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Cardiovascular Emergencies. LIN LING ED , ICU SIR RUN RUN SHAW HOSPITAL. Table of contents. 1. 2. Acute coronary syndrome. Acute heart failure. 3. 4. Hypertensive emergencies. Cardiac arrhythmias. Table of contents. 1. 2. Acute coronary syndrome. Acute heart failure. 3. 4. - PowerPoint PPT Presentation
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Cardiovascular Emergencies
LIN LING
ED , ICU
SIR RUN RUN SHAW HOSPITAL
LIN LING
ED , ICU
SIR RUN RUN SHAW HOSPITAL
SIR RUN RUN SHAW HOSPITAL 2/41
Table of contents
1
Acute coronary syndrome2
Acute heart failure3
4
Hypertensive emergencies
Cardiac arrhythmias
SIR RUN RUN SHAW HOSPITAL 3/41
Table of contents
1
Acute coronary syndrome2
Acute heart failure3
4
Hypertensive emergencies
Cardiac arrhythmias
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Hypertensive emergency is defined as the acute and progressive
decompensation of damage of vital organ function caused by an elevated blood pressure
CONCEPT
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Major organs affected by hypertension are the brain,kidney, heart, and vascular system.
Need to be carefully evaluated ,be monitored, and have their blood pressure controlled.
The important issue is clinical situation,not the severity of BP level.
CONCEPT
No degree of hypertension by itself defines an emergency
No degree of hypertension by itself defines an emergency
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Usually referring to markedly elevated BP and without symptoms.
No longer widely used.Can be managed on an outpatient
basis.Do require increased vigilance, the pts
are at high risk of nearterm complications from their uncontrolled hypertension,especially those pts with a history of previous end-organ disease.
Hypertensive urgency
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Hypertensive encephalopathyAccelerated malignant hypertensionCerebrovascular accidents
stroke
Cardiovascular crisis Pulmonary edema Heart failure
Renal crisesOther emergencies
Preeclampsia/eclampsia
Hypertensive emergencies
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A-B-Caccurate measurements of
BPHistoryPEDiagnositc studies
ED EVALUATION
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Several separate BP measurements : Initially elevated Bp frequently decrease
spontaneously by a second reading Evaluated in both armsSeated with the arm at the level of the
heart and the cuff bladder should cover at least 80%of the arm circumference
Accurate measurement of BP
Base clinical decisions on correctly measured and repeated BPBase clinical decisions on correctly measured and repeated BP
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Start with the target organ Dyspnea,chest pain,neurologic
complaints ,visual changesDuration and severity of
preexisting hypertensionThe degree of previous success
with BP controlThe presence of target organ dz
history
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Directed toward identifying signs of target organ damage
funduscopic examinationretinal hemorrhage or papilledema is
sufficient to diagnose accelerated malignant hypertension
Cardiovascular Neurologic :
PE
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Based on the pt’s symptomsCXRHead CTECGUrine screen and Serume
cratinine
Diagnostic studies
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The goal of therapy is a reduction in the mean MAP by 20%to 25% in 1 to 2 hrs.
NOTE:Reducing BP too quickly or too low a level.----can result in inadequate cerebral or cardiac blood flow leading to stroke or myocardial infarction.
ED Management
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All hypertensive emergencies require admission to a monitored setting .
Close BP monitoring ,preferably with an A-line.
Pts with preeclampsia/eclampsia require emergent obstetric consultation
ED Management
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Search for and correct underlying causes of an elevated BP (e.g.pain,hypoxia,bladder distension
Avoid relative hypotension or dropping BP in the absence of an indication.
Treat the BP according to specific indications.
