C30 Cardiology and Cardiac Surgery Toronto Notes 2023
Major Complications
• cardiac: high grade AV block requiring permanent pacemaker (less risk with cryoablation), new or
worsening arrhythmia, tamponade, pericarditis
• vascular:hematoma, vascular injury, thromboembolism, TIA/stroke
• pulmonary: Ft
Ischemic Heart Disease
Epidemiology
• refer to CCS guidelines - 2014 Stable Ischemic Heart Disease Guidelines for Diagnosis and
Management for more information
• most common cause of cardiovascular morbidity and mortality
• patients may have asymptomatic orsymptomatic disease
• silent myocardial ischemia may be a predictor of adverse coronary events and cardiac mortality
• needs to be monitored via intracardiac monitoring of physiological and hemodynamic
parameters, metabolic indicators of ischemia in the coronary sinus, and hemodynamic factors
optimal medical therapy (reduction of HR and BP) and myocardial revascularization
• atherosclerosis and thrombosis are the most important pathogenetic mechanisms
• M:F=2:1 with all age groups included (Framingham study), 8:1 for age <40, 1:1 for age >70
• CHD incidence in women triples shortly after menopause
• peak incidence of symptomatic IHD is age 50-60 (men) and 60-70 (women)
• for primary prevention of ischemic heart disease see Family Medicine. FM8
HTN DM Smoking Dyslipidemia Rheumatoid Arthritis
J I
Endothelial injury
I
Monocyte recruitment
Enhanced LDL permeability
Monocytes enter into initial space and dillerentiate into macrophages - LDL is converted into oxidized-LDLI0X-L0LI
I
Macrophages take up OX-LDLvia scavenger receptors to become foam cells ('
fatty streak'
and lipid core of plaque)
I
Cytokine and growth factor signalling Irom damaged endothelium and macrophages promote medial smooth muscle
cell migration into the intima,proliferation (intimal hyperplasia),and release ol matrix to form the fibrous cap of plaque
-rupture depends on balance of pro- and anti
-proteases,magnitude of necrosis,and location ol plaque (bifurcation
sites are exposed to greater shear stress)
T t T l
Calcification Plaque rupture Hemorrhage into plaque Fragmentation Wall weakening
I I
;
Increased vessel Thrombosis Emboli Aneurysm
wall rigidity
Figure 35. Pathophysiology of atherosclerosis
Lumen narrowing
Table 9. Risk Factors and Markers for Atherosclerotic Heart Disease
Non-Modifiable Risk Factors Modifiable Risk Factors 5 Markers of Disease
Elevated high-sensitivity C- reactive protein (hsCRP)
Coronary artery calcification
Carotid IMl/plaque
Ankle - brachial index
Age Hyperlipidemia'
Male, postmenopausal female HIM'
Family history (FHx) of Ml *
first degree male relative «55 yr Cigarette smoking*
First degree female relative *65 yr Psychosocialstress
Abdominal obesity
Sedentary lifestyle
Heavy alcohol intake
Mot consuming fruits and vegetables daily
Elevated lipoprotein(a)
Hyperhomocysteinemia
DM'
r “t
iJ
* Major risk factors
S Modlliablo risk factors account tor >90% olMis
+
C31 Cardiology and Cardiac Surgery Toronto Notes 2023
Chronic Stable Angina
Definition
• symptom complex resulting from an imbalance between oxygen supply and myocardial oxygen
demand in the myocardium
Chronic stable angina is most olten
due to a fixed stenosis caused by an
atheroma
ACSs ate the result of plaque rupture
which causes a cascade resulting in
thrombosis
Etiology and Pathophysiology
• factors that decrease myocardial oxygen supply:
decreased luminal diameter:atherosclerosis, vasospasm
decreased duration of diastole:tachycardia (decreased duration of diastolic coronary perfusion)
decreased hemoglobin:anemia
decreased Sa02: hypoxemia
congenital anomalies
• factors that increase myocardial oxygen demand:
• increased HR: hyperthyroidism, exercise, anemia, pregnancy
increased contractility: hyperthyroidism
• increased wall stress: myocardial hypertrophy, AS
Signs and Symptoms
• typical
Canadian Cardiovascular Society (CCS)
Functional Classification of Angina
• Class I: ordinary physical activity
(walking, climbing stairs) does not
cause angina:angina with strenuous,
rapid, or prolonged activity
• Class II:slight limitation of ordinary
activity: angina brought on at >2
blocks on level or climbing >1flight of
stairs, or by emotionalstress
• Class III: marked limitation of
ordinary activity:angina brought on
at <2 blacks on level or climbing <1
flight of stairs
• Class IV: inability to carry out any
physical activity without discomfort:
angina may be present at rest
1. retrosternal chest pain,tightness or discomfort radiating to left (± right)shoulder/arm/neck/
jaw,associated with diaphoresis,nausea, anxiety
2. predictably precipitated by the “3Es": exertion, emotion, eating
3. brief duration,lasting <10-15 min and typically relieved by rest and nitrates
• atypical/probable angina (meets 2 of the above)
• non-cardiac chest pain (meets none or I of the above)
• Levine’
ssign:clutching fist over sternum when describing chest pain
• anginal equivalents: dyspnea, acute LV failure, flash pulmonary edema
• ischemia may present differently in understudied populations
Clinical Assessment
• history including directed risk factor assessment and physical exam
• labs:Hb,fasting glucose, fasting lipid profile, HbAlc,renal function tests, liver function tests, and
thyroid function test
• 12-lead ECG (at rest and during episode of chest pain if possible)
• CXR (suspected HI'
, valvular disease, pericardial disease,aortic dissection/aneurysm,or signs/
symptoms of pulmonary disease)
• stress testing (see Stress Testing,C15 ) or angiography
• echo for other causes of chest pain:
• aortic dissection
valvular heart disease
-
HCM
LV dysfunction and/or wall motion abnormality
Pericardial disease/effusion
Differential Diagnosis
• see Differentia] Diagnoses of Common Presentations, C5
Treatment of Chronic Stable Angina
refer to 2019 European Society of Cardiology guidelines for more information Initial Invasive or ConsenratneStrategy for
Stable Coronary Disease (ISCHEMIA)
NEJM 2020:382:1395 1«?
Purpose: Assess clinical outcomesin stable coronary
if lease treated with Invasive pins medical lberapps.
medical therapy alone.
Methods: 5119 patents were randomliedto invasive
therapy (angiography and revascularization} plus
medical therapy or medical therapy alone plus
angiography upon failure of initial conservative
approach.Ihe primary outcomewas a composite ol
mortality from CV causes.Ml. hospitalitation for UA.
