CARDIAC PT 1

what is blood pressure? CO? systemic vascular resistance (SVR)?

• BP: force that results from blood pulsing from the heart against the walls of the arteries

  • indicates cardiovascular health

• CO: amount of blood pumped from the ventricle in 1 min

• SVR: force in blood vessels opposing blood movement (overcome force to move forward)

  • BP = CO + SVR

causes of HTN

1. increased peripheral resistance → age related stiffness/atherosclerosis

2. renin angiotensin aldosterone system overactivity (vasoconstricts → increase BP)

3. sympathetic nervous overactivity → trigger BP to go up

HTN pathophysiology, what is it known as, how to diagnose?

• excessive tensing or vasoconstriction of the blood vessels → greater SVR → greater pressure

• most common BP alteration

• often symptomatic until severe (known as the silent killer b/c people walk around with it)

• diagnosis requires two or more incr. BP readings at diff times

what is considered normal, elevated, stage 1, stage 2 hypertension?

1. normal: systolic <120, diastolic <80

2. elevated: systolic 120-129, diastolic <80

3. stage 1: systolic 130-139, diastolic 80-90

4. stage 2: systolic >140, diastolic >90

what is primary hypertension? what are the modifiable & unmodifiable factors?

• most common cause of HTN & idiopathic, lifestyle related

• modifiable

  • incr. BMI/obesity

  • sedentary lifestyle

  • poor diet

  • excessive alcohol use

  • excessive sodium intake

  • tobacco use

  • uncontrolled diabetes & hyperlipidemia → irritates vessels → vasoconstrict

  • medications (ex. NSAIDs)

    • NSAIDs impact the kidneys, which will impact BP (any meds in general that impacts the kidneys)

  • incr. stress

• unmodifiable

  • age, family hx, genetics, ethnicity, gender

what is secondary hypertension? how does it occur?

• occurs secondary to other medical conditions

• renal disease

  • kidneys & heart work together

  • glomerulonephritis, renovascular disease

• obstructive sleep apnea

  • activates SNS to increase BP

• neurologic disorders

  • brain tumors, quadriplegia, traumatic brain injury

  • sending wrong signals about BP → increases BP

• pregnancy induced

• coarctation of the aorta

  • narrowing in one area → increases BP

• endocrine disorders

  • hormones sending wrong signals → increase BP

  • pheochromocytoma, cushing syndrome, thyroid disease, primary hyperparathyroidism, primary hyperaldosteronism

what are the complications of untreated hypertension? what organs does it impact?

• untreated hypertension → decreased vital organ perfusion → increases risk for damage to the

  • brain

    • stroke or TIA (cerebrovascular disease)

    • elevated BP in the vessels in the brain can cause cognitive decline

  • eyes

    • retinal damage, retinal hemorrhage

    • tiny vessels in the eyes get stressed out d/t high BP → retinopathy, blindness

  • heart

    • coronary artery disease, myocardial infarction, hypertensive heart disease, left ventricle hypertension, heart failure

    • stressing out vessels in the heart → damages heart

  • peripheral vessels

    • think peripheral vascular diseases

  • kidneys

    • chronic kidney disease, kidney failure

    • need the most blood flow

    • very sensitive to pressure

what is resistant hypertension?

even through treatment it does not get better

what are the contributing factors to resistant hypertension?

• increasing obesity

• inadequate medication dosing

• lack of medication adherence

  • education deficit, side effects, socioeconomic status

• oral contraceptives

  • impacts RAAS system

• sympathomimetic drugs (any drugs that increase SNS)

  • decongestants → increases SNS & BP

• cocaine, amphetamines

• corticosteroids, NSAIDs

what is the treatment for hypertension (drugs, secondary hypertension)

• medication management

  • ACE inhibitors (PRIL)/ARBS (SARTANS) → blocks vasoconstriction & reduces peripheral vascular resistance, works w/ the kidney to decrease sodium & water

