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**Anatomy and Physiologyof the Heart
- =>Three layers of the heart:
- Endocardium: inside, innerlaying
- Myocardium: muscle
- Epicardium: outer layer, compromises itself with more layers that adds to pumping action by lubrication
- Four chambers
- Heart valves
- Coronary arteries
- Cardiac conduction system
- Cardiac hemodynamics
**Structure of the Heart-
blood gets into heart through IVF and SVF -> R Atrium -> Tricupside valve -> R vent -> pulm valve -> R/L pulm artery (deoxygenated) -> lungs (oxygen exchange occurs)-> pulmonary VEINS-> Left Atricum -> Mitral valve-> L ventricle -> Aorta -> Circulatory System.
-breakdown can occur in valves: inadequate backflow of bloow then mix of oxygenated and deoxygenated blood and no adequate circulation.
-Breakdown of structural system (muscle) where if there's no adequate pumping action due to weak muscles then we're not going to receivve adequate circulatory system oxygenation
- **Coronary Arteries-feeds the heart:coronary arteries an veins.
- -interventions to open up cardiac muscles and interventions in the heart: now we can replace valves endoscopically in the cath lab.
**Conduction System (focus)
- =>Electrical impulse/action potential
- -generates capability of muscle to contracct and relax; starts in SA node
- Starts at the SA node: located in R atrium; Depolarization of cells: Exchange of electrolytes
- Travels from atrium to the AV node
- - travels down septal valve between left and right ventricle in bundle brach (Bundle of His) and then to the..Walls of ventricles to Purkinje fibers causing a contraction=> there can be conduction problems anywhere in this electrical system. Physicians that specialize in this are electrophysiologist (cardiologist expertise); look at diagnostics and determine what electrical pathway problem is causing a dysarrythmia. => -conduction process relies on exchange of electrolytes within the cell membrane so it's important to look an Na, K, Ca, MG levels. All of that is required for that electrical system to work. So when we have this change between the cell membranes, that creates firing potential.
-negative action potential (no exchange of electricity) to a positive potential (allows AP to initiate the firing/beating of the heart)
**Cardiac Action Potential (Picure)
- -Phase 0: Rapid Depolarization
- -phase 1: apid repolarization
- -Phase 2 Plateu(high na and ca levels entering cell)
- -Phase 3: Final Repolarization(drop in k and na leaving cell membrane)
- -Phase 4: Resting.
P wave (atrial activity): initation of electrical activity in the SA node. Firing of the SA node creates the P wave. then there's travel time so there's a gap. Once it hits AV node..
QRS (ventricular activity): Depolarization from the AV node (which picks it up)throughout the ventricles, corrleation to second squiggly line. To the BUNDLE of his to Purkinje Fibers where blood goes into the system then it rests. aV and SA node repolarization which allows a resting phase so that it can accept another charge. T wave (ventricular asystole): Repolarization of the ventricles when the activity is done.
U wave:Usually not seen but may indicate delayed ventricular repolarization or hypokalemia
QRS; represents time taken for depolarization/contraction of both ventricles (systole)
S-T Segment: represents the time between ventricular depolarization and repolarization (diastole), should be isoelectric (flat)
- T wave: rep time for ventricular repolarization
12 lead is for us to visualize this electrical activity, put grounding wires all over patient 9chest,arms,legs) hook it to machine. The machine will look at electrical conduction through diff views, from top to bottom, sides, from back. Electrophysiologist that can tell on where that lead and changing on conduction about what portion of heart may be damaged due to inadequate oxygenation to the muscle (MI-heart attack)
**Interpreting an EKG
- Determine Regularity
- Determine Rate
- Determine Intervals-are the beats regular, the rates and the intervals
-PR Interval: the space when the p wave starts (beginning of the P) to the beginning of the Q wave. That length of time should be certain distance. If too long, then something's blocking it. The QRS should be a certain width also.
-QT: beginning of Q to the end of the T. each tiny box is .04 seconds across. So five boxes makes .2.the bold lines happen every five boxes, that's .2 seconds.
Check if complexes look alike and are equally spaced-see if the QRS complexxes and the P-P rates, make sure the beat initiated from the P wave and in timing and in sync
white on right, on top of green (clouds over trees)
Black on the left over red (smoke over fire)
Brown in the middle, close to the heart (chocolate near to our heart)
-this is generateing impulses that teletech is going to see, can switch views on the monitors.
