CVD Diseases Flashcards

1
Q

Management for Primary Hypertension

Pharmacological

A

Which drugs are used are dependant upon the severity of hypertension and any undyling disorders

  • ß-blockers: Class II Antiarrhythmic
  • ACE Inhibitors
  • Duiretics
  • Calcium Channel Blockers
  • Nitroglycerin/Nitroprusside
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2
Q

ß-blockers: Class II Antiarrhythmic

A
  • Reduce HR and force of contraction (not a desirable side effect), by blocking B1 receptors on the heart.
  • Used in angina and to treat hypertension.
  • Sympatholytic Drug
    • Opposes the downstream effects of postganglionic nerve firing in effector organs innervating the sympathetic nervous system (fight or flight)
    • Ex. Metoprolol
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3
Q

Diuretics

A

Help your kidney to get rid of extra water and salt from you body through your pee

Because there is less overall fluid in your blood vessels the pressure will be lower

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4
Q

Diuretics

Examples

A

Hydrochlorothiazide

Furosemide

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5
Q

Calcium Channel Blockers

A

Block the entry of calcium into the muscle cells of the heart and arteries

Calcium is critical to help pass electrical signals in the heart as well as constrict the arteries

By blocking calcium it will in turn dilate the arteries and decrease the force of contraction in the heart

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6
Q

Calcium Channel Blockers

Examples

A

Verapamil

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7
Q

Nitroglycerin/Nitroprusside

A

Potent vasodilators

Used in acute management

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8
Q

Causes of Secondary Hypertension

A

Renal Disease

Excess Adrenosorticosteroids

Co Arctation of the Aorta

Pregnancy

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9
Q

Secondary Hypertension

Renal Disease

A
  • Responsible for majority of 2° HTN
  • Usually atherosclerotic (hardening and narrowing of arteries) in origin
    • Decreased blood flow to the kidneys
  • Results in the retention of salt and water (due to the stimulation of RAA system)
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10
Q

Secondary Hypertension

Excess Adrenosorticosteroids

A

Seen in primary hyperaldosteronism and Cushing’s syndrome

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11
Q

Secondary Hypertension

Co Arctation of the Aorta

A

Coarctation of the aorta —Is a narrowing of the aorta, meaning your heart must pump harder to force blood through the aorta.

Coarctation of the aorta is generally present at birth (congenital). The condition can range from mild to severe, and might not be detected until adulthood, depending on how much the aorta is narrowed.

It will reduced blood flow to the kidney’s triggering the RAA system which results in water retention and HTN results

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12
Q

RAA System

A
  • When blood volume or sodium levels in the body are low, or blood potassium is high, cells in the kidney release the enzyme, renin.
  • Renin converts angiotensinogen, which is produced in the liver, to the hormone angiotensin I.
  • An enzyme known as ACE or angiotensin-converting enzyme found in the lungs metabolizes angiotensin I into angiotensin II.
  • Angiotensin II causes blood vessels to constrict and blood pressure to increase. Angiotensin II stimulates the release of the hormone aldosterone in the adrenal glands, which causes the renal tubules to retain sodium and water and excrete potassium.
  • If the renin-angiotensin system becomes overactive, consistently high blood pressure results.
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13
Q

Secondary Hypertension

Pregnancy

A
  • Pregnancy induced hypertension (PIH)
    • Elevated blood pressure throughout pregnancy
  • Precampsia
    • Serious disorder characterized by the onset of acute hypertension after 24thweek
    • Accompanied by proteinuria and edema
  • Eclampsia
    • Life threatening form of toxemia cause severe convulsions, coma, kidney failure, and possibly death
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14
Q

Treatment of Secondary Hypertension

A

Treat the underlying cause

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15
Q

Malignant Hypertension

A

AKA Hypertensive Crisis

Occurs when someone with second degree hypertension develops an accelerated and potentially fatal form of the disease

Characterized by a sudden marked elevation in blood pressure with systolic pressure (>180 mmHg) and diastolic pressure (>120 mmHg)

Causes severe damage to the vascular system

Can result in encephalopathy, cerebral edema, coma, convulsion, and stroke and organ damage

Manifests as headache, confusion, motor and sensory deficit and visual disturbances

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16
Q

Hypertension Pathphysiology

Plaque does not rupture

A
  1. Damage to vascular endothelium
  2. Healing plaque formation
  3. Lumen narrowing
  4. Decreased blood flow distally
  5. Decreased blood flow to kidney
  6. Stimulation of RAA system
  7. Increased blood volume
  8. Increased blood pressure
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17
Q

Hypertension Pathphysiology

Plaque Ruptures

A

Thrombus

Lack of blood flow to organ

Ischemia/Infarction to area distal to blockage

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18
Q

Target Organ Damage

Hypertension

A
  • Heart
    • Hypertrophy of LV, risk of ischemia/MI
  • Cerebrovascular
    • Increased risk of stroke (2°bleed or clot)
  • Peripheral Vascular
    • Development of atherosclerosis and arteriosclerosis
  • Renal
    • Stimulation of renin-angiotensin system (which worsens HTN)
  • Retinal
    • Damage to vasculature and resulting vision problems, increased intraocular pressure can cause retinal separation
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19
Q

Hypertension

Clinical Manifestation

A

Increased BP!

