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Cardiovascular
Emergencies
LIN LING
ED,ICU
SIR RUN RUN SHAW HOSPITAL
Table of contents
1
Hypertensive emergencies
2
Acute coronary syndrome
3
Acute heart failure
4
Cardiac arrhythmias
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Table of contents
1
Hypertensive emergencies
2
Acute coronary syndrome
3
Acute heart failure
4
Cardiac arrhythmias
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CONCEPT
Hypertensive emergency
is defined as
the acute and progressive decompensation
of damage of vital organ function caused by
an elevated blood pressure
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CONCEPT
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.
No degree of hypertension by itself
defines an emergency
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Hypertensive urgency
 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 endorgan disease.
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Hypertensive emergencies
 Hypertensive encephalopathy
 Accelerated malignant hypertension
 Cerebrovascular accidents

stroke
 Cardiovascular crisis
Pulmonary edema
 Heart failure

 Renal crises
 Other emergencies

Preeclampsia/eclampsia
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ED EVALUATION
A-B-C
accurate measurements of BP
History
PE
Diagnositc studies
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Accurate measurement of BP
Several separate BP measurements :
 Initially
elevated Bp frequently decrease
spontaneously by a second reading
 Evaluated in both arms
 Seated with the arm at the level of the heart
and the cuff bladder should cover at least
80%of the arm circumference
Base clinical decisions on correctly
measured and repeated BP
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history
Start with the target organ
 Dyspnea,chest
pain,neurologic
complaints ,visual changes
Duration and severity of
preexisting hypertension
The degree of previous success
with BP control
The presence of target organ dz
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PE
Directed toward identifying signs of
target organ damage
funduscopic examination
 retinal
hemorrhage or papilledema is
sufficient to diagnose accelerated malignant
hypertension
Cardiovascular
Neurologic :
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Diagnostic studies
Based on the pt’s symptoms
CXR
Head CT
ECG
Urine screen and Serume
cratinine
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ED Management
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.
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ED Management
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
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ED Management
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.
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The ideal drug
Rapid onset
Rapid maximal effect
Rapid offset
Easy titrationof BP
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PARENTERAL DRUGS
DOSAGE
ONSET/DUR ADV.EFFE
Nitroprusside
0.2510mcg/kg/min
Instant/1-2min.
Thiocyanate,cyani
de poisoning
Nitroglycerine
5-100mcg/min
1-5min/3-5min
Flushing,headach
e,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,1.255MG1Vq6hr
20-30min/6hr
Hypotension,renal
failure,hyperkalemia
Fenoldopam
0.10.3mcg/kg/min
5min/10-15min
Flushing,headache,t
achy
DRUG
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PARENTERAL DRUGS
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.avoidheart failure,asthma
Esmolol
(b-1 selective
blocker)
200-500
mcg/kg/min for
4min,then 150300mcg/kg/min
1-2min/10-20min
Hypotension,avoidheart failure,asthma
Phentolamine
(a1 blocker)
5-15mg iv
1-2min/3-10min
Tachycardia,flushing
,headache
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SPECIFIC TREATMENT
Hypertensive Encephalopathy
 Goal
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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SPECIFIC TREATMENT
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.
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SPECIFIC TREATMENT
SAH
 Nimodipine decreases vasospasm
that occurs due to chemical irritation
of arteries by blood.
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SPECIFIC TREATMENT
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.

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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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Specific Treatment
MI:
 NTG,b-blockers,ACE
Acute LVF:
inhibitors.
 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.
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Specific Treatment
Renal insufficiency:
 is
a cause and effect of high BP.
 Goal is to prevent further renal
damage by maintaining adequate
blood flow.
 Nitroprusside effective.
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Common pitfalls
 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.
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Table of contents
1
Hypertensive emergencies
2
Acute coronary syndrome
3
Acute heart failure
4
Cardiac arrhythmias
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Acute coronary syndrome
Is a spectrum of myocaridal ischemia ,
which most often due to disruption of
vulnerable atherosclerotic plaques,
Including
 UA
 NSTEMI
 STEMI
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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
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DIAGNOSIS
•symptoms
•With or
without ECG
changes
•No cardiac
biomarkers
UA
•symptoms
•ST depression
or T-wave
inversion
•Positive Cardiac
biomarker
•Symptoms
•ST-elevation
•Positive Cardiac
biomarker
STEMI
NSTEMI
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symptoms
Ischemic chest pain/chest discomfort

