Health and Illness 3: Exam 1

September 14

Formula for Cardiac Output

HR (BPM) x Stroke Volume = CO (L/min)

• Normal range 5-6 L/min

Diastole vs Systole

Diastole: All chambers of heart relax, blood flows in

Systole: Heart contraction - pushing blood out

Ischemia vs Infarction

Ischemia: Blood supply available but decreased

• NSTEMI, unstable angina

Infarction: Death of tissue r/t lack of blood supply (ie M.I)

• STEMI

Flow of Blood Through the Heart

Deoxygenated blood enters

Vena Cava

Right Atrium

Right AV valve (tricuspid)

Right Ventricle

Pulmonary valve/arteries

Lungs

Oxygenated blood enters via

Veins

Left Atrium

Left AV valve (mitral/bicuspid)

Left Ventricle

Aortic valve/aorta

Body

Patient Lifestyle Management for Hypertension

• Reduce weight by 5% (1 kg = 1 mmHg down)

• DASH eating plan

• <1500 mg/day of sodium (if substituting salt, watch for potassium if on a potassium sparing diuretic (spironolactone))

• No alcohol

• Increased exercise (150 min/week)

Stage 1 (130/80): Diet/lifestyle mods (try for 3-6 months before adding med if low risk) + one medication

Stage 2 (140/90): Diet/lifestyle mods + two medications

Medications for Hypertension (1st Line)

1. Thiazide diuretics (hydrochlorothiazide)

2. ACE inhibitor (lisinopril)

3. CCBs (amlodipine)

4. ARBs (losartan) - can cause renal problems if used alongside ACEs

Hypertensive Crisis

>180/120

Urgency

• May require hospitalization

Emergency

• Evidence of target organ damage

• Hospitalization

S/S

• Severe HA

• Blurry vision

• Dizziness

• Epistaxis

• Vomiting

Often caused by not taking HTN medications, or abrupt stopping of meds

Hypertensive Emergency Treatment

1. Vasodilators - Sodium Nitroprusside IV

2. Nicardipine IV (CCB)

3. Labetalol (BETA blocker)

Bring down BP by 20-20% in first hour - not less than 140/90

• BP monitoring q 5-15 min (ART line?)

• Neuro assessment (pupils, LOC) ( can cause hypertensive encephalopathy, intracranial hemorrhage)

• Cardiac status assessment (can cause MI, aortic aneurysm, HF)

• Measure UOP

  • High Creatinine, High BUN - RENAL FAILURE

MAP Calculation

SBP + 2 (DBP) / 3 = MAP

What Causes Hypertension

• Increased CO (from increased fluid/SV, from increased cardiac activity/HR)

• Increased resistance/SVR, PVR (from vasoconstriction, RAAS system activation)

Hypertension Medications that Reduce SV (and in turn reducing CO)

1. If cause of increased CO is from high fluid/SV in body

Diuretics to get fluid out

• Furosemide - strongest, loop, K wasting (watch for digoxin tox!) - not first line

• Hydrochlorothiazide - thiazide - watch for hypokalemia

• Spironolactone - potassium sparing - blocks aldosterone instead of providing direct diuresis - watch for hyperkalemia

Hypertension Meds that reduce HR (and in turn reduce CO)

2. If cause of increased CO is from increased cardiac activity (HR)

Decrease HR/cardiac activity

• Metoprolol - cardioselective (beta - 1 only- only affects heart)

• Propranolol - non- cardioselective (affects heart and lungs beta 1 and 2) - caution with asthma

• Diltiazem - CCB - decreases HR and contraction strength - use for HTN, NOT HF! - No grapefruit

• Clonidine - CCB - stops SNS system - mostly used to decrease SVR but can also decrease HR - DONT stop abruptly - rebound htn

Hypertension Meds that Decrease Resistance (SVR, PVR) - Inhibitors of RAAS System

3. If cause of increased resistance is due to RAAS system activation

• Lisinopril - ACE inhibitor - stops angiotensin 1-2 conversion which leads to vasoconstriction - Stops RAAS system - Monitor creatinine and BUN for kidney function

• Losartan - ARB - Blocks angiotensin receptors preventing vasoconstriction - Stops RAAS system