Usually an asymptomatic disease (especially initial few decades)

Occasionally can result in headaches

Often the first symptoms are due to complications of the HTN

E.g., Chest pain, stroke symptoms, CHF symptoms

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20
Q

Coronary Artery Disease

A

A narrowing of one or more coronary arteries due to a build-up of fatty deposits within the arterial wall

This will result in a reduced blood flow and subsequently less oxygen and nutrients delivered to the heart muscles that are reliant upon the affected arteries

Lack of blood flow will lead to ischemia of the heart

CAD is also known as ischemic heart disease

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21
Q

Atherosclerosis

A

Atherosclerosis- Plaque build up in the arteries

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22
Q

Ischemia vs Infarction

A

Ischemia-When blood flow to the heart muscle is obstructed

Infraction is caused by ischemia and is an area of tissue/organ necrosis

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23
Q

Coronary Artery Disease

Risk Factors

A
  • Increased cholesterol
  • Diabetes
  • Hypertension
  • Smoking
  • Age
    • Men > 45 y
    • Women > 55 y
  • Family history
  • Physical inactivity
  • Obesity
  • Stress
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24
Q

Coronary Artery Disease

Prevention

A
  • Lifestyle changes!
    • “Heart-healthy” diet, regular exercise, quit smoking, limit alcohol intake
  • Control blood pressure
  • Control blood sugars
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25
Atherosclerotic Process
* Cholesterol and calcium is deposited beneath the endothelium in the lining of the artery to develop fatty streaks * Scar tissue formation at these sites will result in plaques * Plaques have a firm outer layer with a soft inner core of cholesterol * This deposition of cholesterol and calcium is a natural part of the aging process, however, having risk factors accelerates it.
26
What is the Pathopyshiology of CAD
1. Atherosclerotic Process 2. Luman Narrowing 3. Plaque Rupture
27
CAD Pathyphysiology Lumen Narrowing
Results in decreased blood flow to the myocardium, resulting in ischemia which can cause chest pain Chronic ischemia can lead to myocardial fibrosis and can decrease ventricular wall compliance
28
CAD Pathophysiology Plaque Rupture
When there is a plaque rupture it will expose the lipid core resulting in platelet adherence (clot development) The clot development will further narrow the lumen and can result in a complete occlusion and myocardial infarction This is the etiology of most myocardial infarctions
29
CAD Clinical Manifestations
* These are “non-specific” and can appear gradually as the coronary arteries slowly narrow. * Heartburn * Palpitations * Dizziness or fainting * Nausea or vomiting * Diaphoresis * Exertional Angina * SOBOE * Jaw/back/arm pain * Especially left-sided
30
CAD Lab Findings
* **Non-Diagnostic** * High cholesterol levels * High levels of CRP * C-Reactive Protein which is a protein produced in the liver in response to inflammation
31
CAD ECG
May reveal ischemia, MI or rhythm disorders
32
CAD Cardiac Stress Test
ECG may show exertional myocardial ischemia
33
CAD Thallum Stress Test
Combines nuclear imaging of the blood flow to the myocardium at rest and under exertion
34
CAD Coronary Angiography
**Gold Standard**-The best way to diagnose CAD and evaluate the extent and locations of the blockages. This is the only test that indicates **whether treatment should include angioplasty or CABGs** Uses a catheter inserted into an artery (usually femoral) and threaded up the aorta to the openings of the coronary arteries Dye is injected at this point and fluoroscopy captures the image of the blood flow
35
CAD Treatment
* Non-Invasive * Lifestyle Changes * Medical Management * Invasive * Angioplasty * Stenting * CABG
36
The drop in heart disease is due to
The phenomenal drop in the heart disease death rate over the past 30 years has been due more to reducing risk factors than to advances in treatment.
37
CAD Medical Management
* **Daily Low Dose Aspirin** * ​Will help to prevent clotting * Statins * Calcium Channel Blockers * Nitoglycerin * B-Blockers * ACE Inhibitors
38
**Drug:** Statins
Chemical which makes cholesterol Ex. Atorvastatin (Lipitor)
39
Angioplasty
Angioplasty=Percutaneous Transluminal Coronary Angioplasty (PTCA) If necessary if it often done at the same time as an angiography A balloon tippe catheter is threaded into the affected coronary artery. When the **balloon is positioned at the blockage it will be inflated.** This will result in a widening of the artery as the plaque will be flattened against the arterial wall. Arteries treated with angioplasty alone can **still undergo restenosis** (1/3 of cases within 6 months)
40
**Drug:** B-Blockers
Beta blockers, also known as beta-adrenergic blocking agents, are medications that **reduce your blood pressure.** Beta blockers work by **blocking the effects of the hormone epinephrine**, also known as adrenaline. When you take beta blockers, your **heart beats more slowly and with less force**, thereby reducing blood pressure. Beta blockers also **help blood vessels open up to improve blood flow.** Beta blockers aren't usually prescribed for blood pressure until other medications, such as **diuretics, haven't worked effectively.** Beta blockers generally **aren't used in people with asthma** because of concerns that the medication may trigger severe asthma attacks.
41
B-Blockers Examples
**Will end in -olol** Acebutolol (Sectral) Metoprolol (Lopressor, Toprol-XL) Nadolol (Corgard) Propranolol (Inderal LA, InnoPran XL)
42
ACE Inhibitor
Angiotensin converting enzyme inhibitors (ACE inhibitors) are medications that **slow (inhibit) the activity of the enzyme ACE**, which **decreases the production of angiotensin II**. As a result, **blood vessels enlarge or dilate, and blood pressure is reduced.**
