OXY/CIRC N3 Lecture ORIGINAL

Inflammation of the heart's inner lining and valves

Usually caused by an infective agent (bacteria, fungi, viruses)

Streptococcus

Staphylococcus

IV drug abusers

Valve replacement recipients

Structural cardiac defects

Pharyngitis

Positive blood culture (usually strep)

Murmurs

S3 and S4 present

Fever/chills

Malaise, fatigue

Anorexia, weight loss

S3, S4 sounds

Chest pain

Petechiae

Splinter hemorrhages (see top left in pic)

Osler's nodes (see top right)

Janeway's lesions (see middle pics)

murmurs may be present in infective endocarditis due to damage to the heart valves

Heart failure

Systemic embolization

Sepsis

Heart blocks

Presents with:
- Edema
- Fatigue
- Shortness of breath
- Crackles

Left-sided heart embolizations:
- Brain
- Limbs
- Kidney
- Liver
- Spleen

Right-sided heart embolizations:
- Pulmonary embolism

Antibiotics --> high dose IV 4-6 weeks (not for viral infections UNLESS there is a secondary bacterial infection)

Adequate pain control

Surgical management if antibiotics don't work

Remove infected valves

Repair damaged valves

Repair shunts

Drain abcesses

Assess for HF: tachycardia, fatigue, SOB, edema, crackles

Balance activities --> adequate rest vs mobility

Monitor for the presence of murmurs or additional murmurs

Adequate pain control

Report to provider STAT: recurrent fever, fatigue, SOB, weight loss or gain

Antibiotic prophylaxis --> 4-6 weeks of therapy (some may have to take for life)

Focal or diffuse inflammation of the myocardium

Inflammation of the heart muscle (caused by virus, bacteria, radiation, pharmacologic, or chemical factors)
↓
May lead to hypertrophy, fibrosis (hardening), and inflammatory changes to the myocardium and conduction system
↓
Heart muscle weakens --> Contractility decreases
↓
Left ventricular dysfunction leads to pulmonary venous and arterial hypertension, pulmonary edema (think left-sided heart failure)

Cardiomyopathy

Fever

Fatigue, malaise

Myalgias (muscle pain)

Pharyngitis

Dyspnea

Lymphadenopathy (swollen lymph nodes)

Nausea/Vomiting

Pleuritic chest pain

Pericardial friction rub

Pericardial effusion

S3 heart sound

Dysrhythmias

Crackles

JVD

Syncope --> due to not enough oxygenated blood reaching brain

Peripheral edema

Angina

Think HEART FAILURE

Assess cardiac function:
- ECG --> ST changes
- Nuclear scans (MRI)
- Echocardiography

Confirm Diagnosis:
- Endomyocardial biopsy --> DEFINITIVE

O2

Bed rest, restricted activity (space activity and rest) --> don't overwork heart

Semi-Fowler's position --> help with breathing

ACE Inhibitors/Beta Blockers --> decrease preload

Diuretics --> decrease fluid volume, decrease preload

nitroprusside and milrinone --> reduces afterload, improve cardiac output

digoxin --> improve contraction, reduce HR

Anticoagulants --> for patients with low ejection fraction (EF)

AVOID NSAIDs FOR PAIN CONTROL

MOA: prevent conversion of angiotensin I to angiotensin II (which is a potent vasoconstrictor) --> decreased vasopressor activity and decreased aldosterone secretion

Side Effects: hypotension, hyperkalemia, cough

Contraindications: allergy, renal impairment (excreted by kidneys)

MOA - competitive antagonism of catecholamines at peripheral and cardiac adrenergic receptors --> reduces HR, cardiac contractility, and at higher doses, relaxes vascular smooth muscle, lowering the BP

Side Effects: hypotension, bradycardia, dizziness

Contraindications: severe bradycardia, cardiogenic shock, systolic BP <100 mmHg

nitroprusside and milrinone

Reduces afterload, improves cardiac output

Caution for Hypotension

Improves contraction and reduces HR

Side Effects: yellow-green visual discoloration, nausea, vomiting, cardiac dysrhythmias

Digoxin Toxicity is exacerbated by hypokalemia

Check apical pulse for 60 seconds before administration

For patients with low ejection fraction (for the blood that doesn't get pumped out and pools in the heart)

Heparin for acute myocarditis

Warfarin for chronic

Volume of blood in the ventricles at the end of diastole (heart relaxation)

When the volume of blood in the ventricles increases, the heart's stroke volume increases in response.

More cardiac muscle stretch = stronger contraction force

Resistance left ventricle must overcome to circulate blood

Condition in which pericardium around the heart becomes inflammed

Pericardial tissue is damaged by bacteria, fungi, virus, or another substance that releases chemical mediators of inflammation into surrounding tissue
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Chemical mediators dilate blood vessels and increase vessel permeability
↓
Vessel walls leak fluids and proteins, causing extracellular edema

Bacteria, virus, fungi infectie agent (usually respiratory)

Post MI syndromes

Connective tissue disease

Acute Pericarditis: 48-72h post MI

Dressler's Syndrome: 4-6 weeks post MI

Pericardial friction rub --> hallmark sign

Pericardial effusion --> presents as dyspnea/tachypnea

Sharp, severe radiating chest pain (made worse by inspiration and lying down, relieved by sitting)

Elevated WBC, high fever

ST elevation, Afib

Sitting upright

Leaning forward

Depends on the cause
- If bacterial: antibiotics 4-6 weeks
- if not baterial: corticosteroids
- if due to malignancy: radiation or chemo

Pericardiocentesis

Monitor for worsening pericardial effusion:
- Risk for cardiac tamponade
- Ineffective heart pumps

ECG monitoring

Hemodynamic measurements

Post op: watch for recurrence of tamponade

MEDICAL EMERGENCY

Accumulation of fluid in the pericardial space = reduced ventricular filling --> decreased CO, shock, death