HF or resuscitated cardiac arrest.
Jesuits: Ovei a median ol 3.2 yr. 318 and 352 primary
outcome even Isoccurred In the uvasive strategy and
cotiscrvatlve-strategy groups, respectively.It 5 yr,
the cumulative event rate was16.4% and18.2% in the
invasive-strategy and coaservatne -strategy groups,
respectively.
Conclusion:In
ifcease, there was no evidence thatan initial invasive
strategy reduced ischemic CV eventsor death from
any cause ove r a median of 3.2 yr.compared with
initial conservative medical therapy.
1.General Measures
• goals:to reduce myocardial oxygen demand and/or increase oxygen supply
• lifestyle modification (diet, exercise,smoking cessation)
treatment of risk factors:e.g.statins (see Endocrinology, E5, family Medicine. 1 Ml 1 for target
lipid guidelines), antihypertensives
pharmacological therapy to stabilize the coronary plaque which will prevent rupture and
thrombosis
2. Antiplatelet Therapy (first-line therapy)
• ASA
dopidogrei when ASA contraindicated
• low dose rivaroxaban in combination with ASA (based on COMPASS trial)
pt
3. p blockers (first-line therapy improvessurvival in patients with HTN)
increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)
cardioselective agents preferred (e.g. metoprolol, atenolol) to avoid peripheral effects (inhibition
of vasodilation and bronchodilation via 02 receptors)
avoid intrinsic sympathomimetics (e.g. acebutolol) which increase demand
patients with chronic stable coronary
+
C32 Cardiology and Cardiac Surgery Toronto Notes 2023
4.Nitrates(symptomatic control, no clear impact on survival)
decrease preload (venous dilatation) and afterload (arteriolar dilatation), and increase coronary
perfusion
maintain daily nitrate-free intervalsto prevent tolerance (tachyphylaxis)
5.Calcium Channel Blockers (CCBs,second-line or combination)
increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)
caution:verapamil/diltiazem combined with p-blockers may cause symptomatic sinus
bradycardia or AV block
contraindicated in patients with LV systolic dysfunction
6.Renin-Angiotensin-Aldosterone System Blockade
angina patients tend to have risk factors for CV disease which warrant use of an ACE1 (e.g. HTN,
DM, proteinuric renal disease, previous Ml with LV dysfunction)
• ARB can be considered in patients intolerant to ACEI
benefit in all patients at high-risk for CV disease (e.g. those with concomitant DM, renal
dysfunction, or LV systolic dysfunction)
7. Invasive Strategies
revascularization (see Coronary Revascularization,C37)
VARIANT ANGINA (PRINZMETAL’S ANGINA)
• myocardial ischemia secondary to coronary artery vasospasm with or without atherosclerosis
• uncommonly associated with infarction or LV dysfunction
• typically occurs between midnight and 8am, unrelated to exercise, relieved by nitrates
• typically ST elevation is observed on ECG
• diagnosed by provocative testing with ergot vasoconstrictors(rarely done)
• treat with nitrates and CCBs
• strongly recommend patient to stop smoking
SYNDROME X
• typical symptoms of angina but normal angiogram
• may show definite signs of ischemia with exercise testing
• thought to be due to inadequate vasodilator reserve of coronary resistance vessels
• better prognosis than overt epicardial atherosclerosis
Acute Coronary Syndromes
Definition
• ACS includes the spectrum of UA, NSTEM1, and STEM)
:this distinction aids in providing the
appropriate therapeutic intervention
UA is clinically defined by any of the following:
accelerating pattern of pain:increased frequency, increased duration, decreased threshold of
exertion,decreased response to treatment
angina at rest
new-onset angina
angina posl-MI or post-procedure (e.g. PCI, CABCi)
Ml (STEM1/NSTEM1) is defined by evidence of myocardial necrosis and is diagnosed by a rise/fall
of serum markers plus any one of:
symptoms of ischemia (chest/upper extremity/mandibular/epigastric discomfort:dyspnea)
ECG changes(ST-T changes, new BBB, or pathological Q waves)
imaging evidence (myocardial loss of viability, wall motion abnormality, or intracoronary
thrombus)
if biomarker changes are unattainable, cardiac symptoms combined with new ECG changes
issufficient
NSTEM I meets criteria for Ml without ST elevation or BBB
• STEMI meets criteria for Ml characterized by ST elevation or new BBB
• possible ACS in women, diabetics, and older adults is more likely to present with “atypical” symptoms
such as dyspnea or weakness even in the presence of acute coronary-related ischemia
Efficacy a ltd Sif etyof L
Myocardial Infarction (COICOI)
HE JM 2019:381:2497 2S0S
Purpose lo determine if colchicine hwnsrisk of
futureCVevtntsfollowinq Ml.
Methods: Pat ents|n -IMS) who had an Ml within
the last 30 d were randoanted to colchicineonce
daily or placebo.Ihe primary efficacy endpoml was
a composite of death from CV canes,resuscitated
cardiac arrest.Ml.stroke,or urgent hospitaktation
for angina.
Results:Median folow up was 22.0 mo.Ihe preiory
endpoint occurred in 5.5
*
and f.1% of patientsin the
coichicme and placebo groups,respettuely (P-0.02).
Pneumonia was observed In 0.9% of the patentsin
the colchicine group and in 0.4% of patients m the
placebo group (P-0.03).
Conclusion In patients with recent Ml.colchicine
lowered the risk of subsequent CV eventsas
compared to placebo.
on Oose Colchicine after
Investigations
• history and physical
• note that up to 30% of Mis are unrecognized or “silent"due to atypical symptoms more common
in women, patients with DM, elderly, post-heart transplant (because of denervation)
. EGG
. CXR
+
C33Cardiology and Cardiac Surgery
ch as dyspnea or weakness even in the presence of acute coronary-related ischemia
Efficacy a ltd Sif etyof L
Myocardial Infarction (COICOI)
HE JM 2019:381:2497 2S0S
Purpose lo determine if colchicine hwnsrisk of
futureCVevtntsfollowinq Ml.
Methods: Pat ents|n -IMS) who had an Ml within
the last 30 d were randoanted to colchicineonce
daily or placebo.Ihe primary efficacy endpoml was
a composite of death from CV canes,resuscitated
cardiac arrest.Ml.stroke,or urgent hospitaktation
for angina.
Results:Median folow up was 22.0 mo.Ihe preiory
endpoint occurred in 5.5
*
and f.1% of patientsin the
coichicme and placebo groups,respettuely (P-0.02).