    • watch for sodium, electrolytes, make sure BP is not too low

  • beta adrenergic blockers (OLOLs) → lowers HR & contractility of the hart

    • SE: super tired at first but gets better

    • watch for HR

  • calcium channel blockers → lowers BP by vasodilation & sodium channels in the kidneys

  • diuretics

    • may hold if HR & BP is too low, watch for electrolytes

• individualized tx

• secondary hypertension → diagnose & tx underlying cause

what is the first intervention for HTN?

lifestyle changes then meds if needed

client teachings for HTN

• lifestyle modifications

  • dietary changes

    • DASH diet

    • low sodium, cholesterol, saturated dats

  • BMI reduction

  • regular exercise

  • alcohol in moderation

  • tobacco cessation

  • stress management

  • need for follow up visits & health screenings

  • ambulatory BP monitoring for “white coat” HTN

  • how to measure BP

  • importance of med adherence

what is hypertensive crisis? how does it occur? what are the s/sx of an emergency?

• when BP >180/120

• life threatening emergency!

• occurs if someone who has not been dx w/ HTN & stopping meds abruptly

• s/sx of emergency:

  • looking for end organ damage

  • brain** → encephalopathy → BP w/ headache, confused, blurry vision → seizures, stroke, or death

  • heart → MI, heart failure

  • kidneys → acute kidney disease

  • eyes → blindness

  • vessels → aortic dissection if pressure is too high

hypertensive emergency vs urgency?

• emergency: very high BP + organ damage

• urgency: very high BP + no organ damage

do we lower BP fast or slow? why?

• slow b/c fast can have the opposite effect

• drop no more than 25% per hour

what is the nursing priority for hypertensive emergency?

IV meds, gradual BP reduction, ICU monitoring

what is heart failure? is it reversible? what underlying medical conditions cause it?

• when the heart is unable to pump enough blood to meet the body’s oxygen & nutrient needs

• structural or functional cardiac disorder leads to

  • abnormal cardiac output, can’t pump effectively

• chronic & progress, but reversible

  • starts from the left progresses to the right

• underlying medical conditions:

  • hypertension (COMMON), atheroscleorsis, cardiomyopathy, valvular disorder, kidney failure, viral, ischemia, toxins, postpartum

pathophysiology of heart failure

• inability of the heart to maintain adequate cardiac output to meet the metabolic needs of the body

• diminished cardiac output → inadequate peripheral tissue perfusion

• congestion of the lungs & periphery will occur depending which side is failing

what is ejection fraction?

measurement of the % of blood leaving the left ventricle each time of contraction

what makes the heart work?

• electrical conduction system (electrical wiring)

• muscle mass & function (walls)

• valves (doors)

• vessels (pipes)

  • volume (effective circulating volume)

  • O2/CO2 changes sensed by chemoreceptors

  • pressure changes sensed via baroreceptors (monitors stretch of the vessels)

what is cardiac preload, cardiac afterload, cardiac output & index?

1. cardiac preload

• known as left ventricular end diastolic pressure (amount of ventricular stretch at the end of diastole)

• the heart loading for the next squeeze of the ventricles during systole

• decrease preload (dehydrated)→ decrease CO

• high preload (fluid overload)

2. cardiac afterload

• known as systemic vascular resistance (SVR) → amount of resistance the heart overcomes to open the aortic valve & push blood volume into systemic circulation

• increase afterload → decrease CO

3. cardiac output & index

• CO: volume of blood heart pumps per min

• cardiac index: a calculation of CO divided by the person’s body surface area (BSA)

what additional sound do you hear when the heart muscles are dilated vs hypertrophy?

• dilation → thin & weak walls →S3 sound

• hypertrophy →thick & stiff walls → S4 sound

what are the 3 ways to classify heart failure?

1. based on time

• acute (ex. MI) vs chronic (ex. heart muscle build up d/t HTN)

2. based on location

• right sided (caused by worsening left side, so fluid backs up the entire system) vs left sided (heart overworking to overcome HTN → blood backs up to the lungs b/c left ventricle is not working as well)

3. based on pathophysiology

• HF w/ reduced ejection fraction (systolic)

• HF w/ preserved ejection fraction (diastolic)

what is left sided HF? symptoms/features?

