HTN Cardiomyopathy CHF Flashcards

1
Q

hypertension

A

-Elevation of BP at 2 or more office visits after an initial screening (3 total)
-With 2 or more readings at each office visit
-If there is a disparity in category between the systolic and diastolic pressures, the higher value*determines the stage
-normal- <120/<80
-prehypertension- 120-129/<80
-hypertension (stage 1)- 130-139/80-89
-hypertension (stage 2)- >140/>90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

primary hypertension- essential

A

Description:
-90-95% of cases, no identifiable cause
-no treatable cause
-Hypothesized factors:
-SNS hyperactivity, abnormal renal development

Exacerbating factors:
-Alcohol, tobacco, sedentary lifestyle
-NSAIDs
-Polycythemia vera: thicker blood
-Males, African American
-Diet
-Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

secondary hypertension

A

5-10% of cases

Causes: “bella PORCH drives on the PCH -> shes just a secondary thought (forgotten influencer”
- parenchymal renal ds
- obstructive sleep apnea
- Renal artery stenosis
- coarctation of aorta
–hormone use
-pheochromocytoma
-cushing’s syndrome
-hypothyroidism

-coarctation of aorta - - (hypertensive on the left)- congential abnormality
-parenchymal renal ds - Angiotensin cascade
-Renal artery stenosis - Angiotensin cascade
-pheochromocytoma
-cushing’s syndrome
-hormone use
-hypothyroidism
-obstructive sleep apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

reasons to screen for secondary HTN

A

-new/abrupt or uncontrolled HTN
-presence of drug resistant or drug induced HTN
-onset of HTN in young person <30
-exacerbation of previously controlled HTN
-disproportionate target ORGAN DAMAGE for the degree of HTN
-accelerated or malignant HTN
-onset of DIASTOLIC HTN in older adults >65
-unprovoked or excessive HYPOKALEMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hypertension complications

A

Cardiovascular:
-Coronary artery disease
-heart failure
-valvular disease
-left ventricular hypertrophy
-aortic aneurysm/dissection
-peripheral vascular disease

Nephro: Renal sclerosis

Neuro:
- TIA
- CVA
- encephalopathy
- aneurysms

Optic:
- Retinopathy
- retinal hemorrhage
- blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hypertension initial testing

A

-12 lead EKG: Left ventricular hypertropy (LVH)

Labs: Rule out secondary causes
-Potassium
- blood glucose (diabetes)
- creatinine/BUN kidney
-Pheochromocytoma: 24 hour urinary metanepharine and normetanephrine
-Thyroid and parathyroid disease- TSH, T3/T4, serum PTH
-Primary aldosteronism: 24 hour urinary aldosterone level
-Lipid profile- Atherosclerosis risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

echocardiogram

A

echocardiogram
-2-D echocardiogram (Transthoracic):
-Ultrasound technology allowing to view cardiac structures including atria, ventricles, and valves

-Transesophageal echocardiogram (TEE):
-Ultrasound technology through esophagus allowing better visualization of the mitral valve and left atrium
-Left atrial appendage thrombus*
-Mitral regurgitation
-best way to see aortic and mitral valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ejection fraction normal values

A

-Ejection fraction = percentage of blood ejected from left ventricle
-Normal: 55%
-Low normal: 50-55%
-Low: 45% and less
ICD at < 35%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

hypertension goal BP and lifestyle management

A

Goal BP:
-DM or CKD < 130/80
-All others <140/90

Lifestyle management:
-1. Weight loss- BMI 18.5-24.9** best tx to lower BP
-2 Dietary Approach to Stopping Hypertension (DASH diet)- Low salt, low saturated fat, increasing fruits and vegetables
-<2000mg salt for low salt diet
-3. Aerobic exercise- 30 mins or more, 5 days or more
-4. Limitation of alcohol consumption- 2 or less drinks daily for men, 1 or less drinks daily for women
-STOP SMOKING **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hypertension: pharm modifications