43
ACE Inhibitor Examples
**Ends in -pril** benazepril (Lotensin) lisinopril (Prinivil, Zestril, Qbrelis) perindopril (Aceon) ramipril (Altace)
44
Retenosis
the recurrence of abnormal narrowing of an artery or valve after corrective surgery.
45
Stenting
* If necessary can be done at the same time as an angiography * Stents are used more often than not. * The goal is to help prevent restenosis, or at least lengthen the time before restenosis occurs * Use of drug-impregnated stents reduces risk of restenosis.
46
Angioplasty vs. Stent
In an angioplasty the balloon will be expanded several times in order to force the plaque against the wall and then will be **completely removed from the body** In a stent the mesh will **remain in the body**
47
CABG
Used to treat severe CAD or CAD that has not responded to medical therapy or PTCA The blocked arteries will be bypassed through grafting a vessel above and below the blockage The vessels that are used most often for grafting are most commonly the saphenous vein, internal mammary artery or radial artery
48
What are the different CABG Methods
Traditional Approach Off Pump or Beating Heart MICABS/MICS
49
CABG Methods Traditional Approach
Full sternotomy, heart is stopped and heart-lung bypass is used Pros: still heart; Cons: “pump time”
50
Median Sternotomy
Median sternotomy is a type of surgical procedure in which a vertical inline incision is made along the sternum, after which the sternum itself is divided, or "cracked".
51
CABG Methods "Off-Pump" / Beating Heart
Full sternotomy but heart is not stopped (no bypass machine is required)
52
CABG Methods MICABS/MICS
MI-Minimally Invasive ## Footnote No sternotomy; access through the intercostal region Typically for front of the heart vessels; 1 or 2 vessels
53
CABG Surgeries
These surgeries are generally very successful with low rates of complications.
54
Myocardial Infarction
Blood flow to the heart decreases or stops, damaging the heart muscle, which can help in Decreased ejection fraction Shortness of breath
55
Myocardial Infarction Risk Factors
* **Most MI’s are caused through a ruptured atherosclerotic plaque** * The risk factors for the development of CAD are also risk factors for an MI * Age * Smoking/illicit drugs * Hyperlipidemia * Diabetes mellitus * Poorly controlled HTN * Type A personality * Family history * Sedentary lifestyle
56
Myocardial Infarction Decreased Supply of O2
A decreased supply of oxygen can result from a lack of sufficient blood flow or an absence of blood flow Plaque rupture and thrombus formation Vasospasm of coronary artery Hypoxia Profound Hypotension Embolus to coronary arteries Aneurysm of coronary artery Arteritis
57
Aneurysm
An aneurysm is a **localized, abnormal, weak spot on a blood vessel wall** that causes an outward bulging, likened to a bubble or balloon. Aneurysms are a result of a weakened blood vessel wall, and may be a result of a hereditary condition or an acquired disease.
58
Increased O2 Demand
* Inotropic Drugs * Increased contractility * Because the heart is working harder there is an increased demand of oxygen * Cocaine and Amphetamines * Beta and alpha receptors * Sympathetic receptors for an increased sympathetic response * Ephedrine * Stimulant * Often used as a medication for hypotension and spinal anesthesia * Exercise
59
Myocardial Infarction Pathophysiology
* Regardless of etiology, whether it be a lack of blood supply, decreased blood supply, or increased O2 demand, there will be an area of myocardium that is deprived of oxygen * This lead to the development of ischemia, then an area of injury, and then finally an infarction * Ischemia will be on the outer border * During an area of injury there is the ability for the muscle to repair itself, but it will not be 100% repaired as there is a lot of extra fibrinogen, fat deposits, etc * Reperfusion injury is also an important component of the pathophysiology.
60
Area of Infarction
The area of infarction can be described as transmural or subendocardial based on the thickness of the injury Transmural-Full thickness of myocardium Subendocardial-Partial thickness of myocardium
61
Myocardial Infarction Time Frames
* 0-30 Minutes * Reversible injury * 1-2 Hours * Onset of irreversible injury * 4-12 Hours * Beginning of necrosis * There will continue to be necrosis and development of scar tissues occurs up until 8th week post infarct * The risk for myocardial rupture is greatest at days 4-7 post infarct * As the tougher fibrotic scar tissue starts to form 7-10 days post infarct
62
Myocardial Infarction Atypical Presentation
Common among women, elderly and longstanding diabetics Results in higher mortality Can be mistaken with a GI problem such as reflux or heart burn
63
Myocardial Infarction Clinical Manifestations
* Pain/Discomfort * Dyspnea * Nausea +/- vomiting * Anxiety– impending doom * Lightheadedness * Syncope * Cough * Pale * Diaphoresis * Dysrhythmias * Hypertension * 2° to anxiety or pain * Hypotension * Indicates ventricular dysfunction and failure
64
Myocardial Infarction Clinical Manifestations-Pain and Discomfort
Tightness, pressure or squeezing Usually substernal and radiating down left arm Can involve the jaw, right arm, epigastrum (right above stomach) and back Often perceived as GI!
65
Myocardial Infarction Types of blood markers
Myoglobin CK-MB Total CK Troponin I
66
Myocardial Infarction Blood Markers-Myoglobin
Very sensitive and early marker of myocardial necrosis, but is not specific for MI Levels will begin to rise within 1 hour with peaks within 4-8 hoursWill return to normal by 36 hours
67
Myocardial Infarction Blood Markers CK-MB
Levels will begin to rise within 4 hours and peak at 24 hours Levels will subside by 3 days Not specific to MI
68
Myocardial Infarction Blood Markers Total CK
Enzyme of cardiac damage
69
Myocardial Infarction Blood Markers Troponin I
