity of obstruction
  • Early peak: benign murmurs and aortic sclerosis
  • Late peak: severe aortic stenosis

• Abnormal flow between two chambers that have different pressures throughout systole
• Plateau configuration
• Mitral or tricuspid regurgitation
• VSD
• Always abnormal!

• Mitral valve prolapse
• Often preceeded by mid-systolic click
• Tends to crescendo until S2
• Always abnormal!

• Semilunar valve regurgitation
• Begins with S2 and has decrescendo pattern
• Duration correlates with chronicity
  • Acute MR: short murmur
  • Chronic MR: long murmur
• Murmur of AR is high pitched
• Murmur of PR is low pitched
• Murmur of pulmonary HTN = Graham Steele murmur
• Always abnormal!

• Mitral or tricuspid valve stenosis
• Severe aortic regurg (Austin Flint murmur) due to premature MV closure
• Increased flow across normal valve (ASD)
• Low pitched
• Augments in late diastole with atrial contraction
• Always abnormal!

• Patent ductus arteriosus, fistula
• Flow from high pressure to low pressure throughout cardiac cycle
• Often high pitched, "machinery" type
• Normal variants too

• Grade I-II/VI early peaking systolic ejection murmur (often at LSB)
• No other abnl on CV exam
• No cardiac sx or limitation in functional capacity
• Young patient (<50)
• Normal ECG
• Does not require additional evaluation, treatment, or endocarditis prophylaxis

Grade I: not immediately audible

Grade II: heard with each cardiac cycle but not loud

Grade III: loud murmur without a thrill

Grade IV: loud murmur with a thrill

Grade V: very loud murmur

Grade VI: may be heard with stethoscope off the chest

• focal thickening of valve cusps with normal excursion and no obstruction to flow
• common (25% of >65 yo)
• causes early peaking systolic ejection murmur at RUSB
• pathophys similar to atherosclerosis
• increases risk of coronary events x 2
• may progress to aortic stenosis

• 1-2% of population (4M:F)
• can develop aortic stenosis, regurg, or both
• ~25% of pts require surgery
• moderate risk for endocarditis
• systolic ejection click on exam
• associated with aortic dz (indep of valve dz/fx)
  • ascending aortic aneurysm in 50%
  • coarctation in 10% (30-50% with coarct have bicusp valve)
  • aortic dissection

• Severe, symptomatic AS
• Severe, asymptomatic AS with LV systolic dysfunction (EF<50%)
• Severe, asymptomatic AS at the time of CABG, aorta, or mitral valve surgery

Anything that causes atrial dilatation!

(incl: AV valve regurg or stenosis)

Fluid overload problems & heart chamber volume overload problems:

• AV valve problems (mitral/tricusp regurg/stenosis)
• Constrictive pericarditis
• NOT FOR TAMPONADE

Advantages:

• Low thromboembolic risk
• Good hemodynamics

Disadvantages:

• Relatively short lifespan (10-15 yrs)

Advantages:

• Durability

Disadvantages:

• High thromboembolic risk (requires lifetime anticoag tx)

• Endocarditis
• Structural failure (stenosis and regurg)
• Thromboembolism
• Bleeding on anticoag tx

• alleviate symptoms & improve functional status
• prevent progressive, potentially irreversible LV dysfunction
• prevent progressive, potentially irreversible pulm HTN
• prevent death

• Symptomatic severe valvular dz
• Asymptomatic severe valvular dz w/ evidence of LV dysfunction
• Asymptomatic severe mitral valve dz w/ evidence of significant pulm HTN
• Asymptomatic moderate to severe valvular dz when performing other cardiac surgery (CABG, other valve surgery, etc)

• History of CAD, chest pain, or other evidence of ischemia
• Patients at risk of concurrent CAD:
  • Men >35 yo
  • Post-menopausal women
  • Pre-menopausal women >35 yo with coronary risk factors
• Patients in whom an autograft (Ross procedure) will be performed

• New onset atrial arrhythmias
• Endocarditis
• Sudden progression of dz (chordal rupture, etc)
• Concurrent ischemic heart disease

Beat-to-beat inconsistency in heart due to poor stability of heart within fluid-filled pericardial sac.

On ECG: every other QRS complex looks different

Highly suggestive of pericardial tamponade

Tamponade

(Treatment goal for tamponade is to increase preload in RV. Diuretics decrease preload.)

