Left Ventricular FailurePathophysiology

Results in increased back pressure into the pulmonary circulation

Causes MI, valvular disease,

chronic hypertension, and dysrhythmias

Right Ventricular FailurePathophysiology

Results in increased back pressure into the systemic venous circulation

Causes Left ventricular

failure Pulmonary

Embolism

Congestive Heart FailurePathophysiology

Reduction in the heart’s stroke volume causes fluid overload throughout the body’s other tissues Starling’s law no longer able to compensate

Manifestation In the acute setting, pulmonary edema,

pulmonary hypertension, or myocardial infarction

In the chronic setting as cardiomegally, left ventricular failure, or right ventricular failure

Field AssessmentCheck ABC’s and manage life threatsChief Complaint

OPQRST Paroxysmal Nocturnal Dyspnea (PND)

Medications: Diuretics Medications to increase cardiac contractile force

Lanoxin Home oxygen

Mental StatusMental status changes indicate impending

respiratory failure Breathing

Signs of labored breathingTripod positioning“Number of pillows”

SkinColor changesPeripheral and/or sacral edema

ComplicationsPulmonary edema may lead to respiratory

failurePulsus paradoxus

Systolic blood pressure drops more than 10 mmHg with inspiration

Pulsus alternans Pulse alternates between weak and strong

ManagementGeneral management:

Avoid supine positioning Avoid exertion such as standing or walking

Maintain the airway Administer oxygen

Administer Nitroglycerine as soon as possible

CPAP

Monitor ECG Establish IV access

Limit fluid administration Consider medication administration:

NitratesAngiotensin-converting enzyme (ACE)

inhibitor Catopril Enalopril

AlbuterolVasopressor

Dopamine Avoid patient refusals if at all

possible

Continuous Positive Airway Pressure (CPAP)Can often prevent

the need for endotracheal intubation and mechanical ventilation

© Scott Metcalfe

Continuous Positive Airway Pressure (CPAP)Maintains a constant pressure within the

airway throughout the respiratory cycle CPAP will force excess fluid out of the alveoli PEEP is applied only during expiration

Use the lowest effective pressure when applying CPAP A pressure of 2.5–5 cm/H2O is adequate

Asthma, COPD, pulmonary edema, CHF, or pneumoniaAwake and able to

follow commands>12 years old and

able to fit the CPAP mask

Able to maintain an open airway

Exhibits two or more of the following A respiratory rate

greater than 25 breaths per minute

SpO2 of less than 94% at any time

Use of accessory muscles during respirations

Any patient who is in respiratory arrest or apnea

Pneumothorax or has suffered trauma to the chest

Tracheotomy Patient who is actively vomiting or

has upper GI bleeding

Epidemiology and PathophysiologyPathophysiology

Result of fluid accumulation between visceral pericardium and parietal pericardium

Increased intrapericardial pressure impairs diastolic filling

Typically worsens progressively until correctedEpidemiology

Acute onset typically the result of trauma or MI Benign presentations may be caused by cancer,

pericarditis, renal disease, and hypothyroidism

Field AssessmentPatient History

Determine precipitating causes Patient relates a history of dyspnea and

orthopneaExam

Rapid, weak pulse Decreasing systolic pressure Narrowing pulse pressures Pulsus paradoxus Faint, muffled heart sounds Electrical alternans

Less than normal voltage in waveforms

ManagementMaintain airwayAdminister oxygenEstablish IV accessConsider medication administration:

Morphine sulfate Nitrous oxide Furosemide Dopamine/dobutamine

Rapid Transport Pericardiocentesis

Pericardiocentesis is the definitive treatment Insertion of a cardiac needle and aspiration of

fluid from the pericardiumProcedure should be performed only if

allowed by local protocolProcedure should be performed only by

personnel adequately trained in the procedure

Hypertensive EmergencyCauses

Typically occurs only in patients with a history of hypertension

Primary cause is noncompliance with prescribed antihypertensive medications

Also occurs with toxemia of pregnancy Incidence

Risk Factors Age-related factors Race-related factors

Field Assessment Initial Assessment

Alterations in mental stateSigns and Symptoms

Headache accompanied by nausea and/or vomiting

Blurred vision Shortness of breath Epistaxis Vertigo Tinnitus

HistoryKnown history of hypertensionCompliance with medications

ExamBP >160/90Signs of left ventricular failureStrong, bounding pulseAbnormal skin color, temperature, and

conditionPresence of edema

ManagementMaintain airwayAdminister oxygenEstablish IV accessConsider medication administration:

Nitroglycerin Sodium nitroprusside (Nipride) Labetalol (Trandate, Normodyne)

PathophysiologyGeneral

Inability of the heart to meet the body’s metabolic needs

Often remains after correction of other problems Severe form of pump failure High mortality rate

Causes Tension pneumothorax and cardiac tamponade Impaired ventricular emptying Impaired myocardial contractility Trauma

Field Assessment Initial AssessmentChief Complaint

Chief complaint is typically chest pain, shortness of breath, unconsciousness, or altered mental state

Onset may be acute or progressiveHistory

History of recent MI or chest pain episode Presence of shock in the absence of trauma

Mental StatusRestlessness progressing to confusion

Airway and BreathingDyspnea, labored breathing, and coughPND, tripod position, accessory muscle

retraction, and adventitious lung sounds ECG

Tachycardia and atrial dysrhythmias Circulation

HypotensionCool, clammy skin

ManagementMaintain airway

CPAPAdminister oxygen Identify and treat underlying problemEstablish IV access

Consider aggressive fluid therapyConsider medication administration:

Dopamine, dobutamine, norepinephrine

Click here to view the Cardiogenic Shock diagram.