Troponin I is detectable at 3-6 hours with peaks at ~26 hours and remains elevated for up to 14 days This is a highly sensitive test The pattern and numbers are important This is a main test (#1 test choice for marker) and a marker of damaged tissue right after an MI where it will have an exponential increase (gotta check over several hours) and then decline over days
70
Myocardial Infarction ECG
Only ~50% of patient will have diagnostic changes on their initial ECG
71
Myocardial Infarction ECG-ST Segments
Depression (ischemia) Elevation (infarction) ST segment elevation is only considered pathologic if it occurs in two or more anatomically contiguous leads!
72
Myocardial Infarction ECG-T Wave
Peaking, flatten, or inversion T waves associated with potassium levels If the T wave is irregular it tends to not be due to an MI but rather it is often caused by hyperkalemia
73
Myocardial Infarction ECG-Q Wave
Deepening and widening of Q Wave Loss of R wave resulting in a deep QS wave
74
Myocardial Infarction 12 Leads and Coronary Arteries
The 12 lead ECG helps to locate areas of ischemia, infarct or injury When a specific coronary artery is blocked it can result in predictable changes of specific leads
75
Myocardial Infarction 12 Leads and Coronary Arteries-Lateral Injury
Leads I, aVL, V5, V6
76
Myocardial Infarction 12 Leads and Coronary Arteries-Inferior Injury
Leads II, III, aVF
77
Myocardial Infarction 12 Leads and Coronary Arteries-Septal Injury
V1, V2
78
Myocardial Infarction 12 Leads and Coronary Arteries-Anterior Injury
V3, V4
79
Classifications of MI STEMI
* The patient’s presentation and ST elevation on 2 or more contiguous leads provides an immediate diagnosis * Without the need of cardiac enzymes * This means that the patient can be considered for re perfusion therapy * Those with STEMI should have reperfusion therapy: thrombolytics or angioplasty
80
Classifications of MI Non- STEMI
The ECG alone will not confirm the MI and we have to rely on the serum markers (the pattern is important)
81
Myocardial Infarction Medical Management
\*ACLS will use the acronym MONA for initial pharmacological therapy * **Morphine** * Analgesic for pain relief and vasodilator effects which results in reduced afterload and systemic pressure * **Oxygen** * Will increase oxygen content and therefore increasing oxygen supply * **Nitrates** * Vasodilator effect to decrease systemic vascular resistance and afterload * **Aspirin** * Reduces platelet aggregation by preventing them from sticking together * **Beta Blockers** * Reduce SNS stimulation (reduce HR) post MI and reduce afterload * Decrease oxygen demand and hypertension
82
Myocardial Infarction Reperfusion therapy
* Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a MI * The goal is to reduce mortality and limit the infarct size * Methods * Thrombolytics * Dissolve blood and platelet clots * Best is used within 60-90 minutes of onset * Should be given by EMT * Risk of bleeding must be considered, because you will have a time period when there is no clotting factors avalible * Percutaneous Coronary Interventions (PCI) * CABG
83
Heart Failure Definition
Inability for the heart to meet the metabolic demands of the body
84
Types of Heart Failure
Right sided-Cor Pulmonale left sided Both sides affected
85
Classifications of heart failure
* High output * Low output * Can be systolic or diastolic in origin
86
Left vs Right Sided Heart Failure
Although the initial event that leads to heart failure may be right-sided or left-sided in origin, long-term heart failure usually involves both sides! Because the circulatory system is a closed system when one side starts getting backed up it will eventually affect the other side
87
Cor Pulmonale
* Cor pulmonale is the **enlargement and failure of the right ventricle** in response to an increased vascular resistance from the lungs * Chronic pulmonary heart disease will usually result in right **ventricular hypertrophy** * Hypertrophy is an adaptive response to a long term increase in pressure as muscle cells will grow thicker in order to increase the contractile force and move the blood against a greater resistance
88
Left Sided Heart Failure
* There is a **failure in the left ventricle to move blood** to the body causing **poor systemic perfusion** * Decreased systemic perfusion will lead to vasoconstriction (increased SVR) * There will be a normal or increased BP that is needed to maintain cerebral and coronary perfusion * Blood will also back up into the pulmonary system causing **pulmonary congestion** and can lead to right ventricular failure as the right side of the heart will pump against the increased PVR which will lead to a decreased RV output * When the RH fails there is a decreased pulmonary congestion giving a false look of improvement
89
Left Sided Heart Failure Hemodynamics
Increased PAWP HR Decreased CO Pulse pressure
90
Right Sided Heart Failure
Due to failure of the right ventricle to pump blood out to the lungs Results in blood backing up into the systemic circulation _Backwards Failure_ Decreased RV output leading to venous congestion _Forward Failure_ Decrease RV output -\> Decreased pulmonary perfusion -\>Decreased LV filling -\>Decreased LV output -\> systemic perfusion
91
Right Sided Heart Failure Hemodynamic Profile
Increased CVP
92
High Output Heart Failure
Uncommonform of heart failure that can occur when there is an excessive need for cardiac output due to an increase in peripheral demand The heart is “supranormal” and yet still inadequate Can occur when there is an increased blood volume (excess water and/or salt), excess fluid, chronic and severe anemia, etc.
93
Low Output Heart Failure
Caused by a disorder that will impair the pumping ability of the heart May be systolic or diastolic in origin Many patient will have elements of both
94
Low-Output Systolic (Systolic Failure)
Heart failure with reduced ejection fraction (HFrEF) Impaired ejection of blood from the heart during diastole
95
Low-Output Systolic (Systolic Failure) Causes
