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CARDIOVASCULAR EMERGENCIES

Erwin Azmar
Cardiology Division Dept of Internal Medicine
Faculty of Medicine University of Sriwijaya
2016
Cardiovascular emergencies

Life-threatening
Immediately recognized
Avoid delayed treatment
Minimize morbidity and mortality
Cardiac anatomy

9. Right Atrium
1.Left Anterior Descending
10. Right Ventricle
2.Left Circumflex
11. Left Atrium
3.Superior Vena Cava
12. Left Ventricle
4.Inferior Vena Cava
13. Papillary Muscles
5.Aorta
14. Chordae Tendineae
6.Pulmonary Artery
15. Tricuspid Valve
7.Pulmonary Vein
16. Mitral Valve
8.Right Coronary
17. Pulmonary Valve
Aortic Valve (Not pictured)
Etiology and underlying diseases
Congenital heart diseases
Valvular heart diseases
Hypertensive heart disease
Coronary artery disease
Cardiac dysrhythmia
Trauma, myopathy, infection, tumor, toxin
Vascular diseases
Systemic diseases
Diagnostic
History : chest pain, shortness of breath,
palpitation, racing heart beat, syncope, dizziness,
epigastric pain, leg pain, vomitus, convulsion,
numbness.
Physical exam : BP HR RR PR consciousness,
Temperature, pallor, sweating, heart sounds,
pulmonary sounds, JVP, pulsation, struma, vessel
dilation.
Modalities : ECG, Echo, Imaging, Blood, cardiac
biomarkes, urinalysis.
Acute cardiac emergencies
Cardiac arrest : anaphylactic, electrocution, hypothermia, drug overdose,
pregnancy
Cardiogenic shock
Peri-arrest arrhythmia : bradycardia, broad-complex tachycardias, narrow
complex tachycardias
Cardiac tamponade : pericardial effusion
Valve and Septal Rupture : after AMI, trauma
Sinus of valsava rupture : congenital aneurysm, infective endocarditis
Acute aortic dissection
Acute prosthetic valve rupture
ACS
Acute cardiac failure
Hypertensive emergency
Vascular thrombosis
Emergency cardiological procedures

Central venous access


Pulmonary artery catheterization
Temporary cardiac pacing
Pericardial aspiration
Intra aortic ballon pump insertion
Intra Aortic Balloon Pump
Indications for IABP therapy
Increase coronary artery
perfusion Reduction in afterload

Refractory unstable angina Ventricular failure


Impending infarction unresponsive to
Acute myocardial infarction pharmacological therapy
Support during PCI Cardiogenic shock
Complications post myocardial Post-surgical myocardial
infarction (VSD, papillary muscle dysfunction/low cardiac
rupture, acute mitral regurgitation) output syndrome
Myocardial contusion Bridge to cardiac
Ischaemia related intractable transplantation
ventricular arrhythmias Bridge to other form of
Bridge to cardiac surgery circulatory support
Cardiac pacing
Central venous accsess
Pulmonary artery catheterization
Pericardial aspiration
CARDIOGENIC SHOCK
Cardiogenic Shock

Hypotension and end-organ hypoperfusion as a result


of low cardiac output
Most common COD after presentation of MI
Occurs in 5% to 8% with STEMI, 2,5% Non STEMI
Incidence of CS has decreased only slightly over time
Mortality rate remains high at near 50%
Etiology

CS after an MI secondary to severe LV dysfucntion


Acute hemodynamic collapse (rupture)
Iatrogenic inappropriate administration of
medications ( Beta-blocker)
Occult hemorrhage due to procedure-related
complication/medication (antithrombotic, antiplatelet,
fibrinolytic)
Differential Diagnosis