Hypertension Meds that Decrease Resistance (SVR, PVR) - General Vasodilators

4. If cause of increased resistance is general vasoconstriction

• Amlodipine, Nicardipine - CCBs - IV used for HTN crisis - Prevents Ca, which is needed for muscle contraction from entering into heart cells

• Diltiazem - CCB

• Hydralazine - Direct vasodilator - causes arterial vasodilation -may be sudden and quick drop

• Nitroglycerin - Direct vasodilator- venous dilation in small doses, arterial vasodilation in larger doses

• Sodium Nitroprusside - Direct vasodilator - used for HTN crisis

Coronary Artery Disease

Caused (usually) by artherscleorotic plauques that narrow the coronary arteries and reduce blood flow to the heart muscle, leading to ischemia and potential heart attacks.

• Angiogenesis may occur - new BV pathways to heart if arteries are blocked - compensatory blood flow occurs - may not be adequate in events such as strenuous exercise which causes angina

Diagnostics for CAD

• ECG

• Coronary CT angiogram/Cardiac Cath - Gold standard for dx

Asses for contrast dye/iodine allergy and for kidney function (BUN, Creatinine) (taking metformin? Hold for 48h)

Keep extremity (usually femoral, radial or brachial) where catheter was inserted straight and flat after

Keep pressure dressing on for 24h

Brace insertion site when coughing, monitor site for bleeding

• Troponin

• CRP/ESR (general inflammation)

• Echocardiogram - Have pt lay on L side

• Increased LDL lab

• Decreased HDL lab

• Cardiac Stress Test - Goal to reach 85% of predicted HR for age - If pt has angina, the test is stopped and dx of CAD is made - if ECG shows ST elevation, depression or arrythmias test is also stopped

Chronic Stable Angina vs Unstable Angina

Chronic Stable Angina:

• Decreased blood flow to heart from CAD

• Often occurs at predictable times (ie during exercise)

• Position pt upright, encourage rest

• Apply O2

• Nitroglycerin (can pre-treat)

• As plaque increases and blood flow decreases over time, unstable angina may occur

Unstable Angina:

• Partial rupture of artery - no permanent damage - a type of acute coronary syndrome

• Often new onset

• Less predictable

• Occurs at rest

• More prolonged and severe >10 min

• Cardiac markers not elevated - distinguishes from NSTEMI and STEMI

• ST segment depression, T wave inversion

STEMI vs NSTEMI

STEMI:

• Classic heart attack - extensive muscle damage

• Occur abruptly from stopped blood flow - usually from disrupted arthroscelertoic plauqe that becomes a thrombus and occludes blood flow

• Cardiac markers are elevated

• ST segment elevation. - appears as tombstones - T wave inversion

NSTEMI:

• Intermediate form of ACS - less extensive heart damage

• Cardiac markers are elevated

• ST segment depression, T wave inversion (also seen in unstable angina)

Proper Nitroglycerin Storage

• Keep away from light, heat

• Once opened, replace in 6 mo

• If long acting (ointment) ensure 10-14 hours nitrate free periods

• Keep in dark bottle

Cardiac Markers

CKMB - enzyme specific to heart muscle - seen within 4 hours

Troponin - seen within 4 hours, eleated for days after

Myoglobin - Heme protein in cardiac and skeletal muscle seen within 1h - most immediate cardiac marker

BNP - from stretching of heart muscle, eval of HF severity and risk of death

• >400 = HF

S/S of Acute Coronary Syndrome (NSTEMI, STEMI)

S/S

• Severe chest pain not relieved by nitro or rest

• Feeling of doom

• Positive levine’s sign (clutching chest)

• Rapid respirations

• Dyspnea

• Increased HR and BP at first, then decreased (uh oh)

• Crackles

• Abnormal heart sounds (S3, S4)

• JVD

• Liver enlargement

• Peripheral edema

• Decreased UOP

• Pale, cool, clammy

• N/V r/t blood shunting away from GI tract

Treatment for ACS

THROMBINS

Thienopyridines (clopidogrel)

Heparin/enoxaparin

RAAS system blockers (ACE inhibitors)

Oxygen

Morphine (pain and vasodilation)

Beta Blocker (decrease O2 demand of heart)

Intervention (PCI, CABG)

Nitroglycerin (SL) if B/P is okay

Stain/Salicylate (high dose)

Time Frames for STEMI and NSTEMI Treatment

STEMI:

• PCI within <90 min

• If no PCI available, thrombolytics in <30 min (TPA)

Thrombolytics cause bleeding EVERYWHERE - Contraindicated in hx of bleeding disorders, ischemic stroke, uncontrolled HTN, ect.

