Cardio 1
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Chapter 17
Cardiovascular Emergencies
Dale A. LeCrone Sr NRPInstructor
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Introduction
Heart disease is the number one killer.
Kills 600,000 Americans each year
About half in ED or before reaching a hospital
During first minutes or hours
Formulate a field impression from assessment, and implement a treatment plan.
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Epidemiology
In 2007, heart disease contributed to about 34% of all US deaths.
Prevention strategies include education and early recognition.
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Anatomy and Physiology
Structure and function Cardiovascular system
Composed of heart and blood vesselsDelivers oxygenated blood and nutrients to
cellsTransports waste products to disposal sites
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The Heart
Sits above diaphragm, behind and slightly left of the retrosternal.
Size of a fist
Circulates 7,000 to 9,000 L of blood daily
Apical thrust or point of maximum impulse (PMI) is located at the fifth intercostals space on the left anterior part of the chest , in the midclavicular line.
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The Heart
Three layers: Epicardium: outmost
layer Myocardium:
muscular middle layer of wall
Endocardium: lines inside of the heart’s cavities
Endocardium
Myocardium
Epicardium
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The Heart Pericardium: sac surrounding
the heart
Protects the heart and provides lubrication
Parietal pericardium (superficial layer)
Visceral pericardium – fused to the epicardium
Potential space between the two layers
Abnormal accumulation of fluid can occur.
Pericardial effusion: Small accumulation
Pericardial tamponade: Large accumulation
VisceralPericardium
ParietalParicardium
Paricardium
Paricardial Cavity
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The HeartLike all cells in the body, myocardial cells require an uninterrupted supply of oxygen and nutrients.
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The Heart
Coronary arteries
Left coronary (LMCA) artery supplies:
Left ventricle
Interventricular septum
Part of right ventricle
Divides into:
Left anterior descending artery (LAD)
Circumflex coronary artery (LCx)
Right coronary artery supplies:
Right atrium
Right ventricle
Part of the left ventricle
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The Heart
Numerous connections (anastomoses) between the arterioles of the various coronary arteries allow for the development of alternative routes of blood flow.
Arterioles merge form
ing
collateral circulation.
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The Heart
Atria are separated from ventricles by atrioventricular (AV) valves: Tricuspid valve Mitral valve Semilunar valves
Pulmonary semilunar valve
Aortic semilunar valve
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The Cardiac Cycle
Represents complete depolarization and repolarization of the atria and ventricles Diastole: atria or ventricles are resting
Atrial diastole: Atrial restVentricular diastole: Ventricular rest
Systole: atria or ventricles contractingAtrial systole: Atrial contractionVentricular systole: Ventricular contraction
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The Cardiac Cycle
Relaxation phase: left atrium fills with blood under venous pressure
Atrial contraction: blood in each atrium is squeezed into respective ventricle
Atrial kick: contribution made by contraction
As ventricular contraction begins:
Ventricles contract. (ventricular systole) last about 0.28s
Semilunar valves are forced open.
Blood from the right ventricle is squeezed into the pulmonary arteries.
Left ventricle blood is pushed into the aorta.
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The Cardiac Cycle
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Blood Flow Through the Heart
The heart acts as two pumps, separated by an interventricular septum.
Right side: low-pressure pump
Superior vena cava collects blood from upper body
Inferior vena cava collects blood from lower body
Left side: high-pressure pump
Pulmonary veins collect blood from the lungs.
Preload: initial stretching of cardiac myocytes prior to left-sided contraction
Afterload: blood is driven out of the heart against systemic arteries
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Blood Flow Through the Heart
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Blood Flow Through the Heart
Two circulations: Systemic circulation
All blood vessels between left ventricle and right atrium
Pulmonary circulation All blood vessels between right ventricle and
left atrium
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Blood Flow Through the Heart
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Blood Vessels
Types of blood vessels: Veins Arteries
Common structures Tunica adventitia Tunica media Tunica intima Lumen
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Blood Vessels
Veins carry deoxygenated blood back to the heart. Venules empty into larger and larger veins. Contain valves to keep blood flowing forward
Capillaries separate arteries and veins.
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Blood Vessels
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The Pump at Work
Skeletal muscle and thorocoabdominal pumps aid venous blood return to the heart.