ED Management
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Rapid onsetRapid maximal effectRapid offset Easy titrationof BP
The ideal drug
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PARENTERAL DRUGS
DRUG DOSAGE ONSET/DUR ADV.EFFE
Nitroprusside 0.25-10mcg/kg/min
Instant/1-2min. Thiocyanate,cyanide poisoning
Nitroglycerine 5-100mcg/min 1-5min/3-5min Flushing,headache,methemoglobin
Nicardipine 5-15mg/hr 5-10min/1-4hr Tachycardia,flushing.avoid-heart failure
Hydralazine 10-20mg 5-15min/3-8hr Flushing,tachy,avoid-A.diss,MI
Enalapril 10-40mg IM,1.25-5MG1Vq6hr
20-30min/6hr Hypotension,renal failure,hyperkalemia
Fenoldopam 0.1-0.3mcg/kg/min
5min/10-15min Flushing,headache,tachy
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DRUG DOSAGE ONSET/DUR ADV.EFF
Labetalol
(a+b blocker)
20-80mgiv bolus every 10 min,2mg.min iv infusion
5-10min/3-6hrs Heart block,ortho hypotension.avoid-heart failure,asthma
Esmolol
(b-1 selective
blocker)
200-500 mcg/kg/min for 4min,then 150-300mcg/kg/min
1-2min/10-20min Hypotension,avoid-heart failure,asthma
Phentolamine
(a1 blocker)
5-15mg iv 1-2min/3-10min Tachycardia,flushing,headache
PARENTERAL DRUGS
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SPECIFIC TREATMENT
Hypertensive EncephalopathyGoal is to reduce MAP by not >25%
or DBP to100mmHg in the first hour.Nitroprussid(widely used in past)is a
powerful arteriloar dilator,so a rise in ICP may occur.
Labetalol,fenoldopam used more now.
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Intracerebral Hemorrhage: CPP=MAP-ICP.As ICP rises,MAP must rise for perfusion
but this raises risk of bleeding from small arteries and arterioles.
MAP guidelines:decrease when MAP>130 or SBP>220
Labetalol,esmolol agents of choice.
SPECIFIC TREATMENT
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SAH Nimodipine decreases
vasospasm that occurs due to chemical irritation of arteries by blood.
SPECIFIC TREATMENT
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Acute Ischemic Stroke: High BP can cause hemorrhagic
transformation of infarct , cerebral edema.But,if CPP is low,ischemic area may enlarged.
AHA guidelines:BP be reduced only if SBP>220 or DBP>120mmHg.(unless end-organ damage is due to BP)
Labetalol,nitroprusside-agents of choice.
For thrombolysis,BP<185/110.
SPECIFIC TREATMENT
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Specific Treatment
Aortic dissection: Immediate reduce BP !!mainly,shear stress(change in BP
with change in time) is essential to limit the extension of damage
Eliminate pain and reduce systolic BP to 100-120 or lower that permits perfusion.
Labetalol / b-blocker + nitroprusside/other vasodilators
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MI: NTG,b-blockers,ACE inhibitors.
Acute LVF: usually associated with pulmonary
edema and diastolic/systolic dysfunction.
IV nitroprusside,NTG agents of choice.
Titrate until BP controlled and signs of heart failure alleviated.
Specific Treatment
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Renal insufficiency: is a cause and effect of high BP.Goal is to prevent further renal
damage by maintaining adequate blood flow.
Nitroprusside effective.
Specific Treatment
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Dianosing a hypertensive emergency when one does not exist. -----Elevated BP with acute end organ dysfunciton.
Reducing BP too quickly or too low a level.----can lead to cerebral or cardiac ischemia
Neglecting to match the antihypertensive agent to the clinical scenario.
Common pitfalls
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Table of contents
1
Acute coronary syndrome2
Acute heart failure3
4
Hypertensive emergencies
Cardiac arrhythmias
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Is a spectrum of myocaridal ischemia , which most often due to disruption of vulnerable atherosclerotic plaques,
IncludingUANSTEMISTEMI
Acute coronary syndrome
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PATHOPHYSIOLOGY OF ACS动脉粥样硬化斑块的破裂和腐蚀Disruption of vulnerable plaques
SIR RUN RUN SHAW HOSPITAL
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DIAGNOSISDIAGNOSIS
•symptoms•With or without ECG changes•No cardiac biomarkers
•symptoms•ST depression or T-wave inversion•Positive Cardiac biomarker
•Symptoms
•ST-elevation
