Cardiovascular Emergencies

Cardiovascular Emergencies

LIN LING

ED ， ICU

SIR RUN RUN SHAW HOSPITAL

LIN LING

ED ， ICU


SIR RUN RUN SHAW HOSPITAL 2/41

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Acute coronary syndrome2

Acute heart failure3

4

Hypertensive emergencies

Cardiac arrhythmias


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4


Cardiac arrhythmias


Hypertensive emergency is defined as the acute and progressive

decompensation of damage of vital organ function caused by an elevated blood pressure

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.

CONCEPT

No degree of hypertension by itself defines an emergency

No degree of hypertension by itself defines an emergency


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


Hypertensive encephalopathyAccelerated malignant hypertensionCerebrovascular accidents

stroke

Cardiovascular crisis Pulmonary edema Heart failure

Renal crisesOther emergencies

Preeclampsia/eclampsia



A-B-Caccurate measurements of

BPHistoryPEDiagnositc studies

ED EVALUATION


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


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


Directed toward identifying signs of target organ damage

funduscopic examinationretinal hemorrhage or papilledema is

sufficient to diagnose accelerated malignant hypertension

Cardiovascular Neurologic :

PE


Based on the pt’s symptomsCXRHead CTECGUrine screen and Serume

cratinine

Diagnostic studies


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


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


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


Rapid onsetRapid maximal effectRapid offset Easy titrationof BP

The ideal drug


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


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


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.


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


SAH Nimodipine decreases

vasospasm that occurs due to chemical irritation of arteries by blood.

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.

SPECIFIC TREATMENT


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


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


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


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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Cardiac arrhythmias


Is a spectrum of myocaridal ischemia , which most often due to disruption of vulnerable atherosclerotic plaques,

IncludingUANSTEMISTEMI

Acute coronary syndrome


PATHOPHYSIOLOGY OF ACS动脉粥样硬化斑块的破裂和腐蚀Disruption of vulnerable plaques



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


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


Cardiac biomarkers

CKMB

Troponin

myosin


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



Pre-hospital

Every pts with chest pain should initially be assumed that the pain is ischemic in origin.——ACS suspected


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


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


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


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


UA/NSTEMI


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


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


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


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


ER managementPharmacoligical therapy ：

Anti-platelet （ aspirin,clopidogrel)

anticoagulants(heparin,LMWH ）

anti-ischemic nitrates 、 β-blockers 、 Ca-

A 、 ACEIstatins

Management of NSTEMI/UA

48


NO benefit of fibrinolytic therapy in UA/NSTEMI pts was clealy demonstrated.

NO FIBRINOLYSIS!!

49


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


ECGDifferentiate diagnosisReperfusion therapyPost-MI complications

STEMI


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


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


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


posterior STEMI


Extensive-Anterial AMI


Inferior infaction


Cause of ST elevation


Differential diagnosis of ST-elevation

Acute pericrditisAcute myocarditisHyperkalemiaBrugada syndromeARVDMassive PEAcute aortic dissectionSAHLV aneurysmEarly repolarization/normal variant


90min球囊扩张

溶栓

Increasing loss of myocyteIncreasing loss of myocyte


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


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


Strategies for reperfusion

FibrinolysisPre-hospital In-hospital

PCIPrimary PCIFacilitated PCIRescue PCI

CABG


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


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


Relative contraindications

Transient ischaemic attack in preceding 6 months

Oral anticoagulant therapyPregnancy Refractory hypertension(>180/110mmHg)Advanced liver diseaseInfective endocarditisActive peptic ulcerCPR>10min


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


Failure to reperfuse

<50% reduction in ST↑at 60min after fibrinolysis

Ongoing symptoms(beware masking effect of analgesics), arrhythmia, haemodynamic instability


ConservativeRepeat fibrinolysisRescue PCI

Options(REACT ）


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)


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


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


Post-MI complications

Cardiogenic shockFail to reperfuse(15%)Post-infarct anginaRe-infarction(30%at 3 mo)VSDSevere MR


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Cardiac arrhythmias


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


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


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


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


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


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


Pulmonary edema


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)


stabilizing the patients’ clinical condition

establishing the diagnosis, etiology, and precipitating factors

initiating therapies to rapidly provide symptom relief

ED MANAGEMENT


receive oxygenIV lineMonitor heart rate and

rhythmElevate the head of the bedContinuous pulse oximetry

All pts with CHF should


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


nitroglycerin:sublingual,oral or transdermalIV furosemideIf SVT is present ,controlling the ventricular

rate

Rx of mild-to –moderate AHF


Morphinehelps with the anxiety, distress, and

dyspnea.decreases preload

Diuretics

Rx of severe AHF


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


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


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


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


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


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


If patient is hypotensive, use of either inotropic therapies and/or in addition to continuous hemodynamic monitoring is indicated.

Rx of severe AHF


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


Inotropes Medications includeAn adrenergic agonist

– (dopamine, dobutamine, epinephrine, norepinephrine),

a phosphodiesterase inhibitor (milrinone, enoximone)

a calcium sensitizer (levosimendan)

: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.

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.

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.

Rx of severe AHF


mechanical circulatory support intraaortic balloon pump extracorporeal membrane

oxygenator left ventricular assist device

Rx of severe AHF


Non-invasive ventilation: BiPAP

Endotracheal intubation if severe hypoxemia does not improved by early treatment.

Rx of severe AHF


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Cardiac arrhythmias


Normal Sinus Rhythm

EKG Characteristics:

Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave


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


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


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


sinus bradycardiadisorders of AV conduction

first-degree AV blocksecond-degree AV block :mobitz

type Ⅰ andⅡthird-degree AV block


Sinus bradycarida


1st Degree AV Block


•Prolongation of the PR interval, which is constant

•All P waves are conducted


Type 1 2nd degree AV block

)


•Progressive prolongation of the PR interval until a P wave is not conducted.

•As the PR interval prolongs, the RR interval actually shortens


Type 2 2nd degree AV block

EKG Characteristics: Constant PR interval with intermittent failure to conduct


3rd Degree (Complete) AV Block


•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


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


is indicated in any hemodynamically unstable bradycardia that fails to respond to pharmacologic therapy

Temporary pacemakers


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



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 .





TACHYCARDIA


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).


Atrial Flutter


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


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.


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


Ventricular tachycarida


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)


Ventricular fibrillation


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


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


Step 3 determine the rateThe more extreme the ventricular rate,the

more likely the pt is to become unstable

ED evaluation


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


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




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


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


Lin Ling E-mail [email protected]

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Cardiovascular Emergencies