Cardiac Em Erg

8/3/2019 Cardiac Em Erg

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Hypertension andPeripheral Vascular Disease

EMS Professions

Temple College


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Hypertension

Resting BP consistently >140

systolic or >90 diastolic


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Epidemiology

20% of adult population

~35,000,000 people

25% do not know they are hypertensive

Twice as frequent in blacks than in

whites

25% of whites and 50% of blacks > 65 y/o


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Types

Primary (essential) hypertension

Secondary hypertension


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Primary Hypertension

85 - 90% of hypertensives

Idiopathic

More common in blacks or with positivefamily history

Worsened by increased sodium intake,

stress, obesity, oral contraceptive use, ortobacco use

Cannot be cured


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Secondary Hypertension

10 - 15% of hypertensives

Increased BP secondary to another

disease process


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Secondary Hypertension

Causes:

Renal vascular or parenchymal disease

Adrenal gland disease Thyroid gland disease

Aortic coarctation

Neurological disorders

Small number curable with surgery


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Hypertension Pathology

Increased BP inflammation, sclerosisof arteriolar walls narrowing of vessels decreased blood flow to major organs

Left ventricular overworkhypertrophy, CHF

Nephrosclerosis renal insufficiency,failure


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Hypertension Pathology

Coronary atherosclerosis AMI Cerebral atherosclerosis CVA Aortic atherosclerosis Aortic

aneurysm

Retinal hemorrhage Blindness


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Signs/Symptoms

Primary hypertension is asymptomatic

until complications develop

Signs/Symptoms are non-specific

Result from target organ involvement

Dizziness, flushed face, headache, fatigue,

epistaxis, nervousness are not caused by

uncomplicated hypertension.


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HTN Medical Management

Life style modification

Weight loss

Increased aerobic activity

Reduced sodium intake

Stop smoking

Limit alcohol intake


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Medications

Diuretics

Beta blockers

Calcium antagonists

Angiotensin converting enzymeinhibitors

Alpha blockers


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Medical management prevents or

forestalls all complications

Patients must remain on drugtherapy to control BP


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Categories of Hypertension

Hypertensive Emergency (Crisis)

acute BP with sx/sx of end-organ injury Hypertensive Urgency

sustained DBP > 115 mm Hg w/o evidence ofend-organ injury

Mild Hypertension

DBP > 90 but < 115 mm Hg w/o symptoms Transient Hypertension

elevated due to an unrelated underlyingcondition


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Hypertensive Crisis

Acute life-threatening increase

in BP

Usually exceeds 200/130


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Hypertensive Crisis

Few Hypertensive Conditions are

Emergencies

Emergent Hypertensive Conditions include:

encephalopathy (CNS sx/sx)

eclampsia

when associated with

AMI or Unstable angina

Acute renal failure

Intracranial injury

Acute LVF

Aortic dissection


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Causes

Sudden withdrawal of anti-hypertensives

Increased salt intake

Abnormal renal function

Increase in sympathetic tone

Stress

Drugs

Drug interactions Monoamine oxidase inhibitors

Toxemia of pregnancy


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Signs/Symptoms

Restlessness,

confusion, AMS

Vision disturbances

Severe headache

Nausea, vomiting

Seizures

Focal neurologic

deficits

Chest pain

Dyspnea

Pulmonary edema


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Hypertensive Crisis Can Cause

CVA

CHF

Pulmonary edema

Angina pectoris

AMI

Aortic dissection


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Hypertensive Crisis Management

Immediate goal: lower BP in controlled fashion

No more than 30% in first 30-60 mins Not appropriate in all settings

Oxygen via NRB Monitor ECG

IV NS TKO

Drug Therapy Targeted at simply lowering BP, OR

Targeted at underlying cause


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Drug Therapy Possibilities

Sodium Nitroprusside (Nipride)

Potent arterial and venous vasodilator

Vasodilation begins in 1 to 2 minutes

0.5 g/kg/min by continuous infusion, titrate toeffect increase in increments of 0.5g/kg/min

50 mg in 250 cc D5W

Effects easily reversible by stopping drip

Continuous hemodynamic monitoring required

Cover IV bag/tubing to avoid exposure to light

Used primarily when targeting lower BP only


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Nitroglycerin

Vasodilator

Nitropaste simplest method

1 to 2 inches of ointment q 8 hrs easy to control effect but slow onset

Sublingual NTG is faster route

0.4 mg SL tab or spray q 5 mins

easy to control but short acting

NTG infusion, 10 - 20 mcg/min

seldom used for hypertensive crisis

Commonly used prehospital when targetingBP lowering only especially in AMI


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Nifedipine (Procardia)

Calcium channel blocker

Peripheral vasodilator

10 mg Sublingual Split capsule longitudinally and place contents under

tongue or puncture capsule with needle and have patientchew

Used less frequently today! Frequently in past!