**Determine Heart Rate:
Count the number of small squares between two QRS complexes (R-R interval) and take that number and...Divide 1500 by the number of small squares to get the HR
Or, count the number of large squares between two QRS complexes (R-R interval)
Divide 300 by the number of large squares to get HR (rough estimate)
count QRS waves for six seconds for irregular beats (five big boxes is one second?)
**Normal Sinus Rhythm
<60: brady>100: tachy
-every interval is equally spacedIf you're missing a p wave, then AV node fired without the conduction initiation from the SA node. Every QRS must be preceded by a P wave.
-basically sinus rhythm but irregular. Every QRS preceded by P wave. only problem is not regular.
IF IRREG: Brady arrythmia-irregular slow HR
**Sinus Bradycardia:conduction pathway is same as sinus rhythm but SA node fires at a rate less than 60 b/p; aerobically normal in trained athletes or while sleeping (regular rhythm)s/s: pale, cool skin, hyptotension, weakness, angina, dizziness, confusion or disorientation and shortness of breath.-atropine & dopamine, intropinBrady arrythmia-irregular slow HR-too slow. By counting the number of boxes.
conduction pathway is same as sinus rhythm but SA node fires at a rate less than 60 b/p; aerobically normal in trained athletes or while sleeping (regular rhythm)
s/s: pale, cool skin, hyptotension, weakness, angina, dizziness, confusion or disorientation and shortness of breath.
-atropine & dopamine, intropin
- Brady arrythmia-irregular slow HR
- -too slow. By counting the number of boxes.
Greater than 100 & regular.
-associated with exercise, fever, hypotension, hypovolemia, hypoxia
-Reduce HR: IV beta adrenergic blocker (metoprolol), ca channel blocker (diltiazem)
You see P before every QRS and a T wave.
=> Irregular with HR > 100 is tachyarrythmia.
=>Super Ventricular Tachy:
where P waves bury into the QRS. (skip in book)
**Premature Atrial Contraction (PAC)
- -ectopic signal strarts in either atrium and travels abnormal pathways creating distorted p wave
- -normal with use of caffeine, alcohol, tobaco
- -normal QRS, not usually regular.
- -abberant beat; just watch the frequencies. Notify physician when we're seeing them.-after that T waves and ressting period, something triggers the SA node to fire too quickly causing a PAC. The QRS complex and SA node shortens and this whole electric process happens faster than normal.
- -Resting process is important, Firing SA node too soon can start a fatal rhythm and vent fatal rhythms.
- -more freq PAC's must find cause: stress, electrolyte imbalance, lack of O2, caused by meds or emotions? Stimulants that could cause it?
- -if you're not giveing adequate relaxing and allowing blood to come in and that pumping process starts due to premature activity then not enough oxygenation and not eough peripheral circulation.
- -beta adrenergics blockers may be used to decrease PACs
*NSR: when you say sinus: the SA node has generated every beat.
**Dysrhythmia vs Arrythmia:
Dys: group of classificaion with abberant beats and rhytms
**Atrial Flutter (Sawtooth)
-atrial tachydysrhytmia; rarely occurs in healthy hearts
-atrial rate: 200-350 with ventricles at 150 b/m (2:1)
-decreased cardiac output-treatment: increase the AV block; ca channel blockers and b adrenergic blockers to control ventricular rate. and/or antidysrhytmia drugs to revert back to NSR
-Means SA node fires more frequently than it should and the electrical conduction isn't being completely caputred every single time by the AV node. Atriums are contracting due to SA node so P wave is there but if electrical conductionisn't going down every single time-Atrial flutter
-ariium accepts blood but only a little bit is going down into the ventricles. when we're not adequately getting o2 blood then we're not adequatly oxygenating our pt.
-flutter or swatooth waves are countable to determine if they're an equal conduction.
-the longer the conduction of the p waves then HR is low and not enough Cardiac output and atrium is overfilling in blood, then blood is clotting. Rhythmically contracting.
**Atrial Fibrillation (Many irregular P’s)
-Fibrillating, muscle is spasming. ; total disorgannization of atrial electrical acctivity because of multiple ectopic foci resulting in loss of effective atrial contraction.
-paroxysmal (begins/ends spontaneously) or persisten (lasts more than 7 days)
-most common and clinically significant dysrhythmia with respect to morbidity.
-Atrial rate: 350-600p waves replaced cy chatoic fibrillatory waves and venti beats 60-100; normal QRS shape
-Sa node fires and creating atrium spasms-centrifuge of blood creating clots in Atrium and every time valves open, clots travel to the lungs and into body. :(
-Loss of CO b/c effective atrial contraction and bloods stasis,embolized clots can travel to brain and cause a stroke.