•Positive Cardiac biomarker
UA NSTEMI
STEMI
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symptoms
Ischemic chest pain/chest discomfort Chest Pain,tightness,or heaviness,pain that
radiates to neck,jaw,teeth,shoulders,backOthers
Dyspnea Indigestion of heartburn,Nausea/Vomitting Weakness,dizziness,or Syncope
Intypical in DM, elder and female pts
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Cardiac biomarkers
CKMB
Troponin
myosin
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Troponin
cTnT,c TnI Highly sensitive and highly specific Detecting cell necrosisHigh specific in cardiac Be detected 4~6hrs after the onset
of symptoms, persistes up to 5 ~14ds
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Pre-hospital
Every pts with chest pain should initially be assumed that the pain is ischemic in origin.——ACS suspected
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Prehospital and ED care
Ischemic chest pain
•Prehospital evaluation•ABC,and Diffibralation available•Monitor,Obtain IV access,oxygen•Aspirinshould be given except for contraindication•nitroglycerin if chest pain is ongoing •Morphin if needed•12-lead ECG
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Initial management
ED <10min
Monitor VS,SpO2 IV 12-LEAD ECG Briefly History and PE Thrombolysis
checklist CBC,cardiac
markers,electrolytes,PT PTT
Portable X ray ( 30min)
ED <10min
Monitor VS,SpO2 IV 12-LEAD ECG Briefly History and PE Thrombolysis
checklist CBC,cardiac
markers,electrolytes,PT PTT
Portable X ray ( 30min)
MONA
Oxygen,SpO2>90% ASA 162~325mg NTG Morphin:chest pain
not relieved
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Chest pain suspected ACS
STEMISTEMI
STABLE STABLE ANGINAANGINA
NON-NON-CARDIAC DZCARDIAC DZ
12-lead ECG12-lead ECG ER ER 10 min10 min
TransferTransferhistory,PEhistory,PECardiac markerCardiac marker
ACSACS
Troponin ELEVATIONELEVATION
Troponin NORNAL
UA NSTEMI
ST-ST-ELEVATOINELEVATOIN
NON-ST NON-ST ELEVATIONELEVATIONNSTEACS
RECHECK IN 10~15MIN
recheck in 6 hrs
SIR RUN RUN SHAW HOSPITAL
TIME IS MYOCARIDIUM ! TIME IS LIFE !
patient transfer In ED reperfusion
symptoms doorCall for help
thrombolysis
PCI
10min 30min D-N 30min
D-B 90min
goal
Pt educationECG ACS
protocolPCI team
Prehospital care
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UA/NSTEMI
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Three principal presentation of UA
SIR RUN RUN SHAW HOSPITAL 43
1997/2001
SIR RUN RUN SHAW HOSPITAL 44Courtesy A Gitt
0.7
0.8
0.9
1
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
after ACS ( mo )
生存率
NSTEMI
STEMI
Although in-hospital mortality of STEMI is high,1-year mortality of NSTEM is equivalent to STEMI
STEMI 与 NSTEMI 比较的 1 年累积死亡率
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Selection of the site of careCoronary care unitStep-down unitOutpatient setting
Selection of the therapy Invasive managemnt strategy
EARLY RISK STRATIFICATIONS OF
UA/NSTEMI
45
SIR RUN RUN SHAW HOSPITAL 46
非 ST 段抬高的 AMI 的危险性分层
High riskAt least 1 of the following
features
Intermediate riskAt least 1 of the
following
Low risk
historyhistory Accelerating of ischemic symptoms in preceding 48h
Prior MI, peripheral or
cererovascular dz,or CABG,prior
ASA use
Character Character of painof pain
Prolonged ongoing(greater than 20min) rest pain
Prolonged(>20min) rest angina,now
resolved,with moderate or high likelihood of CAD
Incrased angina frequency,severity or durationNew onset angina
Risk stratification of UA/NSTEMI
标准不一致时以最高为准
SIR RUN RUN SHAW HOSPITAL 47
High risk Moderate risk Low risk
Clinical findings
Pulmonary edema, new or worsening MR murmur, ,hypotension,>75ys
Age greater than 70ys
ECG
Angina at rest with transient ST-changes, new BBB,sustained VT
T-wave changes, pathological Q
waves
Unchanged ECG
Cardiac markers
Elevated cardiac biomarkers
Slightly elevated(eg.
0.1>cTnT>0.01ug/l
normal
Risk stratification of UA/NSTEMI
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ER managementPharmacoligical therapy :
Anti-platelet ( aspirin,clopidogrel)
anticoagulants(heparin,LMWH )
anti-ischemic nitrates 、 β-blockers 、 Ca-
A 、 ACEIstatins
Management of NSTEMI/UA
48
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NO benefit of fibrinolytic therapy in UA/NSTEMI pts was clealy demonstrated.
NO FIBRINOLYSIS!!