- Re-occlusion is a big concern - Heparin drip!

• If PCI does not work - CABG

NSTEMI:

• If manifestations are controlled, schedule heart cath

• NO thrombolytics

Percutaneous Coronary Intervention (PCI)

Catheter threaded into artery - blockage visualized with contrast - balloon catheter into narrowed vessel and inflates to open the artery - stent placement

• If radial artery used - no lifting >5 lbs for 48 hours

• No submersion of cath site

• If bleeding occurs, pressure for 10 min

• Report new or worsening bruising and pain

• Similar management to coronary angiogram insertion site

Pre-Procedure

• Labs/ECG

• Allergies (contrast?)

• Prior meds (metformin??)

• Kidney function

• IV access - conscious sedation (fentanyl and midazolam) (heparin and direct thrombin inhibitors)

• NPO

• Clean skin/shave

Post-Procedure

• EKG- watch for reperfusion arrhythmias! Very common

• UOP, fluid volume status/labs

• Monitor for bleeding at puncture sites q15 min for first hour

• IV fluids

• IS, OOB, ambulation ASAP

• Dual antiplatelet therapy (clopidogrel, ticagrelor) for at least 1 year s/p procedure

• ASA for life (prevents stent clotting)

• Assess neurovascular status of involved extremity q15 min for 1st hour

CABG

Usage of transplanted mammary or radial artery, saphenous vein in leg to bypass blockage

• Takes 3-6 hours

• Requires median sternotomy and bypass to circulate blood while heart is stopped during surgery

• NPO after midnight

• Anticoagulant discontinuation

Post-Op Care for CABG

• Continuous ECG - reperfusion arrhythmias (A-fib most common)

• Arterial Blood Pressure via Arterial Line

• Pulmonary Artery Pressure (PAP) and cardiac output via swan-ganz catheter

• Central venous pressure (CVP) aka right atrial pressure RAP via central venous catheter

• Mechanical ventilator weaning

• Chest tubes, pacing wires for emergency

• UOP monitoring

• Diuretics/titration of IV meds (vasopressors and vasodilators)

• Ambulation, IS, TCDB with splinting incision

• Aspirin forever

• Clopidogrel for 1 year

• Beta Blockers to decrease O2 demand and prevent reperfusion arrhythmias

• Statins to lower cholesterol, long term maintenance

Potential Complications:

• Dysrhythmias

• Bleeding

• Cardiac tamponade (if chest tube clogged) Muffled heart sounds, JVD, hypotension (dx with echocardiogram)

• Hypothermia r/t bypass

• Stroke

• Cardiogenic shock

• Infection (sepsis)

• Heart failure

• Renal problems

• Repeat MI :(

Medications for CAD

1. Decrease cholesterol

• Statins - atorvastatin - liver damage/rhabdomyolysis (rare)

• Niacin/vitamin B3 - flushing, purritis

• Gemfibrozil - GI issues (cholesterol is part of GI tract, so decreasing it can cause GI issues, applicable for all meds)

2. Keep blockages from forming

• Aspirin

• Plavix - longer half life

• Warfarin - narrow therapeutic range

Preload

Degree of stretching of the ventricular muscle at the end of diastole (volume of blood is highest in the ventricle at end of diastole - ie stretching of the muscle is the greatest)

• Can be estimated by measuring pulmonary capillary wedge pressure (PCW)

• Preload affects stroke volume (SV) and ultimately CO

Afterload

Resistance/pressure the ventricle must overcome to eject the blood into circulation during ventricular contraction

• Smaller BVs increase afterload as seen in hypertension

• Directly affects arterial BP

• Also affects SV and CO

Contractility

Force the myocardium generates during contraction

• Affected by SNS

• Positive inotropic meds increase, and negative inotropic meds decrease

• Also affects SV and CO

• Increased contractility = INCREASED O2 DEMAND

Heart Failure Pathophysiology and Symptoms

Insufficient blood supply/oxygen to tissues and organs

Can be associated with

• HTN

• CAD + MI

• Valve defects

• Heart rhythm disorders

• DM

• Kidney disease

• Stimulant drugs

S/S:

• SOB (how many pillows do you sleep on?)