-we can give meds to slow it down and control it. Anticoagulation; maze therapy and cryoablation (cold therapy)
-aV node can intrisically fire on it's own but it's only 40-60 beats per hour (too slow) so get a pacemaker..
**Premature Ventricular Contractions (PVC’S-Uni/Multifocal)
-defined as three or more pvcs, occurs when ectopic focus repeatedly fire and ventricle takes control as the pacemaker
-vent rate: 150-25- beats with regular or irregular rhythm-p wave buried in QRS and PR interval not measurable. PVC without a pulse is MEDICAL EMERGENCY! Treated like V. Fib.
-This is when AV node fires with no initiation from SA nodes. Ventricles are contracting without blood so no Cardiac Output.
-Wide QRS complex, "wide and bizarre".
-unifocal and multifocal. Focal: where is it coming from?-coming from different areas then multifocal.
-once in a while normal for us due to caffeine..or stress or exeercise.But if Frequent, then cause should be found. Progresses could lead to Vent tachycardia
**Ventricular Tachycardia (V-tach/Regular)
-run of three or more PVCs defines VT. Occurs when an aecvtopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker.
-sustaineded (longer than 30 seconds) or nonsustaine (less than 30)
- -omnimous sign, lifife threatening b/c of decreased CO and possiblity of VF. -Asdsociated with MI, CAD, signifcant electorlye imbances, mitral valve proplapse, long QT interval.
- -independent P waves with vent contraction of 150-250 b/m
-can be stable (pt has pulse) or unstable (without pulse-LIFE THREATENING and treated like VF)
**Ventricular Fibrillation (V-fib/irregular)
ACLS: how do you respond to lethal rhythms. V Fib:: like A fib, no blood is getting in or out. MEDICAL EMERGeNCY. Requires shocking.can be course or finer.
-severe derangment of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude. Represents the firing of multiple ectopi foci in the ventricle. Mechanically, the ventricle is simply quicering with no contraction and no CO. LETHAL MEDICAL EMERGENCY.
-occurs in acute MI and myocardial ischemia and in chrnoic diseases: HF and cardiac myopathy
-HR and rhythm isn't measurable, nothing is measureable!
-Treatment: ADvanced Cardiac Life Support and Defibrillation and definite drug therapy (epi, vasopressin)
**Asystole (Absent Electrical Activity)
-good CPR will save the patient with medications but can't shock! Can't shock b/c nothing to stop or start, NO electrical activity ):
-total absence of ventricular electirc activity. Occasional P waves are seen
-VF can masquerade as asystole
-result of advanced cardiac diseas, a severe cardiac conduction system disturbance or end
-Generally the pt with asystole has end stage heart disease or has a prolonged arrest and cannot be reuscitated.
-Treatment: consists of CPR w/ initation of ACLS measures + drugs (epi)
**Nursing Process: The Care of the Patient with a Dysrhythmia:
- Assess indicators of cardiac output and oxygenation: Level of consciousness.
-bring in vitals signs if rhythms have changed, ask a/o, have they felt anything, how they're feeling. Check peripheral pulses!
- =>Physical assessment:
- Rate and rhythm of apical and peripheral pulses & look for edema
- Assess heart sounds Blood pressure
- Signs of fluid retention: Labs, Weight
- => Health history:
- Presence of coexisting conditions
- Previous cardiac occurrences
**Nursing Process: The Care of the Patient with a Dysrhythmia: Diagnosis
Decreased cardiac output
- Anxiety- chest pain, impending doom
- Deficient knowledge of the knew arrythmia
Collaborative Problems/Potential Complications-cardiac arrest. Alterations in baselines, we need to get there right away.
- Cardiac arrest
- Heart failure
- Thromboembolic event
- Atrial fibrillation
**Nursing Process: The Care of the Patient with a Dysrhythmia: Planning
Goals: Eradicating or decreasing the occurrence of the dysrhythmia They can have stable arrythmia as long as it's managed medically and watched for any complications
- =>Maintain cardiac output
- Stable B.P (for that pt)
- Stable Pulse
- SaO2 > 92%
- Minimize anxiety
- Verbalize/demonstrate knowledge regarding the dysrhythmia and its treatment
**Nursing Process: The Care of the Patient with a Dysrhythmia: Interventions
=>Cardiac Output: Monitoring: ECG monitoring & assessment of signs and symptoms
Administration of medications and assessment of medication effects
Adjunct therapy: cardioversion (they have an unstable dysrythmia, still stable and orient, may not have best CO. They may shock with light voltage to reset the heart), defibrillation (rhythm is vtack or vfib, unresponsive and shocked with higher voltage), pacemakers (either in SA node or placed in ventricles to allow AV node to do conduction, demand pacemakers)
**Nursing Process: The Care of the Patient with a Dysrhythmia: Interventions
- Use a calm, reassuring manner.