Beck's Triad:
1. Hypotension with narrowed pulse pressure
2. JVD
3. Muffled heart sounds

Pulsus paradoxus - BP drops on inspiration

Tachycardia --> bradycardia (if not treated fast enough)

Dyspnea

Electrical alternans (alternating QRS amplitude from high-low-high-low)

Pericardiocentesis

Pericardial drain (if there isn't that much fluid)

Hemodynamic monitoring

Supportive therapy: O2, vasopressors, close monitoring for reoccurence

Aortic Stenosis (can't open fully)

Aortic Regurgitation (can't close fully)

Mitral Stenosis (can't open fully)

Mitral Regurgitation (can't close fully)

Congenital Bicuspid Valve Defect

Rheumatic Fever

Atherosclerosis degenerative disease

Rheumatic fever

Endocarditis

Enlargement Aortic root

Rheumatic fever

Congenital defect

Infective Endocarditis

Rheumatoid arthritis

Myocardial Infarction

SLE (systemic lupus erythematosus)

Fatigue

Dyspnea on exertion, Orthopnea (difficulty breathing while flat)

Paroxysmal nocturnal dyspnea (patient suddenly wakes up with SOB)

Hemoptysis (coughing blood)

Hepatomegaly

JVD

Pitting Edema

Rumbling, apical diastolic murmur

Fatigue

Dyspnea on exertion, orthopnea

Palpitations

Atrial fibrillation

JVD

Pitting edema

High-pitched, holosystolic murmur @ apex

Fatigue

Dyspnea on exertion, orthopnea

Paroxysmal nocturnal dyspnea

Angina

Syncope on exertion --> due to reduced CO

Harsh, systolic crescendo-decrescendo murmur

Fatigue

Paroxysmal nocturnal dyspnea

Othopnea

Palpitations

Angina

Sinus Tachycardia

Blowing, decrescendo diastolic murmur

Aortic --> second right intercostal space, right sternal border

Pulmonic --> Second left intercostal space, left sternal border

Erb's point --> Third left intercostal, left sternal border

Tricuspid --> Fourth left intercostal, left sternal border

Mitral --> Fifth intercostal, left mid-clavicular line

Same meds for heart failure
- Diuretics
- Beta blockers
- ACE inhibitors
- Vasodilators
- Anticoagulants
- Digoxin
- Prophylactic antibiotics

Oral health --> limit infections

Balance rest vs. exercise --> progressively increase activity to increase cardiac tolerance

Balloon valvuloplasty

Transcatheter Aortic Valve Replacement (TAVR)

Valvuloplasty
- Open fused valves --> allows for greater blood flow
- Does NOT reverse damage
- Does NOT prolong life, but provides symptom relief, improve ADLs and quality of life
- Indication: when ADLs are affected

Valve Replacement
- Requires lifelong anticoagulation --> check PT/INR, PTT

monitoring for warfarin therapy (lifetime treatment)

PT = 11-13.5 seconds

INR = 0.8 - 1.1

monitoring for heparin therapy (short term)

PTT = 30-40 seconds

PTT (with DVT therapy) = 50-90 seconds

Monitor for bleeding

Monitor for signs of regurgitant valve --> heart murmur, cardiac output, heart rhythm

Monitor for signs of systemic emboli

Monitor respiratory status

Monitor renal function --> BUN/Creatinine, urine output > 30 ml/hr

BUN = 6-20 mg/dL

Creatinine = 0.6-1.2 mg/dL

Assess for s/s of complications

encourage early ambulation

provide adequate pain control

Ensure home environment can provide rest

Increase ADLs as soon as pt can tolerate

Drug adherence - anticoagulant treatment

Home care aide to assist with ADLs

Incision care

Notify provider if: history of defective heart valve, any invasive dental work

Notify provider STAT if: fever, petechiae, SOB

Lifetime anticoagulant treatment (Warfarin for prosthetic valves) --> bleeding precautions, avoid dark green leafy veg

Permanant localized dilation 2x its normal diameter

Common in males age 65+

Common locations include:
- Thoracic aortic aneurysm
- Abdominal aorta

Arteriosclerosis - hardening of arteries

Atherosclerosis - narrowing due to plaque buildup

Tobacco use, HTN, Hyperlipidemia

CAD

Congenital anomalies --> Marfan's syndrome (breakdown of vascular tissue), Ehlers Danlos syndrome (collagen defect)

Penetrating or blunt trauma --> less common

CT w/ contrast --> assess size and location

Ultrasound

MRI

Aortic arteriography

Chest X-ray --> "eggshell appearance" = aortic dissection

Asymptomatic --> usually found during routine exams

If present --> difuse chest pain that extends to interscapular area

Hoarseness --> due to pressure in laryngeal nerve

Dysphagia --> pressure in esophagus makes it difficult to speak

Neck Vein Distention --> due to pressure in superior vena cava

Asymptomatic --> detected on routine exam

Pulsatile abdominal mass

Bruit over the aneurysm

Symptoms mimic abdominal and back disorder --> epigastric + back pain, altered bowel elimination

Rupture

Dissection

HTN --> MOST COMMON CAUSE OF RUPTURE

Assess for severe radiating back/flank pain (mimics kidney stone pain)

Assess for pulsation and bruit on xiphoid and umbilicus --> DO NOT PALPATE

Assess for s/s hemorrhagic shock --> hypotension, tachycardia, dysrhythmia, diaphoresis, oliguria, decreased LOC

if AAA:
- Abdominal distention
- Grey Turner Sign (back and flank bruising)

if TAA:
- SOB
- Hoarseness
- Dysphagia

Monitor + Maintain BP --> antihypertensive drugs

Monitor size --> CT scan, ultrasound

Educate:
- S/S of impending rupture
- Medications and follow-up

Elective:
- Endovascular Aneurysm Repair (EVAR) procedure

Emergent:
- Resection or repair (aneurysmectomy)
- Endovascular stent grafts

Graft Occlusion --> Monitor distal pulses (dorsalis pedis and post tib)