Non ischemic and extracardiac


Acute myocarditis ec infection or toxin
Apical balloning syndrome (Takotsubo
cardiomyopathy acute LV dysfunction, as a
response to emotional/physical stress)
Acute aortic dissection, coronary artery dissection,
aortic rupture, tamponade
Myocardial depression ec septic shock
Pathogenesis
Predominant LV failure (SBP < 90 mmHg, normal to
elevated LV filling pressure, evidence of end-organ
hypoperfusion )
RV failure (infarction of territory supplied by cute
marginal branches of RCA ( hypotension, clear lung
fields, bradyarrhytmic complication)
MR
Ventricular Septal Rupture
Free Wall Rupture
Pathophysiology
Clinical Presentation
Derive from underlying pathophysiology
Chest pain, nausea, emesis,restlessness, agitation
Cool and clammy peripheries
Decreased of urine output
Mental status changes
Pulmonary edema,dyspnea, tachypnea, bilateral
rales,respiratory failure
Clinical Presentation
Hemodynamic collapse
Diffuse point of maximal impulse
Loud S3 gallop, elevated JVP
Rales
New holosystolic murmupresence of cardiac
tamponade
Diagnostic Approach

Clinical signs and symptoms of CS


Echocardiography
Management and Therapy
Optimum treatment ( to stabilize oxygenation, BP
and rhythm while proceeding urgently to coronary
angiography )
Hemodynamic monitoring with SGC
IABP (creates a vacuum effect during systole
reduces afterload on LV, augment DBP increase
coronary perfussion pressure )
Early reperfusion of occluded coronary artery
Avoiding treatmen errors
Future Directions

Persistent shock Poor prognosis


Adequate CO prevent end-organ dysfunction
Cardiac tranplantation
Mechanical support (devices implanted
percutaneously)
Stem cell therapy
Cardiac dysrhythmia
Dis- /Arrhythmias :

Disorders of the regular rhythmic beating the heart.


Common 2.2 million Americans are living with AF
(one type of rhythm problem).
Can occur in a healthy heart and be of minimal
consequence.
Also may indicate a serious problem and lead to
heart disease, stroke or sudden cardiac death.
The goal : ultimately reduce disability and death from
heart disease and stroke.
Causes
Common : heart disease, high BP, DM, smoking,
excessive alcohol or caffeine, drug abuse, stress
Scarring most commonly, from a previous heart
attack disrupt the initiation or conduction of
electrical impulses.
In a healthy person with a normal, healthy heart, a
sustained arrhythmia to develop caused by outside
trigger: an electrical shock or the use of illicit drugs.
Any pre-existing structural heart condition
can lead to arrhythmia development due to:
Inadequate blood supply.

It can alter the ability of heart tissue including


the cells that conduct electrical impulses to
function properly.

Damage or death of heart tissue.


This can affect the way electrical impulses spread in
the heart.
These pre-existing heart conditions may
include:

Coronary artery disease (CAD).


Cardiomyopathy.

Valvular heart diseases.


Complications
Stroke.
When your atrial chambers fibrillate, they're unable
to pump blood effectively. Stagnant blood in the atria
can form blood clots. If a clot breaks loose, it can
travel to and obstruct a brain artery, causing an
ischemic stroke. This may damage or kill a portion of
your brain or lead to death.

Congestive heart failure.


This can result if your heart is pumping ineffectively
for a prolonged period due to a bradycardia or
tachycardia, such as AF. Sometimes, controlling the
rate of an arrhythmia that's causing CHF can lead to
improved heart function.
SUMMARY
Ventricular Arrhythmias
Rules of Malignancy for PVCs :

Frequent PVCs
Consecutive PVCs
Multiform PVCs
R-on-T phenomenon
Any PVC occurring during an acute
myocardial infarction (or in any patient with
underlying heart disease)
RBBB

Sinus rhythm with a normal PR interval


RSR1 pattern in V1
The dominant R wave is characteristic of RBBB, and does not
indicate RV hypertrophy
Wide and slurred S wave in V6
LBBB

Sinus rhythm
Broad QRS complexes with notch in the R wave in I, VL, V5, V6
Inverted T waves are associated with bundle branch block, and
have no other significance.
Acute coronary syndrome
Hypertensive crise
Clinical Vignette
65 y/o M with past medical history of Type II DM (on oral
hypoglycemics), presenting with headache, chest pain and
shortness of breath that developed after lunch the day of
admission; non-exertional; no alleviating factors.
Physical Exam:
Vitals: 37.3, 195/125, 92, 24, 93% on RA
HEENT: Decreased A:V on retinal exam (<25%)
Heart: S4 heard on exam, no m/r/g
Lungs: mild resp distress, otherwise clear to auscultation

Whats the diagnosis and next best step in management?