- Measures to maximize patient control to make episodes less threatening
- Communication and teaching, "
- =>Knowledge Deficit
- Include family in teaching
- Teaching modalities
- Community Support: life and near death,
**Nursing Process: The Care of the Patient with a Dysrhythmia: Evaluation
- =>Cardiac Output
- ABG’sLabs: electrolytes, BNP for heart failure, cardiac enzymes
- Cooperative with care
- Reports decreased in anxiety
- V/S WDL’s
- V/U: Diagnosis, Procedures, Labs
- Demonstrates compliance: Meds, Activity, Diet
**Coronary Artery Disease (CAD)
Cardiovascular disease is the leading cause of death in the United States for men and women of all racial and ethnic groups.
CAD (coronary artery disease) is the most prevalent cardiovascular disease in adults.
Atherosclerosis-arteries filled with fat and fibrous tissues so not a good pathway for blood, narrowed arteries. Deposits have affinity to the heart arteries. /:
Abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen.
In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium.
**Risk factors for CAD
- Sex:women have higher risk of CAD after menopause due to lack of hormones not maintaining cholesterol well.
- Race:Family history/tenedncies
:Hyperlipo-proteinemia: manage lipid and cholesterol
- Dietary patterns
- Glucose intolerance: blood sugar
- Cigarette smoking
- Personality and life-style: high stress job and Type A personality.
**Risk Factors for CAD: Health Promotion (Cont’d)
=>Cholesterol-lowering drug therapy (three kinds)
- Health-promoting behaviors
- =>Physical fitness: FITT (Freq, Intensity, Type & Time) formula: 30 minutes >5 days/week
- Regular physical activity contributes to:
- Weight reduction: if you have a regular physical activity will reduce systolic BP greater than 10 percent
- Reduction of >10% in systolic BP
- In some men more than women, an increase in HDL cholesterol (better)
Your Personal Fitness Center at www.justmove.org Choose to Move at www.choosetomove/org
- =>Health-promoting behaviors: Nutritional therapy: Therapeutic lifestyle changes Omega-3 fatty acids (help with cholesterol management)
- -eat clean, green,
- -Decrease cholesterol and saturated fat intake.
- Omega-3 fatty acids have been shown to lower cholesterol. Found in fatty fish and soy products. There are also nutritional supplements claiming to be high in omega-3 fatty acids.
- =>Cholesterol-lowering drug therapy (three kinds)
- Drugs that restrict lipoprotein production: Statins, niacin
- Drugs that increase lipoprotein removal: Bile acid sequestrants (RH?)
- Drugs that decrease cholesterol absorption: Ezetimibe (Zetia)
- Health-promoting behaviors:
- Antiplatelet therapy
Ideal over plavix and cheaper but it has GI upset (enteric will help)
especially if they've had stents in the past. Different mechanisms.. *book?
- Strategies to reduce risk factors are effective but often underprescribed
- Necessary to modify guidelines for physical activity
- Two points when elderly may consider lifestyle change(s):When hospitalized When symptoms result from CAD and not normal aging- they don't change until a life or death situation
**Development of Atherosclerosis
-stage 1: asymptotmatic: fatty streaks, fibrous atheromatous plaque; can't tell what's going on.
-stage 2: complicated plaque, fibrous plaque calcifies; may start to feel some changes during exercise and stress (morejusts angina)
-stage 3: complications include MI, Brain infarction, gangrene, aneurysm. Full blown occlusion and pt notices acute chest pain
-high blood pressure builds quicker?
Lipid panel and cholesterol levels
Elevated lipid levels found to be one of the four most established risk factors for CAD.
Risk associated with serum cholesterol level of >200mh/dl or fasting triglyceride level of >150 mg/dl.
LDL’s have more cholesterol than any other type. Has affinity for arterial walls.
-we can also see internally in the cath lab.
- Refer to table 34-2-angina and comorbidities without compliance then medication therapy right away
=>HMG-CoA Reductase Inhibitors (statins)
Cholesterol-lowering Medications (Table 34-6)
Blocks cholesterol synthesis and ↑ LDL receptors in liver
Monitor liver enzymes and assess for muscle weakness or muscle pain.