Constrictive pericarditis

(poor mid-late diastolic filling of ventricles due to inability to expand)

• A: risk for development of LV dysfx
• B: asymptomatic LV dysfx
• C: symptomatic LV dysfx
• D: drug refractory LV dysfx

• Confirm the diagnosis of CAD
• Assess functional capacity
• Assess the response to treatment
• Risk stratification:
  • How severe is the ischemia?
  • How much myocardium is jeopardized?
  • How many vessels are involved?
  • What is the LV function?
• Screen for occult CAD (?)

• Unstable symptoms
• Severe, symptomatic aortic stenosis
• Uncontrolled hypertension
• Decompensated CHF
• Uncontrolled arrhythmias
• Uncooperative patient

• Left main stenosis >50%
• 3 vessel disease, especially with LV dysfx
• 2 vessel disease involving proximal LAD
• Multi-vessel disease in diabetics
• Impaired LV function

• Exercise (treadmill, bicycle) *THE MOST INFORMATIVE*
  • ECG
  • Echo
  • Myocardial perfusion imaging ('nuclear')
• Pharmacologic
  • Dobutamine (beta agonist, incr HR/contractility)
  • Vasodilator (adenosine, dipyridamole)
  • Pacing (with pacemaker)

85% of age predicted maximal heart rate (220-age):

= 0.85 (220 - age)

Functional capacity (METS)

• <6 METS is poor capacity (worst prognosis)
• 6-10 METS is average capacity
• >10 METS is good capacity (best prognosis)

• Target heart rate
• BP response
• Heart rhythm response
• Functional capacity (METS)
• Symptoms (time of onset, severity, accompanying evidence of ischemia)
• ECG (ST segment changes)
• Heart rate recovery

≥1mm horizontal or downsloping ST depression

• Magnitude: more is worse
• Timing: earlier is worse
• Duration: longer is worse
• Number of leads: more is worse
• Associated angina, drop in BP, arrhythmia
• Also ≥1mm ST elevation (in leads without pathologic W waves)

• Inability to complete stage II of Bruce protocol (7 METS)
• Angina at low workload (<6 METS)
• Failure to achieve 80% of target HR or HR >120
• Fall in BP >10mmHg with progressive exercise (accompanied by other evidence of ischemia)
• Ischemic ST depression
  • ≥2mm (esp. downsloping)
  • occurring at a low workload or HR (<6 METs)
  • Occurring in multiple leads
  • Lasting >5 min into recovery
• ST elevation ≥1mm (non-infarct lead)
• Sustained ventricular tachycardia

• Pt is unable to exercise
• Abnormal baseline ECG
• Known CAD (prior infarct, cath, etc)

• Perfusion defects in multiple coronary territories
• Large reversible perfusion defect in single territory (LAD)
• Transient ischemic LV dilatation
• Increased lung uptake (with abnormal perfusion)
• Abnormal LV function (EF<40%)

• Wall motion abnormalities in multiple coronary territories
• Large inducible wall motion abnormalities in single territory
• LV dysfunction (EF<35%)

• Persistent symptoms despite medical therapy
• Non-invasive test results suggesting high risk CAD
• Equivocal or non-diagnostic non-invasive test results
• (High risk occupation)

• Indications: ongoing ischemic pain of <12 hrs duration with ≥1mm ST elevation in contiguous leads in a coronary distribution OR new LBBB
• Advantages:
  • readily available at all times of day
  • can be given quickly
• Disadvantages:
  • contraindicated in ~15% of otherwise eligible patients
  • fails to restore adequate blood flow in up to 50% of patients
  • life threatening bleeding (ICH in ~1%)

• Any history of ICH or known intracerebral mass lesion
• Prior ischemic stroke within 3 months
• Active internal bleeding (excludes menses)
• Known bleeding diathesis
• Recent surgery or biopsy within 2 weeks
• Pregnancy
• Severe HTN (BP>180/110)
• Suspected aortic dissection

• Indications: ongoing ischemic pain of <12 hrs duration with ≥1mm ST elevation in contiguous leads in a coronary distribution OR new LBBB
• Advantages: achieves adequate blood flow in >90% of cases lower risk of life-threatening bleeding allows delineation of coronary anatomy & risk stratification
• Disadvantages: not widely available time delays

3 vessel disease with LV dysfunction

>50% stenosis of the left main coronary artery

2 vessel disease involving the proximal LAD

Constrictive pericarditis

(early diastolic filling is not restricted, but late diastolic filling is restricted → very steep & brief Y descent)

isometric hand grip exercise

squatting