Pneumonia was observed In 0.9% of the patentsin
the colchicine group and in 0.4% of patients m the
placebo group (P-0.03).
Conclusion In patients with recent Ml.colchicine
lowered the risk of subsequent CV eventsas
compared to placebo.
on Oose Colchicine after
Investigations
• history and physical
• note that up to 30% of Mis are unrecognized or “silent"due to atypical symptoms more common
in women, patients with DM, elderly, post-heart transplant (because of denervation)
. EGG
. CXR
+
C33Cardiology and Cardiac Surgery Toronto Notes 2023
• labs
serum cardiac biomarkersfor myocardial damage (use of high-sensitive cardiac troponin (hscTn) with a validated 0 h/2 h algorithm recommended blood sampling at 0 h and 2 h) (see Cardiac
Biomarkers,C13)
CBC,International Normalized Ratio (lNR)/prothrombin time test (PIT),electrolytes,
magnesium, creatinine, urea,glucose, and serum lipids
• draw serum lipids within 24-48 h because values are unreliable from 2-48 d post-Ml
Complete Revascularization with Hiltivessel PCI
for Myocardial Infarction (COMPLETE)
NUM 2019:381:1411-1421
Purpose: In determine if PCI of non -culpnt lesions, in
addition to culprit lesions,former reduces the risk ol
CV events or Ml In patients with SIEU.
Methods: Patients with SIEMI andmuhivessel CAD
who had undergone culprit-lesion PCI (#’
4041) were
randomized toeither complete revascularization with
PCI (of significant non-culprit lesions)or mfarther
revascularization,the two main outcomes measured
included:t) the composite of CV death or Ml,and 2)
the composite of CV death.Ml.or ischemia-driven
revascularization.
lesults: The fust outcome wasohsetrtd in 7.8%
of the complete revascularization group aad18.5%
of the culprrt-lesion-only PCI group (P-0.004).
Ihe second outcome was observed in 8.9% of the
complete revascularization group aod16.71of the
culprrt-lesion- only PCI group (P’
0.001).
Conclusions:In patientswith STEMI and muliivesse I
CAD.complete revascularization try PCI further
reduced the risk of CV death or Ml as compared to
culprit-leslon-only PCI.
MANAGEMENT OF ACUTE CORONARY SYNDROMES
1.GeneralMeasures
ABCs:assess and correct hemodynamic status first
• bed rest,cardiac monitoring,oxygen
nitroglycerin sublingual (SL) followed by IV
• morphine IV
2. Antiplatelet and Anticoagulation Therapy
• see also 2018 CCS/CAIC Antiplatelet Guidelines, 2012 and 2010 CCS Antiplatelet Guidelines, and
2009 CCS Position Statement on Dual Antiplatelet Therapy in Patients Requiring Urgent CABG
for details(free mobile apps available on iOS and Android platforms in the CCSapp stores).
Also see 2020 ESC guidelines on ACS management in patients without persistent ST-segment
elevation, 2017 ESC guidelines on STEM1 management, and 2019 CCS guidelines on acute STEM1
management (focused update on regionalization and reperfusion)
• ASA chewed
• NSTEM1
ticagrelor + ASA f LMVVH/IV unfractionated heparin (Ul-
'H), unless contraindications
- LMWH, except in renal failure or if CABG is planned, within 24 h
- fondaparinux also commonly used in Canada for initial medical management of
NSTEM1/ UA based on OASIS-5 results
clopidogrel used if patient ineligible for ticagrelor
if PCI is planned:ticagrelor or prasugrel and consider IV glycoprotein Ilb/llla inhibitor (e.g.
eptifibatide, tirofiban)
clopidogrel used if patient ineligible for ticagrelor and prasugrel
prasugrel contraindicated in those with a history of stroke/TI A, and its avoidance or lower
dose is recommended for those >75 yr or weighing <60 kg (T’RITON-TTMI 38)
anticoagulation options depend on reperfusion strategy:
primary PCI: UEH during procedure;bivalirudin is a possible alternative
thrombolysis:LMWH (enoxaparin) until discharge from hospital; can use UFH as alternative
because of possible rescue PCI
no reperfusion: LMWH (enoxaparin) until discharge from hospital
• continue LMWH or UPH followed by oral anticoagulation at discharge if at high-risk for
thromboembolic event (large anterior Ml,severe LV dysfunction, CHI'
, previous DVT'
or PE, or
echo evidence of mural thrombus)
in patients with APib (CHA2DS2-VASc score 21 in men and 2 in women), use triple
antithrombotic therapy for up to I wk and then transition to dual antithrombotic therapy
(using a NOAC and an antiplatelet agent (preferably clopidogrel))
3. (3-blockers
• STEMI:contraindications include signs of HE, low output states, risk of cardiogenic shock, heart
block, asthma, or airway disease;initiate orally within 24 h of diagnosis when indicated
• if p-blockers are contraindicated or if (3-blockers/nitratesfail to relieve ischemia, nondihydropyridine CCB (e.g. diltiazem, verapamil) may be used assecond-line therapy in the
absence ofsevere LV dysfunction or pulmonary vascular congestion (CCB do not prevent Ml or
decrease mortality)
4. Invasive Strategies and Reperfusion Options
UA/NSTEM1:early coronary angiography ± revascularization if possible isrecommended with
any of the following high-risk indicators:
diagnosis of NSTEMI
recurrent angina/ischemia at rest despite intensive anti-ischemic therapy
CHE or LV dysfunction
hemodynamic instability
high (>3) Thrombolysis in Myocardial Infarction (T1M1) risk score (tool used to estimate
mortality following an ACS)
GRACE risk score >140
sustained ventricular tachycardia
dynamic ECG changes, transient ST-elevation
high-risk findings on non-invasive stress testing
PCI within the previous 6 mo
repealed presentationsfor ACS despite treatment and without evidence of ongoing ischemia
or high-risk features
note: thrombolysis is NOT administered for UA/NSTEM1
TIMI Risk Score for UA/NSTEMI
Characteristics Points
Historical
Age e6Sgrr
>3risk factors for CAD
Known CAD (stenosis zS0%)
Aspirin
‘
useinput 7 d
Presentation
Recent(<24 h)severe angina
ST-segment d eriation >0.5star
Increased cardiac marker
1
1
1
1
LJ
1
1
1
tthk Score = Total Pujols
IITIMIrisk sure >3.toiaidnurlyLMWHamt
anpogrnplty
IIMI
- IliiomUolysA In iwyourMMwttion
IAA •unstable angina
JAMA 2000:284:83S-S42
I
C34 Cardiology and Cardiac Surgery Toronto Notes 2023
• ST EMI
after diagnosis ofSTEM1is made, do not wait for results of further investigations before
implementing reperfusion therapy