Graft Rupture --> Monitor for increasing abdominal girth, hypovolemic shock (↓BP, ↑HR)

Embolization

Paraplegia

Activity restriction --> 6-12 weeks; no stair climbing, no heavy lifting

Incisional care

Pain management

Aortic Dissection

Aortic Rupture

Inner wall of the aorta is damaged or torn --> can lead to less blood flowing to organs and limbs

Can lead to aortic rupture --> not good

Many people who have an ascending aortic dissection or severe descending aortic dissection do not survive

Atherosclerosis, chronic HTN, congenital heart defects

Hereditary Connective Tissue Disorder (Marfans, Ehlers-Danlos)

Vascular inflammation (syphillis, Takayasu's arteritis)

Trauma (such as motor vehicle crash, falls)

Iatrogenic events ( cardiac catherization, cardiopulmonary bypass)

Pregnancy (rare)

Crack cocaine use

Basically anything that threatens the integrity of the vessel wall

Varies with size, location, and stem of dissection --> most common site is ascending aorta

Sudden onset of severe tearing pain
- Substernal = ascending dissection
- Intrascapular = descending aorta

Hypertension --> Hypotension

Diastolic murmur secondary to aortic regurgitation

Damage to aortic valve

Impaired coronary blood flow

Cardiac tamponade

Laryngeal nerve compression

Bleeding into pleural space

Diastolic murmur

Due to the associated impaired coronary blood flow:
- Chest pain indicative of MI

Due to the associated impairment of cardiac tamponade:
- Muffled heart sounds
- Hypotension
- Tachycardia
- JVD

Hoarseness associated with laryngeal nerve compression impairment

Dyspnea

Hemothorax

Reduced blood flow to the brain

Interruption of cervical sympathetic ganglia

Impaired brachiocephalic flow

- Syncope
- Altered mental status
- Horner syndrome --> ptosis (eyelid drooping), miosis (pupil constriction), anhidrosis (absence of sweating on one side of the face)

Blood pressure differential

Asymmetric pulses in upper extremities

Spinal Cord Ischemia

Mesenteric Artery Ischemia (the artery that supplies blood to ur intestines)

Due to spinal cord ischemia
- Limb paresthesia/paralysis

Due to mesenteric artery ischemia
- Acute abdominal pain
- Melena (gi bleed)
- Hyperactive bowel sounds

Renal artery ischemia

Lower limb ischemia

- Flank pain
- Oliguria

Diminshed/absent pulses in lower extremities

Chest X-ray --> wide mediastinum

12 Lead ECG --> lack of ischemic changes (unless dissection affects coronary arteries)

Troponin and Creatine Kinase --> elevated if coronary arteries affected

CT scan

Transesophageal electrography (TEE)

MRI

Smooth muscle myosin --> elevated

Establish baseline assessment

Serial assessments to detect changes in LOC, motor/sensory function, ischemic changes

Assess bilateral pulses, BP, urinary output --> priority (BP should be evaluated bilaterally to rule out "psuedo" hypotension created by dissection into brachiocephalic vessel)

Monitor Oxygen saturation --> hypoxemia is common post op

IV meds to decrease BP and HR

Administer analgesics and sedation PRN --> dissection creates pain, which can exacerbate BP and HR

Continuously monitor core temperature (use Pulmonary Artery catheter)

Warm air blankets for temperature < 36C

Meperidine prn for shivering

Fluid warmers may be useful (esp if blood products are administered)

Control hemorrhage

Maintain patency of chest tubes

Maintain MAP of 70-80 --> increased pressure puts stress on suture lines and cannulation sites

Monitor H&H, platelet, PT/INR, PTT

Administer medications for bleeding (warfarin, heparin) --> have vitamin K, protamine sulfate on hand to reverse

Replace volume: blood products, volume expanders (dextran, albumin)

Impaired perfusion to brain and spinal cord may occur during period of circulatory arrest, emboli, or debris from surgical procedure

Allow patient to awaken ASAP to evaluate neuro status

Assess cognitive function, as well as gross motor movement and sensation

Potential for ischemic complications related to location of aortic injury, surgical approach, and preexisting disease

Continuous ECG monitoring (esp. ST segment monitoring)

Administer perioperative beta blockers as ordered --> decrease incidence of MI in pts with vascular disease

Optimize perfusion to spinal cord by maintaining adequate BP --> MAP > 80 mmHg

If lumbar drain --> maintain system @ prescribed level and drain CSF pressure < 10 mmHg

Q.1h Neuro check --> numbness/tingling, weakness in lower extremities

Cross-clamping or emboli may compromise flow to lower extremities

Perform neurovascular checks --> motor function, sensation, capillary refill, distal pulses (palpation or Doppler)

Renal failure may occur secondary to perioperative hypotension, hypovolemia, use of contrast dye, cross-clamping, or preexisting renal disease

Monitor urine ouptut q.1H --> > 30 ml/hr

Monitor filling pressures and maintain preload with fluids PRN

Maintain adequate blood pressure for renal perfusion

Patients are at risk for an ileus postop, esp. w/ repairs of abdominal aorta

Maintain NG tube to low continuous suction until bowel sounds are present

Monitor pt for s/s of ischemic bowel, including abdomnial pain and distention, persistent acidosis, elevated WBCs, diarrhea

Related to post surgery risk for atelectasis

Monitor O2 Sat PRN

Maintain mechanical ventilation PRN

Reposition frequently

If extubated: Deep breathing exercises and incentive spirometer q.1-2H

Splinting with pillow during cough

Provide adequate pain medication to promote activitiy without inducing respiratory depression

Goal is to stabilize to prevent rupture

Control BP (systolic 100-110 mmHg) --> beta blockers, ACE inhibitors, vasodilators