Definitions:
Hypertension:
Stage I: 140-159/90-99
Stage II: >160/100

Hypertensive Urgency:
Systolic
BP >180 or Diastolic BP >120 in the absence
of end-organ damage
Definitions Continued:
Hypertensive Emergencies:
SBP>180 OR DBP>120 in the presence of end-organ
damage
Malignant Hypertension: End-organ damage--eyes, kidneys,
brain (hemorrhage/infarct) affected
Hypertensive encephalopathy: Cerebral edema leading to
neurological symptoms
Signs and Symptoms:
Hypertensive Urgency:
Can be completely asymptomatic
Some symptoms include:
Severe headache
Shortness of breath
Nosebleeds
Severe anxiety
Signs:
Elevated BP on consecutive readings
S&S Continued
Hypertensive Emergencies
Symptoms:
nausea, vomiting (cerebral edema)
Chest Pain
SOB
Blurry vision
Confusion
Loss of consciousness
Signs:
Retinal hemorrhages, exudates, or papilledema
Renal involvement (malignant nephrosclerosis) with AKI,
proteinuria, hematuria
Cerebral edema seizures and coma

Pulmonary Edema

Myocardial Infarction

Hemorrhagic Stroke, lacunar infarcts


Treatment Options
Hypertensive Urgency:
Goal: Reduce BP to <160/100 over several hours to
day
Elderly at high risk of ischemia from rapid reduction of BP,
therefore slower reduction in BP in this patient population
Previously treated hypertension:
Increase dose of existing med or add another med
Reinstitution of med in non-compliant patients
Treatment continued
Hypertensive Urgency continued:
Previously untreated hypertension:
Slowreduction of BP (one to two days): Amlodipine,
Metoprolol XL, lisinopril (po anti-hypertensives usually
enough)
Experts recommend: Initiate two agents or a combination
agent (one being a thiazide diuretic)
Rationale: Most patients with BP >20/10 above goal will require
two agents to control their BP
Treatment Continued
Hypertensive Emergency:
Goal: Lower Diastolic BP to approximately 100-105 over 2-
6 hours; max initial fall not to exceed 25%
More aggressive decrease can lead to ischemic stroke and
myocardial ischemia
If focal neurological sx presentobtain MRI to r/o acute
stroke (rapid BP correction contraindicated)
Parenteral antihypertensives (IV Drip) recommended over
oral agents in hypertensive emergency
Treatment
Recommended parenteral antihypertensive agents
(IV drip) for Hypertensive Emergencies and
admission to ICU
Nitroprusside (cautious about cyanide toxicity),
Nicardipine, and Labetalol.
Once BP controlled, switch to oral anti-hypertensives
and follow-up closely
Summary
Hypertensive Crises are common
Differentiate Hypertensive Urgency from Emergency
on the basis of end-organ damage
Can treat hypertensive urgency with oral
antihypertensives, but parenteral medications
required for hypertensive emergencies
25% reduction in diastolic BP over 2-6 hours for
hypertensive emergencies
Dont forget to start Oral antihypertensives and
follow-up closely!
Heart failure
DEFINITION
The situation when the heart is
incapable of maintaining a cardiac
output adequate to accommodate
metabolic requirements and the
venous return."
E. Braunwald
PUMP
DYSFUNCTION MYOCARDIAL
HORMONAL REMODELING

CIRCULATORY NEUROREGULATORY
CYTOKINE
INSUFFICIENCY

HEART FAILURE
PATHOPHYSIOLOGY
Heart Failure is a Dropsical Condition with
Generalized Edema from Fluide Retention.
Heart Failure is Due to a Central Cardiac Pump inadequacy.
Heart Failure is Precipitated by Decompansated Ventricular
Hypertrophy.
Heart Failure is due to Circulatory Dysfunction.
Heart Failure is an Endocrinopathy.
Heart Failure is a Fever
DIAGNOSIS