Chest Pain,tightness,or heaviness,pain that
radiates to neck,jaw,teeth,shoulders,back
 Others
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 necrosis
High 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)
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MONA




Oxygen,SpO2>90%
ASA 162~325mg
NTG
Morphin:chest pain
not relieved
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Chest pain suspected ACS
Transfer
history,PE
ER
12-lead ECG
10 min
Cardiac marker
ACS
NONCARDIAC
DZ
STABLE
ANGINA
NON-ST ELEVATION
NSTEACS
Troponin
NORNAL
UA
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RECHECK IN
10~15MIN
Troponin
ELEVATION
recheck
in 6 hrs
NSTEMI
ST-ELEVATOIN
STEMI
TIME IS MYOCARIDIUM!TIME IS LIFE!
symptoms
door
Call for
help
patient
transfer In
thrombolysis
ED
reperfusion
PCI
goal
10min
30min
D-N 30min
D-B 90min
Pt education
ECG ACS
PCI team
Prehospital
protocol
SIRcare
RUN RUN SHAW HOSPITAL
UA/NSTEMI
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Three principal presentation of UA
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1997/2001
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Although in-hospital mortality of STEMI is high,
1-year mortality of NSTEM is equivalent to STEMI
1
STEMI与NSTEMI比较的 1 年累积死亡率
生存率
NSTEMI
0.9
STEMI
0.8
0.7
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
after ACS (mo)
Courtesy A Gitt
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EARLY RISK STRATIFICATIONS
OF UA/NSTEMI
Selection of the site of care
 Coronary
care unit
 Step-down unit
 Outpatient setting
Selection of the therapy
 Invasive
managemnt strategy
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Risk stratification of UA/NSTEMI
High risk
At least 1 of
the following
features
Intermediate risk
At least 1 of the
following
Accelerating of
Prior MI,
ischemic
peripheral or
非ST段抬高的AMI的危险性分层
symptoms in
cererovascular
preceding 48h dz,or CABG,prior
ASA use
Prolonged
Prolonged(>20min)
ongoing(greate
rest angina,now
Character r than 20min)
resolved,with
of pain
rest pain
moderate or high
likelihood of CAD
Low risk
history
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SHAW HOSPITAL
标准不一致时以最高为准
Incrased angina
frequency,severit
y or duration
New onset angina
46
Risk stratification of UA/NSTEMI
Clinical
findings
ECG
Cardiac
markers
High risk
Pulmonary edema,
new or worsening
MR murmur,
,hypotension,>75ys
Age greater than
70ys
Angina at rest with
transient STchanges, new
BBB,sustained VT
Unchanged
T-wave changes, ECG
pathological Q
waves
Elevated cardiac
biomarkers
Moderate risk
Slightly
elevated(eg.
Low risk
normal
0.1>cTnT>0.01ug/l
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Management of NSTEMI/UA
 ER management
 Pharmacoligical therapy:
 Anti-platelet(aspirin,clopidogrel)
 anticoagulants(heparin,LMWH)
 anti-ischemic
nitrates、β-blockers、Ca-A、ACEI
 statins
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NO FIBRINOLYSIS!!
NO benefit of fibrinolytic therapy in
UA/NSTEMI pts was clealy demonstrated.
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Early invasive strategy in UA/NSTEMI
is indicated in
UA/NSTEMI pts who have refractory
angina
Hemodynamic or electrical instability ;
High risk pts and ineffective with
pharmacologic therapy
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STEMI
ECG
Differentiate diagnosis
Reperfusion therapy
Post-MI complications
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Information from the ECG
Diagnosis
 Is
the ST elevation requiring reperfusion Rx?
Prognosis
 Infarct
size
 How many mm ST elevation?
 How many leads show ST elevation?
 Infarct
location
Complications
 arrhythmia
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STEMI –ECG Treatment Criteria
ST elevation
in 2 continuous leads V1~V3 or
 > 0.1mV in at least 2 continuous other leads
 >0.2mV
LBBB
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ECG-localize infarct territory