• Edema (specifically peripheral)

• Fatigue

• Chest congestion

Left Sided HF

HF where the left ventricle cannot effectively pump blood to the body, leading to fluid buildup in the lungs.

• LEFT is for LUNGS

• Crackles

• Nocturnal dyspnea

• Cough w/ frothy, pink sputum (pulmonary congestion)

• Tachypnea

• Cyanosis

• Displaced apical pulse r/t hypertrophy (LV becomes dilated and hypertrophied over time - remodeling causes dysrhythmias)

• S3 heart sound (gallop)

Can have reduced or preserved ejection fraction (% of blood in LV pumped out with each contraction)

• Normal EF = 55-65%

Right Sided HF

Right ventricle not pumping into lungs effectively - fluid backs up into the body

• Most common cause is LHF, second most common cause is cor pulmonale (r/t COPD, pulmonary fibrosis)

• JVD

• Edema (dependant peripheral)

• Ascites

• Weight gain

• Polyuria

Nursing Management for HF

• Oxygen therapy + high fowler’s position

• Structured exercise program (associated with better outcomes)

• Renal monitoring (EKG, UOP)

• Avoid aspirin, NSAIDs - may cause increased sodium retention which can worsen HF

• Low sodium diet

• DASH diet

• Fluid restriction (maybe) <2L/day

• Daily weights at same time, same clothes (report wt gain of 3lb in 2 days or 3-5lb in 1 week)

Cardiogenic Shock

Heart cannot pump enough blood to vital organs - catastrophically low CO

Mainly caused by

• MI

• Severe HF

S/S

• Pulmonary congestion

• Pallor, cool, clammy skin (r/t blood shunting)

• Decreased UOP r/t decreased renal perfusion

• Dyspnea

• Tachycardia

• Hypotension

Treatment:

• Vasopressors

• Positive Inotropes (ie digoxin) to increase CO

• Diuretics low and slow, after BP is OK

• Nitrates if BP is OK

Medications for HF

1. Reduce afterload (lowers heart workload)

Via vasodilation

• ACEs/ARBs - Stop RAAS system - Monitor creatinine and BUN for kidney function

• Nitrates

• Hydralazine

• Valsartan

• CCBs (not diltiazem)

2. Reduce preload (lowers heart workload)

• Diuretics

3. Inhibit SNS

• BETA blockers

4. Improve Contractility (Makes heart beat BETTER, not faster) (+ Inotropes)

• Dobutamine (increases contraction strength and vasodilates)

• Milrinone (increases contraction strength and vasodilates)

• Digoxin (watch potassium lab!) (if on furosemide or HCTZ especially) (low K = digoxin toxicity)

• Norepinephrine and epinephrine - weaker but used to vasoconstrict during shock

Cellulitis

Bacterial infection (usually of subcutaneous tissue) r/t a break in the skin (wounds, radiation)

• Usually staphylococci or streptococci

S/S:

• Heat

• Redness

• Tenderness

• Fever, chills, malaise

• Edema

Can lead to systemic/septic infection if not treated (blood, joints, bone, heart, thrombophlebitis, necrotizing fasciitis, death)

Dx:

• Ultrasound to rule out DVT

• CT if deep infection suspected

May be chronic or acute, mark borders with sharpie - spreading quickly can be indicative of necrotizing fasciitis

Tx:

• Moist heat

• Elevation, immobilization

• Antibiotics (PO) - amoxicillin, cephalexin, clindamycin

• IV Abx: Penicillin-G, Nafcillin, cefazolin, ceftriaxone

• Severe IV Abx Tx: Vancomycin + piperacillin/tazobactam

• May need surgical irrigation and debridement

Urinary Tract Infection (UTI)

Can be lower (bladder, urethra), upper (renal and pelvic), or cause urosepsis (systemic and life threatening)

• Uncomplicated

• Complicated - occurs with underlying disease (obstruction, stones, catheters, DM, abx resistance, pregnancy)