Management of hypercholesterolemia; smoking cessation

Regular follow up --> monitor size progression

ICU care for suspected dissection
- Aggressive BP control and monitoring
- Prep for surgery as warranted
- Psycho/emotional support for patient and family

Heart Enlargement = inefficient pump

Two types: Dilated Cardiomyopathy (DCM), Hypertrophic Cardiomyopathy (HCM)

Can lead to HF, dysrhythmias, sudden death if left untreated

mostly unknown

Bombay university uno

HTN

Chronic excessive alcohol intake

Pregnancy complications

Systemic infection

Echocardiography

Angiocardiography

ECG --> T wave inversion, ST segment depression

Fibrosis of myocardium/endocardium

Dilated chambers

Prevalent mural wall thrombi (thrombi that sticks to the wall)

Fatigue, Weakness, Dizziness, Syncope --> could be onset of deadl arrhythmia

Heart failure; left side

Dysrhythmias or heart block

Systemic or pulmonary emboli

S3 and S4 gallops

Moderate to severe cardiomegaly (enlarged heart)

Hypertrophy of all walls

Hypertrophied septum

Relatively small chamber size

Dyspnea, fatigue --> lungs need to work harder to adequately oxygenate

Angina (kinda obvious ngl)

Syncope --> due to decreased cardiac output

Palpitations

Mild cardiomegaly (enlarged heart)

Ventricular dysrhythmias (i wonder why)

Heart failure (no shit)

Sudden death is common

Same as nonobstructed EXCEPT there is obstruction of left ventricular outflow tract associated with hypertrophied septum and mitral valve incompetence

Same as nonobstructed

Mitral regurgitation murmur

Atrial fibrillation

O2 therapy

Drug Therapy:
- Diuretics --> insert foley, I&O
- Morphine --> reduces venous return (preload)
- Vasodilators
- Digoxin

Control of dysrhythmias

Report dizziness or fainting --> indication of onset of lethal dysrhythmia

Avoid alcohol, strenuous exercise

Surgery --> heart transplant

For both obstructive and nonobstructive

Drug Therapy:
- Beta Blockers
- Antidysrhythmic drugs
- Nitrates and other vasodilators are contraindicated in the obstructed form --> CO is already low, don't wanna make it worse

Conversion of afib

Automated implantable cardioverter defibrillator

Genetic Counseling

Surgical management:
- Ventriculomyotomy or muscle resection with mitral valve replacement

The pumping ability of left ventricle fails and cardiac output decreases
↓
Blood backs up into the left atrium and lungs, causing pulmonary congestion
↓
If left untreated, left-sided heart failure leads to right-sided heart failure

Ineffective contractile function of the right ventricle
↓
Blood backs up in right atrium and peripheral circulation
↓
Peripheral edema and engorgement of kidneys and other organs

HTN

CAD

Cardiomyopathy

Valvular disease

Cardiac infections

DM

Family history

Acute myocardial infarction

Hyperthyroidism

Substance abuse

Congenital defects

Dysrhythmias

Alcohol/Tobacco use

Severe lung disease

Decreased Cardiac Output and Systemic Blood Pressure
Baroreceptors in the left ventricle, aortic arch, and carotid sinus are activated
↓
Vasomotor regulatory center in medulla is stimulated
↓
Sympathetic nervous system activated
↓
Increase in catecholamines (epinephrine and norepinephrine
↓
Vasoconstriction --> increase in afterload, blood pressure, HR
↓
Impaired contractility = decreased cardiac output

RAAS system activated
↓
Angiotensin II --> leads to vasoconstriction
↓
Aldosterone released into the kidneys --> retain more sodium and water

Hypertrophy and dilation of ventricles
↓
Impaired contractility = decreased cardiac output

Crackles secondary to pulmonary edema

Increased HR, S3 and S4 present

Fatigue, Dyspnea, Orthopnea, Nocturnal Dyspnea --> Do NOT lay flat

Nocturia

Pulsus Alternans (alternating pulses: strong -> weak0

Dry, hacking cough

Peripheral edema

Increased HR

Fatigue

Ascites (fluid in abdomen)

Anasarca (general swelling around body)

Weight Gain

JVD

Hepatomegaly --> right upper quadrant pain

Right pleural effusion

Anorexia, GI bloating, Nausea

Detect underlying etiology

History and Physical

chest xray

12 Lead ECG

Detect Ejection Fraction --> echocardiogram, stress test, cardiac catherization

BNP (brain natriuretic peptide) --> increased in HF (should be under 100 pg/mL)

Cardiac enzymes (troponin and creatine kinase)

BMP, CBC

LFT

Thyroid function studies

When the heart works harder to pump blood, it releases BNP

BNP signals blood vessels to widen and kidneys to remove water and salt

Increased in heart failure

Sodium and fluid restrictions; I&O

O2 therapy

Biventricular pacemaker

Implantable cardioverter-defibrillator

Circulatory Assistive Devices --> Intra-aortic balloon pump, ventricular assist device

Cardiac Transplantation

End of life care

Decreases preload

Decreases systemic vascular resistance --> increases cardiac output and improves tissue perfusion

Decreases heart rate --> decreases heart O2 demand

Milrinone

Improves contractility --> improves cardiac output

Dopamine, Dobutamine, Levophed (norepinephrine)

digoxin

Improve contractility, decrease HR

Vasodilation

Decrease preload

Avoid Viagra

Decrease preload, anxiety, work of breathing

Relaxes blood vessels, slows the heart, and slows breathing down

Since they aren't as physically active and also blood is not effectively moving and is stagnant, anticoagulants may be required to prevent thromboembolisms

Life expectancy less than 1 year

Age < 65

Normal or slightly elevated pulmonary vascular resistance

Absence of active infection

Stable psychosocial status

No evidence of current drug or alcohol abuse

monitor for bleeding --> s/s of cardiac tamponade

medications to support HR and maintain CO

Caution to change position slowly (orthostatic hypotension)

Pacemaker

Monitor for transplant protocol --> s/s of rejection (flu-like symptoms, swelling); immunosuppressants

Strict I&O

Monitor for signs of fluid overload --> daily weights (1-2 lb increase); breath sounds, SOB (how many pillows needed?)