* Results from conditions that either * Impair contractility of the heart * Produce a volume or pressure overload on the heart * Ex. CAD, previous MI, A-Fib, Valve disease/dysfunction, alchol, infection, cardio myopathy, etc
96
Low-Output Systolic (Systolic Failure) Results
Results in a decreased stroke volume and in turn a decreased ejection fraction
97
Low-Output Diastolic (Diastolic Failure)
Heart failure with a preserved ejection fraction (HFpEF) Ejection fraction will remain the same at 50% or become lower Impaired relaxation of the heart during diastole Will result in a decreased stroke volume There will be an increase in muscle mass without dilating
98
Low-Output Diastolic (Diastolic Failure) Causes
Restrict diastolic filling Increase ventricular thickness Thus decrease chamber size Delay diastolic relaxation (fibrosis) Ex. Ventricular hypertrophy from long term HTN or aortic stenodid, diabtese, constrictive pericarditis
99
Direct Causes of Heart Failure
* Most Common * Myocardial ischemia * Myocardial infarction * Arrhythmias * The heart is not pumping in proper sequence (ex. A-fib) so blood does not pump well and will stay in the atrium * Clots can also form if the heart is pulling for some time * Heart valve lesions * Opening and closing problems * Congenital malformations * Pericarditis * Inflammation of sac around the heart * Cardiomyopathies
100
Indirect Causes of Heart Failure
* Fluid overload * Renal failure * Sepsis * Biggest issue * Causes membrane variable of well weaken, so fluid will enter more easily * Vasodilation of blood vessel * Causing RHF (Cor Pulmonale) * \*\*Nitric Oxide * COPD * PE * Pulmonary HTN
101
Left Sided Heart Failure Clinical Manifestations
* Exertional Dyspnea * Orthopnea * The heart is not pumping when the patient lying down and fluid will back up into the lugs * Peripheral Edema * Late stage * Paroxysmal Nocturnal Dyspnea (PND) * The heart is not pumping properly when sleeping or when the body is relaxing and fluid will back up into the lungs so when the patient wakes up they will have SOB and wheezes * Cough * Frothy, blood tinged sections * Fluid backs up from the vasculature bringing up RBC * Frothy because of surfactant (creates bubbles) * Cyanosis * Increase PAWP * Backed up pressure from the left ventricle due to fluid overload * Distinguishes heart failure and non-cardiac infections * ~4-12 mmHg
102
Left Sided Heart Failure On Auscultation
Fine/Coarse crackles due to the fluid “Cardiac” wheezes
103
Left Sided Heart Failure Clinical Manifestation
* Peripheral/dependent edema * Dependant Edema=Gravity related swelling in the lower body * Fatigue * JVD * Hepatomegaly * Due to a backup of blood in the liver * Ascites * Abnormal accumulation of fluid in abdominal (peritoneal) cavity * When the right side of the heart loses its pumping power, blood will back up into the veins * Cyanosis * Increased CVP
104
Heart Failure Inadequate Cardiac Output
This is the end result of different etiology’s This is what will trigger different compensatory mechanisms
105
Heart Failure Compensatory Mechanisms
Frank-Starling Mechanism Increased SNS activity Renin-Angiotensin Mechanism Myocardial Hypertrophy
106
Frank-Starling Mechanism
* In a normal heart this will be the mechanism that is responsible for the heart pumping the blood it receives and matching the output of the two ventricles * Increased preload will increase stretch which increases force of contraction and ultimately increase stroke volume * During heart failure this mechanism is responsible for maintain normal CO in the face of end diastolic volumes * This is reflected by an increase in PAWP and CVP * This mechanism become ineffective when the myocardial fibers become overstretched * Thus CO can not increase with an increase in physical activity
107
Compensation Mechanism for HF Increased SNS Activity
* SNS will be stimulated through a decrease in SV and CO * Leads to (all of the below is an attempt to maintain perfusion to vital organs) * Systemic vasoconstriction * This may lead to increased afterload and further increase in myocardial demand * Stimulation of the heart * Increased HR * Increased contractility * Norepinephrine * Increases SVR
108
Renin-Angiotensin Mechanism
* Decreased SV and CO will result in a decrease perfusion to the kidneys * The kidneys will respond through releasing renin which will activate the renin angiotensin aldosterone system * End result * Aldosterone will cause sodium and water retention resulting in an increase in blood volume * Angiotensin II causes vasoconstriction * Because this mechanism results in an increase in blood volume there will also be an increase in end-diastolic volume * Indirectly this is activating the frank starling mechanism and increase CO
109
Myocardial Hypertrophy
* A long term compensatory mechanism in response to increase work demand * The heart is working harder building muscle which will decrease the size of the ventricle * Less preload and less fluid that can be ejected * This results in an increased in the number of contractile fibers in the myocardium * While this mechanism allows for the ventricle to do more work it also results in an increase in myocardial demands and increase myocardial oxygen requirements
110
Decompensated Heart Failure Increased SVR
Further increase myocardial demand
111
Decompensated Heart Failure Increased HR
Increase myocardial demand Shorten diastole
112
Decompensated Heart Failure RAA System
Further increase filling pressure Further contributes to fluid overload worsening clinical manifestations
113
Decompensated Heart Failure Frank Starling Mechanism
Ineffective due to over stretched myocardial fibers
114
Decompensated Heart Failure Myocardial Hypertrophy
Increase myocardial oxygen requirements May reduce chamber size cause a diastolic failure
115
Exam Findign for Heart Failure CXR
* Cardiomegaly * Left sided heart failure * Diffuse bilateral infiltrated (butterfly pattern) * Pleural effusion
116