A

hypertension: pharm modifications
-DM, CKD, and patient without comorbidities who have failed non-pharmacologic modifications
-Diuretics are first-line for all pt w/o comorbidities (hydrochlorothiazide) **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HTN: pharmacologic modifications for pts with comorbidities or those who have failed non-pharmacological modifications

A

Diabetes mellitus + Chronic Kidney Disease (stage I, II) + Cerebral Vascular Disease
- ACE inhibitors (-prils) or ARB

Coronary artery disease (post-MI)
- beta blockers or
- ACE inhibitors or
- ARB

Heart failure:
- beta blocker or
- ACE inhibitors or
- ARB or
- diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is first line pharmacologic treatment for patients with out comorbidities with hypertension?

A

Dieuretics
-THIAZIDE: HCTZ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Angiotensin 2 receptor (ARB)

A

MOA:
- vasodilation by inhibiting activation of angiotensin 2 receptor
-decrease preload/afterload

ADR:
- angioedema** BAD -> switch med
- hyperkalemia
- cough (less common)
- renal impairment

Drug names: -sartan drugs
-Valsartan
-Candesartan
-Losartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ACE inhibitors MOA, ADR, drug names

A

MOA:
-vasodilation by inhibiting angiotensin-converting enzyme
-decrease preload/afterload
-category X in preg

ADR
- hyperkalemia**
- angioedema (mouth and lips) = BAD
- cough due to bradykinin production
- renal impairment

Drugs: -prils (X)
-Ramipril
- Lisinopril
-Enalipril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

beta blockers

A

MOA:
-antagonists
-block receptor sites of epinephrine and norepinephrine on adrenergic beta receptors

ADR
- bronchospasm**
-> if bronchospams try a cardioselective b1
- hypotension
- fatigue (normal for 2 weeks)
- bradycardia

Drugs: -olol
- Metoprolol - beta 1 selective
- Bisoprolol - nonselective
- Propanerol -nonselective
- Carvediolol- mixed alpha and beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

calcium channel blockers

A

MOA
-decrease smooth muscle contraction and cardiac monocyte contraction by blocking calcium entry
-non-DHP have less vasodilation, selective to myocardium
-can cause dizziness when you stand - ask

ADR
- peripheral edema**
- fatigue
- hypotension
- muscle cramps (K shift)

Drug names:
- Amlodipine*
- Nifedipine*
- Verapamil
- Diltiazem

“think muscle and periphery with CCBs”
- non-DHP is more central but ADR causes PERIPHERAL EDEMA + muscle cramps, hypotension, fatigue”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

diuretics

A

MOA:
-increase sodium excretion
-increasing water extrication

ADR
- hypokalemia
- hypochloremia
- hypotension
- renal failure
- pancreatitis

Thiazide :HCTZ (htn tx)
Loop: Flurosemide (Lasix) (HF symptomatic tx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

alpha blockers- HTN med; MOA, ADR, drug names

A

MOA:
-block alpha receptors in smooth muscle causing vasodilation
-only use when they are on meds and cant get BP down

ADR
- orthostatic hypotension**
- dizziness
- somnolence: excess sleepiness
- headache

Drugs:
-Clonidine
-Terazosin
-Doxazosin

“alpha males CANT stand up or lower BP
- only use when other meds arent working
- ADR: orthostatic hypotension”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

meds to avoid with comorbities:
Chronic kidney disease (stage 3, 4),
Hyperkalemia, Hyponatremia, Asthma, gout, Angioedema, 2nd/3rd degree heart blocks, bradycardia

A

Chronic kidney disease (stage 3, 4):
- ACE inhibitors or ARB

Hyperkalemia
- ACE inhibitors or ARB
- aldosterone antagonist

Hyponatremia
- thiazide diuretics

Asthma
- beta blockers

Gout:
- thiazide and loop diuretics (first toe pain)

