cardio 1

Chapter 17

Cardiovascular Emergencies

Dale A. LeCrone Sr NRPInstructor

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.

Epidemiology

In 2007, heart disease contributed to about 34% of all US deaths.

Prevention strategies include education and early recognition.

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

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.

The Heart

Three layers: Epicardium: outmost

layer Myocardium:

muscular middle layer of wall

Endocardium: lines inside of the heart’s cavities

Endocardium

Myocardium

Epicardium

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

The HeartLike all cells in the body, myocardial cells require an uninterrupted supply of oxygen and nutrients.

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

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

collateral circulation.

The Heart

Atria are separated from ventricles by atrioventricular (AV) valves: Tricuspid valve Mitral valve Semilunar valves

Pulmonary semilunar valve

Aortic semilunar valve

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

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.

The Cardiac Cycle

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

Two circulations: Systemic circulation

All blood vessels between left ventricle and right atrium

Pulmonary circulation All blood vessels between right ventricle and

left atrium

Blood Vessels

Types of blood vessels: Veins Arteries

Common structures Tunica adventitia Tunica media Tunica intima Lumen

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.

Blood Vessels

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%

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

The Pump at Work

CO = SV × HR Must increase output to meet changing demand Increases output by:

Increasing SVIncreasing rateBoth

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

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

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

Specialized conduction tissue propagates electrical impulses to the muscular tissue. Pacemaker: area where electrical activity arises

Sets rate for cardiac contraction

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

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.

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

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

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.

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.

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

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

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.

Measuring the heart’s electrical conduction activity Show as a

series of waves and complexes on ECG

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

Autonomic nervous system conductors: Sympathetic nervous

system Speeds up the heart

Parasympathetic nervous system Regulates vegetative

functions

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

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

Sympathetic nervous system Adapts to changing demands

Increases heart rateStrengthens cardiac muscle contraction forceOther adaptive responses to increase CO

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.

Drugs that Act on the Sympathetic Nervous System

Classified by the receptors with which they interact (alpha and beta receptors)

Sympathomimetic drugs imitate actions of naturally occurring sympathetic chemicals

Isoproterenol: pure beta agent

Phenylephrine: pure alpha agent

Other drugs have varying degrees of alpha and beta activity.

Beta-sympathetic agents classified as: Beta-1 adrenergic agonists: work on cardiac beta receptors Beta-2 adrenergic agonists: work on pulmonary beta

receptors

Sympatholytic blockers work by beating agents to receptor sites.

Beta adrenergic blockers occupy beta receptors.

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

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

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

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)

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

Patient Assessment

Cardiovascular common complaints:Chest painDyspneaFaintingPalpitationsFatigue

Scene Size-Up

Ensure scene safety. Anticipate the need for other resources. Look for clues to identify the potential

problem.

Primary Assessment

Form a general impression.Observe general appearance.Assess for apparent life threats.Determine level of consciousness.

Primary Assessment

Airway and breathingDetermine airway patency.Check open airway for rate, quality, and

effort of breathing.Consider oxygen therapy initiation.

Primary Assessment

CirculationCheck pulse:

Conscious: radial pulseUnconscious: carotid pulse

Note rate, regularity, and overall quality.Assess skin color and condition.

Primary Assessment

Transport decisionsDetermine if immediate transport is

needed.If unsure, continue assessment until

answer can be determined.

History Taking

Chest pain is often the presenting symptom of AMI.Use OPQRST.

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?

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?

History Taking

Palpitations: sensation of abnormally fast or irregular heartbeatOften caused by dysrhythmiaInquire about:

Onset, frequency, and durationPrevious episodes

History Taking

Patients may also report:Feeling of impending doomFeeling nausea or having vomited

Inquire about medical history.

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.

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

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

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

Calcium channel blockers Block influx of

calcium ions into cardiac muscle

Relieves angina Hypotension may

be a side effect.

Antidysrhythmic agents Control chronic cardiac rhythm disturbances Monitor carefully.

Diuretics Used for chronic

fluid overload and hypertension

Helps excrete sodium and water

Also excretes more potassium Patient may

become depleted.

Antihypertensive agents Treat hypertension. Difficult to regulate

dosageMay cause

hypotensionCheck BP in both

recumbent and sitting positions.

Anticoagulant drugs (blood thinners) Slow ability to clot

Antiplatelet drugs Used in managing myocardial infarctions Keeps platelets from sticking together

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.

Physical Exam

Begin with inspection, auscultation, and palpation. Inspect neck and tracheal position. Inspect adjacent structures (neck veins, etc.).

Estimate jugular venous pressure.

Physical Exam

Inspect/palpate chest. Surgical scars Nitroglycerin patch Pacemaker or ACID Chest enlargement Crepitus

Listen with a stethoscope.

Physical Exam

Heart sounds

Physical Exam

S1: correspond to carotid artery pulse Decreased sounds can indicate:

Mitral valve subject to fibrosis or is calcifiedObesityEmphysemaCardiac tamponade

Physical Exam

S2: correspond with pulmonary and aortic valves closing Louder: chronic high BP or pulmonary

hypertension Decreased: hypotension Split: right bundle branch

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

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

Physical Exam

Pulse Irregular: disturbance in cardiac rhythm Very rapid: anxiety, secondary to severe pain, or

cardiac dysrhythmia Weak thread: reduction in CO

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

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

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

Physical Exam

Monitoring devices ECG monitor-defibrillator records:

3-lead ECG tracing12-lead ECGs

Attach the cardiac monitor, waveform, capnography, or pulse oximeter.

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.

Electrophysiology

Cardiac dysrhythmia: disturbance in normal cardiac rhythm Evaluate in context

with overall condition

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.

cardio 1

left ventricle blood

blood volume

percentage of blood

deoxygenated blood

blood vessels veins

heart pericardium

heart atria

heart acts

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