Kerley B lines
Seen in the CXR with left sided heart failure These are 1-2 cm thin lines in the peripheral of the lungs They are peripheral to and external to the pleural surface They represent thickened subpleural interlobar septal and are unlikely seen at the lung bases Suggesting pulmonary edema
117
Exam Findings ## Footnote Echocardiography
Useful to diagnose cause of heart failure
118
Heart Filaure Exam Findings ECG
May diagnose cause (MI, arrthymia)
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Pharmacological Treatment for Preload Reduction
* Diuretics * Used to target hypervolemia * Inhibit sodium and water reabsorption * Will reduce intravascular volume, decrease CVP, decrease right and left heart filling pressures * Nitroglycerin * Causes systemic venodilation decreasing preload * Morphine
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Pharmacological Treatment for Afterload Reduction
* β-Blockers * Inhibit sympathetic nervous system and block alpha 1 adrenergic vasoconstrictor activity * Slow down HR and dilate blood vessels * Nitroglycerin, Nitroprusside * ACE inhibitors
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Pharmacological Treatment for Inotropic Support
* Use with caution * Ex. Milrinone, Inamrinone, digoxin, Dobutamine, Dopamine, and Norepinephrine * Increase contractility and can increase oxygen as a result * Inotropic agents will help to restore organ perfusion and reduce congestion
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What to treat for acute pulmonary edema
Oxygen & NIPPV!!
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Treatment for Severe Heart Failure
Intra-aortic Balloon Pump Left Ventricular Assist Device Heart Transplant
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Heart Failure and NIPPV
* CPAP is the 1st line of therapy * BiPAP if hypercapnia or continued dyspnea * The increase FiO2 and Pmean will improve oxygenation * The increase intrathoracic pressure and increase PVR due to PPV will cause blood to back up on the right side * This will cause distension of the RV and a shift of the septum towards the left side * The effectively reduced preload on the left side of the heart and improved output (Frank-Starling Curve) * The increased intrathoracic pressure will also reduce transmural pressure resulting in a decreased afterload * Will help to open alveoli and get oxygen * This pressure will push fluid in the alveoli back to the vasculature
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General/Long Term Treatment for Heart Failure
Restriction of dietary sodium Diuretics Nitroglycerin or long-acting nitrates ACE Inhibitors/β-blockers Cardiac rehabilitation
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What is the best predictor of mortality in heart failrue
Ejection fraction is the best predictor of mortality! The lower the EF the worse the prognosis!
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Valvular Disorders mechanical disruptions
* Stenosis: This is a narrowing of a valve so that it does not open properly * Obstruct blood flow * Incompetence: This is a distortion of the valve so that it unable to close completely; results in regurgitant flow.
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Valvular Disorders Etiology
* Congenital defects * Trauma * Ischemic damage * Degenerative changes * DM and hypercholesteremia are risk factors * Inflammation/Infection * Rheumatic heart disease * Auto-immune diseases (Rheumatoid Arthritis) * Endocarditis 2°bacterial infection (IVDU) * Neoplasm * Connective tissue diseases Eg. Marfan Syndrome
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Valvular Disorders Pathophysiology
1. Damage or inflammation of the heart valve leaflets 2. Healing results in increased collagen content and scaring 1. Valve leaflets heal together 1. Valve cannot open properly (Valve stenosis) 2. Valve leaflets become retracted 1. Valve cannot close properly (regurgitant valve)
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Stenotic Valve
Distension of the chamber that pumps the blood thru the diseased valve (and thus an increase in pressure) Impaired filling of the chamber that receives the blood (and thus decrease pressure)
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Regurgitant/Incompetent Valves
There is backward flow thru the valve This causes distension of the chamber prior to the diseased valve (and thus increase pressure here!) This places increase work demands on this chamber
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Valvular Disorders Clinical Manifestations
* Mild valvular disorders may not produce any signs or symptoms other than a heart murmur. * History of heart murmur (or newly developed) * Exertional dyspnea\*\* * Orthopnea and paroxysmal nocturnal dyspnea * Effort-induced fatigue * Angina 2°ischemia * Palpitations * Syncope * Signs of heart failure (S & S depend on whether L or R heart failure)
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Valvular Disorders Diagnostic Tests Auscultation of Heart Sounds
Valve dysfunction results in turbulent flows replacing the normal laminar flows and result in “murmurs” being heard Depending on the valve affected there may be extra heart sounds heard
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Valvular Disorders Diagnostic Tests Echocardiogram
Allows for viewing of the internal structures of the heart and blood flow patterns The transesophageal echo is particularly effective in identifying valve disorders
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Valvular Disorders Management
* Medical management of associated heart failure * Surgical intervention * Replace or repair valve– put in pig valve * Only done in severe cases * Ideal prosthetic valve is not yet invented * Percutaneous balloon valvuloplasty * For treatment of stenotic valves
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Cardiomyopathies