The absence of ventricular contraction Immediately results in systemic

circulatory failure Sudden death is any death that

occurs within 1 hour of symptom onset

Severe atherosclerotic disease is common Risk factors

Acid-base imbalance

Drowning Drug intoxication Electrocution Electrolyte

imbalance End-stage renal

disease

Hyperkalemia (high levels of potassium)

Hypothermia Hypoxia Pulmonary

embolism Stroke Trauma

Patients who suffer a cardiac arrest resulting from ventricular fibrillation go through several phases leading up to biological death ElectricalCirculatoryMetabolic

Prehospital intervention required depends on the phase the patient is in

Electrical PhaseBegins at the time of the cardiac arrest

and ends at approximately 3 to 4 minutes post-arrest

Adequate oxygen at the level of the myocardial cells Cells are able to maintain energy production

through aerobic metabolismThe only beneficial treatment is

immediate defibrillation

Circulatory Phase4–10 minutes post-arrest Oxygen levels in the myocardial cells are

inadequate Shift to anaerobic metabolism

Survival from cardiac arrest during this phase is better if at least 90 seconds of CPR is provided before the application of defibrillation Epinephrine beneficial

Metabolic PhaseBegins approximately 10 minutes after

the onset of cardiac arrest Failure of the sodium-potassium pump

Sodium begins to diffuse into the cell Water follows sodium Cellular swelling and eventually lysis

Current resuscitative measures do not improve survival during the metabolic phase

Field Assessment Initial Assessment

Unresponsive, apneic, pulseless patientECG

DysrhythmiasHistory

Prearrest events Bystander CPR “Down time”

ManagementTerms

Resuscitation Return of Spontaneous Circulation Survival

Role of Basic Life SupportGeneral Guidelines

Manage specific dysrhythmias CPR Advanced airway management Establish IV access

Pharmacological considerationsAmiodaroneAtropine sulfateEpinephrineLidocaineMagnesium sulfateVasopressin

Follow medications in arrest with a bolus of fluid

Click here to view the Cardiac Arrest diagram.Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary

Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-59. © 2005 American Heart Association.

Manage dysrhythmias and problems as presented.Be alert for PEATransport rapidly:

Take care to protect intubation and IV access

Withholding resuscitationRigor mortisDependent lividityDecapitation, decomposition, incinerationValid advance directive

Terminating Resuscitation Inclusion criteria for termination of

resuscitation: Patient over 18 years old Cause is presumed cardiac in origin Successful endotracheal intubation ACLS standards applied throughout the arrest On-scene effort >25 minutes, or four rounds of

drug therapy ECG remains asystolic or agonal

Terminating ResuscitationExclusion Criteria:

Patient under 18 years old Arrest is of a treatable cause Present or recurring VF/VT Transient return of a pulse Signs of neurological viability Witnessed arrest Family or others opposed to termination of

resuscitationAlways follow local protocols related to

termination of resuscitation

AtherosclerosisPathophysiology

Progressive degenerative disease of the medium-sized and large arteries

Results from the buildup of fats on the interior of the artery

Fatty buildup results in plaques and eventual stenosis of the artery

ArteriosclerosisClaudication

AneurysmPathophysiology

Ballooning of an arterial wall, usually the aorta, that results from a weakness or defect in the wall

Types Atherosclerotic Dissecting Infectious Congenital Traumatic

Abdominal Aortic AneurysmOften the result

of atherosclerosisSigns and

symptoms: Abdominal pain Back/flank pain Hypotension Urge to defecate

Dissecting Aortic AneurysmCaused by degenerative changes in the

smooth muscle and elastic tissueBlood gets between and separates the

wall of the aortaCan extend throughout the aorta and into

associated vessels

Acute Pulmonary EmbolismPathophysiology

Blockage of a pulmonary artery by a blood clot or other particle

The area served by the pulmonary artery failsSigns and Symptoms

Dependent upon size and location of the blockage

Onset of severe, unexplained dyspnea History of recent lengthy immobilization

Acute Arterial OcclusionPathophysiology

Sudden occlusion of arterial blood flow due to trauma, thrombosis, tumor, embolus, or idiopathic means

Frequently involves the abdomen or extremities

VasculitisPathophysiology

Inflammation of the blood vessels Commonly stems from rheumatic diseases and

syndromes

Noncritical Peripheral Vascular ConditionsPeripheral Arterial Atherosclerotic Disease

Can be acute or chronic Often associated with diabetes Extremities exhibit pain, coldness, numbness,

and pallorDeep Venous Thrombosis

Blood clot in a vein Typically occurs in the larger veins of the thigh

and calf Swelling, pain, and tenderness, with warm, red

skinVaricose Veins

Dilated superficial veins, common with pregnancy and obesity

General Assessment and Management of Vascular DisordersAssessment

Initial Assessment Circulatory Assessment

Pallor Pain Pulselessness Paralysis Paresthesia

Assessment (cont.)Chief Complaint

OPQRSTPhysical Exam

Prior history of vascular problems Differences in pulses or blood pressures

ManagementMaintain the airwayAdminister oxygen if respiratory distress

or signs of hypoperfusion presentConsider administration of analgesicsTransport rapidly if signs of hypoperfusion

present

Assessment of the Cardiovascular Patient

Management of Cardiovascular Emergencies

Managing Specific Cardiovascular Emergencies