• LEFT = LUNG CONGESTION

• left HF = heart overworking to overcome HTN → blood backs up to the lungs b/c left ventricle is not working as well

3. based on pathophysiology

4. clinical features:

   • pulmonary edema: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, crackles

   • cough w/ pink, frothy sputum

   • crackles/rales

   • weakness & fatigue

   • cold, clammy skin

   • increased HR

   • weight gain (not obvious)

   • cyanosis

what are the causes for left sided HF?

• systemic hypertension

• myocardial injury

• left sided valve problems

• dysrhythmias (more acute)

what is right sided heart failure? clinical features?

• right sided HF → caused by worsened left sided HF & fluid backs up to the whole system

• clinical features

  • distended neck veins

  • hepatomegaly, splenomegaly

  • ascites

  • peripheral edema

  • weight gain (more obvious)

what are the causes of right sided HF?

• left HF (most common)

• lung disease (cor pulmonale)

• right sided valve problems

• right ventricle muscle problems

what is heart failure w/ preserved ejection fraction (HFpEF)? also known as? what is it characterized by? common with?

• also known as diastolic HF

• a compliance abnormality often d/t hypertensive cardiomyopathy, where ventricular relaxation is impaired (EF >= 50% aka normal)

• think of heart working really hard & is now hypertrophied, struggles to fill

• characterized by

  • thickened muscle wall

  • little filling of blood in ventricles

  • less cardiac output

  • common w/ hypertension

what is heart failure w/ reduced ejection fraction (HFrEF)? also known as? what is it characterized by? common with?

• also known as systolic HF

• inotropic abnormality (decreased contractility) often d/t MI or dilated cardiomyopathy resulting in diminished systolic emptying (EF <= 40% aka low)

• think problem with squeeze, struggles to pump

• characterized by

  • thin wall muscle

  • large amount of blood filling the ventricles (decreased pumping)

  • less cardiac output

  • common w/ myocardial damage

    • scar tissue replaces ventricular myocardiocyte & scar tissue can’t pump effectively

can diastolic & systolic coexist in a pt? what can both lead to?

• yes

• leads to decreased CO & HF symptoms but mechanisms diff

what is cor pulmonale? key symptoms? nursing focus?

• right sided HF d/t lung disease → think hypertrophy

• key symptoms: dyspnea, JVD, peripheral edema

• nursing focus: support oxygenation & manage right HF symptoms

how does the ventricles remodel after an acute MI?

if no interventions are taken, the ventricles will remodel →tissues die → atrophy so dilated → permanent change

what is the activation of neurohormonal mechanism during myocardial dysfunction?

• decreased CO

  • activation of baroreceptors in the SNS → detects drop → release NOREPI to increase HR, contractility → incr. BP

  • activates renin-angiotensin aldosterone system (RAAS) → detects decreased renal perfusion → kidney release renin → converts angiotensinogen to antgiotensin 1 to angiotensin II → vasoconstriction to increase BP, HR, afterload ALSO release aldosterone to ask kidneys to retain sodium & water

• naturetic peptides counteract what is happening by releasing BNP & ANP for fluid overload to drop BP (vasodilate) & excrete out sodium & water (inhibit RAAS), inhibits SNS, decrease aldosterone levels

what is the problem with activation of neurohormonal mechanism in the long term?

short term can help temporarily maintain perfusion but long term can cause harm b/c ventricular hypertrophy & remodeling, fluid overload (edema, pulmonary congestion), increased workload can worsen HF progression

what medications target the neurohormonal mechanisms: RAAS, SNS, fluid overload, H2O & sodium retention?

• ACE inhibitors/ARBs/ARNI → block RAAS

• Beta blockers → block SNS overstimulation

• diuretics → relieve fluid overload

• Aldosterone antagonists → stop Na+/ fluid retention

what are the diagnostic studies for HF?