goal is to re-perfuse artery:thrombolysis (“EMS-to-needle”) within 30 min or primary PCI
(“EMS-to-balloon”) within 90 min (if available)
Newer, more accurate risk quantification
scoresfor UANSTEMI east such asthe
GRACE Risk Score:however.TIMI isstil
PCI used most often
- early PCI (<12 h aftersymptom onset and <90 min after presentation) improves
mortality vs.thrombolysis with fewer intracranial hemorrhages and recurrent Mis
- primary PCI:without prior thrombolytic therapy method of choice for reperfusion in
experienced centres
- rescue PCI:following failed thrombolytic therapy (diagnosed when ST segment
elevation failsto resolve below half its initial magnitude after thrombolysis and patient
still has chest pain)
thrombolysis
- assuming no contraindications, use if <12 h since symptom onset and primary PCI
cannot be conducted within 120 min of STEMI diagnosis
- note: benefit of thrombolysis is inversely proportional to time from symptom onset;
in patients meeting the above criteria, the later the presentation (>3 h ), the more one
should consider using primary PCI instead (depending on clinical circumstances)
HTN DM Smoking Dyslipidemia Rheumatoid Arthritis
I
Endothelial injury
*
Monocyte recruitment
Enhanced LDL permeability
Monocytes enter into initial space and differentiate into macrophages-LDL is converted into oxidized-LDLIOX-LDL)
Macrophages take up OX-LDLvia scavenger receptors to become foam cells ('
fatty streak' and lipid core of plaque)
*
Cytokine and growth factor signalling from damaged endothelium and macrophages promote medial smooth muscle
cell migration into the intima. proliferation (intimal hyperplasia), and release of matrix to form the fibrous cap of plaque
-rupture depends on balance of pro- and anti-proteases,magnitude of necrosis, and location of plaque (bifurcation
sites are exposed to greater shear stress)
j i i i
Calcification Plaque rupture Hemorrhage into plaque Fragmentation Wall weakening
* *
I I
T
1
Increased vessel - L.i; Emboli Aneurysm
wallrigidity
Lumen narrowing
Figure 36. Reperfusion strategy in STEMI
Table 10. Contraindications for Thrombolysis in STEMI
Absolute Relative
Prior intracranial hemorrhage
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Significant closed-head or facial trauma(s3 mo)
Ischemic stroke (<3 mo)
Active bleeding
Suspected aortic dissection
Chrome,severe,poorly controlled HIN
Uncontrolled HIN|sSP >180. d8P >110)
Current anticoagulation
Noncompressible vascular punctures
Ischemrc stroke (>3 mo)
Decent internal bleeding (<2-4 wk)
Prolonged CPR or major surgery (<3 wk)
Pregnancy
Active peptic ulcer disease
Long-Term Management of ACS
• risk of progression to Ml,or recurrence of MI, or death is highest within 1 mo
• at 1-3mo after the acute phase,most patients resume a clinical course similar to that in patients with
chronic stable coronary disease
• pre-discharge workup:ECG and echo to assess residual LV systolic function
• drugs required in hospital to control ischemia should be continued after discharge in all patients
• other medicationsforlong-term management of ACS are summarized below
r n
.General Measures
• education
risk factor modification
+
C35Cardiology and Cardiac Surgery Toronto Notes 2023
2. Antiplatclct and Anticoagulation Therapy
see also CCS Antiplatelet Guidelines 2018 for details (free mobile apps available on iOS and
Android platforms in the CCS app stores)
• ECASA 81 mg daily
ticagrelor 90 mg BID or prasugrel 10 mg daily (at least 1 mo, up to 9-12 mo;if stent placed at least
12 mo)
clopidogrel 75 mg daily can be used as alternatives to ticagrelor and prasugrel when indicated
± warfarin x 3 mo if high-risk (high-risk patients include those with large anterior Ml,LV
thrombus, LVEF <30%, history of VTE,chronic Alib)
» rivaroxaban 2.5 mg BID (based on COMPASS trial)
Is this Patient having a Ml?
From Ilie RationalCImical iin naton
JAMA 1998:381(14):1256-1263
Study:Systematic review of articlesassBS'igthe
accuracy and precision ol ttiedincaleun ia the
diagnosis oi an acute Ml.
Results: h patients with normal onton-dagnostic
ECG, no estattished CAO.and prolonged or recurrent
chest pam typical of their usual discomfort,radiation
of pain to the shoulder OR troth anus had the highest
positive likelihood ratio (-LR) of 4.1ard a negatne
likelihood raho (-LR) of 0.68.Radiatmntothe right
arm had a HR of 3.8 and -IR of 0.86.vomitmg had a
HR of 3.5 and -IR of 0.8)
. while radutionto the left
arm only hod a HR oft.3 and a -IRof 0.1.
Conclusions lire most compe ng teatsres that
inc lease likelihoodo!an III areSi-segment and
cardiac eniyme elevation, new 0-wave, and presence
of an S3 heartsound . In patients where the dagnosis
of Ml is uncertain, radiation of pan to the shoulder OR
both arms, radiation to the right arm.and nor ibng
had the best predictive values,while radiation to the
leftarm isrelatively non-diagnostic.
3. (3-Blockers(e.g. metoprolol 25-50 mg BID or atenolol 50-100 mg daily)
4. Nitrates
alleviate ischemia but do not improve outcome
• use with caution in right-sided Ml patients who have become preload dependent
5.Calcium Channel Blockers ( NOT recommended as first line treatment, consider as alternative to
P-blockers)
6. ACEIs
prevent adverse ventricular remodelling
recommended for asymptomatic high-risk patients (e.g. diabetics), even if LVEF >40%
recommended for symptomatic CHE, reduced LVEF (<40%), anterior Ml
* use ARBsin patients who are intolerant of ACE1; avoid combining ACE1 and ARB
7.± Aldosterone Antagonists
if already on ACE1 and P-blockers,svith and LVEF <40% and CH F or DM
significant mortality benefit shown with eplerenone by 30 d
8. Lipid Lowering Therapy Statins (early, intensive, irrespective of cholesterol level; e.g. atorvastatin 80
mg daily)
• atorvastatin 80 mg daily (ezetimibe or PCSK9 inhibitor if LDL <2 mmol/L)
9. Invasive CardiacCatheterization if indicated (risk stratification)
Post-Infarction Risk Stratification
1
;
i
High Risk (30 Intermediate/Low-Risk (65-70%)
-35%)
•Prior Ml
•CHF
•Recurrent Ischemia
•High-Risk Arrhythmia
I
Noil-Invasive Stress Testing
1
f
Ischemia or Poor
Functional Status
Normal Results
Cardiac Catheterization j
!