HISTORY.
PHYSICAL EXAMINATION.
APPROPRIAT INVESTIGATION.
1. SYMPTOMS OF HEART FAILURE(AT REST OR DURING EXERCISE).
2.Objective evidence of cardiac dysfunction.
3.Response to treatment directed towards heart failure.
CRITERIA FOR CONGESTIVE HEART FAILURE

MAJOR CRITERIA MINOR CRITERIA


1.Paroxysmal nocturnal dyspnea 1.Ankle edema.
or orthopnea. 2.Night cough.
2.Rales. 3.Dyspnea on exertion.
3.Cardiomegaly. 4.Pleural effusion.
4.Acute pulmonary edema. 5.Vital capacity decreased 1/3 from
5.S3 Gallop. maximum.
6.Increased venous pressure>16 cm of 6.Tachycardia (rate>120/min).
water.
MAJOR OR MINOR
7.Circulation time>25 sec.
Weight loss>4.5 Kg in 5 days in
8.Hepatojugular reflux. response to treatment.
Symptomatic classification of exercise tolerance
New York Heart Association (NYHA)

NYHA Class I: No complaints under


heavy physical load.
NYHA Class II: Complaints under
heavy physical load.
NYHA Class III: Complaints under light
physical load.
NYHA Class IV : Complaints at rest.
Descriptive terms in heart failure

Acute vs Chronic heart failure.

Systolic vs Diastolic.

Right vs Left heart failure.


Etiology of Chronic Heart Failure

It is important to know the etiology


of heart failure.
Look for other diseases that may an important
influence on management of heart failure.
Identify potentially reversible exacerbatiry factor.
Causes of ChronicHeart Failure

Systolic dysfunction:
Coronary artery disease.
Hypertension.
Dilated Cardiomyopathy.
Myocarditis.
Causes of Chronic Heart Failure cont.

Diastolic Dysfunction:
Coronary artery disease.
Systemic Hypertension.
Diabetis Mellitus.
Aortic stenosis.
Hypertrophic cardiomypathy.
Infiltrative cardiomypathy
Endocardial fibrosis.
Normal aging process.
Causes of worsening Heart Failure
Non- cardiac:

Non compliance to the prescribed


regimen(salt,liquid,medication).
Recently co-prescribed drugs
(antiarrhythmic,beta-blockers,non steroidal anti-
inflmatory drugs,verapamil,diltiazem).
Renal dysfunction.
Infection.
Pulmonary embolism.
Thyroid dysfunction.
Anemia.
Alcohol abuse.
Causes of worsening Heart Failure cont.
Cardiac:

Atrial fibrillation.
Other supraventricular or ventricular arrhythmias.
Bradycardia.
Appearance or worsening mitral or ticusped
regurgitation.
Myocardial ischaemia.
Excessive preload reduction(diuretics,ACE inhibitors).
The Heart Failure Milieu :
Clinical Presentation Physical findings
Peripheral edema
Disease Ascites
process Vascular congestion
Jugular venous distension
Rales
Ventricular Tachycardia
dysfunction
Hypotension
Cachexia
Disease-specific findings
Hemodynamic
abnormalities
Physical findings
Azotemia Metabolic
Hyponatremia changes
Hypocalemia Compensatory
Hypomagnesemia mechanisms Symtoms and
Symptoms
Hyperuricemia physical findings Fatique and weakness
Acidosis/alkalosis Dyspnea and fluid
Hypoxia/O2 desaturatuion retention syndromes
Decreased MVO2 Nocturia
Gastrointestinal symptoms
Diminished mentation
The Heart Failure Milieu :
Disease
End-Organ Failure and Death
process
Systemic organ failure
Renal failure
Ventricular Hepatic failure
dysfunction
Respiratory failure
Multi-organ failure
Pulmonary embolism
Hemodynamic Peripheral (cerebral embolism)
abnormalities