49
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UA/NSTEMI pts who have refractory angina
Hemodynamic or electrical instability ;
High risk pts and ineffective with pharmacologic therapy
Early invasive strategy in UA/NSTEMI is indicated in
50
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ECGDifferentiate diagnosisReperfusion therapyPost-MI complications
STEMI
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Information from the ECG
Diagnosis Is the ST elevation requiring reperfusion
Rx?Prognosis
Infarct sizeHow many mm ST elevation?How many leads show ST elevation?
Infarct locationComplications
arrhythmia
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STEMI –ECG Treatment Criteria
ST elevation> 0.2mV in 2 continuous leads V1~V3 or > 0.1mV in at least 2 continuous other
leads
LBBB
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ECG-localize infarct territory
Antero-septal(LAD) : V1-3Anterior wall(LAD) : V1-6, Ⅰ 、
aVL Inferior(RCA) :Ⅱ、Ⅲ、 aVFPosterior(LCx): V7-9(ST
depression in V1-V4)RV(RCA) : V3R-5R
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posterior STEMI
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Extensive-Anterial AMI
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Inferior infaction
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Cause of ST elevation
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Differential diagnosis of ST-elevation
Acute pericrditisAcute myocarditisHyperkalemiaBrugada syndromeARVDMassive PEAcute aortic dissectionSAHLV aneurysmEarly repolarization/normal variant
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90min球囊扩张
溶栓
Increasing loss of myocyteIncreasing loss of myocyte
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Immediate management
Aspirin 300mg to chewIf age <75,clopidogrel 300mgOxygen by mask esp if SpO2
<90%,LVF,shockMorphine 4-8mg iv ot achieve
analgesiaIV NTG or beta blocker for
analgesis,↓ BP and ↓ischaemia
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For pts with STEMI within 12h after symptom onset and with persistent ST-elevation or new LBBB,early PCI or pharmacological reperfusion should be performed
Indication of reperfusion
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Strategies for reperfusion
FibrinolysisPre-hospital In-hospital
PCIPrimary PCIFacilitated PCIRescue PCI
CABG
SIR RUN RUN SHAW HOSPITAL
Fibrinolytic Medicationsmed dose usage 90min
reperfusion rate
StreptoKinase
1.5mil U 30-60min iV 55-64%
UroKinase
1.5-2mil U 60min iv 31-55%
rtPA 15mg bolus iv 82-87%
0.75mg/kg 30min iv
0.5mg/kg 60min iv
Up to 100mg
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Absolute contraindications
Haemorrhagic stroke or SAHIschaemic stroke in preceding 3monthsCentral nervous system trauma or
neoplamsRecent major trauma/surgery/head injury
with preceding 3 wksGastrointestinal bleeding within the last
monthKnown bleeding disorderAortic dissection
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Relative contraindications
Transient ischaemic attack in preceding 6 months
Oral anticoagulant therapyPregnancy Refractory hypertension(>180/110mmHg)Advanced liver diseaseInfective endocarditisActive peptic ulcerCPR>10min
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Benefits of Fibrinolysis in STEMI
Pain to Rx <3hrs,fibinolysis with fibrin specific agent=PCI
Onset of pain <6hrs,prevent 30deaths per 1000 pts Rx’d
Onset of pain <12hrs,prevent 20deaths per 1000 pts Rx’d
Onset of pain >12hrs,little evidence of benefit
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Failure to reperfuse
<50% reduction in ST↑at 60min after fibrinolysis
Ongoing symptoms(beware masking effect of analgesics), arrhythmia, haemodynamic instability
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ConservativeRepeat fibrinolysisRescue PCI
Options(REACT )
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Primary PCIAngioplasty and /or stenting without prior or
concomitant fibrinolytic therapyFacilitated PCI
Pharmacologic reperfusion treatment delivered prior to a planeed PCI in order to bridge the PCI-related time delay
Rescue PCIPCI performed on a coronary artery which
remains occluded despite fibrinolytic therapy
PCI(Percutaneous coronary interventions)
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PCI of door-to-balloon and mortality
0%
4%
8%
12%
16%
20%
<60min 61-75min 76-90min >90min no PCI
死亡率
Time to PTCA 30day mortality
SIR RUN RUN SHAW HOSPITAL
PCI and fibrinolytic therapy
mortalitym
orta
lity
(%
)
p<0,05 p<0.02
Gibbons R.J.,N.Engl.J.Med.(1993)328:685
n=645
2,6
6,5
5,1
12,0
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Post-MI complications
Cardiogenic shockFail to reperfuse(15%)Post-infarct anginaRe-infarction(30%at 3 mo)VSDSevere MR
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Table of contents
1
Acute coronary syndrome2
Acute heart failure3
4
Hypertensive emergencies
Cardiac arrhythmias
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Heart failure is a syndrome manifesting as the inability of the heart to fill with or eject blood due to any structural or functional cardiac conditions.