Technical terms: Cardiac output (CO): Amount of blood pumped by
either ventricle. Normally 5-6 L/min for an average adult
Stroke volume (SV): Amount of blood pumped by either ventricle in a single contraction normally 60-100 mL can increase by at least 50%
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The Pump at Work
Technical terms (cont’d): Heart rate (HR): Number of contractions per
minute (pulse rate) Ejection fraction (EF): Percentage of blood leaving
the heart on each contraction
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The Pump at Work
CO = SV × HR Must increase output to meet changing demand Increases output by:
Increasing SVIncreasing rateBoth
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The Pump at Work
Preload is influenced by the blood volume returned to the heart. More blood is returned when more oxygen is
demanded.Frank-Starling mechanism is used to achieve
normal resting CO in a diseased heart
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The Pump at Work
Degree of contract can vary without change in the stretch this is known as contractility
With a constant SV, CO can be increased by increasing number of contractions per minute Positive chronotropic effect
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The Electrical Conduction System of the Heart
Cardiac cells have four properties: Excitability: allows response to electrical impulse Conductivity: ability to pass on electrical impulses Automaticity: can generate own electrical
impulses Contractility: ability to contract
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The Electrical Conduction System of the Heart
Specialized conduction tissue propagates electrical impulses to the muscular tissue. Pacemaker: area where electrical activity arises
Sets rate for cardiac contraction
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The Electrical Conduction System of the Heart
Sinoatrial node
Located in right atrium
Receives blood from the RCA
Fastest pacemaker
Impulses are spread through intermodal pathways, causing depolarization of the atrial tissues.
Occurs in about 0.08s
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The Electrical Conduction System of the Heart
Sinoatrial node (cont’d): Electrical impulses move from SA node to the
atrioventricular (AV) node Impulse conduction is delayed so the atria will
empty into the ventricles.
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The Electrical Conduction System of the Heart
Conduction pathways that allow current to bypass AV node: James fibers in the intermodal pathways Mahaim fibers extend into ventricles Bundle of Kent enables early depolarization of
ventricular tissue
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The Electrical Conduction System of the Heart
If atrial rate becomes rapid, not all impulses go through AV junction
Normally impulses pass: Into bundle of His Into right and left bundle branches Into Purkinje fibers This takes about 0.8s
Dromotropic effect: effect on conduction velocity
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The Electrical Conduction System of the Heart
Depolarization: muscle fibers are stimulated to contract Occurs through changes in concentration of
electrolytes across cell membranesMyocardial cells bathed in electrolyte solutionChemical pumps maintain ion concentrations
within the cells creating an electric gradient across the cell wall.
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The Electrical Conduction System of the Heart
Depolarization (cont’d) Cell receives stimulus from conduction
Permeability of the cell wall changes to allow sodium ions in
Calcium ions also enter. Depolarization spreads, causing a mechanical
contraction.
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The Electrical Conduction System of the Heart
Repolarization begins with the closing of sodium and calcium channels. Sodium ions pumped out and potassium ions in
Active transport: ions are moved against the natural gradient
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The Electrical Conduction System of the Heart
Myocardial cells must be fully polarized to respond normally to electrical stimulus. Refractory period: cell is depolarized or in the
process of repolarizingAbsolute refractory period: completely
depolarizedRelative refractory period: partially repolarized
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The Electrical Conduction System of the Heart
Secondary pacemakers Any conduction system component can act as a
secondary pacemaker if the SA node is damaged.The farther removed from the SA node, the
slower the intrinsic rate of firing.
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The Electrical Conduction System of the Heart
Measuring the heart’s electrical conduction activity Show as a
series of waves and complexes on ECG
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The Electrical Conduction System of the Heart
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The Autonomic Nervous System and the Heart
Autonomic nervous system controls involuntary actions Works with the
voluntary nervous system to allow body functions to proceed smoothly
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The Autonomic Nervous System and the Heart
Autonomic nervous system conductors: Sympathetic nervous
system Speeds up the heart
Parasympathetic nervous system Regulates vegetative
functions
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The Autonomic Nervous System and the Heart
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The Autonomic Nervous System and the Heart
Parasympathetic nervous system Sends messages through vagus nerve, which can
be stimulated by:Pressure on carotid sinusStraining against a closed glottis (Valsalva
maneuver)Distention of a hollow organ
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The Autonomic Nervous System and the Heart
Parasympathetic nervous system (cont’d) If brain senses the heart should slow its pace:
Electrical impulse travels to the SA nodeCauses release of acetylcholine (ACh)Signals node to slow heartAnother ACh molecule travels to the AV node
of as a reminder
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The Autonomic Nervous System and the Heart
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The Autonomic Nervous System and the Heart
Sympathetic nervous system Adapts to changing demands
Increases heart rateStrengthens cardiac muscle contraction forceOther adaptive responses to increase CO
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The Autonomic Nervous System and the Heart
Sympathetic nervous system (cont’d) In response to need for more oxygen:
Brain sends message through nerves to heartCommands conveyed through release of
norepinephrineHeart speeds up to prevent lactic acid buildupEpinephrine is used if intense stimulation
occurs.