Safety --> progressive mobility

Energy conservation

Follow-up care

S/S to report --> SOB, swelling in legs, ankles, feet, chest pain, etc.

Morphine --> decrease preload

Diuretics --> decrease preload

Vasodilators --> decrease afterload

Amiodarone --> control dysrhythmia

Digoxin --> improve contractility

Intra-aortic Balloon Pump --> balloon is deflated during systole. inflated during diastole (rest)
- Balloon inflation during diastole allows the heart to fill

HeartMate II Ventricular Assist Device (Thoratec) --> used as bridge to heart transplant

when your heart cannot pump enough blood and oxygen to the brain and other vital organs

Inability of the heart to pump blood forward

Ex: MI, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary HTN, myocardial depression

Inability of the heart to fill

Ex: Cardiac tamponade, ventricular hypertrophy, cardiomyopathy

Bradydysrhythmias

Tachydysrhythmias

Vavular stenosis or regurgitation

Ventricular Septal Rupture

Tension pneumothorax

Systolic BP < 90 mmHg, HR >100 bpm

Weak, thready pulse

Chest pain, dysrhythmias

Tachypnea

S3,S4, Crackles

JVD

Decreased O2 saturation

Cool, pale, moist skin

Urine output <30 mL

Decreased cardiac output

Change in sensorium

Pharmacological agents to maintain cardiac output
- Inotropic agents (dobutamine, milrinone) --> increases contractility
- Vasopressors (dopamine)
- Diuretics --> reduce preload
- Vasodilators --> reduce preload and afterload
- Antidysrhythmic agents

Intubation and mechanical ventilation --> sedate + paralyze

IABP (intra-aortic balloon pump)

Ventricular Assist Device

Early identification --> facilitate earlyl reperfusion treatment

Close monitoring (q.10-15 minutes)

Limit myocardial O2 demands --> administer pharmacological agents

Maintain respiratory status

Monitor for complications

First choice for cardiogenic shock

Vasopressor support

Some positive inotropic effects

Minimum doses should be used and systemic vascular resistance should be monitored during administration

Vasopressor support with some positive inotropic effects

May increase pulmonary artery occlusion pressure

Minumum dose should be used; systemic vascular resistance should be monitored

produces positive inotropic effect by increasing cardiac index

also decreases afterload (through vasodilation)

Used to induce peripheral vasodilation and provide inotropic support

Decrease preload and afterload

Amiodarone --> for sustained ventricular or atrial tachyarrhythmias

SA node (main pacemaker; 60-100 bpm)
↓
AV node (backup pacemaker; 40-60 bpm)
↓
Bundle of His (super backup pacemaker; 30-40 bpm)
↓
Purkinje fibers

represents depolarization (contraction) of the atria

represents depolarization (contraction) of the ventricles

Represents repolarization (back to resting state) of the ventricles

amount of time it takes for electrical signal to move from SA to AV nodes

Rhythm is regular

P wave: abnormal; inverted or hidden

PR interval < 0.12 seconds when P wave precedes QRS

QRS is normal

CAD, HF, cardiomyopathy

Electrolyte imbalances

Inferior wall MI

Rheumatic heart disease

SA node disease (i.e. Sick Sinus Syndrome)

Drugs (such as digoxin, amphetamines)

Vagal simulation

Cardiac surgery

May be asymptomatic

Lightheadedness, palpitations

Effort intolerance, chest heaviness

Neck tightness or pounding

SOB, weakness

Hypotension, Bradycardia

Altered LOC, blurred vision

Treat the underlying cause

Discontinue meds causing the arrhythmia

If caused by Digitalis toxicity
- Administer Digoxin Immune Fab
- Check serum potassium (potentiates dig toxicity)

Atropine --> increase HR

Temporary or permanent pacemaker

Ablation

Interruption in conduction between atria and ventricles

differentiated by PR Interval:
- 1st degree --> impulses reach ventricles
- 2nd degree --> some impulses do not reach ventricles
- 3rd degree --> no sinus impulses reach ventricles (Complete Heart Block)

R is far from P --> PR interval greater than 0.2 seconds (one box)

Most common form of heart block

Impulse conduction between atria and Bundle of His is delayed at the level of the AV node

MI or ischemia

Medications: digoxin, Ca Channel Blockers (amlodipine, diltiazem), beta blockers

Myocarditis

Degenerative changes of the heart

Asymptomatic

Dizziness, syncope

Longer, Longer, Drop --> PR interval continues to increase untill impulse is not conducted (QRS complex is dropped)

Risk: Reduced cardiac output, progression to 3rd degree

CAD, Inferior wall MI

Rheumatic fever

Increased vagal stimulation

Medications: propanolol, digitalis, verapamil

Some P's don't get through --> atrial rhythm is regular, ventricular rhythm is irregular (dropped/non-conducted beats)

More lethal than Mobitz I

Risk: Reduced cardiac output, Progression to 3rd Degree Heart Block

Anterior MI

Medications (like digoxin)

Changes of the heart

CAD

Lyme disease

P's and Q's don't agree --> impulses from atria are completely blocked at AV node (can't be conducted to the ventricles

Most serious type

Risks: Progression to asystole; rate is too slow and ineffective

Congenital condition

CAD

Acute MI, inferior wall MI

Degenerative changes of the heart

Digitalis toxicity

Severe fatigue

Dyspnea

Chest pain

Decreased LOC

Hypotension

Pallor

Diaphoresis

ECG

Echocardiogram

Electrolytes

Drug Level

Purpose is to figure out the cause

If asymptomatic --> continue to monitor, treat the underlying cause

Goal: Raise HR to improve cardiac output, improve ventricular rate

Oxygen therapy; bed rest

Medications: atropine, epinephrine, Isoproterenol, Dopamine

Temporary or transcutaneous pacemaker --> until rhythm resolves

Holter Monitor

think of it as a "portable ECG monitor"

