cardiac exam 1 - my version

coronary artery disease (CAD)

preventable disorder characterized by progressive occlusion of coronary arteries

• altered perfusion of myocardium

• impaired cardiac function

• reduced cardiac output

• decreased perfusion

cardiac output =

stroke volume x heart rate

cardiac output norm

5-7 L/min

stroke volume

volume of blood ejected by left ventricle with each contraction in mL PER HEARTBEAT

stroke volume norm

50-100 mL

ejection fraction

PERCENT of volume in left ventricle ejected with each contraction

easier to measure + more clinically relevant

ejection fraction norm

50-70%

factors that affect cardiac output

preload, afterload, contractility

preload

• VOLUME of blood in ventricles before contraction/systole (end diastole)

  • IF IT AFFECTS VOLUME WITHIN VESSELS = AFFECTS PRELOAD

afterload

• RESISTANCE the left ventricle must pump against

  • WORKLOAD

contractility

• FORCE of myocardial/muscle contraction

progression of CAD

arteries are blocked and occluded by plaques (cholesterol deposits)

CAD nonmodifiable risk factors

• age

• gender

• ethnicity

• genetics + family history

CAD modifiable risk factors

• high serum lipids

• hypertension

• tobacco use

• lack of regular exercise

• obesity (BMI > 30 kg/m2)

CAD contributing risk factors

• diabetes

• metabolic syndrome

• psychological factors: stress, depression, anxiety, anger

• coagulopathy

• elevated homocysteine level, c-reactive protein level

• substance disuse disorders (stimulants: cocaine + meth)

coronary arteries locations

main coronary artery

left descending artery (LAD)

• widowmaker

• travels to left ventricle

  • LV pumps to body

CAD disease progressions

stable angina

unstable angina

non-ST wave elevation myocardial infarction

ST-wave elevation myocardial infarction

workload is affected by

preload and afterload

increased preload

• fluid volume overload

• increased venous return

decreased preload

• hypovolemia

• venous dilation

• shock

increased afterload

• hypertension

• valve stenosis (stiff valves, heart pumps harder)

• pulmonary hypertension

• hypotension

• systemic vasodilation

drugs that reduce preload

• diuretics

• ACE inhibitors

  • reduce aldosterone production

  • reduce water retention

drugs that reduce venous return to heart that reduce preload

nitroglycerine

drugs that vasodilate reduce afterload

antihypertensives

• dec bp, hr

• vasodilate

stable angina care

PHARMACOTHERAPY: antiplatelet, nitrate, ACE/ARB, BB, CCBs, anti-lipid (statin most common)

RISK FACTOR MODIFICATION/LIFESTYLE CHANGES: high priority placed on patient education- goal is to prevent progression

POSSIBLE REPERFUSION:

• angioplasty/stent

• bypass surgery

the oddball angina: prinzmetal’s

• AKA variant angina

• NOT caused by CAD or OCCLUSION

  • caused by coronary artery vasospasm

  • pain predictable, typically occurring late at night/very early AM

  • relieved with activity

  • associated with Reynaud’s Syndrome + migraine headaches caused by temporal artery spasm (impaired BF)

• common at rest, midnight- 8 AM for 5-30 minutes

  • inc demand during REM

• chronic prinzmetal’s angina treated with CCBs

ACS diagnosis

CARDIAC BIOMARKERS: myoglobin, CKMB, troponin

ECHOCARDIOGRAM:

• functional loss in affected area

• reduced ejection fraction

• reduced cardiac output (estimated)

ACS: diagnosis- NSTEMI

ST depression confirmed in 2 or more leads of 12-lead ECG

• indicated ISCHEMIA of heart muscle

• ECG changes not always present in NSTEMI

• DAMAGE NOT DEATH

NSTEMI ECG findings

infarct: tissue damage

ST depression

STEMI ECG findings

infarct: tissue death

ST elevation

DEATH

ACS: diagnosis- STEMI

ST elevation confirmed in 2 or more leads of 12-lead ECG

• indicates tissue death

ACS immediate/urgent treatment goals

• preserve heart muscle

• treat pain

• anticipate + manage complications

ACS long term treatment goals

• coping with illness

• cardiac rehabilitation

• lifestyle modification

ACS clinical manifestations

• chest pain not relieved by rest, nitrates

• hypertension + tachycardia

• cool, clammy skin, ashen appearance of darker skin tones

• abnormal heart sounds: S3-S4

• n/v

• fever

ACS clinical manifestations

if area of infarct grows (esp if LV affected), s/s of significantly impaired cardiac output or shock may appear