Antero-septal(LAD):V1-3
Anterior wall(LAD):V1-6, Ⅰ、aVL
Inferior(RCA):Ⅱ、Ⅲ、aVF
Posterior(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 pericrditis
Acute myocarditis
Hyperkalemia
Brugada syndrome
ARVD
Massive PE
Acute aortic dissection
SAH
LV aneurysm
Early repolarization/normal variant
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球囊扩张
90min
溶栓
Increasing loss of myocyte
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Immediate management
Aspirin 300mg to chew
If age <75,clopidogrel 300mg
Oxygen by mask esp if SpO2
<90%,LVF,shock
Morphine 4-8mg iv ot achieve analgesia
IV NTG or beta blocker for analgesis,↓
BP and ↓ischaemia
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Indication of reperfusion
For pts with STEMI within 12h after
symptom onset and with persistent STelevation or new LBBB,early PCI or
pharmacological reperfusion should be
performed
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Strategies for reperfusion
Fibrinolysis
 Pre-hospital
 In-hospital
PCI
 Primary
PCI
 Facilitated PCI
 Rescue PCI
CABG
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Fibrinolytic Medications
med
dose
usage
90min
reperfusion
rate
StreptoKi
nase
1.5mil U
30-60min iV
55-64%
1.5-2mil U
60min iv
31-55%
15mg bolus
iv
82-87%
0.75mg/kg
30min iv
0.5mg/kg
60min iv
UroKinase
rtPA
Up to 100mg
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Absolute contraindications
 Haemorrhagic stroke or SAH
 Ischaemic stroke in preceding 3months
 Central nervous system trauma or neoplams
 Recent major trauma/surgery/head injury with
preceding 3 wks
 Gastrointestinal bleeding within the last month
 Known bleeding disorder
 Aortic dissection
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Relative contraindications
 Transient ischaemic attack in preceding 6 months
 Oral anticoagulant therapy
 Pregnancy
 Refractory hypertension(>180/110mmHg)
 Advanced liver disease
 Infective endocarditis
 Active peptic ulcer
 CPR>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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Options(REACT)
Conservative
Repeat fibrinolysis
Rescue PCI
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PCI(Percutaneous coronary interventions)
Primary PCI
 Angioplasty
and /or stenting without prior or
concomitant fibrinolytic therapy
Facilitated PCI
 Pharmacologic
reperfusion treatment
delivered prior to a planeed PCI in order to
bridge the PCI-related time delay
Rescue PCI
 PCI
performed on a coronary artery which
remains occluded despite fibrinolytic therapy
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PCI of door-to-balloon and mortality
20%
16%
12%
死亡率
8%
4%
0%
<60min
61-75min 76-90min
>90min
no PCI
Time to PTCA 30day mortality
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PCI and fibrinolytic therapy
mortality
p<0,05
p<0.02
n=645
mortality (%)
12,0
6,5
5,1
2,6
Gibbons R.J.,N.Engl.J.Med.(1993)328:685
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Post-MI complications
Cardiogenic shock
Fail to reperfuse(15%)
Post-infarct angina
Re-infarction(30%at 3 mo)
VSD
Severe MR
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Table of contents
1
Hypertensive emergencies
2
Acute coronary syndrome
3
Acute heart failure
4
Cardiac arrhythmias
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INTRODUCTION
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.
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CLINICAL PRESENTATION
Due to excess fluid accumulaiton
Left HF
Rihgt HF
Dyspnea
Orthopnea
Paroxysmal
nocturnal
dyspnea
Cardiac
asthma
Edema
hepatic
congestion
Ascites
Nocturia
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Due to reduction
in cardiac output
Fatigue
weakness
altered mental
state
 low BP
Acute pulmonary edema
 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.
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NYHA Class