A group of disorders that affect the heart muscle and diminishes cardiac performance It can develop as a primary or secondary disorder
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Cardiomyopathies Main Types
Dilated Restrictive Hypertrophic Arrthymogenic right ventricular dysplasia
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Cardiomyopathies Primary Causes
* Idiopathic * Genetic * Infectious * Viral, bacterial, protozoal * Toxic * Drugs, poisons, ETOH
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Cardiomyopathies Secondary Causes
* Other CV disorders * Ischemia \*\* * Hypertension * Valvular disorders * Metabolic disorders: * DM, hyperthyroidism… * Collagen Vascular Disease * SLE, RA
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Dilated Cardiomyopathy
* Most Common * This type causes the heart to become enlarged and the myocardium to become weak, thin and floppy * Most often idiopathic in origin * The affected ventricle is unable to pump the blood it receives, thus, * If LV is affected ggLeft heart failure and its manifestations * If the RV is affected ggRight heart failure and its manifestations * Results in a systolic dysfunction
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Hypertrophic Cardiomyopathy
* Hallmark is inappropriate, disorganized proliferation of myocardial cells and is caused by a genetic disorder * Affects the left ventricle, frequently in the interventricular septal area * Results in an obstruction of outward flow * Results in both a systolic and diastolic dysfunction * Because the left ventricle is smaller * The leading cause of sudden cardiac death in pre-adolescent and adolescent children. * We don’t know about this until afterwards
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Restrictive Cardiomyopathy
* This type causes the walls of the ventricles to become stiff but not necessarily thickened * It impairs the filling of blood as the ventricle doesn’t relax normally * If LV is affected * Left heart failure and its manifestations * If the RV is affected * Right heart failure and its manifestations * Results in a diastolic dysfunction * This is the least common cardiomyopathy and is often due to infiltration by foreign materials
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Arrhythmogenic Right Ventricular Dysplasia
* Rare * Genetic * Two patterns: Autosomal Dominant and Autosomal Recessive * Can affect left or right wall * Loss of myocardium of the right ventricular free wall (free wall is the ventricle wall that is not the septum * Right Ventricular muscle is replaced by fat and fibrous tissue (scar tissue) * Scar tissue will affect the conduction of the hert * Right ventricle has poor dilating and contracting ability * Highly associated with ventricular arrhythmias
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Cardiomyopathies Clinical Manifestations
* Ventricular arrhythmias * Palpitations * Dizziness, lightheadedness, syncope * SOBOE * Heart Failure * Abnormal ECG * Sudden Cardiac Arrest
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Cardiomyopathies Diagnosis
MRI CT scan
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Cardiomyopathies Treatment
Antiarrhthmic drugs Catheter Ablation- Will damage the pace maker cells in order to prevent the off firing of the heart Implantable cardioverter defibrillator
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Cardiomyopathies Antiarrhythmic Drugs
* Class I (Na Channel Blocker) * Lidocaine, Phenytoin * Class II (B-Blocker) * Sotalol * Slows down HR and helps to decrease SVR * Class III (K Channel Blockers) * Amiodarone * The big problem is that this drug is toxic and will affect the lung (pulmonary fibrosis)
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Pericarditis
* An inflammation of the pericardium (sac that surrounds the heart) * Can be acute or chronic * The inflammation can lead to the accumulation of fluid in the pericardial sac * Characterized by chest pain, pericardial friction rub and serial ECG changes.
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Pericarditis Etiology
* Idiopathic * Infectious * Viral, bacterial, fungal, TB * Prior MI * 7-10% of MI patients develop this complication * Kidney failure * Cancer * Rheumatoid Arthritis/Scleroderma/SLE * Chest trauma * Rheumatic Fever * Inherited disorder * About 1/1000 hospitalized patients are diagnosed with this disorder. Many more are likely to have an mild form that goes undiagnosed.
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Pericarditis Pathophysiology
1. Etiological Agent 2. Infiltrations of WBCs 3. Pericardial Vasculitis 1. Pericardial Effusion 1. Formation of cardiac tamponade 1. Exudative: Serous, fibrinous, hemorrhagic, purulent, or chylous 2. Fribrinous, retractions, and adhesion formation 1. Constrictive pericarditis 3. Formulation of granulomas 1. Seen with TB, RA, sarcosiodosis, fungal infections
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Pericarditis Clinical Manifestation
* Chest pain * Cardinal Symptom * Pericardial rub * Dyspnea (2° to pain) * Dry cough * +/- Fever * Chills * Weakness * Signs of tamponade if large effusion present * Becks Triad: Distended neck veins, distant heart sounds, hypotension
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Three Main Signs of Percarditis
Chest pain Dyspnea secondary to pain Dry cough Fourth possible sign: Kussmauls sign
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Constrictive Pericarditis
Scarring of the pericardium after one or more episodes of pericarditis The pericardium becomes thickened and stiff making it hard for the percadium to expand Results in impaired filling of the heart, thus, diastolic dysfunction
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Constrictive Pericarditis Clinical Manifestations
Because this results in blood backing up into the extremities and lungs you will see S & S similar to heart failure Kussmaul’s sign is often seen! (Swelling JVD during insp).