• hypotension

• oliguria

• crackles in lungs

• peripheral edema

ACS: collaborative care

• 12 lead ECG, continuous telemetry monitoring

• IV access

• oxygen therapy

pharm: NTG, MS, ASA, BBs, ACE, ARBs, statins

unstable angina + NSTEMI collaborative care

• antiplatelet

• anticoagulant

• reperfusion: PCI or CABG

STEMI collaborative care

• PCI or CABG

• thrombolytic therapy

• antiplatelet

• anticoagulant

ACS collaborative treatment: TIME

TIME = HEART MUSCLE —> myocardial cells viable for approximately 20 minutes before damage permanent

• NSTEMI: reperfusion intervention recommended within 72 hours

• STEMI: reperfusion intervention needed within 90 minutes of onset of pain

  • doesn’t mean intervention won’t be attempted if over 90 minutes but degree of permanent damage greater

ACS collaborative treatment: URGENT/EMERGENT CARE

• 12 ECG: what changes would we look for?

• continuous cardiac monitoring

• serial cardiac biomarkers: typically q8h x 24-48 hours then daily

• MONA: Morphine, Oxygen, Nitroglycerine, Aspirin

• anticoagulant

  • may be delayed fpr anticipated cardiac cath or CABG
    

ACS: reperfusion

PCI: angioplasty + stenting

coronary artery bypass graft surgery:

thrombolytic therapy

PCI: angioplasty + stenting

• breaks plaque

• stent maintains patency of coronary artery—impregnated with anticoagulant

coronary artery bypass graft surgery

vessels harvested from internal mammary arteries and/or saphenous (leg) veins “bypass” plaque

thrombolytic therapy

IV admin of drug capable of dissolving clot that’s occluding artery

• cannot disrupt plaque

• indication: when is this treatment choice used?

ACS complications

• dysrhythmias very common

  • “reperfusion arrythmias” within 24-48 hours following successful reperfusion intervention

  • myocardium irritable

• heart failure

  • most common following MI affecting LV

• cardiogenic shock

  • more common following very extensive MIs or if LV sustains significant damage

• valve incompetency, esp mitral

• LV aneurysm

• pericarditis

nursing care: discharge planning

PATIENT TEACHING:

• psychosocial support: anxiety, fears, support systems

• activity: encourage cardiac rehab program for safe, gradual inc in activity post- MI

• avoid vagal stimulation: prevent constipation, no rectal temps, avoid weight lifting that causes “bear down”

• resumption of sexual activity: no ED meds if on nitrates!

• diet modification

• reportable signs and symptoms

coronary artery disease patho

• cholesterol adheres to endothelium of coronary artery

• damaged endothelium stimulates inflammatory process

• RBCs, platelets, clotting factors increase plaque size

• arterial lumen narrows reducing perfusion to myocardium

  • occlusion gets bigger, blood flow dec

MEN clinical manifestations of MI

• chest pain + pressure

  • “heavy” or “crushing”, weight on chest

  • radiate to jaw +/or left arm

• SOB (esp w/ exertion)

• nausea with/without vomiting

• diaphoresis

• palpitations

• fatigue

WOMEN clinical manifestations of MI

• chest pain/pressure

  • may radiate to both arms, stomach, abdomen, back or jaw

  • “heartburn” “acid reflux”

  • some women have no chest pain

• SOB

• extreme fatigue

• sudden dizziness (syncope)

stable angina

• predictable

• occurs w/ activity

• resolves w/ rest and/or admin of NTG

• no ECG changes

• CHEST PAIN FIXED WITH REST

• CAD w/ mild, partial occlusion

unstable angina

• unpredictable

• chest pain w/ activity or at rest

• s/s not reliably resolved w/ rest and/or NTG

• no ECG changes

• may/may not exhibit other symptoms

NSTEMI (non-ST segment elevation MI)

• unpredictable: may have sudden onset

• chest pain w/ activity or at rest

• not reliably resolved w/ rest or NTG

• may/may not have ECG changes

• may/may not exhibit other symptoms

• death to heart muscle, partial occlusion, can progress

STEMI

• typically sudden onset of severe chest pain/pressure

• pain not resolved with rest or NTG

• typically exhibits other s/s (more severe)

• subjective feeling of “impending doom”

• ST elevation in 2 or more leads on ECG

CAD diagnosis

cardiac biomarkers + physiology of ST changes

cardiac biomarkers/enzymes (panel of 3)

MYOGLOBIN: indicates muscle injury/breakdown

• least specific

• drawn at same time; several times within 24-48 hours

• repeated every # of hours

CK-MB: specific to injury to heart

• inflammation: inc = problem in heart

TROPONIN (cTnT): more specific subtype of troponin

• most specific for MI

• gold standard for MI!!