-breaks down myoglobulins in all muscle and experience generalized muscle pain and weakness--> d/c them immediately-
Statins: Less cholesterol is manufactured by the body, and more LDL is “caught” and stored by the liver. Then there’s less LDL to deposit cholesterol on arterial walls.
**Cholesterol-lowering Medications (Table 34-6)
=> Fibric acid derivatives (gemfibrozil, fenofibrate)↓
=>Cholesterol absorption inhibitor Zetia
- Inhibits synthesis and secretion of VLDL and LDL.
- Can cause painful flushing-feel it in their kidney's
- => Fibric acid derivatives (gemfibrozil, fenofibrate)
- ↓ hepatic synthesis and secretion of VLDL, which reduces triglycerides.
- May ↑ effects of warfarin and the adverse effects of statins.
- Coumadin-monitor lab values could potential or increase bleeding time.
=>Cholesterol absorption inhibitor Zetia
- =>Bile-acid sequestrants
- Binds with bile acids in intestine, causing excretion of LDL and cholesterol in the feces.
- Interferes with absorption of some medications.
- Inhibits intestinal absorption of cholesterol. GI upset very common
- Can cause mild GI distress.
- watch their Liiver Function Tests and any changes
- Should not be used w/pts with liver impairment.
**CAD Clinical Manifestations
- Symptoms are due to myocardial ischemia. Feel like they have crushing, chest pain-may radiate. May be a pattern. May awaken from their sleep. Typical signs.
- Symptoms and complications are related to the location and degree of vessel obstruction.
- Angina pectoris
- Myocardial infarction
- Sudden cardiac death
- **CAD “The Silent Killer”
- The most common symptom of myocardial ischemia is chest pain; - complete, can manifest as Heart failure. Chest pain is most common. Can be atypical in woman (fullness in stomach, epigastric pain, lightheadedness)
- however, some individuals may be asymptomatic or have atypical symptoms
Atypical symptoms are more common in women and in persons who are older or who have a history of heart failure or diabetes.
- Includes GI symptoms: Nausea, heartburn, epigastric pain
- Respiratory symptoms: SOB, dyspnea
Others: Fatigue, weakness (Weakness: “I couldn’t stand up.” “I couldn’t get out of bed.” )
-stable vs unstable
-what's causing it? maybe ischemic or anginal episode. Labs, EKG, work them up. They'll take them to the cath lab for any blockage. Occurs when myocardial oxygen demand exceeds the supply
- Chest pain
- Radiating discomfort to the arm, jaw or back
- =>Frequently associated with:
- Extreme cold or hot temp
- Heavy meals:
- -because blood is being shunted from heart to the stomach and it pains the pt.
- =>Stable Angina
- Intermittent pain (3-5 min)-brief & PredictableSubside when precipitating factor is relieved (exertion)
- Pain at rest is unusualControlled with meds (Nitroglycerine)
- =>Unstable Angina
- New onset, occurs at rest, or has worsening pattern
- Increasing frequency, easily provoked
- Can occur during sleep or at total rest
- Associated with once stable artherosclerotic plaqueCan progress to MI (IMPORTANT because muscle is starting to die and it can't regenerate SO important to catch these events)
- Treated like MI: with ASA, heparin, Beta Adrenergic blockers; woke them up during sleep
- =>Antiplatelet aggregation therapy
- ASA 325mgTiclid
- Dilate arteries and vessels EVERYWHERE. Once anginal event, the dilation makes BP and HR drop and they might get headach
- Sublingual (fastest acting), paste, patch on their chest changed every 6-8 hours-brown bottle so that light doesn't change characteristics of the medications. Don't keep in glove compartment b/c it's hot. Keep it with them at all times, look at expiration. Stinging censation under tongue.
- -patch applied to a non hairy chest
- =>B-Adrenergic blockers “-lols”
- Decrease oxyenated myocardial contractility, HR, SVR, and B/P reducing the myocardial O2 demandrests the heart. Put them right away
- =>Calcium channel blockers
- Systemic vasodilation with decreased SVR (syst vasc resistance)
- Decreased myocardial contractility'
- Coronary vasodilation
- =>Percutaneous Coronary intervention (PCI): Angioplasty
- -if they don't find cause-cath through groin all the way through heart
Placed during angioplasty, wired mesh product fits inside lumen to keep it open. Stays forever, need antiplatet therapy and/or switched to aspirin therapy after so many months.