Pt Education:
- Keep diary of activities and symptoms
- Do NOT shower while on monitor

Stimulate a heartbeat if HR drops too low

Usually initiates pacing stimulus if ventricular rate drops below the preset level (usually 72 bpm)

Two types: Temporary (transcutaneous) and Permanent

Treat temporary problems (duh)
- Heart surgery
- Overdose of medicine
- Emergencies

Long-term rhythm problems

Keep site dry and clean for a week

Bed rest for first 12 hours

Avoid lifting for one week

Avoid high output generators (like an MRI)

Teach patient how to take a pulse --> if set at 72 bpm, pulse should be at 72 bpm

Low HR = pacemaker failure

Carry a pacemaker info card

Watch for pre-implementation S/S --> chest pain, diaphoresis, dizziness

Atrial pacing "spikes" followed by P waves

Ventricular pacing "spikes" followed by wide, bizarre QRS complexes

QRS will look wide and bizzare --> this is because impulse is generated in the ventricle (does not follow normal pathways from atria)

Danger is potential for pacer spike to land on T wave

Although unlikely, it can cause Ventricular Fibrillation

Originates above Bundle of His

Triggered by a Premature Atrial Contraction (PAC)

HR: 100 - 300 bpm

P wave is hidden in preceding T wave; PR interval is shortened or normal; QRS is usually normal

If HR > 180 bpm and sustained --> low cardiac output, hypotension

Overexertion

Emotional stress

Stimulants (like caffeine)

Rheumatic Heart Disease

Digitalis toxicity

CAD

Vagal stimulation --> Valsalva, coughing

Cardioversion

Ablation --> radiofrequency catheter ablation

Implantable Cardioverter Defibrillator

Medications (adenosine, diltiazem, amiodarone)

IV adenosine --> Administer IV rapidly (1-2 seconds), causes brief asystole (place on heart monitor)

Antiarrhythmics --> Diltiazem, amiodarone

More life-threatening than atrial dysrhythmias

Result from increased irritability of the ventricles

CHF, COPD, MI (esp. anterior MI)

Anemia

Hypokalemia --> #1 cause
- PVC's, prolonged PR interval, T wave inversion
- Patient complains of N/V

Hypomagnesemia

Anesthesia, Infection, Surgery

Stress, Nicotine, Caffeine, Alcohol

Assess the patient --> are they symptomatic or asymptomatic

Check how many PVCs per minute --> if less than 6, continue to monitor

Are the PVCs the same shape?

If >10/min with symptoms --> treatment time

Oxygen

Prevent progression to VTach --> assess and treat cause

Lidocaine IVP --> 1 mg/kg

PVC occuring on a T wave

Can trigger a lethal arrhythmia

Repetitive firing at 150-250 bpm

Can be preceded by PVCs

MI, CAD, HF

Hypokalemia, Hypomagnesemia

Valve defects

Digitalis toxicity

Cardiomyopathy

Determined by a presence of a pulse

Lidocaine + Amiodarone --> be aware of seizures for lidocaine

Synchronized cardioversion --> avoid R on T phenomenon

Ablation --> for chronic cases

Defibrillation - Unsynchronized

CPR/ACLS

Elective procedure --> Obtain informed consent

Patient is awake and sedated

Synchronized with QRS

50-200 Joules

ECG Monitor

Emergency --> pulseless VTach or VFib

Patient has no cardiac output; patient is unconscious

Begin with 200 Joules; may go up to 360 Joules

ECG monitor

Used for sustained and nonsustained VTach, VFib

Also used for atrial dysrhythmias

IV or PO

Many side effects --> hypotension, corneal microdeposits (visual disturbances; most common)

Most serious concern is Pulmonary Toxicity

Result of electrical chaos in ventricles --> no CO = no systemic perfusion

Rhythm is fatal if not successfuly ended in 3-5 minutes

Accidental elective shock (R on T phenomenon)

Hyper/Hypo Kalemia

Hypoxemia --> esp from MI, CAD, cardiomyopathy, etc.

Acidosis

Drug toxicity

Defibrillation

ACLS measures

1. 30:2 ratio compressions to ventilations

2. Shock once at effective setting (~360 Joules) --> resume CPR after shock

3. Start IV and put on O2

4. If still no pulse, IVP epinephrine 1mg q. 3-5 minutes

5. When ready, intubate or LMA (laryngeal mask airway)

6. Rhythm check q.2min; Epinephrine 1mg Q.3min

AKA ventricular standstill

Complete absence of any ventricular rhythm

No electrical activity

Electrical activity on ECG monitor but no ventricular activity (no pulse)

Account for 50% of trauma deaths

Blunt trauma (non-penetrating), penetrating (like stabs or gunshot wounds)

Emergency approach --> Remember the ABC's (airway, breathing, circulation)

Bruising of lung secondary to blunt trauma or rib fracture

Intra-alveolar hemorrhage = Interstitial edema = ↓ pulmonary compliance, ↓ gas exchange, ↓ lung perfusion = ventilation perfusion imbalance

May be asymptomatic first 24-48 hours

Hypoxemia, SOB

Blood-tinged sputum

Crackles, wheezes

Atelectasis

Chest X-Ray --> pulmonary infiltrate, hazy opacity

Goal: Aggressive Respiratory Care
- O2, deep breathing exercises, incentive spirometry
- Adequate pain control
- Semi Fowlers
- If side lying, good lung down
- Noninvasive Positive-Pressure Vent (NPPV)
- Mechanical ventilation with PEEP (positive end-expiratory pressure)