• detectable in blood for up to 2 weeks after event

• inc troponin = MI

• can take a while to show up in blood (4-8 hrs after MI)

ST depression =

ischemia

ST elevation =

necrosis

shock

• SEVERE COMPLICATION OF MI

• life threatening alteration in perfusion

  • reduced blood flow to tissues

    • insufficient to meet oxygen + metabolic demands

  • cell death

  • multisystem organ failure

types of shock

• hypovolemic

• neurogenic (ex. spinal cord injury)

• septic

• cardiogenic

• distributive vs obstructive

traditional 4-stage classification

• early/initial

• compensatory (compensations used against us)

• progressive

• refractory (untreatable)

progression of shock

TISSUE HYPOXIA, ACID/BASE/ELECTROLYTE IMBALANCES, TOXINS FROM CELL DEATH = MULTISYSTEM ORGAN FAILURE

• variety of compensatory mechanisms maintain hemodynamic stability for limited time

• cellular function thru anaerobic metabolism (w/out O2)

  • can be maintained only for limited time

• build up of lactic acid + other toxins contribute to cell death

• sodium-potassium pump disrupted

  • increased K+ out of cells

  • hyperkalemia = ASYSTOLE

cardiogenic shock

• left ventricular dysfunction (PUMP PROBLEM)

• severely compromised CO

• impaired systemic perfusion

cardiogenic shock causes

• MI (esp in LV)

• heart failure exacerbation

• arrythmia

• end-stage cardiomyopathy (structural problems)

• myocarditis (inflam. of myocardium)

• tamponade (external force on heart + can’t contract)

cardiogenic shock patho

• dec CO

• SNS inc, catecholamines = inc contractility

• RAAS activation: systematic vasoconstriction

• aldosterone: inc fluid retention

GOOD THINGS BUT INC CARDIAC WORKLOAD AND O2 DEMANDS

cardiogenic shock treatment goals

• maintain systemic perfusion (maintain MAP + help pump)

• improve cardiac output

• dec cardiac workload

• improve oxygen delivery to myocardium

cardiogenic shock nursing care

INTENSIVE CARE

• monitor VS, urine output, peripheral perfusion (peripheral pulses, cap refill), bowel sounds (d/t shunting)

• med admin: vasoconstrictors, inotropic drugs, diuretics, nitrates

• assist w/ placement + management of invasive hemodynamic monitoring: arterial line, Swan-Ganz catheter (pulmonary artery pressure, central venous pressure)

• semi-fowler’s position to reduce venous congestion + improve oxygenation

• multi-disciplinary collab based on patient needs + treatment response (cardiologists, specialists, dieticians)

meds that maintain SYSTEMIC PERFUSION (cardiogenic shock)

VASOCONTRICTOR DRUGS/VASOPRESSORS

INC/TITRATE TO MAINTAIN MAP 60 MMHG+

DOWNSIDE = INC WORKLOAD

• epinephrine

• norepinephrine

• high-dose dopamine

• vasopressin

meds that support cardiac output (cardiogenic shock)

+ ISOTROPES

HELP PUMP OR CONTRACTILITY

DOWNSIDE = INC WORKLOAD

• dopamine

• dobutamine

• milrinone

• amrinone

meds that decrease cardiac workload (cardiogenic shock)

VASODILATORS

• ACE inhibitors (suppress RAAS)

MECHANICAL SUPPORT (short term, buys time)

• intra-aortic balloon pump

• impella heart pump

meds that improve oxygenation

IV NITRATES (for chest pain; dilates CA + venous system, dec blood to heart, dec preload, dec workload, dec O2 demands)