S/S

• Dysuria

• Frequency

• Spasms, abd pain

• Flank pain, chills, fever (upper UTI)

• Confusion and cognitive impairment in older adults

• Non- localized abd pain in older adults

Prevention for CAUTI:

• Position foley bag below bladder with no kinks or “dependant loops”

• Empty if over 400 mL

Dx:

• Dipstick UA (+ Leukocytes)

• Urine C/S

• CBC w/ Diff

• Ultrasound, CT urogram, pyelogram

Tx:

• Abx r/t C/S

• Nitrofurantoin, fosfomycin (shorter course, uncomplicated)

• Longer tx for complicated (7-14 days)

• Phenazopyridine (AZO)

• Increased fluid intake

Pathophysiology of Shock

Massive vasodilation in the presence of endotoxins and other mediators

1. Inflammatory cytokines are released in the presence of sepsis

• Cytokines damage internal layers of blood vessels

• Clotting mechanisms are triggered

2. Other proinflammatory mediators are released such as histamines, serotonin, and bradykinin

• This negative feedback loop initially increases CO

• Increase in CO causes blood flow to bypass capillaries, which decreases perfusion to organs

• CO decreases, hypotension occurs

Stages of Shock

1. Initial Stage

Homeostasis is altered (in a cellular level) due to a decrease in CO. This causes the bodies cells to change from aerobic to anaerobic metabolism

• SIRS response is activated, but not yet affecting VS

2. Compensatory Stage

SNS is activated - body tries to re-perfuse vital organs - tachycardia, tachypnea, RAAS activation, oliguria, dim bowel sounds, cool skin

3. Progressive Stage

Compensatory actions begin to fail. CO is low and decreasing. Ischemia, lactic acid release (causes acid base imbalances like metabolic acidosis) hypotension, dysrhythmias, liver dysfunction, renal dysfunction, anuria, absent bowel sounds, low GCS

4. Refractory Stage

Irreversible cellular damage from hypoperfusion and lack of oxygen - multiple organs fail - ARDS, DIC, MODS (failure of 2 or more organ systems)

Systemic Inflammatory Response Syndrome (SIRS)

A systemic immune response to a harmful stressor (injury or infection)

NOT Sepsis (but infectious SIRS is sepsis)

Infection + SIRS = Sepsis

Criteria: Two or more

1. Heart rate >90

2. Temp >100.4

3. RR >20 or PaCO2 <32

4. WBC >12,000 or <4,000

Sepsis vs Septic Shock vs MODS

Sepsis: Systemic infection and response - life threatening

Septic shock: Presence of sepsis with hypotension despite fluid resuscitation

MODS: Multiple organ dysfunction syndrome - failure of 2 or more organ systems

Manifistations of Sepsis

Labs:

• Increased CRP

• Increased procalcitonin

• Increases coagulation parameters

• Increased creatinine

• Thrombocytopenia (low platelets)

• High lactate level (measures anaerobic metabolism) (>2)

S/S:

• AMS

• Hyperglycemia r/t stress induced hypermetabolism

• SBP <100

• Significant edema

• Decreased UOP

• Ileus (r/t decreased GI motility)

• Mottling

• ABG may be alkaline at first, acidotic in end

Sepsis 1-Hour Bundle

1. Measure lactate levels (repeat if >2)

2. Draw blood cultures (2 sets peripherally from different sites) (drawn before antibiotics)

3. Administer antibiotics

4. Fluid resuscitation (isotonic crystalloids LR or NS) (30mL/kg)

5. Vasopressor administration if fluids fail to restore a MAP >65 (norepinephrine, epinephrine, vasopressin)

Nursing Management for Septic Shock

1. Maintain MAP >65

2. High flow oxygen ie 100% non-rebreather face mask

3. Prepare to intubate, have resuscitation equipment ready

4. Insert indwelling catheter for strict I&O measurement

5. Maintain large bore patent IV access

6. May place pt in trendelenburg (supine with legs elevated above head)

Complications of Septic Shock

• MODS - often begins in lungs causing ARDS and can extend to kidneys and heart and GI tract

• DIC - Assess for bleeding around gums, IV sites, MM - Obtain clotting labs - prepare to admin blood