Angioedema-
ACE inhibitors

2nd/3rd degree heart blocks, bradycardia
- beta blockers
- non-dihydropyridine calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hypertensive urgency definition

A

Definition:
-Blood pressure reading of systolic BP>180 mmHg and/or diastolic BP >120 mmHg
- WITHOUT evidence of end organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

hypertensive urgency management

A

Management:
-Gradual reduction of mean arterial pressure- Reduction should be no more than 25% over 24-48 hour period
-Oral Meds: goal is less than or equal 160/100mmHg
-Labetolol - Beta-blocker
-Nicardipine – Calcium channel blocker
-Captopril – ACE inhibitor

“need to go on a Norwegian Cruise Line (NCL) urgently”
-nicardipine (Calcium)
-labetolol (beta)
-catopril (ACE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hypertensive emergency definition

A

Definition:
-Systolic >220
-Diastolic >120
-WITH END ORGAN DAMAGE -> may not be reversible
- NEED IMMEADIATE reduction of bp*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hypertensive emergency : Signs of end-organ damage

A

“UM I feel CRAPPIE this is an emergency!!-> we need to immediately reduce my BP or else i might get irreversible damage”

-Unstable angina (w/o exertion)
-MI
-CHF
-Renal Failure
-Aortic Dissection
-Papilledema
-Pulmonary edema
-Intracranial hemorrhage
-Encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

causes of hypertensive emergency

A

-Noncompliance*

No CAp Victor we in a PINCHER = Hypertensive emergency

-Noncompliance*
-Alcohol withdrawal
-Vasculitis
-Polycystic kidney disease
-Illicit drug use
-Noncompliance*
-Cushing’s syndrome
-Hyperaldosteronism
-Eclampsia
-Renal artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hypertensive emergency tx

A

-Reduce mean arterial pressure (MAP) by 25% in 1-2hrs*
-Quick reduction of BP can lead to ischemic CVA**

IV agents:
-Esmolol, Labetolol
-Hydralazine
-Nitroglycerine
-Nitroprusside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MAP definition

A

MAP = average blood pressure during a single cardiac cycle:
-Cardiac output
-systemic vascular resistance
-central venous pressure “preload”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

white coat hypertension

A

Definition: consistently elevated office blood pressure readings with out of office readings that do not meet criteria for hypertension
- In office elevated bp but then out of office they dont meet criteria for HTN
-Difficult to differentiate
-Increased risk of developing hypertension
-Ambulatory and home blood pressure monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

hypotension definition

A

-Systolic BP < 90 mm Hg and/or diastolic BP < 60 mm Hg
-Significant if symptoms are present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

causes of hypotension

A

Medications:
-Beta-blockers
-Alpha-blockers
-Calcium channel blockers
-Nitrates

Hypovolemia:
-Blood loss
-Excessive diuretic use
-Dehydration
-Anemia

Low cardiac output:
-Myocardial infarction
-Bradycardia
-Heart failure

30
Q

hypotension symptoms

A

-Dizziness/lightheadedness
-if they are getting up fast or bending down and getting lightheaded -> not vasoconstricting enough to compensate when they move quick -> are they on a vasodilator?
-Fatigue
-Weakness
-Syncope
-Shortness of breath
-Exertion dyspnea
-Chest pain
-Palpitations
-Headache
-Cough- compensation to increase preload
-Seizures- no blood flow to brain

31
Q

orthostatic hypotension

A

Decrease in BP upon standing:
>20 Systolic
>10 Diastolic

32
Q

causes of orthostatic hypotension: non-drug related

A

-Cardiac Arrhythmias
-Dehydration*

-Parkinson’s
-Diabetes
-Endocrine disorders
-Hypoaldosterosterism
-Hypothyroidism
-Anemia

“A DROP”:

Arrhythmias
Dehydration
Regulatory problems (Parkinson’s)
Other Endocrine disorders (like hypoaldosteronism and hypothyroidism)
Poor blood volume (Anemia)

meds:
-alpha blockers
-diuretics
-narcotics
- MAOIs
- TIAs

33
Q

causes of orthostatic hypotension: medications

A

-Alpha-blockers: Terazosin, tamsulosin, doxazosin -> vasodilators!
-Diuretics: Furosemide, hydrochlorathiazide
-Nacrotics: Morphine
-MAOIs: Rasagiline
-TIAs: amitriptyline

34
Q

orthostatic hypotension dx and tx

A

Dx- blood pressure measurements -> lying, sitting, standing

Tx:
-Increase oral HYDRATION and salt INTAKE
-Slow positional changes- pump legs before you stand -> muscular pump
-Compression stockings
-Exercise
-Treat underlying cause

Medication tx:
-Fludrocortisone- glucocorticosteroid
-Midodrine- alpha agonist (dont give to HTN pt)
-Droxidopa (dont need to know)

give “FLUDRO and MIDODRINE”

35
Q

cardiogenic shock

A

-Definition: Cardiovascular failure causing loss of tissue perfusion
-End-organ tissue lack of perfusion
-Hypotension refractory to volume resuscitation
-Systolic BP < 90 mm Hg
- urine output < 20mL/hr

36
Q

cardiogenic shock causes

A

-Acute MI - MC cause**
-Cardiac tamponade
-Pneumothorax
-Arrhythmias
-PE
-Cardiomyopathies
-Heart failure
-Cardiac contusion
-Valvular and septal abnormalities

“youre so cute you SHOCKED me”
- aCUTE MI = cardiogenic SHOCK”

37
Q

clinical features of cardiogenic shock

A

-Hypotension!
-Oliguria/anuria!
-Tachycardia!
-Altered mental status!

-Cool extremities- organs not perfused
-Decreased capillary refill
-Weak peripheral pulses
-Jugular venous distension- volume overload or right HF
-Pulmonary congestion

38
Q

cardiogenic shock tx

A

First step for all patient with shock = ABCs **
-Airway, breathing, circulation
- 2 large bore needles, central line arterial line

Vasopressors: positive ionotropic agents
-Dopamine
-Dobutamine
-Norepinephrine*
-Intra-aortic balloon pump

Identify and treat underlying cause
-Acute MI:
-Aspirin, heparin, nitrates, etc
-Emergent revascularization – coronary angiogram
-bypass, stent
-Cardiac tamponade- Pericardiocentisis, pericardial window
-Arrhythmias: ACLS protocol

39
Q

heart failure

A

-CHRONIC and PROGRESSIVE disease in which the heart is unable to meet the body circulatory demands
-Results in abnormal RETENTION OF FLUID due to reduced efficiency of the heart
- venous congestion due to a pathologic change

40
Q

heart failure classification

A

High output vs. low output (CO)

Diastolic vs. systolic
- systolic: decrease in LV ejection fracture (<45%)
-diastolic: normal LVEF but cannot RELAX myocardium

Right sided vs. left sided
- right sided: periphery and systemic backup
- left sided: pulmonary vascular congestion

41
Q

high output CHF causes

A

“the PATH to be a PA is high workload (high output)”
- Pregnancy
- Anemia
- Thyrotoxicosis
- Hemachromatosis
- Paget’s ds
- AV Fistula

-High-output: Increase in cardiac output
-this is not usually problem with heart -> more compensation for something else
—-

-Anemia (anemic pts compensate -> increase HR, hypertrophy)
-Thyrotoxicosis - excess of thyroid hormones
-Hemachromatosis - iron metabolism issue
-Pregnancy
-Wet beriberi (dont need to know)
-Paget’s disease of the bone
-AV fistulas

42
Q

low output CHF causes

A

Low-output: decrease in cardiac output
- MC compared to high output
- cant contract, cant fill, or the valves are injured

Causes:
-Decrease in myocardial contractility
-Cardiomyopathies - heart diseases
-Valvular disease- stenosis -> back flow -> improper filling
-Diastolic dysfunction