Metabolic Death
changes
Compensatory
Sudden
mechanisms End-Organ Death
Failure

Lethal arrhythmia Symtoms and


Electrolyte abnormalities physical findings
Elevated catecholamine levels
Ischemia
Drug-proarrhythmia
Responses to Hemodynamic Overload

Pressure overload Volume overload

Systolic wall stress Diastolic wall stress

Mechanical transducers

Intracellular signals

Ventricular remodeling

Paralel sarcomeres Series sarcomeres

Concentric hypertrophy Normal Eccentric hypertrophy


Evaluation of heart failure patient

Physical
Laboratory
Examination
tests

History

Diagnostic
studies
Assessment of heart failure

Patient history: Physical examination :


Cardiac Cardiac
Pulmonary Pulmonary
Gastrointestinal Abdominal
Renal Neurological
Neuro-psychatric Systemic

Diagnostic studies:
Laboratory tests,ECG,Chest X ray,Echo,Exercise testing,
Cardiac catheterization,Radionuclited studies
Investigation :Laboratory
Complete Blood Count.
Serum electrolytes, blood urea nitrogen,serum creatinine.
Liver function test.
Prothrombin time.
Lipid profile.
Thyroid function test.
Anaemia evaluation.
Arterial blood gases.
Serum drug levels(digoxin,phenytoin).
Atrial natriuretic peptides.
Urin analysis.
Chest X- ray
Other investigation
Transthoracic Echocardiography.
Stress Echo.
Exercise stress testing.
24- hour Holter monitoring.
Nuclear imaging,thallium perfusion scan,cardiac
MRI.
Coronary angiography
Chronic Congestive Heart Failure

EVOLUTION OF
CLINICAL STAGES
NORMAL
No symptoms
Normal exercise
Asymptomatic
Normal LV fxn LV Dysfunction
No symptoms
Normal exercise
Compensated
Abnormal LV fxn CHF
No symptoms Decompensated
Exercise
Abnormal LV fxn CHF
Symptoms
Exercise
Refractory
Abnormal LV fxn CHF
Symptoms not controlled
with treatment
TREATMENT OBJECTIVES

Survival
Morbidity
Exercise capacity
Quality of life
Neurohormonal changes
Progression of CHF
Symptoms
Treatment Options
Non-pharmacological.
General advice and measures.
Exercise and exercice training.
Pharmacological therapy.
Angiotensin-converting enzyme inhibitors(ACI).
Beta-adrenoreceptor antagonists.
Cardiac glycosides.
Diuretics.
Vasodilators(nitrats,hydralazine).
Antiarrhythmic agent.
Anticoagulantion.
Oxyggen.
Divices and surgery.
Revascularization.
Pacemaker.
Implantable cardioverter defibrillator(ICD).
Cadiac trnsplantation.
Ultrafiltration,haemodialysis.
TREATMENT
Correction of aggravating factors

Pregnancy Endocarditis
Arrhythmias (AF) Obesity
Infections Hypertension
Hyperthyroidism Physical activity
Thromboembolism Dietary excess
MEDICATIONS
TREATMENT
PHARMACOLOGIC THERAPY

DIURETICS

INOTROPES

VASODILATORS

NEUROHORMONAL ANTAGONISTS

OTHERS (Anticoagulants, antiarrhythmics, etc)


Normal
TREATMENT
Asymptomatic
LV dysfunction
EF <40%
Symptomatic CHF
ACEI NYHA II Symptomatic CHF
Diuretics mild NYHA - III
Neurohormonal Symptomatic CHF
inhibitors Loop
Diuretics NYHA - IV
Digoxin?
Inotropes
Specialized therapy
Transplant
Secondary prevention
Modification of physical activity
Take Home Messages
Cardiac emergencies is the life threatening
condition
Many etiologies and underlying diseases
Dx base on history, Physical Exam, Additional exam
Management is depend on the etiology
Early Dx and treatment reduce morbidity and
mortality
Reaching Level of competence need a good skill
and knowledge
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