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Drugs that Act on the Sympathetic Nervous System
Classified by the receptors with which they interact (alpha and beta receptors)
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Drugs that Act on the Sympathetic Nervous System
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Drugs that Act on the Sympathetic Nervous System
Sympathomimetic drugs imitate actions of naturally occurring sympathetic chemicals
Isoproterenol: pure beta agent
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Drugs that Act on the Sympathetic Nervous System
Phenylephrine: pure alpha agent
Other drugs have varying degrees of alpha and beta activity.
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Drugs that Act on the Sympathetic Nervous System
Beta-sympathetic agents classified as: Beta-1 adrenergic agonists: work on cardiac beta receptors Beta-2 adrenergic agonists: work on pulmonary beta
receptors
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Drugs that Act on the Sympathetic Nervous System
Sympatholytic blockers work by beating agents to receptor sites.
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Drugs that Act on the Sympathetic Nervous System
Beta adrenergic blockers occupy beta receptors.
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Drugs that Act on the Sympathetic Nervous System
Major autonomic agents: Atropine: Parasympathetic blocker
Used to speed the heart Norepinephrine: Sympathetic agent
Used to increase blood pressure Isoproterenol: Sympathetic agent
Used to increase CO and dilate bronchi
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Drugs that Act on the Sympathetic Nervous System
Major autonomic agents (cont’d): Epinephrine: Sympathetic agent
Used for peripheral vasoconstrictor effect Dopamine: Sympathetic agent
Used to increase renal perfusion, increase rate and force of myocardial contraction, and constrict peripheral blood vessels
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Drugs that Act on the Sympathetic Nervous System
Major autonomic agents (cont’d): Albuterol: Sympathetic beta-2 agent
Used to induce bronchodilation. Propranolol: Sympathetic beta blocker
Used to slow the heart rate, decrease chronic angina pain, and to depress irritability in the heart
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Sympathetic Nervous System and Blood Pressure Regulation
Body tries to maintain constant BP BP is influenced by CO and resistance of
arterioles: BP = CO × peripheral vascular resistance (PVR)
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Sympathetic Nervous System and Blood Pressure Regulation
Body balances flow and resistance to maintain stable BPIf one variable is altered, the body
compensates by changing another variable.
CO = BP ÷ PVR
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Patient Assessment
Cardiovascular common complaints:Chest painDyspneaFaintingPalpitationsFatigue
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Scene Size-Up
Ensure scene safety. Anticipate the need for other resources. Look for clues to identify the potential
problem.
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Primary Assessment
Form a general impression.Observe general appearance.Assess for apparent life threats.Determine level of consciousness.
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Primary Assessment
Airway and breathingDetermine airway patency.Check open airway for rate, quality, and
effort of breathing.Consider oxygen therapy initiation.
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Primary Assessment
CirculationCheck pulse:
Conscious: radial pulseUnconscious: carotid pulse
Note rate, regularity, and overall quality.Assess skin color and condition.
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Primary Assessment
Transport decisionsDetermine if immediate transport is
needed.If unsure, continue assessment until
answer can be determined.
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History Taking
Chest pain is often the presenting symptom of AMI.Use OPQRST.
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History Taking
Dyspnea is another chief complaint of ACS. A first indicator of left-sided heart failure
When did it start? Suddenly or gradually?Continuous or intermittent?During activity or at rest?Does any position make it better or worse?Ever had it before?Cough? Associated symptoms?
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History Taking
Fainting occurs when CO declines. To determine if it is from cardiac causes, ask:
Under what circumstances did the fainting occur?
Were there any warnings?What position was the patient in?Has the patient fainted before?Associated symptoms?
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History Taking
Palpitations: sensation of abnormally fast or irregular heartbeatOften caused by dysrhythmiaInquire about:
Onset, frequency, and durationPrevious episodes
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History Taking
Patients may also report:Feeling of impending doomFeeling nausea or having vomited
Inquire about medical history.
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Medications for Patients with Cardiovascular Diseases
Patients may be taking a wide variety of medications.
It is not always possible to identify the problem based on medications.