4
'note: echo done routinely post
-MI
No further testing
at this time
Figure 37. Post-MI risk stratification
Prognosis following STEMI
• 5-15% of hospitalized patients will die
• risk factors
infarct size/severity
age
comorbid conditions
development of HF or hypotension
• post-discharge mortality rates
6-8% within first year, half of these within first 3 mo
• 4% per year following first yr
• risk factors
LV dysfunction
« residual myocardial ischemia
ventricular arrhythmias
history of prior Ml
Complications of Ml
CRASH PAD
Cardiac Rupture
Arrhythmia
Shock
Hypertension/Heart failure
Pericarditis/Pulmonary embolism
Aneurysm
DVT
r -1
L J
Resting LVEF is a useful prognostic factor
+
C36 Cardiology and Cardiac Surgery Toronto Notes 2023
Table 11. Complications of Ml
Complication Etiology Presentation Therapy
Treatment of NSTEMI
Arrhythmia
1. tachycardia
2. Bradycardia
Myocardial Rupture
1.LV free wall
2. Papillary muscle (
* MR)
3.Ventricular septum (• VSD)
Shock/CHF
itt Jbihytlimias. CIO
BEMOAN
p blocker
Enoxaparin
Morphine
Sinus. AFib,VI.Vfrb
Sinus. AV block
First 48 h
First 43 h
Oz Surgery
Surgery
Surgery
Inolropes. intra aortic balloon
pump
Aggressive medical therapy
PCIorCABG
Aggressive medical therapy
PCIorCABG
Anticoagulation
Transmural infarction
Interior infarction
Septal Infarction
Infarction or aneurysm
1-7 d
ASA
1-7 d Nitrates
1- 7 d
Within 48 h
Post-Infarct Angina Persistent coronary stenosis
Multivessel disease
Reocclusion
Anytime
Recurrent Ml Anytime
Thromboembolism Mural/apical thrombus 7-10 d. up to 6 mo
DVI
Pericarditis
Dressler's Syndrome
Inflammatory
Autoimmune
1- 7 d ASA
2-8 wk
Treatment Algorithm for Acute Coronary Syndrome
Symptoms Indicating Possible
Acute Coronary Syndrome (ischemia or infarction) Contraindications to nitrates:seveie aortic stenosis,
hypertrophic cardiomyopathy,suspected right
ve ntricular infarct,hypotension,marked bradycardia
or tachycardia,and recent use of phosphodiesterase
S inhibitors.
T
EMS and Pre-Hospital Care
1. Monitor support ABCs.Readiness for CPR and/or defibrillation
2 Obtain 12 Lead ECG; STEMI ST olovation should bo roportod to the recoiving facility
3 Medications to give ASA, oxygon. SL nitroglycorino, and morphino
4 Hospital should proporo to respond to STEMI
MUST BE
PERFORMED
IMMEDIATELY
- -
MUST BE
PERFORMED
IMMEDIATELY
Immediate ED Assessment and Treatment
12 Lead ECG (if not done pre hospital)
Obtain vital signs; 02sat
Oxygen if 0:sat <94%; 4 L then titrate
Piovido ASA160 325 mg
Piovido nitroglycorino sublingual or spray coagulation tosts
Establish IV and givo morphino (if noodod) Puitablo chost x ray (<30 min)
Perform brief,targeted Hx and physical exam
Review fibrinolytic checklist.Check
contraindications
Obtain cardiac marker lovols, electrolyte, and MUST BE
PERFORMED
IN LESS THAN
10 MINUTES
READ ECG
T
j ( ST Depression (NSTEMI)
( ] c ST Elevation (STEMI) Normal ST Segment
11 i r
• Sturt uppropriuto thorapios:
heparin,NTG.pbtockors
* Roporfusion therapy STAT
Elevated Troponin or
High-Risk Patient
Signs for invasive therapy:
• Continued chest discomfort
• Continued ST deviation
• Unstable hemodynamics
• Heart failure
Ventricular tachycardia
• Possible admission: monitor
serial ECG and cardiac markors
• Considor non invasive testing
(treadmill or thallium stress tost)
NO
Symptoms <12 h YES
'Develops 1 or more:
• ECG changes (ST elevation/
depression)
• Troponin olovutod
• Worsening chost discomfort
^
or arrhythmias
YES
•Goal lor stent placement or
balloon inflation should bo
within 90 min
• Goal lor fibrinolysis should be
30 min
Adjunctive Therapies
• Nitroglycerine (IV/PO)
• Heparin (IM/IV)
• Possibly:
^
blockers, clopidogrel.
^
glycoprotein llb/llla inhibitor
^
UN0
• Abnormal results from
non invasive diagnostic tests
• Abnormal results from ECG or
troponin
r1
L J
• Admit to monitored bod
• Continue ASA. hopurin, and
other indicated thorapios
• ACEI/ARB
• Statin therapy
• Expert consultation to assess
cardiac risk factor
YIS WN0
Discharge and schedule
follow-up +
Figure 38. AHA ACLS acute coronary syndrome algorithm
Adopted from: Jeffery Medio Productions 201C. Amsterdam EA. Wenger NK, Brindis RG.ct al. 2014 AHA/ACC guideline for the management of patients
with noit
'
ST'Ulevdtlon acute coronary syndromes. Circulation. 2014 Jun LCIR-0000000000000134
C37 Cardiology and Cardiac Surgery Toronto Notes 2023
Coronary Revascularization
PERCUTANEOUS CORONARY INTERVENTION
• interventional cardiology technique aimed at relieving significant coronary artery stenosis
• main techniques: balloon angioplasty,stenting
• less common techniques: rotational/directional/extraction atherectomy
Indications
• medically refractory angina
• NSTEMI/UA with high-risk features (e.g. high T1M1 risk score)
• primary/rescue PCI for STEM!
