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PAT202 > WEEK 2 - COMPLICATIONS OF MI AND ALTERATIONS OF FUNCTION > Flashcards

WEEK 2 - COMPLICATIONS OF MI AND ALTERATIONS OF FUNCTION Flashcards

1
Q

What is HF?

A
  • pathophysiologic condition when heart is not able to generate adequate cardiac output
  • heart is unable to pump enough blood to meet bodys requirements
  • inadequate circulatory volume and pressure
  • results in inadequate perfusion of tissues
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2
Q

Some causes of HF

A
  • CAD and MI - affects supply of O2 and nutrients to cardiac muscle
  • Chronic and sustained HTN - heart must pump more powerfully to eject blood
  • diabetes mellitus - insulin resistance, hyperinsulinemia, hyperglycemia - effects cardiovascular system including endothelial damage, also associated with dyslipidemia
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3
Q

what accelerates macrovascular disease in diabetes?

A
  • hyperlipidemia
  • hypertension
  • smoking
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4
Q

Diabetes and accelerated atherosclerosis

A
  • diabetes with its associated hyperglycemia, leads to endothelial dysfunction, Reduced NO, increased platelet aggregation, expression of adhesion molecules, adhesion and subendothelial migration of macrophages, formation of macrophage foam cell, smooth muscle cell migration and proliferation, fibrous plaque, complicated athero plaque
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5
Q

Risk factors for HF

A
  • Ischemic heart disease
  • HTN
  • age
  • smoking
  • obesity
  • diabetes
  • renal failure
  • valvular heart disease
  • cardiomyopathies
  • myocarditis
  • congenital heart disease
  • excessive alcohol use
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6
Q

How to prevent HF

A
  • Excersise
  • eat a healthy diet
  • dont smoke (?)
  • effective management of CAD, HTN and DM (Diabetes mellitus)
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7
Q

Pathophysiology of HF

A
  • Myocardium becomes weakened and heart cannot eject all blood it recieves
  • Can be left, right side or both
  • Left side - blood accumulates in left ventricle - increase preload , blood backs up into lungs - cough, SOB
  • Right side - blood back up into peripheral veins - JVD, Peripheral edema, engorgement (congestion) of organns (liver)
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8
Q

Why does the myocardium thicken in left heart failure

A

its called hypertrophy actually 🤓 - does this to compensate for extra blood in the chamber

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9
Q

How are inflammatory cytokines involved?

A
  • inflammatory cytokines - endothelial hormones - endothelin is a potent vasoconstrictor and is associated with a poor prognosis in individuals with HF
  • TNF-α - elevated in HF and contributes to myocardial hypertrophy (remember the left heart?) and remodeling, it down regulates synthesis of vasodilator NO (leads to hypertension), induce myocyte aoptosis (cell death) and may contribute to weight loss and weakness in individuals with HF
  • IL - 6 - elevated and cardiogenic shock and may contribute to further harmful immmune activation
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10
Q

Sys LAC

How is HF classified

A

SYS- systolic vs diastolic
- systolic - decreased contractility leading to decreased ejection fraction
- diastolic - normal contraction but abnormal relaxation
Location:
- Left
- right
Acute
- pronounced response in HF
- rapid sympotms
- requires immediate care
Chronic
- more subtle responses in HF
- many compensatory mechanisms operating

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11
Q

Systolic HFrEF

A
  • reduced ejection fraction
  • EF less than 40% , normal is around 65%
  • heart cannot generate adequate CO to perfuse tissue and organs
  • hemodynamic, neurohymoral, inflammatory and metabolic processes - interaction of these processes results in gradual decline in myocardial function
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12
Q

Evaluation and management of HFrEF

A

Evaluation (PISCES):
Physical exam
Invasive catheterization
Serum troponin
Chest X ray
Echocardiography
Serum BNP levels
Management:
- Interreput worsening cycle of decreasing contractlitity, increasing preload and increasing afterload
- block neurohormonal mediators of myocardial toxicity

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13
Q

Diastolic HF (HFpEF)