Concern for rapid reduction of BP resulting in organischemia


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Furosemide (Lasix)

Loop Diuretic

initially acts as peripheral vasodilator

later actions associated with diuresis

40 mg slow IV or 2X daily dose

most useful in acute episode with CHF or LVF

Often used with other agents such as NTG


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Hydrazaline (Apresoline)

Direct smooth muscle relaxant

relax arterial smooth muscle > venous

10-20 mg slow IV q 4-6 hrs; initial dose 5 mgfor pre-eclampsia/eclampsia

Usually combined with other agents such asbeta blockers

concern for reflex sympathetic tone increase

Most useful in pre-eclampsia and eclampsia


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Metoprolol (Lopressor), or

Labetalol (Normodyne)

decrease in heart rate and contractility

Dose Metoprolol: 5 mg slow IV q 5 mins to total ~15 mg

Labetalol: 10-20 mg slow IV q 10 mins

Metoprolol is selective beta-1

minimal concern for use in asthma and obstructiveairway disease

Labetalol: both alpha & beta blockade

Most useful in AMI and Unstable angina


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Avoid crashing BP to hypotensiveor normotensive levels!

Ischemia of vital organs mayresult!


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Must assure underlying cause ofBP isunderstood

HTN may be helpful to the patient

Aggressive treatment of HTN may be harmful

What patients may have HTN as acompensatory mechanism?


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Syncope

Sudden, temporary loss of

consciousness caused by

inadequate cerebral perfusion


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Vasovagal Syncope

Simple fainting occurring when upright

Increased vagal tone leads to peripheral

vasodilation, bradycardia which lead to:

Decreased cardiac output

Decreased cerebral perfusion

Causes

Fright, trauma, pain

Pressure on carotid sinus (tight collar,shaving)


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Cardiogenic Syncope

Paroxysmal Tachyarrhythmias (atrial or

ventricular)

Bradyarrhythmias Stokes-Adams attack

Valvular disease

especially aortic stenosis Can occur in any position


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Postural Syncope

Due to decreased BP onstanding or sitting up

Orthostatic hypotension


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Postural Syncope

Drugs - usually antihypertensives

Diuretics

Vasodilators

Beta-blockers

Volume depletion

Acute hemorrhage

Vomiting or diarrhea

Excessive diuretic use

Protracted sweating

Neuropathic diseases - diabetes


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Tussitive Syncope

Coughing

Increased intrathoracic pressure

Decreased venous return

Vagal stimulation

Decreased heart rate


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Micturation Syncope

Urination

Increased vagal tone

Decreased cardiac output

Frequently associated with

Volume depletion due to EtOH Vasodilation due to EtOH


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Syncope History

What were you doing when you fainted?

Did you have any warning symptoms?

Have you fainted before? Under what circumstances?

Any history of cardiac disease?

Any medications? Any other past medical history?


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Syncope Management

Supine position - possibly elevate lowerextremities

Do not sit up or move to semi-sitting

position quickly Airway - oxygen via NRB

Loosen tight clothing


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Syncope Management

Vital signs, Focused Hx & Physical exam

Assess for injuries sustained in fall

Attempt to identify cause Based on history/physical, Consider:

ECG Monitor

Blood glucose check Vascular access

Transport for further evaluation


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Peripheral Vascular Disease

Peripheral Atherosclerotic Disease

Deep Vein Thrombophlebitis

Varicose Veins


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Peripheral Atherosclerosis

Gradual, progressive disease

Common in diabetics

Thin, shiny skin Loss of hair on extremities

Ulcers, gangrene may develop


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Intermittent Claudication

Deficient blood supply in exercising

muscle Pain, aching, cramps, weakness

Occurs in calf, thigh, hip, buttocks onwalking

Relieved by rest (2 - 5 minutes)


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Acute Arterial Occlusion

Sudden blockage by embolism, plaque,thrombus

Can result from vessel trauma The 5 Ps of acute occlusion

Pain, worsening over several hours

Pallor, cool to touch

Pulselessness

Paresthesias, loss of sensation

Paralysis


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Inflammation of lower extremities, pelvicveins with clot formation

Usually begins with calf veins

Precipitating factors

Injury to venous endothelium

Hypercoagulability

Reduced blood flow (venous stasis)


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Signs/Symptoms

May be asymptomatic

Pain, tenderness

Fever, chills, malaise

Edema, warmth, bluish-red color

Pain on ankle dorsiflexion during

straight leg lifting (Homans sign) Palpable cord in calf

clotted veins


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May progress to pulmonary

embolism!!!