43
Q

systolic heart failure

A

Issue:
-Difficulty with myocardial contractility -> Failure to contract
-Reduced left ventricular ejection fraction (LVEF)
-45% or less* -> dx with HF

Causes:
-MC- Coronary artery disease** -> Post MI (weakened heart cant contract)
-HTN
-Valvular disease
-Myocarditis
-Alcohol abuse
-Radiation treatment

“THink why can the heart not squeeze?
- CAD - not enough blood and post-MI makes it weak
- HTN
- alcohol or radiation
- myocarditis
- valvular issue -> hard to push out blood

44
Q

diastolic heart failure

A

-Preserve LVEF with impaired ventricular filling
-Difficulty with relaxation myocardium
-Failure to relax

Causes:
-Left ventricular hypertrophy: MC cause of diastolic dysfunction** (chronic HTN could cause LVH)
-Valvular disease
-Restrictive cardiomyopathy: heart wall stiffens ( -osis diseases)
-Amyloidosis- fat deposits in heart tissue
-Sarcoidosis- inflammatory
-Hemachromatosis

45
Q

left sided heart failure

A

main issue: Pulmonary vascular congestion
-Dyspnea
-Orthopnea
-Paroxysmal nocturnal dyspnea
-Cough- frothy clear fluid
-Confusion
-Fatigue

Signs:
-Rales, decreased breath sounds at bases -> sometimes nothing
-Tachypnea
-S3 heart sound – ventricular gallop

Tx- lower volume

46
Q

right sided heart failure

A

-Systemic vascular congestion

Sx: based on liver dysfunction and congestion
-Anorexia- volume compressing stomach
-Nausea/Vomiting
-Jugular venous distention -> JVD reflex
-Hepatomegaly
-Ascities
-Peripheral pitting edema
-ABSENCE OF LUNG FLUID IF ONLY RIGHT SIDED
-Left heart failure is the most common cause of right*

47
Q

congestive heart failure
dx, labs and chest x-ray

A

CLINICAL DIAGNOSIS!

Labs:
-CBC, CMP, TFTs,
-B-type natriuretic peptide (BNP)- Released from the ventricles: volume OVERLOAD or EXPANSION

Chest radiography:
-Cardiomegaly
-Kerley B lines – interstitial edema- Horizontal lines at periphery of lungs
-Pulmonary dilations
-Pleural effusions- Blunting of costophrenic angles

48
Q

congestive heart failure
EKG, echocardiogram and other tests

A

EKG – nonspecific
Echocardiogram:
-reduced LVEF
-Valvular abnormalities
-Pericardial effusion

Stress test – identification of ischemia
Cardiac angiogram

49
Q

IVC US

A

-pleuthoric state of congestion with blood: there is NO IVC MOVEMENT
-hypotensive pt -> check IVC sniff test -> HF pt with overload will have NO IVC collapse
-pt with dehydration: IVC will completely COLLAPSE
-normal- 50% collapse during inspiration
-if you assume the pt with hypotension needs volume and they are really in HF -> you make it worse…

50
Q

common triggers of elevated BNP and NT - proBNP

A

BNP will increase in anything that makes it feel like it has too much volume

Cardiac conditions:
- HF
- valvular heart disease
-CAD
- HTN

Pulmonary ds:
- acute pulmonary embolism
- pulm HTN
- obstructive sleep apnea

Neurologic:
- stroke

critical illness:
- sepsis
-cirrhosis

toxins
- chemo
- snake bites

Others:
-renal insufficiency
- anemia
-hyperaldosteronism

51
Q

classification of HF: A-D

A

A/1:
- no cardiovascular ds
-no sx of limitations with activity

B/2:
- minimal CVD
- slight limiations with physical activity
- GOING UP STAIRS, carrying heavy packages
- no sx with rest

C/3:
- mod-servere CVD
- marked limitation with physical activity
- DOING ACTIVITIES (GETTING DRESSED, walking across a room ETC)
- only comfortable w rest