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Constrictive Pericarditis CXR
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Pericarditis Diagnostics
* Lab Studies * Infectious Etiology * Increase WBC and blood cultrues * Cardiac Enzyme * Increased if myocardial infarction * CXR * May show pericardial effusion * Expanded look at the heart * White out * ECG * 4 classic stages for pericarditis * Echocardiography * Diagnosed type of effusion * CT Scan * Diagnosed type of effusion * Analysis of Pericardial Fluid
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Classic Stages of Pericarditis Stage 1
Elevation in all leads PR segment is depressed Depression between the end of the P wave and the beginning of the QRS complex
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Classic Stages of Pericarditis Stage 2
Pseudonormalisation with t wave flattening (transition) The PR segment will return to normal
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Classic Stages of Pericarditis Stage 3
Inverted T waves
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Classic Stages of Pericarditis Stage 4
Normalization If it gets normal because the electrical conduction is adapting
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Pericarditis Management
* Treatment depends on etiology * E.g. Antibiotics for bacterial pericarditis * E.g. Kidney failure causing uremic pericarditis is treated with dialysis * Due to the overload of volume * Viral will just have to take its course * General * Analgesics for pain management * Steroids for inflammation
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Pericarditis Management if Effusion if present
* Percardiocentesis * Fluid is aspirated from the pericardium * Pericardial window * A small part of the sac around the heart is removal in order to remove drained excess fluid * Pericardiodesis * Percardiectomy
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Pericardiectomy
Excision of part of the pericardium Done for constrictive pericarditis or for chronic recurring pericarditis Usually only done in severe cases! 30% of patients will have a recurrent episode of pericarditis within 2 years
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Cardiac Tamponade
* A life-threatening condition in which elevated intra-pericardial pressures impair the filling of the heart during diastole * The increased pressure results from an accumulation of fluid in the pericardial sac * Results in decreased SV and CO * The severity of the condition depends on the amount of fluid present and the rate at which it accumulated
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Cardiac Tamponade Etiology
* Trauma * Ex. GSW, MVC * Cardiac Surgery * Cardiac Rupture secondary to MI * Pericarditis * All the etiology’s * Neoplasm
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Cardiac Tamponade Pathophysiology
The pericardial space normally contains 20-50 mL of fluid Rapid accumulation of as little as 150 mL of extra fluid can markedly reduce CO However 1-2L of fluid accumulating slowly may not have any significant effect on CO due to the adaptive stretching of the pericardium The effusion can be serous, serosanguineous, hemorrhagic, or chylous
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Acute Pericardial Effusion
Increased Pericardial Pressure ► Decreased Diastolic Filling of the Heart ► Decreased SV and CO ►Signs and Symptons of Shock or Heart Failure
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Chronic Pericardial Effusion
Streching of the Pericardium ► Signs and Symptons of Pericardial Effusion the streaching of the pericardium can lead to additional accumulation of pericardial effusion lead to the acute pathology of pleural effusion
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Cardiac Tamponade Clinical Manifestations
* Beck Triad * Tachycardias * Decreased pulse pressure * Pulsus paradoxus * May be present with PEA * This is life threatening! Patient will present in acute shock!
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Beck Triad
Hypotension Increased Jugular Venous Pressure Diminished heart sounds
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Cardiac Tamponade Treatment
* Pericardiocentesis * ACUTE * Subxiphoid percutaneous drainage with an 18 gauge needle * Less Acute * Will use fluoroscopy/echo to aid * Treatment of underlying causes * For recurrent tamponade secondary effusions * Pericardial window * Pericardiodesis * Agents introduced into pericardial sac to sclerose the tissue * Pericardiectomy * If untreated it is rapidly and universally fatal!
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Disseminating Intravascular Coagulation
A paradox in the hemostatic sequence and is characterized by widespread coagulation and bleeding A stimulus causes hyperstimulation of the clotting pathways This results in formation of diffuse clots in the microvasculature and depletion of the clotting factors, which can now result in generalized bleeding
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Disseminating Intravascular Coagulation Etiology
DIC is not a primary disease it occurs as a complicationof a wide variety of conditions * **Infections**-Bacterial, Viral, Rickettsial, Parasitic * **Shock**, Septic, Hypovolemic * **Trauma**-Burns, Severe Head Injury, Snake Bites, Heatstroke * **Surgical Procedures** * **Other Disease States**-Malignancy, Liver Disease, Pancreatitis, SLE * **Obstetric Conditions**-Abruptio placenta, Retained dead fetus, Amniotic fluid embolism * **Hematologic Conditions**- Incompatible Transfusion, Massive Transfusion
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Disseminating Intravascular Coagulation
1. Stimulus 2. Hyperactivation of Clotting Pathways 1. Consumption of Clotting Factors 1. Bleeding 2. Diffuse clotting and micro emboli 1. Organ and tissue ischemia 1. Organ Failure 2. Widespread Fibrinolysis
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