• echocardiogram for structural defects & assessing ejection fraction

• serum brain (B type) natriuretic peptide

  • good marker for HF b/c released when ventricles stretch out d/t volume overload

  • higher BNP = worse HF

• chest xray to determine pulmonary edema & pleural effusions

• ECG for coronary artery disease & dysrhythmias

what is the new york heart association classification system for HF? how many classes (brief explanation)? what does each class require? what are the symptoms to note of for classification?

• pt reported based on activity tolerance

• 4 classes

  • class 1: no limits to physical activity, no sx, can do normal activities

  • class 2: slight limitation, sx w/ normal activities

  • class 3: marked limitation (only moves around home), sx w/ less than normal activities (not going outside)

  • class 4: severe limitation, sx of heart failure at rest

• class 1-3: requires meds & close monitoring (treating & monitoring to prevent decline)

• class 4: high risk, consider palliative care, transplant, advanced therapy (LVAD)

• symptoms: fatigue, dyspnea, palpitations, or angina

how to manage HF symptoms?

can’t cure, relieve them b/c they predict quality of life, morbidity, mortality

common symptoms/classic of HF

• diuretic related (urgency, frequency)

• dyspnea on exertion, fatigue (activity intolerance), weakness, orthopnea, paroxysmal nocturnal dyspnea

• chest pain, peripheral edema

• cognitive impairment: memory loss, decreased attention, concentration (b/c poor perfusion to the brain)

• loss of balance & falling

• trouble sleeping

• weight loss bc fluid in stomach makes you feel & have no appetite

• fear, depression, sadness

heart failure pneumonic

OVERLOAD: orthopnea, ventricular failure, enlarged heart, reported weight gain, lungs congested, output decreased, apprehension (anxiety), dependent edema

why is there frequent readmissions w/ HF? what should we do to prevent?

• frequent b/c of exacerbations

• prevent by help managing them, educate pt to seek help early, follow up w/ cardiology/PCP

how will HF pts show up to the ED (what symptoms)

rales, peripheral edema, dyspnea (SOB)

what is the dry profile vs wet profile of HF?

1. dry profile (poor perfusion problem, no fluid not pumping well)

• decr. exercise tolerance

• fatigue, malaise

• decreased appeptite

• weight loss

• cachexia

• sleep disorders

2. wet profile (fluid overload)

• decr. exercise tolerance

• S3/S4 heart sounds

• dyspnea on exertion

• paraoxysmal noc dyspnea

• orthopnea

• nocturia

• edema, weight gain

• cough (worse at night)

• N/V/A, RUQ pain

hydrostatic vs oncotic pressure, what does imbalance cause?

• hydrostatic pushes fluid out

• oncotic pulls fluids in

• imbalance causes edema

what happens when there is 3rd spacing in HF? what to do?

• third spacing → fluid overload in tissues, volume depletes in vessels

• always check daily weights, lung sounds, BP to assess fluid status

how to rate edema?

• 0+: no pitting edema

• 1+: mild, 2mm & disappears

• 2+: moderate, 4 mm, disappears in 10-15 secs

• 3+: moderately severe, 6mm, lasts more than 1 min

• 4+: severe, 8mm, lasts more than 2 mins

If cardiac output is diminished in heart failure, will peripheral oxygen saturation measurements be accurate? what is more accurate

no b/c pulse O2 looks at saturation wherever you put it on so just on that finger, not accurate b/c entire system is off. ABG is a better indicator.

quickly explain HF & hypervolemia

1. pump fails → decreased CO → decreased renal perfusion → stimulates RAAS

   1. vasoconstriction → incr. BP

   2. aldosterone → Na & water retention → fluid overload

   3. ADH → water retention

   4. venous congestion → incr. hydrostatic pressure → edema aka third spacing

what to do for unstable HF pt w/ acute pulmonary edema? aka what to do first then what

• high fowler’s & oxygen FIRST then IV diuretics to reduce volume

nursing interventions for acute HF (pulmonary edema)

• place the client in high fowler’s position

• administer O2

• assess lung sounds

• establish IV access

• prepare to administer a loop diuretic → watch K+ levels

• monitor strict I & O

• prepare for mechanical ventilator support, if required

emergent actions for pulmonary edema

1. oxygen

2. sit up, legs dependent (hanging down)

3. nitroglycerin SL → dilates blood vessels, reducing workload of the heart

4. furosemide IVP 0.5-1 mg

5. morphine IVP 2-4 mg

what is the outcomes we should aim for/priority for acute heart failure?