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Varicose Veins

Dilated, elongated, tortuous

superficial veins usually in

lower extremities


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Varicose Veins

Causes

Congenital weakness/absence ofvenous valves

Congenital weakness of venous walls

Diseases of venous system (Deepthrombophlebitis)

Prolonged venostasis (pregnancy,standing)


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Varicose Veins

Signs/Symptoms

May be asymptomatic

Feeling of fatigue, heaviness Cramps at night

Orthostatic edema

Ulcer formation


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Varicose Veins

Rupture may cause severebleeding

Control with elevation anddirect pressure


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Aortic Aneurysm

Localized abnormal dilation ofblood vessel, usually an artery

Thoracic

Dissecting

Abdominal


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Thoracic Aortic Aneurysm

Usually results from atherosclerosis

Weakened aortic wall bows out -

lumen distends

Most common in males age 50 - 70


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Thoracic Aortic Aneurysm

Sign/Symptoms

Dyspnea, Cough

Hoarseness/Loss of voice

Substernal/back pain or ache

Lower extremity weakness/paresthesias

Variation in pulses, BP betweenextremities


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Dissecting Aortic Aneurysm

Intima tears

Column of blood forms false passage,

splits tunica media lengthwise Most common in thoracic aorta

Most common in blacks, chronic

hypertension, Marfans syndrome


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Signs/Symptoms

Sudden ripping or tearing pain

anterior chest or between shoulders

May extend to shoulders, neck, lower back, andabdomen

Rarely radiates to jaw or arms

Pallor, diaphoresis, tachycardia,

dyspnea


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Signs/Symptoms

Normal or elevated upper extremity BPin shocky patient

CHF if aortic valve is involved

Acute MI if coronary ostia involved

Rupture into pericardial space or chest

cavity with circulatory collapse


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Signs/Symptoms

CNS symptoms from involvement ofhead/neck vessel origins

Chest pain + neurological deficit =aortic aneurysm


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Abdominal Aortic Aneurysm

Also referred to as AAA or

Triple A

Usually results from atherosclerosis

White males age 50 - 80


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Signs/Symptoms

Usually asymptomatic until large enough to bepalpable as pulsing mass

Usually tender to palpation

Excruciating lower back pain from pressure onlumbar vertebrae

May mimic lumbar disk disease or kidney stone

Leaking/rupture may produce vascularcollapse and shock

Often presents with syncopal episode


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Signs/Symptoms

May result in unequal lower extremitypulses or unilateral paresthesia

Urge to defecate caused byretroperitoneal leaking of blood

Erosion into duodenum with massive GI

bleed


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Aortic Aneurysm Management

ABCs

High concentration O2 NRB

Assist ventilations if needed Package patient for transport in MAST,

inflate if patient becomes hypotensive

IVs x 2 with LR enroute Draw labs

12 Lead ECG enroute if time permits


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Aortic Aneurysm Management

If patient hypertensive consider reducing

BP

Nitropaste

Beta blocker

Consider analgesia

Tolerated best if hypertensive

Consider transport to facility with

vascular surgery capability


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Pulmonary Embolism

Pathophysiology

Pulmonary artery blocked

Blood:Does not pass alveoli

Does not exchange gases


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Causes

Blood clots =most common cause

Virchows Triad

Venous stasis bed rest, immobility,casts, CHF

Thrombophlebitis vessel wall damage

Hypercoagulability Birth control pills,

especially with smoking


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Causes

Air

Amniotic fluid

Fat particles

Long bone fracture more quickly

splinted, less chance of fat emboli

Particulates from substance abuse


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Signs/Symptoms

Small Emboli

Dyspnea

Tachycardia

Tachypnea


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Signs/Symptoms

Larger Emboli

Respiratory difficulty

Pleuritic pain

Pleural rub

Coughing

Hemoptysis

Localized Wheezing


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Signs/Symptoms

Very Large Emboli

Respiratory distress

Central chest pain

Distended neck veins

Acute right heart failure

Shock

Cardiac arrest


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Signs/Symptoms

There are NO findings specific

to pulmonary embolism


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Management

Airway Consider intubation early (if does not cause delay)

Breathing

100% O2

NRB mask

Consider assisting ventilations (if not intubated)

Circulation

IV x 2, lg bore, NS, TKO

May attempt fluid bolus if hypotensive or shock

ECG monitor

Rapid transport

thrombolysis or pulmonectomy may be useful


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Pulmonary Embolism

If the patient is alive when youget to them, that embolus isnt

going to kill them,

BUT THE NEXT ONE THEY

THROW MIGHT!!!

Cardiac Em Erg

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