. UA/NSTEM1 if not aCABG candidate
STEMI when PCI can be performed more rapidly and safely than CABG
Balloon Angioplasty and Intracoronary Stenting
• coronary lesions dilated with balloon inflation
• major complication is restenosis (approximately 15% at 6 mo), thought to be due to clastic recoil and
neointimal hyperplasia
• majority of patients receive intracoronary stent(s) to prevent restenosis
bare metal stent (BMS) vs. drug-eluting stents: PKAM1 trial demonstrated stenting non-culprit
lesions results in 14% absolute risk reduction of cardiac death, nonfatal Ml, or refractory angina
coated with antiproliferative drugs(sirolimus, paclitaxel, everolimus, zotarolimus)
reduced rate of neointimal hyperplasia and restenosis compared to BMS (5% vs. 20%)
complication:late stent thrombosis (5 events per 1000 stents implanted)
Adjunctive Therapies
• ASA and heparin decrease post-procedural complications
• further reduction in ischemic complications has been demonstrated using GPIlb/llla inhibitors
(abeiximab, eptifibatide, tirofiban) in coronary angiography and stenting
• following stent implantation
dual antiplatelet therapy (ASA and clopidogrel) for 6 mo (and up to 1 vr)
consider short-duration DAPT for 1 mo with BMS or 3 mo with DES followed by monotherapy for
12 mo among patients with high ischemic or bleeding risk
ASA and prasugrel can be considered for those at increased risk ofstent thrombosis
Procedural Complications
• mortality and emergency bypass rates <1%
• nonfatal MI:approximately 2-3%
See Landman Caid ac Iriabfor more information oo
EXCELwhidi BetaIsthe long-term efficacy profile of
CUG A.PCI in patientswith left main CAD.
V
ticagrelorwitlior without Aspirin In High-Risk
Patients after PCI
fCJtl 2019:381:2032-2042
Pnrpose: fodeteimine If monotherapy with
Ptagieloi, a P2T12 inhibitor,after a period of dual
antiplatelet therapy reducesthe risk of bleeding
following PCI.
Methods: Patients whowereathigh-rlsk for bleeding
or an ischemic erent underwent PCI and 3 mo ol
treatment with ASA pinsticagrelor.Patie nts(a-7119)
were then randomiied to receive either ticagrelor
plus ASA or ticagaelor pluspfaeebofor a year, lee
primary endpoint was Bleeding Academic (eseaich
Consortium (3ARC) type 2.3.or 5 bleeding.
Results: The primary endpont was obseried in
4.0% of patents n the llcagrebr plus placebo group
and 7.1% of patentsin the bcagrelot plus ASA gioup
(P<0.001).The incidence of death from a ny cause,
nonfatal Ml. or nonfatal stroke was 3.9% in both
groups(P‘
0.001 for nonlnleriority).
Conclusion:Among high-risk bleed patientswho
received PCIand 3mo of dual antiplatelet therapy,
additional ticagrelor monotherapy wasassouated
with lower incidence of bleeding and the same nsk ol
death,as compared to ticagrelor plus ASA therapy.
Safety and Efficacy Outcomes of Double vs.Triple
Antithrombotic Ihcrapy in Patients with Atrial
fibrillation Eolowing PercutaneousCoronary
Intervention
Eur Heart J 2019:40:3757-3767
Puiposc: fo evaluate the safely and efficacy of
double vs. triple antithrombotic theiapy (DAI rs.IAI)
si patientswith Afib and ACS following PCI.
Methods: Systematic review and meta-analysisof 4
Inals with a total o'10234 patents.
Conclusions:DAI was associated with lower risk of
bleeding, hut higher risk of stent thrumhostsand Ml
compared to IAI.There was no significant ifference
m all-cause and caidiovascular death,stroke,and
mayor adverse cardiovascular events.
CORONARY ARTERY BYPASS GRAFT SURGERY
• objective of CABG is complete revascularization of the myocardium
Indications
• >50% diameter stenosis in the left main coronary1
artery
• 270% diameter stenosis in three major coronary arteries
• 270% diameter stenosis in the proximal LAD artery plus one other major coronary artery
• survivors ofsudden cardiac arrest with presumed ischemia-mediated VT caused by significant (270%
diameter) stenosis in a major coronary artery
• 270% diameter stenosis in two major coronary arteries (without proximal LAD disease) and evidence
of extensive ischemia
• 270% diameter stenosis in the proximal LAD artery and evidence of extensive ischemia
• multivessel CAD in patients with diabetes
• LV systolic dysfunction (LVEE 35% to 50%) and with significant multivessel CAD or proximal LAD
stenosis where viable myocardium is present in the region of intended revascularization
• one or more significant (270% diameter) coronary artery stenosis amenable to revascularization and
unacceptable angina despite medical therapy
Contraindications
• CABG may be contraindicated in patients who are:elderly/frail, have multiple comorbidities or, for
any other reason, may notsurvive surgery
• CABG may be contraindicated in patients who do not have myocardial viability
• CABG is contraindicated in patients that lack bypassablc vessels
See LandmarkCardiac Inalsfor more information on
SYNTAX , which details all-cause mortality,stroke.
M o< repeat recastulanialioa12 mofolbwing PCI
vs.CABG
ri
LJ
Results
• perioperative and in-hospital mortality rate after CABG:
-1% for the lowest risk elective patients, and
2% for all patients(depends on patient characteristics and heart function)
• predictive variables for early hospital mortality include older age (>80 yr),female sex, urgency of
operation, left main stem disease, increasing extent of CAD,increasing LV dysfunctions, redo CABG
+
08Cardiology and Cardiac Surgery Toronto Notes 2023
Table 12. Choice of Revascularization Procedure
PCI CABG
Percutaneous Coronary Intervention Versus
Coronary Artery Bypass Crafting in Patients
with Three-vessel or left Main Coronary Artery
Oisease
lancet 2019:394:1325-34
Purpose:Report10-yr all-cause mortality resets as a
10-yr foltow- up totte 2009 SYNTAX trial.
Methods.Ad J!patients with estab ished left
mam CAO or three-vessel coronary disease were
randomlied to receive eithei PCI or CA8C m a 1:1
ratio. Patients with a prior history ol Ml.PCI or CISC
were excluded.The primary study endpoint wasM- yt
all-cause mortality.
Results: tO-yr all-cause mortality rates were
20% and 24% for PCI- and CABG-treated patents,
respectively|tiaiard ratio 1.19; 95% Cl 0.99 to1.43;
p-0.066). In suhgroupanalysis. 10-yr all-cause
mortality was 21% and 21% nr PCI and CABG patents
with three-vessel disease, respectively (hacaid
ratio1.42:95% Cl1.11 to1.81).Ihe same primary
endpoint occurred in patients with left mam coronary
disease at a rate of 27% and 28% in PCI and CABG
patients, respectively (hazard ratio 0.92;0.69to
1.22; P-0.0233.