1. gas exchange

2. cardiac output

3. activity tolerance

4. pain/anxiety

5. self-care education

ABCS then activity tolerance

pharmacological management for heart failure (what class of med & what for)

1. diuretics

• loop diuretic (ex. furosemide)

• potassium sparing diuretic (ex. spironolactone)

• to reduce preload (volume in venous blood)

2. beta blockers → reduce cardiac workload

3. ACE inhibitors → to reduce afterload (BP)

4. digoxin → to increase cardiac contractility

• second line therapy now

• has a narrow therapeutic index of effectiveness & toxicity

• antidote: digoxin immune FAB

2. advise pt to avoid over the counter meds

gold standard therapy for HF (meds)

1. angiotensin receptor neprilysin inhibitor (ARNI) → preferred over ACE/ARB

• sacubtril/valsartan (ENRESTO → 1st line drug)

2. angiotensin converting enzyme (ACE-1) → ends in pril

• decreases afterload → BP

• improves symptoms & overall exercise capacity in pts in the all NYHA classifications

3. angiotensin receptor blocker (ARB) → ends in sartan

• if they can’t tolerate ACE-1 d/t allergy or coughing use this

4. beta adrenegeric antagonists (beta blockers) → end in olol

• uses in systolic or diastolic HF

• be aware of asthma pts b/c of non-selective beta blockers

5. diuretics

• loop (K+ wasting) → ends in -ide (furosemide, butemanide, torsemide)

• thiazide like (HCTZ, chlorothiazide)

• K+ sparing (aldosterone blocker) → ends in -one (spironolactone, eplerenone)

6. SGLT2 inhibitor (sodium glucose cotransporter 2) → new standard

diuretics (mineralcorticoid receptor antagonist → K+ sparing), ARNI/ACE/ARB, beta blockers, SGLT2 (diabetes meds) → known as GDMT

what to watch for in spironolactone (aldactone)? why?

K+ labs b/c it can cause weakness in muscles esp heart, electrolytes in general

will pts with pulmonary disease tolerate beta blockers? why? what should we do?

no b/c they can impact both the heart & lungs if non-selective so we should advocate

what are the big 3 for HF? which 3 is not evidenced for HF? should we use beta blockers if HR is low?

• carvedilol, metoprolol succinate (XL), bisoprolol → big three for HF

• not evidenced → atenolol, propanolol, metroprolol tartrate

• no do not use, hold!

what is the first line drug for HF? why?

Entresto reduces workload on the heart & less risks compare to other drugs

client teaching for HF

• perform daily weights & report gains of

  • 3 lb (1.4 kg) in 2 days

  • 3-5 lb (1.4-2.3 kg) in a week

• gradually transition from lying to standing

• check HR & BP prior to taking meds

• use a pill organized to ensure med adherence

• instruct moderate restriction of sodium in diet (<3 g/day)

  • eat more whole foods

  • less sodium to prevent fluid overload

  • pt can’t be eating canned soups, deli meats, or fast food → red flag!

  • less salt in homemade food compared to outside

• instruct client regarding fluid restriction if prescribed

• increase exercise gradually

• avoid extreme hot (vasodilate) & cold (vasoconstrict)

• educate smoking cessation & limit alcohol use

• symptoms to report

  • difficulty breathing, fatigue, peripheral edema

what to educate pts about daily weights?

• vascular bed can hold 10 lbs of fluid before seeping out to tissues

• 2 lbs = 1 qt of water (use pt pitcher to show)

• use calendar to record weights

• report 2 lb weight gain overnight or 5 lb weight gain in a week (sign of HF)