INTRODUCTION
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CLINICAL PRESENTATION
Left HFDyspneaOrthopneaParoxysmal
nocturnal dyspnea
Cardiac asthma
Rihgt HFEdemahepatic
congestionAscites Nocturia
Due to excess fluid accumulaiton Due to excess fluid accumulaiton Due to reduction in cardiac output Due to reduction in cardiac output
Fatigueweaknessaltered mental state low BP
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Is defined as the sudden increase in PCWP (usually more than 25 mm Hg) as a result of acute and fulminant left ventricular failure.
Is a medical emergency and has a very dramatic clinical presentation. Patient appears extremely ill, poorly perfused, restless, sweaty, with an increased work of breathing and using respiratory accessory muscles, tachypneic, tachycardic, hypoxic and coughing with frothy sputum that on occasion is blood tinged.
Acute pulmonary edema
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I : No symptoms and no limitation in ordinary physical activityII : Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.III : Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m).Comfortable only at rest.IV : Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
NYHA Class
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is used to support a clinical diagnosis of heart failure. to determine
SV, the amount of blood that ejects from the ventricles with each beat
EDV, the total amount of blood at the end of diastole, ejection fraction (EF). SV in proportion to the EDV
Normally, the EF is 50% ~ 70%; in systolic heart failure, it drops below 40%.
Echocardiography can also identify valvular heart disease, and can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo.
Imaging---Echocardiography
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cardiomegaly (visible enlargement of the heart),
cardiothoracic ratio (proportion of the heart size to the chest )↑
vascular redistribution ("upper lobe blood diversion" or "cephalization")
Kerley lines, cuffing of the areas around the bronchi,
interstitial edema.
Chest X-rays
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Pulmonary edema
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to identify arrhythmias ischemic heart disease right and left ventricular hypertrophy,presence of conduction delay or abnormalities
Although these findings are not specific to the diagnosis of heart failure ,a normal ECG virtually excludes left ventricular systolic dysfunction
Electrocardiagram(ECG)
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stabilizing the patients’ clinical condition
establishing the diagnosis, etiology, and precipitating factors
initiating therapies to rapidly provide symptom relief
ED MANAGEMENT
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receive oxygenIV lineMonitor heart rate and
rhythmElevate the head of the bedContinuous pulse oximetry
All pts with CHF should
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Relief of pulmonary congestion by reducing preload
Improvement in systemic tissue perfusion by
improving myocardial contractility or
reducing systemic vascular resistance(afterload)
The main objectives are
Diuretics
Vasodilators
inotropes
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nitroglycerin:sublingual,oral or transdermalIV furosemideIf SVT is present ,controlling the ventricular
rate
Rx of mild-to –moderate AHF
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Morphinehelps with the anxiety, distress, and
dyspnea.decreases preload
Diuretics
Rx of severe AHF
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Vasodilatorsare recommended as first-line therapy for
patients with acute heart failure in the absence of hypotension in addition to diuretic therapy for relief of symptoms.
Vasodilators will decrease preload, afterload, or both.
Rx of severe AHF
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Nitratesare potent venodilators. decrease preload, therefore decreasing LV filling
pressure and relieving shortness of breath. selectively produce epicardial coronary artery
vasodilatation and help with myocardial ischemia. can be used in different forms (sublingual, oral,
transdermal, intravenous). the most common route in acute heart failure is intravenous.
Their use is limited by tachyphylaxis and headache.
Rx of severe AHF
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Sodium nitroprusside a potent arterial and venous vasodilator resulting in a
very efficient decrease of intracardiac filling pressures. requires not only careful hemodynamic monitoring but
also monitoring for cyanide toxicity, especially in the presence of renal dysfunction.
particularly helpful for patients who present with severe pulmonary congestion in the presence of hypertension and severe mitral regurgitation.
The drug should be titrated to off rather than abruptly stopped due to the rebound potential.