MECHANICAL VENTILAITON

cardiogenic shock collab care: ongoing patient management

• stabilize, identify, treat cause

• intensive care setting

• advanced hemodynamic monitoring

• mechanical ventilation

• cautious IV fluids; strict I + O

• indwelling catheter

• nutrition: enteral or parenteral

• maintain skin integrity

• sedation/pain management

pulmonary artery catheter/swan-ganz catheterization

• big bird into pulmonary artery

• advanced, invasive hemodynamic monitor

• continuous monitoring of pulmonary artery pressure: indirect but accurate estimate of left ventricular function

• directs titration of vasoconstrictor + inotropic meds

cardiogenic shock collaborative care

• long-term management of underlying condition

• patient teaching/lifestyle modification

• cardiac rehab

• palliative care

• hospice

ACE inhibitors use + action

• vasodilation + reduce fluid retention

• ACS: lowers myocardial workload + O2 demand by lowering PRELOAD (inhibits fluid retention) + AFTERLOAD (vasodilation)

ACE inhibitors teach

• -prils

• bp monitoring

• fall risk, orthostatic hypotension

• contact provider if edema in feet/hands

• no salt substitutes

• hyperkalemia

• dry cough, angioedema

calcium channel blockers use + action

• vasodilation

• ACS: lower myocardial + oxygen demand primarily thru lowering afterload

calcium channel blockers teach

• -pines except diltiazem

• bp monitoring

• fall risk, orthostatic hypotension

• contact provider if edema in feet/hands

beta blockers use + action

• decrease contractility

• ACS: lowers myocardial workload + oxygen demand by lowering afterload (resistance) + reducing contractility

beta blockers teach

• -lols

• home monitoring bp + hr

• seek urgent care for sob, dyspnea on exertion, chest tightness

• no vagal stimulation; no rectal temps, don’t bear down or strain w/ BMs, no valsalva

• fall risk: orthostatic hypotension

• bradycardia

• watch for bronchoconstriction

nitrates use + action

• dilates coronary arteries and veins

• CAD/ACS: relief of chest pain by coronary artery vasodilation + reduce preload by lowering venous return to heart

nitrates teach

• nitroglycerine

• fall risk: orthostatic hypotension

• ibuprofen + acetaminophen ok for nitrate-induced headache

• no ED meds

• for chest pain, call 911 if first NTG don’t work

anti-platelet use + action

• reduce platelet aggregation

• ACS: reduce risk of MI; prevent progression to STEMI

anti-platelet teach

• ASA, clopridogrel

• s/s of bleeding (GI, emesis w visible blood or coffee ground, dark tarry stools)

• take with food

• report new/worsening abdominal pain

anti-coagulant use + action

• slows down clotting (inhibits synthesis of clotting factors)

ACS/MI:

• prevention in very high risk individuals diagnosed w/ CAD

• reduce likelihood of disease progression from UA to NSTEMI to STEMI

anti-coagulant teach

• heparin + warfarin

• s/s of bleeding

• keep lab appts (warfarin)

• may eat vitamin k-rich foods but keep amounts consistent

thrombolytics use + action

• lyse/dissolve existing blood clots

• ACS: reperfusion if PCI/CABG unavailable/unaccessible within time frame for tx

thrombolytics teach

• -ase

• s/s of bleeding

• no strenuous activities, contact sports

• contact provider/urgent care in fall event, blunt trauma, penetrating wounds, cuts, lacerations that don’t stop bleeding

HMG-COA reductase inhibitors use + action

• reduced cholesterol synthesis by liver inhibits LDL + stimulates HDL

• ACS: prevention in patients diagnosed w/ CAD

HMG-COA reductase inhibitors teach

• -statins

• reportable s/s: muscle aches, abnormal soreness, stiffness, cramps, weakness, dark urine

• no grapefruit/cranberry juice

alternate anti-cholesterol or lipid lowering agents use + action

• reduce amount of cholesterol absorbed from food

• ACS: prevention in patients diagnosed w/ CAD

alternate anti-cholesterol or lipid lowering agents teach

• cholestipol, cholestyramine

apex of the heart is located to

left of the sternum at fifth intercostal space

two atrioventricular valves are

bicuspid (mitral) + tricuspid

semilunar valves are

aortic + pulmonary

two main coronary arteries

left coronary artery + right coronary artery

where do the two main coronary arteries branch off

aorta

primary pacemaker of heart

SA node

travel of heart

impulses begin in SA node

AV node

the bundle of His

left and right bundle branches

Purkinje fibers

sense pressure in arterial vascular system

baroreceptors