ARDs

Emphysema

Pneumonia

Lung abcess

Pulmonary Embolism

due to fracture of 2+ ribs

Characterized by paradoxical chest wall movement --> sucking inward on inspiration; puffing outward on expiration

Absent breath sounds = pneumothorax (air leak between lungs and chest wall)

Severly impairs ability to expand lungs and thus gas exchange

Goal: Vigilant respiratory care - assess for other injuries

Humidified O2

Pain control

Promote lung expansion --> chest tube

Effective oxygenation --> mechanical ventilation (PEEP), Monitor ABGs and vital capacity (how much air they can exhale)

Surgical stabilization of rib fracture

air in the pleural space

Closed = no external wound

Open = penetrating chest wound

Mechanical ventilation

Insertion of subclavian catheter

Perforation of esophagus

Rib Fracture

Blebs or bullae rupture (COPD)

Dyspnea, chest pain (no shit sherlock)

Decreased movement that is involved with chest wall

Diminished/Absent breath sounds on affected side

Hyperresonance to percussion

Vented Dressing (only on 3 sides) --> open the pneumothorax to release air

Stabilize impaling object --> Do NOT remove

Insertion of chest tube

Heimlich (Flutter valve) --> attached to chest tube to release air

Tension Pneumothorax

a life-threatening condition that occurs when air accumulates in the pleural space, putting pressure on the lungs and heart

Open: thoracic cavity is exposed to outside air

Closed: no disruption in thoracic cage

Air gets trapped --> causing lung collapse
↓
Interferes with venous return
↓
Decreased diastolic filling
↓
Compromised cardiac output --> lung is being pushed and the ventricles cannot contract properly

Idiopathic: chest tube is clamped or blocked

Mechanical ventilation, resuscitive efforts

Perforation/trauma

Spontaneous: COPD with ruptured bullae or bleb (literally just pimples of air on the lung)

Mediastinal shift --> asymmetry of thorax, tracheal deviation

Subcutaneous emphysema --> infiltration of air under the dermal layer

Tachypnea, Tachycardia, Hypotension --> hypotension due to decreased CO

Respiratory distress (no shit)

Absent breath sounds on affected side

Distended neck veins, cyanosis

Needle decompression

O2 therapy

Chest tube insertion

Serious condition in which blood collects in the pleural space

>1500 mL of blood in chest cavity

Arterial bleeding requires surgical intervention

Blunt or penetrating chest trauma

Immediate post-op CABG

Hypotension associated with absence of breath sounds

Dullness to percussion on affected side of the chest

Diminished/Absent breath sounds on affected side

Hypovolemic shock

Chest Tube

Auto-transfusion --> transfuse own blood

Thoracotomy --> indicated if >200 ml/hr for 2-4 hours, injuries to major cardiovascular structures

Cardiac Tamponade

Accumulation of fluid in pericardial space --> MEDICAL EMERGENCY

Reduced ventricular filling, hemodynamic compromise = shock, death

Beck's Triad --> Hypotension, JVD, Muffled heart sounds

Pulsus Paradoxus --> sys. BP increases on expiration rather than inspiration

Electrical alternans (QRS alternates going high, low, high)

Tachycardia --> can eventually lead to bradycardia

Dyspnea

Hemodynamic monitoring

Fluid resuscitation

Pericardiocentesis

Pericardial drain --> if there isn't that much fluid to drain

Monitor for recurrence

Presence of bubbles in the water seal

Intermittent air leak = injury to lungs or airway

Continuous air leak = either large injury to lung or airways or a leak in the tubing

Ensure occlusive dressing is tight and intact

Assess for difficulty breathing --> pulse ox

Assess breath sounds for each lung

Check alignment of trachea

Check tube insertion site --> puffiness or crackling may indicate subcutaneous emphysema

Observe site for infection

Pain control

Deep breathing exercises and incentive spirometry

Administer high flow O2 w/ nonrebreather mask

Establish 2 large bore (20 g or 18g) IV catheters --> fluid resuscitation as appropriate

Remove clothing to assess injury --> cover sucking chest wound w/ nonporous dressing taped on 3 sides

Stabilize, don't remove impaling object

Stabilize flail rib segment

After cervical spine injury is ruled out, place in Semi-Fowler's

Monitor vitals, LOC, O2 sat, cardiac rhythm, resp. status, urinary output

If tension pneumothorax develops, release dressing

Collection of pus, necrotic tissue in pleural space --> Infection

Pneumonia

Lung abcess

Infected pleural effusion

Penetrating chest trauma

Iatrogenic factors --> chest surgery, thoracentesis

Fever > 100.4F

Chest pain, dyspnea

Weak cough, inability to clear secretions

Presence of crackles

Weight loss

Night sweats

Chest XRay

CT scan

Treatment: Same for anyone with infection
- antibiotics (if indicated)

Chest tube, thoracentesis --> empty empyema cavity

Decortication (if not resolved with above) --> remove fibrous/infected tissue on lung surgically

Lung re-expansion

Resolution of effective breathing

Improvement of pulmonary function

a serious and potentially fatal lung condition that occurs when the lungs are severely injured, making it difficult for them to supply the body with enough oxygen

Damage to the alveoli reduces blood flow to the lungs, allowing platelets to aggregate. The platelets release substances that inflame and damage the alveolar membrane and increase capillary permeability
↓
Increased permeability of alveolocapillary membranes allow fluids to accumulate in the lung interstitium, alveoli, and small airways, causing them to stiffen
↓
Ventilation is impaired, reducing oxygenation of pulmonary capillary blood
↓
Pulmonary edema worsens. Inflammation leads to fibrosis, which further impedes gas exchange

Pulmonary aspiration

Shock; trauma; serious infection

Embolisms

Sepsis

Drugs OD (heroin, opioids, ASA)

Hemolytic disorders (e.g. bood transfusions)

