- a clinical history of ischemic type chest pain

- serial ECG tracings indicative of MI

- a rise and fall in serum cardiac markers

angina

radiation to jaw, neck and arms

diaphoresis along with N/V

dyspnea

syncope

sense of doom, anxious

pulse changes

hypotension or hypertension

respiratory rate elevation

dysrhythmia

its usually normal, unless the patient has gone into CHF

Then you will start to hear crackles are the bases of the lungs

may show dyskinetic apical pulsation

or possible extra heart sound

or it could be normal

Hgb

fasting glucose

fasting lipid panel

resting ECG, and during chest pain

cardiac markers

Chest X-ray

aspirin

Vital signs

SL Nitroglyceran

O2

12 lead ECG

Morphine

when the hospital doesn't have onsite cardiac surgery facilities

long distance transport is safe as long as its within 3 hours of the sxs onset

dissection

pericarditis

active bleeding

previous cerebral hemorrhage

intracranial neoplasm

cerebral aneurysm

AV malf.

bleeding problems, coag. problem

recent surgery, puncture, trauma etc.

stroke or hemorrhage with 6 months

tPA

streptokinase

reteplase

you use them with STEMI

but not with NSTEMI or unstable angina

immediate angiography reveals anatomy that precludes primary angioplasty

pts in whom angioplasty has failed

pts with VSD, severe mitral regur. or myoc. rupture

LV failure

RV failure

cardiogenic shock (form of CHF)

ventricular wall rupture

VSD

papillary mm rupture

bradydysrhythmia

PVCs

tachdysrhythmia

sudden cardiac death

blocks (1st, 2nd, or 3rd degree)

bundle branch blocks

complication of AMI

inflammatory condition of the heart

a supraventricular tacharrhythmia defined by rapid, irregular atrial activation

results in loss of coordinated atrial contraction; irregular electrial input to the AV node typically leads to sporadic ventricular contractions

With atrial fibrillation CO drops ____%

and you can form _______ in the atria

20-25%

clots

1. irregularly irregular

(fast, slow or moderate)

2. no p waves

Infarction/intoxication            Pericardititis          

Rheumatic HD                       Worry/Stress

recent thoracotomy                ASD  

Endocrine/hyperthy.               Valvular

Geriatric                               Embolus/PE  

Unknown                              Systemic HTN

Lung disease/COPD

ASHD

Reduced O2

IRREGULAR P WAVES

ventricular rate control

cardioversion of AF and subsequent maintenance of sinus rhythm

prevention of thromboembolism

paroxysmal

persistent

permanent

AF that typicall lasts 7 days or less and than converts spontaneously to sinus rhythm

comes and goes

ECG

may also indicate a possible underlying cause

to keep the ventricular rate less than

90/minutes at rest and

180/minute on exercise

beta-blockers

rate-limiting Ca channel blockers

digoxin

amiodarone

radio-freq. ablation of the AC node and pacemaker implantation

consider combining digoxin with a beta-blocker or verpamil

may be particularly useful in exercise induced tachycardia

either treat with warfarin for 3 weeks prior

or

check for clots (bubble test)

recent onset AF

no structural HD

successful txt of any precipitating cause

young age

people with acute AF and severe hypotension

acute HF or unstable angina

synchronize

to go off with the QRS complex

cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm

use of rate-controlling drugs, allowing AF to persist

cause of about 25% of all cases of CHF

assc w/ dec strength of ventricular contraction

resulting in dilatino of LV

common causes: CAD, valvular HD, EtOH, Inf.

dilated cardiomyopathy

95% of the time

what are the 3 leading causes of dilated cardiomyopathy?