D/4:
- severe CVD
- SYMPTOMS AT REST, END STAGE HEART FAILURE. sitting in a chair

-<45% EF -> classify HF
-classification is based of symptoms -> tx is based on EF

52
Q

heart failure lifestyle tx

A

-Treat any underlying cause
- GET THE annual INFLUENZA and PNEUMOCOCCAL vaccines**

Lifestyle modifications
-Low sodium diet- <1800 mg
-Fluid restriction- volume overload
-Weight loss
-Alcohol reduction
-Smoking cessation
-Exercise programs
-Monitor daily weights

53
Q

Heart failure: what are the main medication treatments

A

Diuretics:
- most effective sx relief (loop); thiazides more for HTN
- aldosterone antagonists: potassium sparring; good for advance stages

ACE inhibitors
- REDUCE MORTALITY
- all pts must be on it

Beta blockers:
- decrease mortality with post-MI HF
- must give to pts with atherosclerotic ds

Digoxin:
- severe Afib or reduced EF pt
- second line tx

last resort: other inotropes
- mildirone, dobutamine

sacubitril-vasartan (ARB)
- for systolic HF pts; class II-IV
- blocks Neprilysin -> increases BNP

54
Q

heart failure diuretic tx

A

Diuretics- most effective with symptomatic relief
-Loop diuretics: Furosemide (Lasix)- MOST POTENT
-Thiazide diuretics: Hydrochlorothiazide (not really HF, just keep volume a little lower)
-Aldosterone antagonist: Spironolactone, eplerenone
-Potassium sparing
-Effective in more advanced stages

55
Q

heart failure ACE inhibitor tx

A

-2. ACE inhibitors – REDUCE MORTALITY
-if you have HF YOU NEED TO BE ON THIS
-Decrease LV stress – decrease preload and afterload
-Slow remodeling- All patient with systolic heart failure should be on ACE inhibitor
-monitor K
-Angiotensin II receptors blockers (ARBs) can be used if a pt is intolerant of ACE inhibitors

MOA:
-Causes atrial and venous dilation
ADR:
-Hyperkalermia*
- angioedema*
- cough*- due to bradykinin production

other treatment: diuretics - most effective for symptomatic relief

56
Q

tracking water weight

A

-tell pt to check weight every morning and night
-tell pt to check weight when they are having symptoms
-tell them to take an extra diuretic if symptomatic and weight increased by about 3 lbs -> shows that symptoms are due to volume overload

57
Q

heart failure tx: beta blockers

A

Beta-blockers – proven to decrease mortality with post-MI HF
-Hx of atherosclerotic ds: have to give Beta-blockers

MOA:
-Decreases remodeling
-Slows HR -> decreases the rate of O2 consumption
-Antiarrhythmic and anti-ischemic properties

Drugs:
- metoprolol (Toprolol): beta 1
- carvediolol (Coreg): alpha and beta
-COMET TRIAL showed significant improvement in survival with carvedilol -> especially prior MI

Contraindications:
- caution in patient with pulmonary disease
- Bronchial spams
- could cause drop in BP -> slowly taper up

58
Q

heart failure tx digoxin + signs of digoxin toxicity

A

-useful with patients with reduced EF or severe Afib
-Positive inotropic affects- Increase cardiac contractility
-Has not been shown to decrease mortality -> last resort/ Second-line treatment
-need to check digoxin levels
-Narrow therapeutic range

Signs of digoxin toxicity:
-Green halos around lights* (board question)
-Nausea, vomiting, anorexia
-AV blocks, ventricular arrhythmias
-Disorientation, memory impairment
.