I :No symptoms and no limitation in ordinary physical
activity
II: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.
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Imaging---Echocardiography


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.
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Chest X-rays
 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.
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Pulmonary edema
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Electrocardiagram(ECG)
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
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ED MANAGEMENT
 stabilizing
the patients’ clinical condition

establishing the diagnosis, etiology, and
precipitating factors

initiating therapies to rapidly provide
symptom relief
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All pts with CHF should
receive oxygen
IV line
Monitor heart rate and rhythm
Elevate the head of the bed
Continuous pulse oximetry
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The main objectives are
 Relief of pulmonary
congestion by reducing
preload
 Improvement in systemic
tissue perfusion by
improving myocardial
contractility or
 reducing systemic
vascular
resistance(afterload)

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Diuretics
Vasodilators
inotropes
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Rx of mild-to –moderate AHF
nitroglycerin:sublingual,oral or transdermal
IV furosemide
If SVT is present ,controlling the ventricular
rate
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Rx of severe AHF
Morphine
 helps
with the anxiety, distress, and dyspnea.
 decreases preload
Diuretics
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Rx of severe AHF
Vasodilators
 are
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.
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Rx of severe AHF
 Nitrates
 are 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.
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Rx of severe AHF
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.
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Rx of severe AHF
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.

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Rx of severe AHF
Beta-blockers
 are
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.
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Rx of severe AHF
 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.
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Rx of severe AHF
If patient is hypotensive, use of either
inotropic therapies and/or in addition to
continuous hemodynamic monitoring is
indicated.
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Rx of severe AHF
Inotropes improve short-term symptoms
and hemodynamics in patients with
evidence of cardiogenic shock and endorgan dysfunction.
Inotropes are used for hypotensive pts
who are unable to tolerate preload and
afterload reducing medications.
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:
Rx of severe AHF
Inotropes
Medications include
An adrenergic agonist
– (dopamine, dobutamine, epinephrine,
norepinephrine),
a phosphodiesterase inhibitor (milrinone,
enoximone)
 a calcium sensitizer (levosimendan)
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Rx of severe AHF
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.
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Rx of severe AHF
 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.

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Rx of severe AHF
 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.

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Rx of severe AHF
mechanical circulatory support
 intraaortic
balloon pump
 extracorporeal membrane
oxygenator
 left ventricular assist device
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Rx of severe AHF
Non-invasive ventilation: BiPAP
Endotracheal intubation if severe
hypoxemia does not improved by
early treatment.
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Table of contents
1
Hypertensive emergencies
2
Acute coronary syndrome
3
Acute heart failure
4
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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bradycardia
 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.
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Symptomatic bradycardia
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.
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Cause
Cardiac
 AMI
 Vascular heart dz
 Valvular heart dz
 Degenerative primary
electrical dz
 Drug eg.digitalis,βblockers,calcium
channel blockers,and
amiodrone
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Non-cardiac
 Drug abuse:
 Metabolic or endocrine
issues,especially in the
thyroid
 Electrolyte imbalance
 Neurologic factors
 Autonomic reflexes
 Sleep apnea
 Infectious
sinus bradycardia
disorders of AV conduction
 first-degree
AV block
 second-degree AV block :mobitz
type ⅠandⅡ
 third-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:
www.uptodate.com
•No relationship between P waves and QRS
complexes
•Relatively constant PP intervals and RR intervals
•Greater number of P waves than QRS complexes
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ED evaluation &management
Airway,breathing,and circulation
Monitor,ECG
The urgency and means of treating depend
on how symptomatic the dysrhythmia is .
 Specific
drug therapy OR
 artificial cardiac pacing
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Temporary pacemakers
is indicated in any hemodynamically
unstable bradycardia that fails to respond
to pharmacologic therapy
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Temporary pacemakers
 prophylactic emergency cardiac pacing is
indicated for pts with AMI in the following :
 fist-degree AV block with new-onset bundlebranh block
 second-degree AV block type Ⅱ
 third-degree AV block
 RBBB with left anterior fascicular block or left
posterior fascicular block
 LBBB and placement of a Swan-Ganz
catheter
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Temporary pacemakers
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 .
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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
Characteristics
Rotation of the heart's electrical axis by
at least 180º
Prolonged QT intervals
Preceded by long and short RR-intervals
Triggered by an early PVC (R-on-T PVC)
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Ventricular fibrillation
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ED evaluation
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
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ED evaluation
Step 2 determine stability
 Unstable
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
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ED evaluation
Step 3 determine the rate
 The
more extreme the ventricular rate,the more
likely the pt is to become unstable
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ED evaluation
Step 4 determine the QRS complex width
 Narrow-complex
tachycardias can be assumed to
be supraventricular
 Wide-complex tachycardias are the result of any
ot three distinct pathophysiologic processes
The 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
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ED evaluation
Step 5 assess the regularity of the RR
intervals
 An
irregular narrow-complex tahcycardia
is usually caused by atrial fibrillaiton.
Step 6 determine the presence or
absence of P waves
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The most important
 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.
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The most important
 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.
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Lin Ling E-mail [email protected]
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