“Shaving” off plaque
=> Laser Angioplasty:
Dissolves the blockage, Cold laser
** Collateral circulation
if artery becomes blocked, it'll create tribitaries where another vessel is created and bypasses it. Another route.-still weak.
*Nursing Management (Chest PAIN)
Airway: O2 is key because no oxygen=pain (even if they're at 100%), No order needed. & Vital signs
=> Start IV or ensure patency to give medications for ACLS protocol
=> EKG: If on telemetry, assess rhythm. Need order for 12-lead EKG, unless part of facility protocol.
=>Assess pain, location, duration, intensity, radiation, precipitating factors, relief factors
Nitrates most commonly given to enhance coronary artery blood flow
Other meds depending on EKG findings
Rapid Response Team.
**Nursing Process: The Care of the Patient with Angina Pectoris: Assessment
- Symptomatology and activities that precede and precipitate attacks
- Complete CV assessment
Risk factors, lifestyle, and health promotion activities Patient and family knowledge
Adherence to the plan of care: Current medications
Nursing Process: The Care of the Patient with Angina Pectoris: Diagnosis/Plan
- **Collaborative Problems
- Acute pulmonary edema
- Heart failureCardiogenic shock
- Dysrhythmias and cardiac arrest
- Myocardial infarction
**Nursing Process: The Care of the Patient with Angina Pectoris: Interventions & evaluation
- =>Decrreased perfusion:
- -Stop activity, Medication administrationHOB Up, Immediate O2, V/S, EKG
- -eval: Absence of chest pain, Stable V/S, Stable EKG, Positive peripheral perfusion
- =>anxiety: -Use a calm manner, Stress
- -reduction techniques (administer meds), Patient teaching disease process, Address spiritual needs, Address both patient and family needs
- -eval:Exhibits a calm manner, Denies anxiety, Reports a reduction in anxiety, Patient and family cooperative with care
- =>Knowledge Deficit:-Stress reduction, lifestyle changes, Medications, disease process, When to seek medical care
- -eval:V/U disease process, stress reduction activities, lifestyle change requirements, medication management, disease process, and when to seek medical care
**Core Measures: Acute Myocardial Infarction
The following are measured by the Joint Commission and Centers for Medicare & Medicaid services in order to have a common set of national hospital performance measures.
You MAY see these ordered for patients admitted with angina:Aspirin at arrival Aspirin at discharge
Beta blocker at discharge; CA channel blockers if they can't tolerate blocker
ACE inhibitor for left ventricular systolic dysfunction (LVSD) of the heart
Smoking cessation counseling
- HTN Classification:
- <120 and <80
- PREHypertns: 120-139 & 80-90
- Stage 1: 140-159 & 90-99
- stage 2: >160 & >100
- =>IncidenceWorldwide epidemic 690 million people, US 50 million, 28-31%
- Slightly higher incidence in males
- Incidence increases with age
- Twice as prevalent among the African-American population
** BP Classifications
=>Primary (essential)Accounts for 90% of all casesCause is unknown
- Results from known cause
- Glomerulonephritis, Cushing’s disease, or renal stenosis
**Blood Pressure Pathophysiology
- Systolic blood pressure
- Peak pressure exerted against the arteries when the heart contracts
- Diastolic blood pressure
- Residual pressure of the arterial system during ventricular relaxation
BP=CO x SVR
**Factors that Affect Cardiac Output:
Cardiac output is affected by either the=>Heart rate: Regulated by autonomic nervous system
- =>Stroke volume
- Preload of the blood volume
- Contractility ofheart
**Regulation of the Cardiovascular System
=>Autonomic Nervous System Sympathetic Nervous System“Fight or Flight” response
Release of epinephrine and norepinephrine attaching to specific receptor sites (B-adrenergic receptors) in the heart
Alpha adrenergic receptors located in vascular smooth muscles: Stimulation of receptor sites causes vasoconstriction & Blocking agents cause vasodilation do decrease BP
- => Parasympathetic Nervous System
- Mediated by the vagus nerve affecting the SA node and slowing the heart (bearing down lowers BP and they pass out)
- Located in aortic arch and carotid sinus
- Sensitive to stretch or pressure in the arteries
- Sends signal to the vasomotor center in the brainstem: Inhibition of the SNS, Enhancement of PNS (Decreased HR and peripheral vasodilation)
- => Chemoreceptors
- Located in aortic arch and carotid bodyChange HR and arterial pressure in response to decreased arterial O2 pressure, increased arterial CO2 and decreased plasma pH
- Stimulate the vasomotor center to increase cardiac activity
**Blood Pressure is Factored By:
- Arterial baroreceptor
- Chemoreceptors system
- Fluid volume regulation
- Renin-angiotensin system (located in kidneys)
- Vascular autoregulation
=> Drop in blood pressure stimulated kidney to release renin as liver releases angiotensinogen.