Conclusions CABG provided a significanta i cause
survival benefit m patients with three-vessel disease,
compared to PCI in the same population,this effect
was not observed m patients with left main CAO or m
the pooled study sample.
Greater ability to achieve complete revascularization
Decreased need for repealed revascularization
procedures
Clinical characteristics
Diabetes
Reduced IV function (IT <35%|
Contraindications to 0AP1
Recurrent diffuse in stent restenosis
Anatomical and technical aspects
MVD with SYNfAX score > 23
Anatomy likely resulting in incomplete
revascularization with PCI
Severely calcified coronary artery lesions limiting
lesion expansion
Need for concomitant interventions
Ascending aorlic pathology with indication for
surgery
Concomitant cardiac surgery
lessinvasive technique
Decreased pcriprocedural morbidity and mortality
Shorter periprocedural hospitalization
Clinical characteristics
Severe comorbidity
Advanced age/frailly/reduced life expectancy
Reslrided mobility and conditions that affed
rehabilitation
Anatomical and (cchnicalaspcds
MVO with SYNTAX score < 23
Anatomy likely resulting in incomplete
revascularization with CABG due to poor quality or
missing conduits
Severe chest deformation orscoliosis
Sequelae of chest radiation
Porcelain aorta
Advantages
Factorsfavouring
Revascularization Procedure
Note:Table reflects guidelinesfrom the European Society olCardiology that have been taught toCanadian cardiac surgery residents
Table 13. Conduits for CABG
Graft Occlusion /Patency Rate Considerations
At 10 yr: 50% occluded. 25% stenotic, 25%
angiographically normal
90-95% patency at 15 yr
Saphenous Vein Grafts (SVG) Used to be commonly used, but arterial conduits have
proven lobe superior
Considered the standard conduit for CABG
Excellent patency
Almost always used to bypass LAD
Improved event-free survival (angina. Ml)
Decreased lale cardiac events
Used in bilateral IIAIIMA grading
Palienls receiving bilateral IIAs/IMAs have less risk ol
recurrent angina,lale Ml. angioplasty
Prone to severe vasospasm postoperatively due to
vascular muscular wall
Left Internal
Thoracic/Mammary Artery (LITA/
LIMA to LAD)
Duration of Dval Antiplatelct Therapy Following
Drug -cluting Steallmplantalion: A Systematic
R eview and Meta-Analysis ol Randomized
Controlled Trials with longer follow up
Catheter Cardiorasc.Inter*
.201); 90:31-7
Purpose:Conduct an updated meta -aralysisto
compa re the efficacy and safely of short-term dual
antiplatelet therapy IS-OAPT) vs. long-term OAPI
(L-OAPfl in patients who uoderwentdiug-etutvig
stent|0fS|implantation,
Methods RCIscorparingeHitacydndlorsafety
outcomes(ov different DAPI durations aftercoronary
DBS imptantatma weie searched m PubMed.ClMAH.
Cochrane CENTRAL.EMBASE.Scopus,and Web of
Science.S-DAPT was defined as <12 mo duration of
aspirin plus P2Y12 receptor inhibitor, while l-DAPI
was defined asthe same combination lor >12 mo
duration after OES implantation,
Results S RCIsmet all eligibility criteria and were
included in Ure final meta-analysis.Outcomes
of interest included all-cause mortality, cardiac
mortality,myocardial infarction,stent thrombosis,
target vessel revascularization,stroke, or major
bleeding.Compared wrth L-DAPI, S-OAPT d d not
significantly increase the rate olstent thrombosis (OR
1.59; 95% Cl 0.1)to 3.27). All-cause mortality,cardiac
mortality, target vessel revascularization and strobe
were also not significantly different between groups.
Rowever.S OAPI was associated with an increased
risk of Ml (OR 1.48:95% Cl 1.04 lo 2.10) and a lowered
risk of major bleeding (OR 0.64:95% Cl 0.41 to 0.99).
Conclusions: In this meta-analysis with a longer
follow- up hue of >24 months.S- DAPI compared
to l-DAPI wasassociated with increased risk of Ml
bul lower ralesol mayor bleeding. No signifcaat
differences were found for all-cause mortality,
cardiac mortabty.stent thrombosis, target vessel
revascularization,or stroke.
Right Internal Ihoracic/Mammary
Artery
(RITAJRIMA)
Radial Artery (free graft)
Pedidcd RIMA patency comparable to LIMA
lower rate of lice RIMA patency
85-95% patency at 5 yr
Right Gastroepiploic Artery 80-90% patency at 5 yr Primarily used as an in situ graft to bypass Ihe RCA
Use limited because of Ihe Iragile qualify of the artery,
technical issues, increased operative time (laparotomy
incision ), and incisional discomfort with associated
ileus
Complete Arterial Revascularization Foi younger patients(<60 y/o)
Preferred due lo longer term graft patency
Indications for redo CABG:symptomatic patients
(disabling angina) who have failed medical therapy,
have stenotic vessels, have viable myocardium, have
suitable distal targets
Risk factors lor redo CABG: poor control of HINT
hypercholesterolermafsmoking. normal IV. 1or 2
vessel disease, no use ol IMA/IIA in initial CABG.
incomplete revascularization in initial CABG.young age
Operative mortality 2-3limes higher than first
operation
10% perioperative Ml rale
Reoperalron undertaken only in symptomatic patients
who have failed medical therapy and in whom
angiography has documented progression ol Ihe
disease
Increased risk with redo-sternotomy secondary to
adhesions which may result in laceration to aorta.
RV. IMAi'IIA.and other bypass gratis, uncontrollable
hemorrhage, arterial bleeding and VFib, venous
bleeding, or failure to arrest heart
Redo Bypass Grafting
Adapted lioin:Chlkwe J. BvddowE.GIerrvllle B. Cnrdiothorock Surgery, tsted. Oxford. UK : Oxford UP. 4000.