A
  • HF with preserved ejection fraction
  • decreased compliance of left ventricle and abnormal diastolic relaxation - ventricle cannot accept filling with blood wthout significant resistance
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14
Q

Evaluation and management of HFpEF

A

Evaluation: CAEE
- Chest x ray
- auscultate
- ECG
- echocardiography
Management:
- improve ventricular relaxtion an d prolonging siastolic filling times to reduce diastolic pressure
- physical training
- improve endurance and quality of life

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15
Q

W2 D2OPE CAN Fuck you up

General manifestations of HF

A
  • Weight gain
  • weakness
  • dyspnea
  • dependant edema
  • orthopnea
  • paroxysmal nocturnal
  • excersise intolerance
  • cough
  • abdominal distention
  • nocturia
  • fatigue
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16
Q

literally think of an unstable avatar

Less common symptoms of HF

A
  • cognitive impairment
  • altered mentation or delirium
  • nausea
  • abdominal discomfort
  • oliguria
  • anorexia
  • cyanosis
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17
Q

LEFT = LUNGS

Left HF

A
  • decreased CO to systemic circulation
  • blood accumulates in left ventricle and backs up into lungs and left atrium
  • this causes increase in pulmonary venous pressure (elevated bp in pulmonary veins)
18
Q

LEFT = LUNGS

causes of left HF

A
  • HTN
  • MI
  • cardiomyopathy
19
Q

LEFT = LUNGS

clinical manifestations of Left HF

A
  • pulmonary congestion/edema (cyanosis, inspiratory crackles)
  • dyspnea, orthopnea, cough with frothy sputum
  • fatigue
  • decreased UO and edema - loss of that blood from heart to be able to excrete it
20
Q

Right HF

A
  • right ventricle unable to push blood into pulmonary circulation
  • when blood not moved forward, backs up into systemic venous system
21
Q

How is right HF caused?

A
  • caused by failure of left HF
  • conditions impending blood flow into lungs and conditions compromising pumping effectiveness of right ventricle (right ventricular MI, cardiomyopathy), left HF
22
Q

clincial manifestations of HF

A
  • JVD, peripheral edema, hepatosplenomegaly (both spleen and liver are enlarged)
23
Q

Treatment goals for Left HF and Right HF

A
  • No care
  • goals are to prevent,treat or remove underlying causes when possible
  • treat sympotms to improve QOL
24
Q

Compensatory mechanisms for HF: SNS activity

A
  • increases SNS activity - catecholamines released - triggered due to decreased SV and decreased CO
  • increases HR and force of contraction, also increases peripheral vascular resistance but combined, cardiac workload is increased (to compensate for decreased CO)
  • this worsens HF - Restraints blood flow and causes arteries to contract leading to underperfusion or ischemia
25
Q

what are catchoalmines

A

found in kidney - released in response to emotional/ physical stress

26
Q

compensatory mechanisms: activation of RAAS

A
  • Kidneys release renin due to decreased cardiac output and this leads to decreased renal perfusion and decreased GFR
  • Promotes vasoconstriction and volume retention and raises BP
  • aldosterone increases preload and angiotensin II increases afterload
27
Q

compensatory mechanisms: ADH

A
  • Causes peripheral vasoconstriction and renal fluid retention but exacerbates hyponatremia and edema (preload) and afterload
28
Q

Compensatory mechanisms: natriuretic peptides

A
  • Secreted in response to increased volume overload and dysfunction
  • ANP from atria
  • BNP from ventricles - biomarker to diagnose and establish severity of HF
  • cause diuresis and reverse negative effects of SNS and RAAS on heart but chronic HF leads to depletion of NPs
29
Q

Frank Starling Law

A
  • increased preload causes increased stretch of mycardial fibres
  • force of each contraction is increased leading to increase in CO
  • but as preload continues to rise repeated stretching of myocardium and dosent snap back forcefully
  • contractility and thus CO is decreased
30
Q