CAD

valvular HD

EtOH

sxs of left or bi-ventricular congestive failure

fatigue/exercise intolerance

dyspnea/orthopnea - LHF

lower extremity edema - RHF

increased urination - RHF

N/V/abd pain

distended neck w/ JVD

hepato-jugular reflux

tachypnea, bi-basilar rales, wheezes

signs of pleural effusion

s3 gallop

large/tender liver, acites

peripheral edema

EKG won't tell you too much

Echocardiography TOC

LV dilation/dysfunction with inc diastolic pressures and low CO

inflammation of the pericardium can be caused by

virus (most common)

bacterial

fungal

TB

causes sharpt pleuritic, retrosternal CP

pericardial effusion

dyspnea, cough

pleuritic/retrosternal CP

Tamponade

pulsus paradoxus

Chest Pain

Friction Rub

EKG changes (diffuse ST elevation)

usually supportive

NSAIDs

steroids

consider non-viral causes

pericardiocentesis

infection of the endocardial surfaces of the heart

usually bacterial

may be acute or subacute

different bugs, different drugs

difference in urgency

pathology is valvular damage

relatively rare

VEGETATION (primary lesion)

primary lesion of infective endocarditis

an infected platelet-fibrin/thrombus located inside the heart

HIV infections

prosthetic heart valves, structural HD

hemodialysis

DM

vancomycin

insidious onset and persists for weeks to months

feve and other non-specific s/s

onset usually abrupt, rigors are common

very high fevers

new heart murmur

cutaneous manifestations

janeway lesions

conjunctival petechiae

pustulonecrotic septic embolic lesions

what is the most important lab for SBE?

positive blood culture for infective endocarditis

2 + cultures drawn < 12 hrs apart or

all of 3 or a majority of 4 cultures drawn within 1 hr

AND

evidence of endocardial involvement

positive echocardiogram

roth spots

oslar nodes

splinter hemorrhages

petechiae

SBE Treatment

antibiotics

blood cultures first

surgical debridement of vegetations

antithrombotic meds

S. aureus

which infective endocarditis is assc with a fever?

ABE txt

empiric ABx txt is appropriate in the face of suspicious ABE

typically 4-6 wks

vancomycin and gentamicin

subsequent changes should be based on blood cultures

stenosis

regurgitation

rheumatic fever

infective endocarditis

congenital abnormality

degeneration

VHD is the most predictable cause of ______

harsh systolic murmur

thrill

murmur can radiate to the neck

valve replacement

balloon dilation

exertional dyspnea

angina

delayed/diminished carotid pulses

exertional dyspnea

widened pulse pressure

water hammer

autin flat murmur

rapid PE

refractory HF

cardiogenic shock

diastolic low-pitched rumbling

snap during mid-diastole

redundant valve tissue often due to connective tissue disorders

mid-systolic click

RVH and or pulmonary HTN

regurg >> stenosis

sounds assc. with valve diseases

MVP = mid-systolic click

Mitral Stenosis = snap during mid-diastole

aortic stenosis = harsh systolic murmur, thrill

aortic regurg = diastolic crescendo

dyspnea

fatigue

fluid retention

decreased exercise tolerance

preload

dilated cardiomyopathy

hypertrophic cardiomyopathy

restrictive cardiomyopathy

arrhythmogenic right ventricular cardiomyopathy

both will

high output = enlarged heart

low output = thickened wall

the structural response to injury

leads to a less efficient pump

CHF NY Heart Assc.

Classification

1: CD w/o resulting limitations of Phys activity

(asymptomatic)

2: slight limitation, comfortable at rest, but ordinary phys activity results in dyspnea, fatigue and angina

3: marked limitation, still comfortable at rest, but less than ordinary phys activity produces sxs

4: inability to carry on any phys activity w/o discomfort of sxs at rest

JVD

Hepatojugular reflux

S3 gallop

tachypnea and tachycardia

inc or dec BP

fever

rales/crackles

use of accessory mm and PE

cough with pink, frothy sputum

beta-blockers

ACEIs

ARBs

diuretics

Beta Blockers for CHF

carvedilol

metoprolol

toprol

counteracts the harmful effects of symp stimulus

improve survival, ejection fraction and quality of life

dec morbidity, hospitalizations, sudden death and slows remodeling

revascularization

valve replacements

mechanical devices

cardiac transplantation

left ventricular assist devices

implantable devices