59
Q

heart failure sacubitril-vasartan tx

A

-Neprilysin inhibitor which increases levels of natriuretic peptide
-increases BNP -> encourages to reduce volume status
-Increasing vasodilation and decreases volume through sodium excretion
-For systolic heart failure patients - With class II-IV heart failure
-Decreases mortality and hospitalizations

60
Q

heart failure implantable cardioverter-defibrillation (ICDs)

A

-Prevention of sudden death (MC cause of death in CHF pts
-indicicated when LVEF <35%
-PPM-AICD options -> combined pacemaker-defib

61
Q

heart failure left ventricular assist device (LVADs)

A

-pt who require frequent hospitalization
-bridge to cardiac transplant* or destination therapy while pts wait for a heart
-need anticoagulation therapy
-very last resort

62
Q

heart failure cardioMEMs tx

A

-monitor pulmonary artery pressures for titration of diuretics

63
Q

dilated cardiomyopathy

A

-Dilation of the ventricles/atria causing a reduction in strength and contraction
-Most common cardiomyopathy (95%)
-Men > females

64
Q

dilated cardiomyopathy causes

A

-Alcohol*
-Ischemia** - CAD
-Idiopathic
-Genetic
-Chemotherapy toxicity
-Post-partum state
-Myocarditis
-Thyroid disease
-Lyme disease
-Diabetes
-Arrythmias
-Cocaine

“CARDIOMYOPAthy”
-CAD/ISCHEMIA*
-Alchohol
-R = genetics lol
- Diabetes
- Idiopathic
- Myocarditis
- Y: ThYroid
- other toxins - chemo
- Post-infection Lyme ds
- Arrythmias
- -toxins - cocaine

65
Q

dilated cardiomyopathy symptoms and dx

A

Symptoms/Signs:
-Heart failure signs and symptoms
-S3 and S4: S3 = volume overload; S4 = noncompliant ventricles
-Cardiomegaly
-Sudden death
Dx:
–Echocardiogram – diagnostic test of choice**
-Chest x-ray
-Genetic testing

66
Q

hypertrophic cardiomyopathy (HCM)

A

-Hypertrophy of the left VENTRICULAR SEPTUM
-Blockage of blood flow out of the left ventricle = hypertrophic obstructive cardiomyopathy (HOCM)
-Men = women
-Common cause of sudden death in people younger than 30 years*

67
Q

hypertrophic cardiomyopathy S&S

A

Systolic ejection murmur at Lower left Sternal Border:**
-Decreases squatting, lying down
-Increases with Valsalva and standing
-Increased carotid pulse (bisferious pulse/ biphasic peaks during systole)

Other sx:
-Dyspnea
-Chest pain
-Palpitations
-Arrhythmias
-Syncope
-Sudden death

68
Q

hypertrophic cardiomyopathy dx

A

-echocardiogram- dx of choice*
-EKG
-genetic testing

69
Q

restrictive cardiomyopathy

A

-Collagen defect infiltrating the VENTRICULAR wall causing reduced relaxation
-“stiffening” of the ventricle
-Impedes ventricular filling

70
Q

restrictive cardiomyopathy causes

A

Cause: anything that increases fibrosis of cardiac muscles
-Amyloidosis
-Sarcoidosis
-Hemochromatosis
-Scleroderma
-Carcinoid Syndrome
-post-radiation/chemotherapy fibrosis
-Idiopathic

71
Q

restrictive cardiomyopathy symptoms and dx

A

Sx:
-dyspnea
-exercise intolerance
-RIGHT sided heart failure S&S: peripheral congestion

Dx:
-EKG: low voltage (low amplitude)
-echocardiogram
-endomyocardial bx

72
Q

cardiomyopathy tx

A

Dilated and restrictive tx:
-Treat underlying cause
-Supportive treatment of congestive heart failure
-defibrillator

Hypertrophic:
-Avoid strenuous activity
-Beta-blockers or calcium channel blockers:to improve diastolic filling
-Septal myomectomy - remove thickened septum
-Alcohol septal ablation - inject alc to cause local necrosis and reduce obstruction

All cardiomyopathies:
-AICD: automatic implantable cardioverter-defib
-Cardiac transplantation