Turns into Angiotensin 1, and in lungs it turns into Angiotensin 2.
This causes thirst and drinking, vasoconstriction, and aldosterone secretion.
Aldosterone secretion causes salt and water retention, keeping the blood volume retained. All this elevates the blood pressure.
**Other Organs that Affect the CV System
- =>Vascular endothelium
- Vessel changes: Sclerotic, tortuous (twist and turn on one another increasing resistance of vessels due to smoking, lack of oxygen, chemo and meds), and weak vessels (overdilated and stretched causes weakness)
- =>Renal system
- Sodium retentionRenin release converts angiotensin I to angiotensin II increasing blood pressure
- =>Endocrine system
- Posterior Pituitary
=> Drop in blood pressure stimulated kidney to release renin as liver releases angiotensinogen. Turns into Angiotensin 1, and in lungs it turns into Angiotensin 2. This causes thirst and drinking, vasoconstriction, and aldosterone secretion. Aldosterone secretion causes salt and water retention, keeping the blood volume retained. All this elevates the blood pressure.
**Mechanism of Action of Aldosterone
Increased aldo -> Increased Na reabsorption -> Increased water reabsoprtion -> Increased Blood volume -> Increased Cardiac Output.
**Risk Factors for High BP & manifestatiions
AgeAlcoholCigarette SmokingDMElevated serum lipidsExcess dietary sodiumGenderFamily historyObesityEthnicitySedentary lifestyleSocioeconomic statusStress
- **Clinical Manifestations High BP
- Reduced activity tolerance
- Silent Killer
- Facial flushing-red noseHistory of nose bleedsElevated BP
- Early HTN is usually completely asymptomatic
**Complications of HTN
- =>Hypertension induced heart disease
- -CAD: increased blood pressure causes micro damage to the cardiac vessels, causing athersclerosis.
- -Left ventricular hypertrophy: Left ventricle working harder to push against the increased pressure. The muscle over-develops, decreasing effectiveness
- -Heart failure
- -> Many of these complications: microvascular damage from the increased pressure against the vessel walls.
- =>Cerebrovascular disease
- =>Peripheral vascular disease
- =>Retinal damage
- =>Insulin resistance
- =>Laboratory studies
- Blood triglycerides
- Cholesterol levels
- Blood lipoproteins
=>CXR: complication: enlarged heart, LVentDiaFailure
=>EKG: dysryhmia, ectopic beats, an old MI
=>Exercise electrocardiography=>Coronary Angiography
- =>Collaborative care
- Assessment of BP-both sides, and treat the higher.Interdisciplinary involvement
- =>Lifestyle changes
- Nutrition: reduced sodium, moderate alcohol consumption, rich in omega-3 fatty acids
- Weight reduction in overweight patients
- =>Drug therapy
- -diuretics change the fluid volume (K sparing or depleting), can cause electrolyte imbalances, changes in BP and output, weight and edema and lung sounds.
- -alpha adrenergic inhibitors: act centrally and peripherally, inhibit norepi release, monitor BP and ortho hypotension changes.
- -peripheral acting ones: orthostatic hypotension
- -central: rebound HTN
- -alpha adrenergin:
- family hx of HTN, DM, CVD, hyperlipidemia, renal disease
- Previous documentation of increased B/PMedical historyDisease or trauma
- Recent weight gain
- Psychological history
**Nursing Considerations for the Elderly
- Comorbities common with increased ageDrug absorption issues
- Metabolism and excretion (kidneys), and liver function
- Lack of compensatory mechanisms
- Hypotension with drug administration
- HTN Pneumonic for Nursing Care
- Patient Education
- Describe what HTN is in lay terms
- Tell the patient their B/P is so they can learn to monitor
- Dietary guidelines
- American Heart Association website
- Medication administration, side effects, etc
- Explain orthostatic hypotension
- Hot baths or jacuzzi, changing position
- Effects of alcohol consumption
**Pharmacology - Diuretics
Also known as the Zides and Ide’s
=>Promote Na & H2O excretion, decrease plasma volume and decrease vascular response to catecholamines
Thiazide (inhibit NaCl reabsorption, deplete K)
Loop diuretics (inhibit NaCl reabsorption, deplete K)
Potassium-sparing diuretics (Minimize K and Na exchange)
-diuretics change the fluid volume (K sparing or depleting), can cause electrolyte imbalances, changes in BP and output, weight and edema and lung sounds.