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Medications for Patients with Cardiovascular Diseases
Digitalis preparations For chronic CHF or certain dysrhythmias
Increases cardiac contractionsToxic effects develop in 30% of patients.Will be sensitive to calcium preparations
and have a decline in serum potassium levels
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Medications for Patients with Cardiovascular Diseases Antianginal agents
NitratesTablets, ointment, or skin patchesDecreases work of the heartTakes 3 to 5 minutes to workCauses significant vasodilation
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Medications for Patients with Cardiovascular Diseases Beta blockers
Block beta receptors
Decrease rate/strength of cardiac contractions
May lead to resistance of beta-stimulating agents
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Medications for Patients with Cardiovascular Diseases
Calcium channel blockers Block influx of
calcium ions into cardiac muscle
Relieves angina Hypotension may
be a side effect.
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Medications for Patients with Cardiovascular Diseases
Antidysrhythmic agents Control chronic cardiac rhythm disturbances Monitor carefully.
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Medications for Patients with Cardiovascular Diseases
Diuretics Used for chronic
fluid overload and hypertension
Helps excrete sodium and water
Also excretes more potassium Patient may
become depleted.
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Medications for Patients with Cardiovascular Diseases
Antihypertensive agents Treat hypertension. Difficult to regulate
dosageMay cause
hypotensionCheck BP in both
recumbent and sitting positions.
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Medications for Patients with Cardiovascular Diseases
Anticoagulant drugs (blood thinners) Slow ability to clot
Antiplatelet drugs Used in managing myocardial infarctions Keeps platelets from sticking together
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Medications for Patients with Cardiovascular Diseases
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Secondary Assessment
Should emphasize cardiac issues LOC is an indicator of cerebral perfusion
Alert and oriented: Enough oxygen Stupor or confusion: Poor CO
Skin color and temperature may indicate circulation problems.
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Physical Exam
Begin with inspection, auscultation, and palpation. Inspect neck and tracheal position. Inspect adjacent structures (neck veins, etc.).
Estimate jugular venous pressure.
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Physical Exam
Inspect/palpate chest. Surgical scars Nitroglycerin patch Pacemaker or ACID Chest enlargement Crepitus
Listen with a stethoscope.
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Physical Exam
Heart sounds
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Physical Exam
S1: correspond to carotid artery pulse Decreased sounds can indicate:
Mitral valve subject to fibrosis or is calcifiedObesityEmphysemaCardiac tamponade
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Physical Exam
S2: correspond with pulmonary and aortic valves closing Louder: chronic high BP or pulmonary
hypertension Decreased: hypotension Split: right bundle branch
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Physical Exam
S3: caused by ventricular wall vibrations Occurs 120 to 170 ms after S2 Generally in young adults and children
S4: heard just before S1 Turbulent filling of stiff ventricle in hypertrophy Possible myocardial infarction
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Physical Exam
Other abnormal heart sounds: Opening snap:
noncompliant valve
Ejection click: dilated pulmonary artery or septal defect
Pericardial friction rub: pericarditis
Murmur: turbulent blood flow
Thrill: frequently occurring and constant vibration
Pericardial knock: thickened pericardium
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Physical Exam
Pulse Irregular: disturbance in cardiac rhythm Very rapid: anxiety, secondary to severe pain, or
cardiac dysrhythmia Weak thread: reduction in CO
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Physical Exam
Pulse (cont’d) Pulse deficit: radial pulse is less than the apical
pulse rate. Pulsus paradoxus: excessive drop in systolic
pressure Pulsus alternans: left ventricular systolic damage
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Physical Exam
Blood pressure Hypertension is indicated by:
Systolic blood pressure of 120 to 139 mg Hg Diastolic blood pressure of 80 to 89 mm Hg
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Physical Exam
Blood pressure (cont’d) Elevated blood pressure: anxiety or pain. Systolic blood pressure lower than 90 mm Hg:
hypotension or shock Increased pulse pressure: arteriosclerosis Reduced SV: cardiogenic shock or cardiac
tamponade
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Physical Exam
Monitoring devices ECG monitor-defibrillator records:
3-lead ECG tracing12-lead ECGs
Attach the cardiac monitor, waveform, capnography, or pulse oximeter.
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Reassessment
Done on way to the hospital Repeat primary assessment. Obtain vitals. Repeat physical exam. Assess intervention effectiveness. Create documentation. STEMI: transmit 12-lead ECG to lab.
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Electrophysiology
Cardiac dysrhythmia: disturbance in normal cardiac rhythm Evaluate in context
with overall condition
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Electrophysiology
Dysrhythmias develop after AMI because: Irritable ischemic heart muscle may cause
abnormal cardiac contractions.Dysrhythmia from ectopic foci is usually a
tachydysrhythmia. ECG analysis should be done on any patient with a
cardiac condition.