Cardiopulmonary bypass

Drowning

Persistent hypoxemia despite 100% O2 --> refractory hypoxemia, a CARDINAL feature

Decreased pulmonary compliance

Dyspnea, tachypnea

Noncardiac bilateral pulmonary edema

Life-threatening

Diaphoresis

Refractory hypoxemia --> low O2 sat despite high oxygen

Restlessness, anxiety, confusion

Dyspnea, Tachypnea

Tachycardia

Cyanosis

Somnolence -->drowsiness

Blood tinged frothy sputum

Pulmonary edema

PaO2 < 60 mmHg on ABG; refractory hypoxemia

Sputum culture (bronchoscopy)

Chest Xray --> diffuse haziness/white-out/Ground glass (see image)

no cardiac involvement on ECG

*Early recognition of high-risk patients*--> patients who aspirated

Mechanical ventilation with PEEP or CPAP

Sedation

Postioning --> Prone, kinetic beds

ECMO for severe ARDs

Nutrition --> can't heal without food (think Maslow's)

Prepare patient and family --> 35-60% mortality rate

Antibiotics

Vasopressors --> support vital signs (like BP)

Vitamin C and E

N-acetylcysteine --> break up mucus

Nitric Acid --> relaxes smooth muscle in pulmonary vessels

Surfactants --> prevent alveolar collapse

Inability to maintain adequate oxygenation for tissues OR adequate removal of CO2 from tissues

Classified as extrapulmonary or intrapulmonary

Can be Ventilation or Oxygenation failure or both

Patient is hypoxemic/hypercapnic due to impaired gas exchange

Most common cause of hypoxemia

Occurs when either the ventilation (airflow) or perfusion (blood flow) in the lungs is impaired, preventing the lungs from optimally delivering oxygen to the blood.

Low V/Q ratio may occur from: decrease of ventilation; overperfusion in presence of normal ventilation

Defect in respiratory control center in brain

Poor respiratory muscle function (esp. diaphragm)

Extrapulmonary causes: CNS depression, CV disorders, Endocrine disorders, Metabolic disorders, airway irritants, thoracic abnormalities

Disorders of the respiratory tract

Hypoxemia, Hypercapnia

Acidosis, dyspnea

O2 sat may be normal but elevated end-tidal CO2 (amount of CO2 on expiration)

Restlessness

Irritability

Agitation

Confusion

Tachycardia

CO2 Narcosis:
Decreased LOC, drowsiness

Lethargy

Seizure

Headache

Performed emergently on patient in cardiopulmonary arrest

Performed electively with impending respiratory failure --> establishes airway, assist in removal of secretions, protects airway from aspiration

Assess breath sounds bilaterally

Symmetrical chest expansion

End Tidal CO2 Detector --> most accurate

Portable Chest X-ray --> most accurate

Preoxygenate with 100% O2 for one minute before

Based on standard procedure to prevent:
- hypoxemia
- airway trauma
- infection
- increased intracranial pressure

In line suction vs. single use suction catheter

Tidal Volume (Vt) --> amount of air delivered with each preset breath

breaths/min

amount of O2 delivered with each breath

duration of inspiration in comparison to expiration

amount of positive pressure added with each expiration

May be due to:
- Increased secretions
- Mucous plug
- Pt coughing, gagging, biting tube
- Pt fighting ventilator
- Condensation in tube

May be due to:
- Leak in tubing (produces a sound) --> check cuff inflation
- Pt stops spontaneous breathing in CPAP/SIMV mode
- Cuff leak in endotracheal tube

Assess tube placement

Breath sounds; chest wall movement

Prevent accidental extubation --> soft wrist restraints, sedation

Check pilot balloon

Nutrition status --> so they can heal up

VAP protocol --> prevent infection

Monitor Urine Output --> ventilators can lead to decreased kidney perfusion

Assess patient FIRST, ventilator SECOND

Monitor patient response

Manage ventilator system

Prevent complications of prolonged intubation

Vocal cord paralysis --> hoarseness

Aspiration --> ventilator associated pneumonia (VAP)

Maintain HOB at 30-45 degrees

Interrupt sedation to assess readiness to wean from ventilator --> "sedation vacation"

Provide prophylaxis for DVT

Administer medications for peptic ulcer disease prophylaxis

Daily oral care with chlorhexidine --> prevent infection

amount of air moving in/out of lungs during a breath

Preset Tidal volume, respiratory rate

Pt triggers breath between vent-initiated breaths

Ensures pt receives adequate ventilation regardless of spontaneous efforts

Similar to AC --> preset tidal volume, respiratory rate

If pt initiates a breath --> delivery of the mandatory breath is synchronized with spontaneousu effort

Keep awake --> must have adequate respiratory drive and tidal volume

Vent has NO mandatory breaths --> Patient performs all work of breathing

Noninvasive pressure support ventilation

Hypotension --> monitor I&O, weight, hydration, S/S of hypovolemia

COPD --> bullae or blebs

Barotrauma --> pneumothorax

Ventilator associated pneumonia (VAP) --> VAP protocol

Ventilator Dependence - wean asap

Nutrition --> Enteral feedings/TPN within 48 hours

Stress Ulcer --> antacids, PPIs (-prazoles)

Muscle Decondition/Atrophy --> passive exercise

Fluid/electrolyte imbalance

Pressure sores

UTIs

Process of going from ventilator dependence to spontaneous breathing

Notice the different suction pressures for age groups?

Tube dislodgement in the first 72 hours after surgery is an EMERGENCY
- Tracheostomy tract --> not matured, replacement is difficult
- Trach tube may end up in subcutaneous tissue --> "false passage" of oxygen

Place trach tube of same type/size (or one size smaller) at bedside

Place trach tray at bedside

O2 and suction units at bedside (if wall unit isn't available)

Air escapes into tissues of neck, chest, and face

Crepitus - puffy with crackling when pressing area involved (like bubble wrap)

Notify physician immediately --> EMERGENCY