=>Side effects: electrolyte imbalance
Nursing considerations: Hypotension, monitor electrolytes
**Pharmacology - Adrenergic Inhibitors
Act both centrally and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels
- Central acting
- Peripherally acting
- Alpha adrenergic blockers
- Beta adrenergic blockers
**Pharmacology - Central Acting Adrenergic Antagonists
=>Reduce the sympathetic nervous system response from the brain: Produces vasodilation & Decreases SVR and BP
=>Nursing considerations: sudden withdrawal can cause rebound HTN
**Pharmacology - Peripheral-acting Adrenergic Antagonists
- =>Prevents peripheral release of norepinephrine
- Produces vasodilation
- Lowers CO and reduces systolic BP
=>Nursing considerations: Orthostatic hypotension
**Pharmacology - Alpha Adrenergic Blockers
- =>The “sin’s”
- doxazosin (Cardura)
- =>Block the alpha adrenergic effects producing peripheral vasodilation
- -peripheral acting ones: orthostatic hypotension
- -central: rebound HTN
=>Nursing consideration: Postural hypotension
**Pharmacology - Beta Adrenergic Blockers
- =>The lol’s
- =>Reduces BP by antagonizing B-adrenergic effects'
- =>Nursing considerations
- Bronchospasm (beta-blocker cough)
AV block: Bradycardia& Monitor for impaired peripheral circulation to where a pt's normal HR is in 40's. Establish that parameter with your physican before not giving the medication
Sudden withdrawal can cause rebound HTN
- watch for peripheral circulation b/c can cause AV block.
- -parameters: <110 hold
**Pharmacology - Combined Alpha and Beta Adrenergic Blocker
-combo drugs, look and Nursin considerations for both
=>Decreased heart rate
=>Reduced CO, SVR, and BP
- Labetalol:: IV push, directly drops it down immediately in HTN crisis
- carvedilol (Coreg)
- Used in pregnancy-induced hypertension
- Post-op hyptertensive crisis
Severe postural hypotension, hepatic toxicity,
**Pharmacology - Angiotensin Inhibitors
=>Angiotensin Converting Enzyme (ACE)
- =>Angiotensin Converting Enzyme (ACE) inhibitors
- “the prils”
=>Prevent the action of angiotension I and II
- =>Nursing Considerations
- Don’t give with ASA or NSAIDS
- Don’t use with K-sparing diuretics
- Can cause a dry cough due to increase in bradykinin.
- => ASA or NSAIDS may reduce drug effectiveness.
- K-sparing diuretics: The drug causes retention of potassium already with the blocking of angiotensin converting enzyme.
- So, additional nursing consideration even if not on K-sparing diuretics: monitor the potassium!
**Pharmacology - Angiotensin Inhibitors
=>Angiotensin II Receptor blockers
=>Angiotensin II Receptor blockers
- the “tans”
- losartan, valsartan
=>Prevent action of angiotensin II, producing vasodilation and increased excrestion of Na and H2O
- =>Nursing Considerations
- Monitor potassium level, can cause hyperkalemia and water
- Full effect may not be seen for 3 – 6 weeks
**Pharmacology - Calcium Channel Blockers
- =>The Pine’s, Zem’s and Mil’s
- Nifedipine, diltiazem, verapamil
Blocks movement of extracellular calcium into cells causing Vasodilation,
Use cautiously in patients with A-V block, nausea, renal disease, electrolyte imbalances
**Hypertensive Crisis Therapy
- =>Hypertensive urgency
- SBP ≥180 or DBP ≥120 (AHA, www.heart.org)
- Blood pressure is very high but no evidence of immediate or progressive target organ damage.
- Usually occurs with pts with poorly controlled or undiagnosed HTN
- =>Hypertensive emergency
- SBP ≥180 or DBP ≥120 (AHA, www.heart.org)
- Can occur at lower BP levels in patients whose BP has not previously been high.
- Must be lowered immediately to prevent damage to target organs.
- Hypertensive Crisis Therapy
- Fast acting
- Sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin
- Given IV
- Reduces SVR and BP by direct arterial vasodilation
=>Nursing considerations:Many serious side effects causing cardiac alterations