Ventricular remodelling

A
  • when contractility decreases, SV falls and LVEDV (Left ventricle End diastolic volume) increases
  • can improve CO but as preload continues to increase, more stretching occurs (hypertrophy) and leads to dysfunction and decreased contractility
  • increased PVR, causes resistance and increase workload for LV
  • heart compensates with hypertrophy of myocardium and initially improves work performance of heart but increase in muscle mass results in increase need for oxygen demand and contractility is compromised
31
Q

disorders of the myocardium - cardiomyopathy

A
  • most are result of remodeling caused by neurohumoral responses to ischemic herart disease or HTN on heart muscle
32
Q

types of cardiomyopathy

A
  • normal
  • dilated
  • hypertrophic
33
Q

Dilated cardiomyopathy

A
  • impaired systolic function, leading to increase in intracardiac volume, ventricular dilation, systolic dysfunction and HF
34
Q

causes of dilated cardiomyopathy

A
  • ischemic heart disease
  • valvular disease
  • diabetes
  • alcohol
  • drug toxicity
  • renal failure
  • hyperthyroidism
  • deficiencies of niacin vitamin D, and selenium
  • infection
35
Q

Hypertensive Hypertrophic cardiomyopathy

A
  • occurs due to increases resistance to ventricular ejection - seen in HTN
  • Hypertrophy of myocytes - attempts to compensate for increased myocardial workload
  • myocyte dysfunction develops over time - first diastoic function, then systolic dysfunction, HF
36
Q

Premature ventricular contractions

A
  • common cause of irregular heart rhythym - not normally serious unless it occurs at high frequency
  • effect - decreased CO from loss of atrial contribution to ventricuar preload for that beat
37
Q

Ventricular Tachycardia

A

regular, rapid, heart beats - often more than 150 bom to 200 bpm, life threatening
- associated with high risk for sudden death
- effect : decresed CO from loss of atrial contribution to ventricular preload, increase in myocardial demand due to tachy

38
Q

Ventricular fibrillation

A
  • complete disorganziation of rhythym - ventricles pump little or no blood , quickly starves tissue of oxygen
  • ventricular fibrillation is now considered cardiac arrest: life threatening, immediate intervention
  • effect: no caridac output, not compatible with life
39
Q

Heart block

A
  • also called AV conduction block
  • classified as first, second and third degree
  • first - AV node conducts impulse slowly, conduction is delayed
  • second - some but not all impulses blocked from leaving AV node
  • third - results in total stoppage of impulses through AV node
40
Q

Deep vein thrombosis

A

Thrombosis/clot in large vein
* flow & pressure are lower in veins than in arteries
Detached thrombus
* thromboembolus can lead to PE
Venous stasis (associated with immobility, obesity, prolonged leg dependency, age, HF)
Tests: D-dimer & Doppler
Symptoms
* pain
* unilateral leg swelling
* dilation of superficial veins
* calf tenderness
* mottled or cyanotic skin
Can be asymptomatic so prevention is crucial

41
Q

Pulmonary embolism

A

PE is occlusion or partial occlusion of pulmonary artery or its branches by an embolus
* conditions & disorders that promote blood clotting as result of venous stasis (immobilization, HF)
Risk factors for PE
* if thrombus is large enough, infarction of lung tissue, dysrhythmias, decreased cardiac output, shock, & death are possible
PE can cause infarction or occlusion
* sudden onset of pleuritic chest pain
* cough
* dyspnea
* tachypnea
* tachycardia
* unexplained anxiety
* occasionally syncope or hemoptysis
* with large emboli, pleural friction rub, pleural effusion, fever, and leukocytosis may be noted
Tests:
* D-dimer & CT arteriography
* serum troponin I levels as risk increases with right ventricular dysfunction

42
Q

Howis MI related to DVT and PE

A

Local disturbances in cardiopulmonary/cardiovascular
circulation after MI may predispose to thrombus formation
* from stasis in pulmonary circulation due to left ventricular dysfunction
* by injury to vascular endothelium
* by activation of coagulation system during acute phase of MI
Atrial fibrillation is a frequent complication after MI
* associated with dysrhythmias
In summary, mechanism(s) secondary to local disturbances in
cardiopulmonary/cardiovascular circulation or
electromechanical activity may be responsible for some of
the DVT and PE risk after MI

PAT202 (4 decks)

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