Operative Issues
• LV function is an important determinant of outcome for all heart diseases
• patients with severe LV dysfunction usually have poor prognosis, butsurgery can sometimes
dramatically improve LV function
• assess viability of non-functioning myocardial segments in patients with significant LV dysfunction
using delayed thallium myocardial imaging,stress echo, positron emission tomography (FED
scanning, or MRI
ri
L J
+
09Cardiology and Cardiac Surgery Toronto Notes 2023
CABG and Antiplatelet Regimens
• refer toCCS guidelines 2018 update on antiplatelet therapy for more information
• prior to CABG, clopidogrel and ticagrelor should be discontinued for 5 d, and prasugrel for 7 d before
surgery
• dual antiplatelet therapv should be continued for 12 mo in patients with ACS within 48-72 h after
CABG
• ASA (81 mg) continued indefinitely (can be started 6 h after surgery)
• patients requiring CABG after PCI should continue their dual antiplatelet therapy
the post
-PCI guidelines
as recommended in
Table 14. Risk Factors for CABG Mortality and Morbidity
Risk Factors for CABG Mortality Risk Factors for CABG Postoperative Morbidity or
Increased Length of Stay
Urgency of surgery (emergent or urgent)
Aeoperalion
Older age
Poor IV function (see below)
female gender
left main disease
Others include catastrophic conditions (cardiogenic shock, ventricular Renal dysfunction
septalrupture,ongoing CPR),dialysis-dependentrenal failure,end- COPO
stage COPD.DM.cerebrovascular
disease,and peripheral vascular disease
Reoperalion
Emergent procedure
Preoperativc intra aortic balloon pump (IA8P)
CHI
CABG •valve surgery
Older age
DM
Cerebrovascular disease
Note:risk factors are listedindecreasing order of significance
Procedural Complications
• CABG using ( P B (see Cardiopulmonary Byp (.r> «s)
stroke and neurocognitive defects (microembolization of gaseous and particulate matter)
immunosuppression
deep sternal wound infection
bleeding
systemic inflammatory response leading to:
myocardial dysfunction
renal dysfunction
neurological injury
respiratory dysfunction
coagulopathies
OFF-PUMP CORONARY ARTERY BYPASS SURGERY
Procedure
• avoids the use of CPB by allowing surgeons to operate on a beating heart
stabilization devices (e.g.Genzyme Immobilizer*) hold heart in place allowing operation while
positioning devices (Medtronic Octopus* and Starfish* system) allow the surgeon to lift the
beating heart to access the lateral and posterior vessels
procedure issafe and well tolerated by most patients; however, this surgery remains technically
more demanding
Indications/Contraindications
• used in poor candidates for CPB who have: calcified aorta, poor LVEF,severe PVD,severe COPD,
chronic renal failure,coagulopathy,transfusion objections(e.g. (ehovah’s Witness),good target
vessels, anterior/lateral wall revascularization, target revascularization in older,sicker patients
• absolute contraindications:hemodynamic instability, poor quality target vessels including
intramyocardial vessels, diffusely diseased vessels, and calcified coronary vessels
• relative contraindications:cardiomegaly/CHF, critical left main disease,small distal targets, recent or
current acute Ml, cardiogenic shock, LVEP <35%
See LandmarkCardiacTrialsfor more information on
ROOBY. which details theS-year dinteal outcomesin
indents undergoing on-pump is.off-pump CABG
Medical Therapy
(optimal)
CASS
ECSS- VACS
COURAGE
ACME MASS II
BARI 2D
ISCHEMIA
[HQ | CABG |
COJ- AC
ACME
'Coronary Artery Surgery Study
futopoon Coronary Surgery Study
VA Coopnrotivo Study
Figure 39. Clinical trials comparing
strategies for stable CAD
Figure recreated with permission
from Dr. Chris Overgaardn
Outcomes
• OPCAB surgery decreases in-hospital morbidity (decreased incidence of chest infection, inotropic
requirement,supraventricular arrhythmia), blood product transfusion, 1CU stay, length of
hospitalization, and CK-MBand troponin 1 levels
OPCAB has been associated with lower graft patency
rn
L J
+
CIO Cardiology and Cardiac Surgery Toronto Notes 2023
Heart Failure
Docs this Dyspntic Patient in the tmergcncy
Department haveCongestive Heart Failure!
JAMA 2005:294:1944-1956
• see also CCS Heart failureGuidelines 2021 for details (free mobile apps available on i
()S and Android
platforms in the CCS app stores) as well as the Canadian Cardiovascular Society (CCS) Heart Failure
Guidelines Compendium available at CCS.ca in * IR - |95S Cl') (95% Cl )
Congestive Heart Failure Initial clinical 4.4
judgment (1.8-10.0] (0.28-0.73)
0.45
PMHx
Low HF 5.8 0.45 -Output HF
due to decreased CO
High-Output HF
due to increased
cardiac demand
(4.1 1.0) (0.38 0.53)
Ml 3.1 0.(9
Systolic Dysfunction Diastolic Dysfunction (2.04.9) (0.58 0.821
Infiltration and
fibrosis
Injury and ischemia CAD 1.8 0.68
in myocardium (1.1-2.81 <0.48 0.96|
*
I
Symptoms
Thick,stiffened
myocardium
Infarction and inflammation PHD 2.6 0.7
I (1.5-4.5) (0.54-0.91)
Thin, weakened muscle Orthopnea 2.2 0.65 I
Ineffective
ventricular filling (1.2-3.91 (0.45 0.92)
Ineffective ventricular
contraction 50806 1.3 0.48
(12-1.4) (0.35-0.671
Increased Cardiac Workload
- Myocardial stress
- Volume overload
• Pressure overload
Physical Eiam
Third heart ff 0.88
sound
Jugular venous 5.1
distension (32-7.9) (0.57-0.771
(4.9 25) (0.83-0.94)
0.86 *
*
Compensation
- Increased HR and
' myocardial contractility
- Increased blood volume
Docomponsation
- Deterioration ol heart(unction
- Heart unable to maintain blood
circulation
Systomic Rosponso
- Activation of SNS and RAAS activity
Rales 2.8 0.51
(1.9-4.1) (0.37-0.70)
Lower
extremity
edena
2.3 0.64
(1.5-32) (0.47-0.871 Left-Sided HF Right-Sided HF Biventricular HF
- Due to long-term left-sided
failure leading to
right-sided failure
- Disorders affecting entire
myocardium
Forward Failure
- Inability to maintain CO
Backward Failure
- Elevated ventricular tilling
pressures
• Vascular congestion in venae
cavae
- Fluid accumulation in lower
extremities (edema in feet,
ankles,legs, lower back,liver,
abdomen),nausea
5
Chest Radiograph
— Pulmonary 12
venous
congestion
Interstitial 12
edena
0.48 5
Backward Failure
- Elevated ventricular filling
pressures
- Pulmonary vascular congestion
- Fluid accumulation in lungs,
apnea,SOB, fatigue,weakness
< s
6 8 21) (0.28 0.831
CO,
S
s
E
o
1 0.68
w
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