Rx of severe AHF
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Oral therapy with ACEI/ARB is usually continued. Adjustment of dose or temporary
withholding may be necessary if hypotension persists and hinders diuresis or if renal functionworsens.
Rx of severe AHF
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Beta-blockersare usually continued in the same
dose or a slightly reduced dose with the exception of the situations requiring intravenous inotropic therapy where they are temporarily stopped.
Usually, beta-blockers are resumed prior to discharge if patient condition allows.
Rx of severe AHF
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If arrhythmia is present and uncontrolled ventricular response is thought to contribute to the clinical scenario of acute heart failure, then either pharmacologic rate control or emergent cardioversion with restoration of sinus rhythm is recommended.
Rx of severe AHF
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If patient is hypotensive, use of either inotropic therapies and/or in addition to continuous hemodynamic monitoring is indicated.
Rx of severe AHF
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Inotropes improve short-term symptoms and hemodynamics in patients with evidence of cardiogenic shock and end-organ dysfunction.
Inotropes are used for hypotensive pts who are unable to tolerate preload and afterload reducing medications.
Rx of severe AHF
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Inotropes Medications includeAn adrenergic agonist
– (dopamine, dobutamine, epinephrine, norepinephrine),
a phosphodiesterase inhibitor (milrinone, enoximone)
a calcium sensitizer (levosimendan)
:Rx of severe AHF
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Dobutamine is a beta-receptor agonist, increases inotropy and chronotropy and
decreases afterload therefore improving end-organ perfusion Doses of 5-10 mcg/kg/min are used although in
the presence of a beta-blocker higher doses may be necessary.
Careful hemodynamic and patient monitoring is required.
Rx of severe AHF
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Dopamine has beta-receptor agonist properties in doses of 5-10
mcg/kg/min and can be used as a positive inotrope. Initiation of it can precipitate arrhythmia due to
inhibition of norepinephrine uptake. Doses of more than 10 mcg/kg/min will produce more
peripheral vasoconstriction via alpha stimulation and can precipitate heart failure.
doses of less than 3 mcg/kg/min, it produces splanchnic vasodilation due to the stimulation of dopaminergic receptors.
Rx of severe AHF
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Milrinone is a phosphodiesterase inhibitor (PDEi) which increases
inotropy, chronotropy and lusitropy acting via cGMP to increase the intramyocardial ATP.
is a vasodilator agent, both veno and arterial, and is used in pts with pulmonary hypertension.
is thought to create less tachycardia since it does not directly stimulate beta-receptors.
0.25 mcg/kg/min ~ 0.75 mc/kg/min. The half-life is 2.4-6 hours
should be adjusted for renal function.
Rx of severe AHF
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mechanical circulatory support intraaortic balloon pump extracorporeal membrane
oxygenator left ventricular assist device
Rx of severe AHF
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Non-invasive ventilation: BiPAP
Endotracheal intubation if severe hypoxemia does not improved by early treatment.
Rx of severe AHF
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Table of contents
1
Acute coronary syndrome2
Acute heart failure3
4
Hypertensive emergencies
Cardiac arrhythmias
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Normal Sinus Rhythm
EKG Characteristics:
Regular narrow-complex rhythm
Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
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Definition:Heart rate <60bpm
seldom symptomatic until the rate drops below 50bpm.Trianed athletes or young healthy individuals may also have a slow resting heart rate. Resting bradycardia is often considered normal if the individual has no other symptoms.
bradycardia
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fatigue, weakness,dizziness, lightheadedness, fainting, mental status changes, syncope, seizures, hypotension, shortness of breath, chest discomfort palpitations and if severe enough,death.
It may cause cardiac arrest in some pts, because those with bradycardia may not be pumping enough oxygen to their heart.
Symptomatic bradycardia
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Cause
Cardiac AMI Vascular heart dz Valvular heart dz Degenerative
primary electrical dz Drug eg.digitalis,β-
blockers,calcium channel blockers,and amiodrone
Non-cardiac Drug abuse: Metabolic or
endocrine issues,especially in the thyroid
Electrolyte imbalance Neurologic factors Autonomic reflexes Sleep apnea Infectious
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sinus bradycardiadisorders of AV conduction
first-degree AV blocksecond-degree AV block :mobitz
type Ⅰ andⅡthird-degree AV block
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Sinus bradycarida
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1st Degree AV Block
EKG Characteristics:
•Prolongation of the PR interval, which is constant
•All P waves are conducted
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Type 1 2nd degree AV block
)
EKG Characteristics:
•Progressive prolongation of the PR interval until a P wave is not conducted.
•As the PR interval prolongs, the RR interval actually shortens
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Type 2 2nd degree AV block
EKG Characteristics: Constant PR interval with intermittent failure to conduct
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3rd Degree (Complete) AV Block
EKG Characteristics:
•No relationship between P waves and QRS complexes
•Relatively constant PP intervals and RR intervals
•Greater number of P waves than QRS complexes
www.uptodate.com
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Airway,breathing,and circulationMonitor,ECGThe urgency and means of treating
depend on how symptomatic the dysrhythmia is .Specific drug therapy ORartificial cardiac pacing
ED evaluation &management
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is indicated in any hemodynamically unstable bradycardia that fails to respond to pharmacologic therapy
Temporary pacemakers
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prophylactic emergency cardiac pacing is indicated for pts with AMI in the following :fist-degree AV block with new-onset bundle-
branh blocksecond-degree AV block type Ⅱ third-degree AV blockRBBB with left anterior fascicular block or
left posterior fascicular blockLBBB and placement of a Swan-Ganz
catheter
Temporary pacemakers
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The advantages are its ease and speed of use and the absence of serious side effects.
the disadvantages include an inability to capture in some pts and the discomfort experinced by conscious pts .
Temporary pacemakers
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TACHYCARDIA
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PSVT
• Abrupt onset and termination of the arrhythmia.
• is different as the remaining beats of the arrhythmia (if a P wave is present at all).
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Atrial Flutter
EKG Characteristics:
Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm
Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75 bpm
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Unmasking of Flutter Waves
In the presence of 2:1 AV block, the flutter waves may not be immediately apparent. These can be brought out by administration of adenosine.
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Atrial Fibrillation
Atrial fibrillation is important because it can lead to:
Hemodynamic compromise;Systemic embolization;
Absent P waves
Presence of fine “fibrillatory” waves which vary in amplitude and morphology
Irregularly irregular ventricular response
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Ventricular tachycarida
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torsade
a rapid, polymorphic ventricular tachycardia with a characteristic twist of the QRS complex around the isoelectric baseline
CharacteristicsRotation of the heart's electrical axis by at least 180ºProlonged QT intervalsPreceded by long and short RR-intervalsTriggered by an early PVC (R-on-T PVC)
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Ventricular fibrillation
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Step 1 be prepared for a cardiac arrest
Be prepared for clinical deterioration in any pt presenting with an acute tachydysrhythmia. A defibrillator and advanced airway equipment should be ready at the bedside
ED evaluation
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Step 2 determine stabilityUnstable is defined as a heart rate and
BP inadequate to maintain vital orgen perfusion and function ,manifested clinically by significant chest pain,pulmonary edema,altered mental status, syncope or severe ypotension.
Electrical cardioversion should be used to treat unstable pts
ED evaluation
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Step 3 determine the rateThe more extreme the ventricular rate,the
more likely the pt is to become unstable
ED evaluation
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Step 4 determine the QRS complex widthNarrow-complex tachycardias can be assumed to
be supraventricularWide-complex tachycardias are the result of any
ot three distinct pathophysiologic processesThe rhythm orginiated in the ventricle with a block conduction below the AV node(BBB)The origin of the tahycardia is supraventricular ,but
there is an accessory conduciton pathway that bypasses the normal conduction pathway
ED evaluation
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Step 5 assess the regularity of the RR intervalsAn irregular narrow-complex
tahcycardia is usually caused by atrial fibrillaiton.
Step 6 determine the presence or absence of P waves
ED evaluation
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If bradycardia produces signs and symptoms of poor perfusion(eg, acute altered mental status, ongoing severe ischemic chest pain,congestive heart failure, hypotension, or other signs of shock) that persist despite adequate airway and breathing, prepare to provide pacing.
For symptomatic high-degree(second-degree or third-degree) atrioventricular (AV) block, provide transcutaneous pacing without delay.
The most important
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If the tachycardic patient is unstable with severe signs and symptoms related to tachycardia, prepare for immediate cardioversion.
Know when to call for expert consultation regarding complicated rhythm interpretation, drugs, or management decisions.
The most important